The Backbone The Official Journal of the W. Montague Cobb Research Laboratory
Winter 2015 • Spring 2016 Volume 2 Issue 1
Cover page credit: We thank Amanda D. Strong for access to this photo of a cadaver from the W. Montague Cobb Research Lab.
The Backbone OFFICIAL JOURNAL OF THE W. MONTAGUE COBB RESEARCH LABORATORY, HOWARD UNIVERSITY ISSN (Online): 2373-3934 ISBN (Print): 2373-3926 Editor-in-Chief: Fatimah Jackson, Ph.D. Production Editor: Nicholas Guthrie Copy Editor: Amanda D. Strong
The Backbone is published twice a year by the W. Montague Cobb Research Laboratory at Howard University. This online, open-access journal accepts original articles, short biohistories, and recent abstracts on scientific considerations of broad aspects of the African diaspora. Manuscripts for publication consideration, comments on the journal, and other inquiries should be sent to: cobbresearchlab@howard.edu
Howard University Š All Rights Reserved
Contents Editorial Resilience Through Research and Publication Fatimah L.C. Jackson
………………………………………………………………………………………………………………………………... 1
Full Articles Chronic Kidney Disease and its Sequelae within the Cobb Collection: Osteological Manifestations and Clinical Record of Evidence Amanda D. Strong, Uzaomaka Nqaogwugwu, M.D., Christopher Cross, M.S., Fatimah Jackson, Ph.D.………..……………………………. 2
Analysis of Potential Treatments for Sickle-Cell Anemia, or Drepanocytosis, in Adults Cameron D. Clarke …………………………………………………………………………………………………….……………………………… 10
Genetic Behavioral Evidence for Autism in the Cobb Collection Jayla Harvey , Fatimah Jackson, Ph.D.……………………………………………………………………………………………………..…….… 16
A Review: Evolutionary Theories of the Pathogenesis of Schizophrenia Nichelle Jackson….……………………………………………………………………………………………………………...……………….……. 19
How might the genetic identification of mental disorders vary across geographical spaces, cross culturally and though time? Sedera Moore ……………………………………………………………………………………………..…………………………………………… 26
Prevalence and Anatomical Evidence of Treponemal Infection in the Cobb Collection Nicholas Guthrie ………………………………………………………………………………………………………..……………………………… 31
Biohistories The Story of CC18 Theodore Meadough, Jermain E. Robertson ……………………………………………………………………………………………………..… 35
The Story of CC112 Turquoisia McNabb, Whitley Hatton ……………………………………………………………………………………………………………….… 39
The Story of CC312 Christine Okaro, Christopher Wilson ………………………………………………………………………………………….………………………42
The Story of CC315 James M. Bryne III, Lopriela Seabrook ………………………………………………………………………………...…………………………… 46
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CONTENTS
The Story of CC331 Jordan Mitchell, Jordan R. Howard ……………………………………………………………………….……………….………………………… 49
The Story of CC437 Rachel Davalos, Mariela A. Martínez …………………………………………………………………………………..…………………………… 52
The Story of CC459 Jasmine Mack, Ambra Palushi ……………………………………………………………………………….……………………………………… 55
Recent Abstracts from W. Montague Cobb Research Laboratory Validation of Cobb Collection Biohistories Davlyn Hollie …………………………………………………………………………………………………………………...……………………… 58
How the Cobb Research Lab succeeds in increasing the number of STEM and STEM-affiliated Students Sherese Taylor ………………………………………………………….…………………………………………………………………...………… 59
Investigation of the Cobb Collection, A Statistical Approach Nicholas Guthrie ……………………………………………………………………………………………………………………………………..… 60
Overview of the Interface of the Cobb Research Laboratory and the Robert Wood Johnson Summer Medical and Dental Education Program (SMDEP) at Howard University Donna Grant-Mills, RDH, M.Ed., DDS ………………………………………………………………………………………….…………………… 61
Comparative Analysis of DNA Extraction Techniques on DNA yield from Ancient Teeth Latifa Jackson Ph.D….………………………………………………………………………………………………………………………………… 62
Geospatial Assessment o Residential and Work Sites for Cobb Collection Individuals Hasan Jackson ………………………………………………………………………………………………………………………………………… 63
Minimally Invasive Method to extract DNA from Dentition using Cobb Collection Human Skeletal Remains Alexis Payne, Christopher Cross, M.S., Latifa Jackson, Ph.D, John Harvey, D.D.D., Fatimah Jackson, Ph.D. …………………….……… 64
Trends and Causes of African-American Osteoarthritis and Osteoporosis within the Cobb Collection Sierra Williams ………………………………………………………………………………………………………………………………….……… 65
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Evidence for Arthritis and Specifically Osteoarthritis in the Cobb Collection Maimouna Traore ………………………………………………………………………………………………………………………...…………… 66
Biohistorical Analysis od Cardiovascular Disease in the Cobb Collection Jameshisa Alexander …………………………………………………………………………………………………….…………………………… 67
Historical Trends of Hypertension and Cardiovascular Disease within the Cobb Collection Janet Mansaray …………………………………………………………………………………………………..………………….………………… 68
The Prevalence and Biohistory of Congestive Heart Failure in the Cobb Collection Kayla Bedeau ………………………………………………………………………………………………………………………………..………… 69
The Correlations between African-American Life Experiences and Type 2 Diabetes Whitney Griffith ………………………………………………………………………………………………….…………………...………………… 70
Prevalence of Cerebrovascular Accident within African Americans of the Cobb Collection Natalia Christian …………………………………………………………………………………………………………..…………………………… 71
Assessment on the Resurgence of Rickets and Scoliosis on African Americans Khristian Ifill ………………………………………………………………………………………………………………………..…………………… 72
Identifying the effects and treatment of Alzheimer’s disease in African Americans Youngho Jung ………………………………………………………………………………………………………….……………………………… 73
Lead in Teeth: Reconstructing Environmental Biohistory and Health at the New York African Burial Ground Using Laser Ablation-Inductively Coupled Plasma-Mass Spectrometry (LA-ICP-MS) Joseph L. Jones, Ph.D. …………………………………………………………………………………………..…………………………………… 74
Profile and initial elemental determination of soil samples collected rom the New York African Burial Ground Remains Candice Duncan, Ph.D. ……………………………………,,,………………………………………………………………………………..……… 75
Analysis of Grave Soil Samples Found in the New York African Burial Ground Keely Clinton …………………………………………………………………………………………………………………………………………… 76
Enhancing Public Access to Recent Research on the African Burial Ground Materials: Grave Soil and Oral Microbiome Analyses Fatimah Jackson, Ph.D. …………………………………………………………………………………………………………….………………… 77
Announcements/Advertisements CobbResearchLab.com/TheBackbone
Winter 2015•Spring 2016
Volume 02 Issue 01
Editorial Resilience through Research and Publication Fatimah L.C. Jackson, Ph.D. Resilience is the process of adapting well in the face of adversity, trauma, tragedy, threats or significant sources of stress. Writing about African American history, studying human biology, and interpreting the past are all activities that can contribute to our resilience as individuals and as a nation. We become vulnerable when we are unfamiliar with our past, when we cannot reconstruct the successes of our ancestors, when we cannot learn from their mistakes and misjudgments. Resilience is primarily a learned attribute. Stress stimulates resilience to subsequently stressful episodes, particularly when it is mild in magnitude and controllable by the individual (Ashokan et al 2016) Research on African American health and lifeways can provide a kind of “stress inoculation” by familiarizing us with what has occurred in the past and how it was responded to. This, in turn can facilitate our psychological adaptations, social connections, life meaning and planning, and ultimately physical wellness. Researching and writing about scientific aspects of the African Diasporas, particularly its transatlantic components, can begin to heal the longstanding wounds of that experience and its sequelae by changing the social context within which these historical facts are understood. The social context is the third pillar linking individual genetic susceptibility, a traumatogenic event, and the phenotypic expression of stress (see Auxéméry, 2012). This issue of The Backbone contains articles on various clinical conditions evident in the Cobb Collection as well as theoretical papers on aspects of human evolutionary biology. As a new feature of The Backbone, we feature a diverse set of short biohistories on specific individuals of the Cobb Collection. These were researched and reconstructed by Summer Medical and Dental Educational Program (SMDEP) student scholars during the summer 2015 research program held at the Cobb Research Laboratory (see Cobb Research Lab News 2(3) Summer 2015). This issue concludes with a flurry of recent abstracts on a range of scientific topics from the Cobb Research Laboratory. These abstracts include topics affiliated with our research on ancient human DNA and our historical studies of health disparities. The abstracts will be given as research papers on April 12, 2016 during a special symposium during Howard University’s Research Week 2016.
Ashokan A, Sivasubramanian M, Mitra R. 2016 Seeding Stress Resilience through Inoculation. Neural Plast. 2016;2016:4928081. doi: 10.1155/2016/4928081. Epub 2016 Jan 5. Accessed February 10, 2016 Auxéméry Y. 2012 [Posttraumatic stress disorder (PTSD) as a consequence of the interaction between an individual genetic susceptibility, a traumatogenic event and a social context]. Encephale. 2012 Oct;38(5):373-80. (in French) doi: 10.1016/ j.encep.2011.12.003. Epub 2012 Jan 24. Accessed February 10, 2016.
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Chronic Kidney Disease and its Sequelae within the Cobb Collection
GENETICS & EPIDEMIOLOGY
Chronic Kidney Disease and its Sequelae within the Cobb Collection: Osteological Manifestations and Clinical Record of Evidence Amanda D. Strong1,2 Uzoamaka Nwaogwugwu, M.D.3 Christopher Cross, M.S.,1,4 Fatimah Jackson, Ph.D.1,2
1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University 3Department of Medicine, College of Medicine, Howard University 4Department of Anatomy, Howard University
Chronic Kidney Disease (CKD) has plagued the African American (AA) community as a frequent result of severe hypertension and diabetes, both diseases that may be instigated by environmental factors or hereditary factors such as genetics. CKD is an ailment that causes a dangerous imbalance of vital minerals and ions, and can cause waste to build up throughout the major organs of the body. In contrast to its prevalence, there is an underrepresentation of CKD when participating in cadaver dependent research; this is the result of major consequences of CKD, such as cardiovascular or neurological symptoms being pronounced the cause of death. The Cobb Research Laboratory’s (CRL) investigation within chronic kidney disease will involve the examination of cadaver skeletons whose deaths have been notably caused by CKD. With the information gathered from these investigations, the CRL team is optimistic for anatomical clues left behind by the disease in the hopes of diagnosing other unknown cases within the Cobb Collection for further research. With the findings of more cases it will be possible to examine the genes that are linked to CKD as well as find explanations that could assist in research on the preventative progression of the disease.
Introduction In the United States, the AA community constitutes approximately 13% of the entire population, yet 32% of all patients receiving treatment for kidney failure are AA,1 this leads to an overall kidney failure rate that is over three times larger than that of our Caucasian counterparts. It has also been shown that AAs require dialysis or transplantation at younger ages.6,7 Chronic kidney disease most often leads to end-stage renal disease (ESRD) in which the kidneys can no longer function at the level necessary to remove all of the waste and excess water from the body.2 AAs have greater incidence rates of ESRD at each decade of life compared with any other racial/ethnic group.6,7 The likelihood for the development of chronic kidney disease is determined by the relationship and interactions between genes and CobbResearchLab.com/TheBackbone
FIGURE 1: RISK FACTORS FOR CKD5
the environment.3 It is key to understand both the genetic and environmental factors so that novel treatments and therapies can be developed. Most importantly, understanding the underrepresentation of CKD and why it plagues our community will aid in developing the preventative measures needed to Winter 2015•Spring2016
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Chronic Kidney Disease and its Sequelae within the Cobb Collection
improve our statistical status on the matter. Socio-
those groups, AA’s have, and have always
environmental, behavioral, biomedical, and predisposing
had, the highest rate of CKD incidents.
factors all work together towards particular health
African Americans and Native Americans share many
outcomes. Once all taken into consideration, real
social environmental stressors that may have aided in
progress can and will be made.
their correlation up until 1999. The quickly accelerating
Background Research
progression of the disease has often be attributed to risk factors such as diabetes, hypertension and obesity;
As reported by the National Kidney and Urologic
however, this has not been able to explain the elevated
Diseases Information Clearinghouse (NKUDIC) and
rate of CKD progressing into ESRD among AAs and other
displayed in Figure 1, African-Americans (red circles)
groups with low socioeconomic status.8 Unfortunately,
have the highest occurrence of ESRD incidents and well
the consequences of the social environment is too often
as the highest exponential increase since the year of
over-looked as a contributing element. Through
1980. In second lead, incidents in Native Americans (blue
behavioral science studies, it has been established that there are psychological and physiological consequences dependent on the environment in which one works and lives.9,10 Social environmental stressors such as poverty and discrimination are proven to adverse the bodies psychological functioning as well as prompt response in regards to the nervous and vascular systems; these complications place individuals at greater risk for developing CKD and cause a lesser ability to prevent the progression towards ESRD.8 From Figure 3, it can be seen that social environmental factors are the beginning of a
FIGURE 2: INCIDENT RATES OF ESRD BY RACE4
chain of risk factors that can contribute to other high risk factors such as psychosocial and behavioral that lead to negative
effects
in
pathophysiological
mechanisms. Social issues such as economic struggle and discrimination often lead to psychological manifests of anxiety, depression and stress. Alone, the psychological state can impact the physiological functions of the body; however, the situation is heightened double-fold when these psychological factors instigate poor habits such as
drug use, poor diet and lowered physical activity. Many studies FIGURE 3: CKD RISK FACTOR FLOW CHART8
have
focused
on
the
effect
of
racial
discrimination and institutionalized racism. It has been suggested that the excess risks for chronic
diamonds) began to rise up until 1999 when a decrease
diseases such as CKD among groups such as African
began. Asians (yellow squares) and Caucasians (green
Americans (and Native Americans) are a function of
triangles) have shown the slightest increase in
economic deprivation. However, racial disparities in the
comparison with the others. Compared to the other
prevalence and progression of kidney disease continue
ethnic groups analyzed and to the overall average of
to persist even when the socioeconomic position at the
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individual and community level is improved and 11,12,13
stable.
Chronic Kidney Disease and its Sequelae within the Cobb Collection
with nondiabetic etiologies of ESRD, there was strong
The main concern given by Figure 1 is in
suggestive evidence for linkage on chromosome 10p,
regards to the continuation of an exponential rise in
specifically.3 Curiously, this is near the D10S1435 marker
ESRD in African-Americans that differentiates them from
that is confirmed to have a consistent presence in
others of same or lower socioeconomical status. These
diabetic families.19 For AA families with a history of type
results lead us to examine the genetic factors as the only
2 diabetic nephropathy, a genome wide scan on sibling
key to understanding why the difference among AAs
pairs showed evidence for linkage on chromosomes 3q,
have the highest risk
10q, and 18q.20 Notably, the type 1 diabetic nephropathy
associated with family history, as do Native Americans15
locus was at the 3q peak in the chromosome. 21 Studying
and Hispanic Americans;16 however, it is observed in case
the close proximity of these chromosomal markers and
studies across the United States that AAs are the only
loci may help to explain the continuous relation between
racial group to have a nine-fold higher risk of developing
diabetes and renal disease beyond the physiological level
ESRD if they already have a first degree family member
and allow for a genetic perspective. This information is
occurs. It is a fact that AAs
17
14
Some studies have concluded racially
extremely useful in determining the cause of CKD
variable susceptibility rate is due to familial clustering of
underrepresentation in the AA community. Essentially,
on dialysis.
3
those with CKD in certain racial groups, but other
there is a considerable amount of evidence that supports
research has indicated a correlation among AA
family history of renal disease, as well as familial
individuals who have a mutation at the location of the
clustering of ESRD, as contribution to the pathogenesis
From newer studies a positive correlation
of chronic kidney failure.3 Identification of causative
between similar genetic mutations and familial clustering
elements located within the genome may enlighten the
has been found, thus combining the two previous
development of innovative gene therapies.3
PKD1 gene.
3,18
theories. In Kidney International studies, it was shown that the location of the PKD1 gene mutation is directly correlated with the severity of renal disease and the onset of 18
ESRD.
In studies regarding rodent renal failure a
correlation was noticed in the Rf-1 gene, the rodent analog of the human chromosome10 To assess any 10
possible linkage between markers on chromosome and ESRD potential, a linkage analysis was performed in African American sibling-pairs. It was shown that in AAs
Osteopathic Research According to Dr. Uzoamaka Nwaogwugwu, MD and DaVita expert, renal osteodystrophy is the most common bone disease associated with kidney failure. This disease causes significant imbalances in calcium, parathyroid hormone, phosphorus and activated vitamin D. The condition further develops to affect the balance of osteoclast
and
osteoblast
development
and
22
production. When the calcium levels in the blood begin to drop a significant amount, the body begins to over activate the parathyroid glands to produce the parathyroid hormone. This hormone will begin to extract calcium from the skeletal system and into the bloodstream in order regain calcium equilibrium. As the calcium is being stripped from the bones they begin to weaken and the texture becomes chalky, rather than the FIGURE 4: OSTEOMALACIA ON BONE23
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natural sturdy form.22 Secondly, kidney disease causes an extremely high amount of phosphorous levels in the Winter 2015•Spring2016
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blood. Because calcium and phosphorous share a
symbiotic relationship, the body will begin to draw calcium from the bones into the blood to create equilibrium between calcium and phosphorous.22 Of course, this causes the same side effect of low blood calcium and diminishes the bone. The kidneys serve an ultimately vital function of activating the vitamin D that courses through our blood to form calcitriol. Calcitriol is acts to assist the body in absorbing calcium and maintaining normal parathyroid hormone levels.22 Unfortunately, when the kidneys begin to fail, they are
no longer able to convert vitamin D into calcitriol and the
FIGURE 5: RENAL OSTEODYSTROPHY X-RAY24
body is no longer able to absorb dietary calcium properly. Again, the body attempts to fulfill its calcium need by stealing from within the bones. The typical symptoms for degradation of the bone include: bone and joint pain, bone deformation and fractures, as well as poor mobility.22 In the case of this research, bone deformation is the key component. When having suffered from long-term renal failure or chronic kidney disease, evidence of the disease is left behind on the skeletal structure. Osteodystrophy, osteomalacia, uremia and metabolic bone disease all alter the visual integrity of the bone. Bone lesions, porousness, thinning or thickening, and the abnormal curving of the bone are
FIGURE 6: EXAMPLE OF LYTIC BONE LESION25
all potential signs that the skeletal system was being robbed of essential minerals and ions. In Figure 4, the abnormal curvature and slight protrusion towards the tips of the bone can be seen. When describing osteomalacia, Dr. Nwaogwugwu described how the bone matrix weakens and the bone begins to flare up towards the joints, where majority of the
damage occurs. Figure 5 shows the lack of mineral density near the joints when suffering from renal osteodystrophy. Renal osteodystrophy has been viewed using an X-ray, even when being viewed as a defleshed cadaver. The symptoms most suitable for observation in the laboratory are related to lesion formation. Lesions can be seen on the bone without using tools, however, this can cause an issue when attempting to differentiate natural deterioration from mechanical damage due to CobbResearchLab.com/TheBackbone
FIGURE 7: X-RAY OF BONE LESIONS26
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Chronic Kidney Disease and its Sequelae within the Cobb Collection
processing. Fortunately, an X-ray picture of the bone
lesions can reveal its true nature and will not be confused with mechanical damage.
Methods and Procedures Extensive research was done on what types of osteological symptoms would be present in order to truly piece together our analysis of cadaver skeletons from the Cobb collection. The beginning step was to completely review the digital Cobb Collection files, with the assistance of our director, Dr. Fatimah Jackson, for all
patients whose cause of death was related to kidney malfunction or kidney disease. The exact cause of death, age, race and body number was noted. It was then that
FIGURE 9: JOINT (1) FROM #693
some of the noted bodies were pulled with guidance of our assistant curator and student
of anatomy,
Christopher Cross. The entire anatomy of a carefully chosen, defleshed cadaver was laid out on the laboratory table and reconfigured for organization and easy access, as shown in Figure 8. Beginning with the bones that survive the most tension and pressure through the lifetime, as well as the highly sensitive joints, we attempted to find signs of lesioning, porosity and abnormal morphology on the femurs. This task became difficult as we faced questions that had not yet posed an issue. During the retrieval of many skeletons from the African Burial Ground (New
FIGURE 8: DEFLESHED CADAVER #693
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FIGURE 10: JOINT (2) FROM #693
FIGURE 11: FEMURS FROM #693
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York), many of the bones were damaged through
biopsies will allow us to insure consistent results by
mechanical digging and treating.
confirming osteopathic symptoms that appear similar
As can be seen in Figure 9 and in Figure 10, it is difficult
also have similar chemical and molecular makeup. This
to categorize the damage on the bone under a specific
will be helpful in proving the exact mineral composition
cause. While it is possible that the damage to the bone
that results from these pathological processes. Along
could be the result of deterioration, it could also be
with Dr. Nwaogwugwu, we hope to make a connection
damage inflicted from machinery or rough handling
with
during transportation.
department in order to gain a more complete
the
Howard
University
Hospital
Pathology
Figure 11 is an example of how normal differences in
understanding of the bone pathologies in this focus. To
midsagittal skeletal structure can be mistaken for the
assist in differentiating what is appropriate for expected
thinning or improper curving of the bone.
The
anatomical difference in the bone versus significant bone
left femur, on the bottom of the figure, appears thinner
curvature or loss (Figure 11), the Howard University
with slightly more curvature than its left counter part. It
Hospital Osteology department will be able to analyze
is expected for the skeletal anatomy to differ slightly
measurements taken in the lab as well as photographs.
when analyzing midsagittal pieces. The question that
In the proceeding research, we will use the
arises is whether or not this difference is significant
information gain to find more cases of osteopathic
enough to note it as an osteopathic symptom. In the lab,
symptoms representing CKD in the Cobb Collection.
we also noticed a difference in the texture and color of
Specifically, we will do this by examining defleshed
the two bones, yet determination of the cause was not
cadavers that have causes of death most often
entirely
associated with CKD (i.e., diabetes, cardiovascular
clear.
All
fragments
in
question
were
photographically captured for future comparison.
disease, nuerological disorders). Not only will this add more sources to our research, but will allow for the W.
Conclusion Ultimately, we were not able to determine as much as had been anticipated through the physical laboratory analysis due to the uncertain observations; however, the flaws in our expectations have been led us to new venues, methods, and resources to continue our hunt for answers. To eliminate misperception between natural deterioration of bone and mechanical damage done to it, we have proposed x-ray scanning. By using a radiographically produced image (Figure 5 and Figure 7), it would allow us to see beyond the outer surface of the bone and deeper into its matrix; for example, dark areas within the bone matrix will indicate significant deterioration, as in renal osteodystrophy whereas patchlike spots on the bone will indicate bone lesions have formed. Utilizing the Howard University Hospital Critical Image and Photo department will allow the W. Montague Cobb Research laboratory access to x-ray machines as well as bone biopsy processes. Bone CobbResearchLab.com/TheBackbone
Montague Cobb Research Laboratory to have a more detailed record for causes of death. Having an extended collection of defleshed cadavers specifically marked for CKD would also allow us to collect DNA samples from a variety of sources in order to analyze the genes and attempt to find common markers and genetic clues. Potentially, finding a common genetic factor amongst all CKD cases in the Cobb Collection could allow for a starting point for gene therapies. We can then extend the research to verify whether CKD is prominent in a
certain sex, age or lifestyle (i.e., profession, family size) within the AA community. By comparing location of deaths, a crude idea of how the social environment impacted composed.
the
progression
of
CKD
can
be
Being that the Cobb Collection contains
African remains dating back to the 17th century, we also hope to find a positive correlation between rising CKD levels and time spent in what is now the United States. We are hoping to find clues that will allow us to Winter 2015•Spring2016
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hypothesize in regards to why AA specifically have 6. Tareen N, Zadshir A, Martins D, et al. Chronic kidney disease in African American and Mexican American populations.
developed predispositions for chronic disease that is not common of our ancestry.
Kidney Int. 2005;68(supplement 97):S137–S140. 7.
Bruce, Marino A., Bettina M. Beech, Mario Sims, Tony N. Brown, Sharon B. Wyatt, Herman A. Taylor, David R.
Discussion
Williams, and Errol Crook. "Social Environmental Stressors,
In all, this research is guided towards to the awareness
Psychological Factors, and Kidney Disease." Journal of
and understanding of how and why chronic kidney disease
Investigative Medicine : The Official Publication of the
affects the African American population at an exponential
American Federation for Clinical Research. U.S. National
rate. Our research could potentially serve as a foundation
Library of Medicine, 18 Feb. 2010. Web.
of knowledge for a disease that is highly neglected on the 8. Fremont A, Bird C. Social and psychological factors, physiological processes, and physical health. In: Bird C,
preventative and treatment level in our community. If we
Conrad P, Fremont A, editors. Handbook of Medical
improve our understanding of what factors place African
Sociology. Upper Saddle, NJ: Prentice Hall; 2000. pp. 334–
Americans at risk for chronic kidney disease, we will be better equipped to avoid those scenarios as preventative measure.
Acknowledgements I would like to thank our director, Dr. Fatimah Jackson, PhD, for allowing us to be apart of the amazing experience of the W. Montague Research Cobb Laboratory. We would also like to thank our curator, Christopher Cross, MS, for
his helpful instruction when analyzing the anatomy of the cadaver skeletons in the Cobb Collection. Finally, I would
352. 9.
Seeman T, Mcewan B. Impact of social environment characteristics on neuroendocrine regulation. Psychosom Med. 1996;58:459–471.
10. Norris K, Nissenson AR. Race, gender, and socioeconomic disparities in CKD in the United States. J Am Soc Nephrol. 2008;19(7):1261–1270. 11. Tarver-Carr ME, Powe NR, Eberhardt MS, et al. Excess risk of chronic kidney disease among African Americans versus white subjects in the united states: a population-based
study of potential explanatory factors. J Am Soc Nephrol. 2002;13:2363–2370.
like to thank Matthew Calhoun for his ideas and 12. Volkova N, McClellan W, Klein M, et al. Neighborhood constructive conversation toward the research. poverty and racial differences in ESRD incidence. J Am Soc Nephrol. 2008;19(2):356–364.
References 1.
"African Americans and Kidney Disease." The National Kidney Foundation. N.p., Apr. 2014. Web.
2.
Miller, Scott, MD, and David Zieve, MD, MHA. "End-stage Kidney Disease: MedlinePlus Medical Encyclopedia." U.S National Library of Medicine. U.S. National Library of
Medicine, 2 Oct. 2013. Web. 3.
"Kidney Disease Statistics for the United States." Kidney Diseases Statistics for the United States. National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC), June 2012. Web.
4.
"3 Risk Factors and Causes of Chronic Kidney Disease." Australian Institute of Health and Welfare. N.p., n.d. Web.
5.
Hsu C-Y, Lin F, Vittinghoff E, et al. Racial differences in the progression from chronic renal insufficiency to end-stage renal disease in the United States. J Am Soc Nephrol. 2003;14:2902–2907.
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13. Freedman, BI, Soucie, JM, McClellan, WM: Family history of end-stage renal disease among incident dialysis patients. J Am Soc Nephrol 1997 8:1942–1945. 14. Pettitt, DJ, Saad, MF, Bennett, PH, et al: Familial predisposition to renal disease in two generations of Pima Indians with type 2 (non–insulin-dependent) diabetes
mellitus.
Diabetologia
1990
33:438–443,
10.1007/
BF00404096. 15. Pugh, J: Diabetic nephropathy and end-stage renal disease in Mexican Americans. Blood Purif 1996 14:286–292. 16. Freedman, BI, Spray, BJ, Tuttla, AB, Buckalew, VM: The familial risk of end-stage renal disease in African Americans. Am J Kidney Dis 1993 21:387–393. 17. Rosetti, S, Burton, S, Strmecki, L, et al: The position of the polycystic kidney disease 1(PDK1) gene mutation correlates with the severity of renal disease. J Am Soc Nephrol 2002 13:1230–1237, 10.1097/01.ASN.0000013300.11876.37.
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Centre for Human Bioarchaeology. N.p., 2005. Web. 26. "Orthopedic Teaching: Bone Lesions Case 2 Answer." Bone Lesions Case 2 Answer : : Feinberg School of Medicine: Northwestern University. Northwestern University Feinburg School of Medicine, n.d. Web
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Potential Treatments for Sickle-Cell
GENETICS & EPIDEMIOLOGY
Analysis of Potential Treatments for Sickle-Cell Anemia, or Drepanocytosis, in Adults Cameron D. Clarke1,2 ,3
1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University 3Department of Health, Human Performance and Leisure Studies,, Howard University
This research paper discusses the clinical and evolutionary history of sickle-cell disease, also known as sickle-cell anemia, or drepanocytosis. It noted the genetic causes and physiological effects of sickle-cell disease, and the evolutionary and environmental factors involved in the disease’s emergence, finding that its proliferation was likely the result of a selective sweep of an adaptation of the red blood cells that had a secondary protective effect against malaria in heterozygous individuals. This also mentioned two of the possible treatment methods that could be used to eliminate or mitigate sickle-cell disease and its symptoms. The first treatment method analyzed was therapy of a patient with sickle-cell disease to increase the production of healthy red blood cells containing fetal hemoglobin. The second involved a bone marrow transplant to replace the defective bone marrow. It was found that while both treatments are effective in reducing the severity of sickle-cell disease, only a bone marrow transplant has been conclusively shown to be able to cure the condition, and even then, has only undergone trial testing amon g children. However, there is currently preliminary clinical research being conducted on gene therapy to promote the body’s continued production of fetal hemoglobin, preventing sickle-cell hemoglobin S from even developing, and curing sickle-cell disease
Clinical Background
Sickle cell disease, also known as sickle-cell anemia or drepanocytosis, is a hereditary blood disorder, characterized by a genetic mutation in the gene that codes for hemoglobin in the red blood cells of the body. Hemoglobin is an iron-based metalloprotein that binds to molecules of oxygen in the capillaries of the lungs, and then carries them through the bloodstream, releasing the oxygen molecules into the somatic cells, and binding to carbon dioxide, which is released back into the lungs with each exhalation.1 This paper will discuss three (3) distinct varieties of hemoglobin: Hemoglobin A (HbA), the normal adult form of hemoglobin; hemoglobin S (HbS), the diseased variety of hemoglobin; and hemoglobin F (HbF), fetal hemoglobin. Sickle cell disease occurs as a result of a mutation at a single nucleotide (A to T) of the β-globin gene, which results in glutamic acid being substituted by valine at position 7 (position 6 under the historic nomenclature. This causes the protein to form Hemoglobin S (HbS) in its final conformation, instead of Hemoglobin A (HbA), normal adult hemoglobin. Under normal conditions, the mutation is generally benign, causing no apparent effects on the secondary, tertiary, or quaternary structures of hemoglobin in conditions of normal oxygen CobbResearchLab.com/TheBackbone
concentration. Under conditions of low oxygen concentration, however, this mutation allows for the polymerization of the HbS itself. When HbS is in conditions of low oxygen saturation, the hydrophobic residues of the valine (formerly glutamic acid) at position 7 of the beta chain in hemoglobin are able to associate with the hydrophobic patch, causing hemoglobin S molecules to aggregate and form fibrous precipitates (Figure 1). These precipitates form long, interlocking strands within the blood cells, elongating and distorting its shape, and causing them to take on the distinctive malformed “sickle-like” shape that gives the condition its name. These “sickle” cells are far less efficient in carrying oxygen than the ordinary rounded cells, additionally, after a cell is sickled, it loses much of its elasticity, becoming much more inflexible. This rigidity makes the cells much more likely to become trapped in the small openings of the capillaries and narrow blood vessels. As cells accumulate in the blocked vessels, they can cause ischemia (oxygen deprivation) and cell death in the affected areas, a complication called a sickle-cell crisis. Sickle-cell crises are often extremely painful, and potentially fatal if the obstruction occurs around a vital organ and causes organ damage or failure. Additionally, the deformation of the cells by the hemoglobin fibers Winter 2015•Spring2016
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Potential Treatments for Sickle-Cell
present itself when the allele for sickle-cell disease is passed from both parents during reproduction. In individuals that are heterozygous for sickle-cell disease (one copy of the diseased allele), also called “carriers,” the sickle cell load is greatly reduced, and symptoms generally only appear after prolonged oxygen
FIGURE 2: MALARIA DISTRIBUTION
FIGURE 1: DIAGRAM OF SICKLE CELLS CAUSING VASO-OCCLUSIVE CRISIS
reduces the integrity of the cell membrane, making the cells much more likely to lyse. This damage is severe, to the extent that while healthy red blood cells may typically function for 90–120 days, sickled cells only last 10–20 days before lysis.2 This rapidly accelerated rate of hemolysis is from where the condition derives its designation as an anemia; although the bone marrow creates red blood cells at increased volume compared to healthy humans, it is simply unable to compensate for the rate of cell destruction. Patients are often left with lower-than-normal levels of erythrocytes, and can exhibit symptoms common to general anemia sufferers, including feeling tired, weakness, shortness of breath, or a poor ability to exercise.3
Evolutionary Background
Sickle-cell disease is an allelic disorder, located on the chromosome 11, at 11p15. It has an autosomal recessive pattern of inheritance, in that the condition will only
CobbResearchLab.com/TheBackbone
FIGURE 3: SICKLE-CELL DISTRIBUTION
deprivation, or severe dehydration. Evolutionarily, the emergence and proliferation of the sickle-cell allele are likely linked to the disease’s protective effect against malaria, a far more expansive and lethal disease, found in a similar range (Figures 2 & 3). This is due to the sickling of the cells interfering with the complex lifecycle of the parasite that causes malaria, Plasmodium malariae. Plasmodium reproduces within the erythrocytes. In a carrier for sickle-cell disease, the presence of the malaria parasite causes the red blood cells with defective hemoglobin to ruptureprematurely, Winter 2015•Spring2016
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making the Plasmodium parasite unable to reproduce. Further, the polymerization of the hemoglobin affects the ability of the parasite to digest hemoglobin in the first place. This reduced efficacy of Plasmodium leads to shorter and less severe infections among sickle-cell carriers. Therefore, in areas with endemic malaria, chances of survival actually increase among heterozygotes. However, this protective effect does not extend to sickle cell homozygotes, or people with the disease, since the premature lysis of infected cells is a common cause of sickle-cell crises. The heterozygote advantage, however, is enough to account for the persistence of sickle-cell disease in areas with high endemic malaria. Analysis of the disease’s genetic history via restriction endonuclease analysis found that it most likely arose spontaneously in several different areas, with a different variant of the mutation emerging in each one. These variants are known as Cameroon, Senegal, Benin, Bantu, and Saudi-Asian. This evidence also supports the hypothesis that the mutation that causes sickle cell arose and proliferated as a result of the widespread malaria that is endemic to the regions.
Fetal Hemoglobin Treatment
Potential Treatments for Sickle-Cell
begin producing adult hemoglobin (HbA) (Figure 4).In
most cases, the switch from fetal hemoglobin to adult hemoglobin is relatively inconsequential. However, since the structure and genetics of fetal hemoglobin differ from those of adult hemoglobin, it is not affected by the same genetic mutations that govern the production of adult hemoglobin. When fetal hemoglobin production is switched off after birth, normal children begin producing adult hemoglobin (HbA). Children with sickle-cell disease instead begin producing a defective form of hemoglobin called hemoglobin S (Figure 5). However, among children
with the sickle-cell trait, where fetal hemoglobin remains the predominant form of hemoglobin after birth, the frequency and severity of sickle-cell crises decrease
FIGURE 4: HEMOGLOBIN A
In addition to corroborative evidence of evolutionary
pressure for the emergence of sickle cell, the restriction endonuclease analysis of the disease also found that in some regions, including Senegal and Saudi-Asia, the sickle-cell mutation has variants that are correlated with increased and persistent production of hemoglobin F, also known as fetal hemoglobin (HbF).4,10 Fetal hemoglobin is the type of hemoglobin that is produced
in the human fetus during the last seven months of development
in
the
uterus.
Functionally,
fetal
hemoglobin differs little from adult hemoglobin, apart from the fact that it has a slightly higher oxygen affinity, and bonds more tightly, but still temporarily, to the oxygen molecules in the capillaries of the lungs.5 This is due to the mixture of oxygenated and deoxygenated blood in the maternal blood that is delivered to the fetus via the umbilical vein. Generally, within six months of
FIGURE 5: HEMOGLOBIN S
relative to those where fetal hemoglobin production has ceased. This protective effect was observed in variants of the sickle-cell mutation in Senegal and Saudi-Asia, where it is believed to be a secondary adaptation, blunting some of the acute complications of sickle cell disease.
birth, humans stop producing fetal hemoglobin, and CobbResearchLab.com/TheBackbone
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Potential Treatments for Sickle-Cell
Fortunately, much progress has been made in a clinical
production of HbF in humans is feasible in order to more
application for this phenomenon.
permanently treat, or even cure, sickle-cell disease.
In a landmark study in the New England Journal of
Preliminary studies have already found that it is possible
Medicine, it was found that not only did treatment of
to completely cure mice of a variant of sickle-cell disease
patients with hydroxycarbamide (hydroxyurea), an
by using gene therapy, and studies in humans have
antineoplastic (tumor-inhibiting) drug, increase the
shown promising results, to the extent that gene therapy
quantity of fetal hemoglobin in erythrocytes, but that it
has moved on to the early stages of clinical trials as a
also appeared to break down cells that were likely to
permanent cure for sickle-cell disease.8,9,11
sickle, further decreasing the risk of vaso-occlusive sickle -cell crises. Additionally, a second study discovered that the treatment of sickle-cell disease with a combination
therapy
of
hydroxycarbamide
and
recombinant
erythropoietin (a hormone involved in red blood cell synthesis) further increased levels of HbF, and further reduced
the
frequency
of
acute
sickle-cell
complications.6 Even more significant, this treatment method was found to have no major adverse side effects, and so would likely significantly improve patient outcomes and quality of life. Important to note, however, is that the study was only conducted on adults, so it is not currently clear how much the success would translate to interventions in children. Additionally, hydroxyurea treatment has only been shown to reduce the frequency of sickle-cell crises, not prevent them entirely. As such, it is only a partially effective treatment, not a cure. It also has not been tested in an attempt to resolve a currently occurring sickle-cell crisis, and so cannot be recommended as an emergency
intervention.
Finally,
the
researchers
involved with the study noted that “there is concern that long-term hydroxyurea therapy may be carcinogenic or leukemogenic, because some other antineoplastic agents
have such effects.”7 As with any medication, additional research is necessary in order to more completely understand the mechanism of hydroxyurea therapy’s function in preventing crises, and its long-term effects on individuals and their children. However, this treatment is already in use in patients suffering from sickle-cell disease, and so far has seen widespread success. On the horizon, researchers have begun testing whether
gene
therapy
CobbResearchLab.com/TheBackbone
to
stimulate
permanent
Hematopoietiec Stem Cell Transplantaion
For all of the promising research on the horizon,
however, a cure for sickle cell disease already exists. Hematopoietic stem cell transplantation (HSCT), also known as bone marrow transplantation, has been shown to permanently cure children of sickle cell disease when it is successful. Allogenic bone marrow transplants, the type used in sickle-cell procedures, are a high-risk procedure, usually involving two people: the (healthy) donor and the recipient (patient). In the procedure, the donor and the recipient must both be tested to determine if they have similar or identical variants of the human leukocyte antigen (HLA) system. This network of
genes is responsible for an individual’s immune response to foreign cells and molecules. If the two individuals are incompatible, or too dissimilar, the transplantation will fail, as the recipient’s immune system will either attack the donor’s stem cells, or the donor’s stem cells will cause an infection in the recipient’s tissues, a condition called graft-versus-host disease . Even if the HLA patterns of the individuals match, in order to minimize the possibility of a rejection, the patient must be subjected to immunosuppressant treatment to destroy their
immune response system. This immunosuppression is part of what makes the procedure so high-risk; patients with compromised immune systems are extremely vulnerable to infection, such that even a relatively mundane disease such as the common cold can be fatal. Once the recipient is immunosuppressed, the donor is placed under general anesthesia, and the hematopoietic stem cells are removed from a large bone of the donor, typically the pelvis, through a large needle that reaches
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Potential Treatments for Sickle-Cell
Discussion
Of the methods described, as a practical solution for patients with mild to moderate sickle-cell disease, with only occasional, infrequent vaso-occlusive crises, the combination therapy of hydroxyurea and recombinant erythropoietin seems to be the ideal currently available treatment, both in terms of relative safety and likelihood of success, and in terms of effectiveness. Of course, as elaborated, all of the treatments require further research to conclusively determine their long-term
FIGURE 6: BONE MARROW HARVEST
health risks and benefits, but currently the risks of
the center of the bone. This technique is referred to as a
hydroxyurea are the most widely studied and well
bone marrow harvest (Figure 6). The cells are then
known. The most promising of the treatments, however,
implanted into the patient’s own bones, and after a few
remains gene therapy, which, unlike hydroxyurea
weeks to allow the cells to multiply, the patient is
therapy, promises to completely cure sickle-cell disease,
removed from immunosuppressants, and the procedure
and without the complex surgery and high-risk
is completed.
immunosuppression
of
hematopoietic
stem
cell
Although HSCT, due to its relatively high risk, is
transplantations. Unfortunately, as this method is still in
generally only attempted in people with conditions that
its earliest stages of clinical trial, it may be years before it
are extremely life-threatening, recent advances in the
becomes available to the average sickle-cell patient. Sickle-cell disease is a stigmatized, misunderstood, and
safety and standardization of the procedure have made it safe
life-altering condition, but it is no longer the death
enough to attempt in individuals with less-threatening
sentence it once was. Hopefully, with additional study,
conditions, such as sickle-cell anemia. In such cases,
evolutionary and clinical research, and public health
however, studies have only been conducted among
outreach, we can make sickle-cell disease no more than
children. A recent study by the New England Journal of
a nuisance, instead of a potentially debilitating condition.
Medicine found that of 22 patients upon whom bonemarrow transplants were performed, 20 survived the procedure itself, and 16 were found to be free of sickle-
References 1.
Maton, Anthea; Jean Hopkins; Charles William McLaughlin; Susan Johnson; Maryanna Quon Warner; David LaHart; Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1.
2.
Maakaron, J. (2014). Sickle Cell Anemia. Medscape. Retrieved April 14, 2015, from http:// emedicine.medscape.com/article/205926-overview
3.
Stedman's medical dictionary (28th ed. ed.). Philadelphia: Lippincott Williams & Wilkins. 2006. p. Anemia. ISBN 9780781733908.
4.
Lanzkron S, Strouse JJ, Wilson R et al. (June 2008). "Systematic review: Hydroxyurea for the treatment of
cell disease in the months following the procedure, survival and event-free survival at four years of 91
percent and 73 percent, respectively. Although these results are promising, a mortality rate of 9%, and with only a 10% mortality likelihood by age 20 is clearly unacceptable, so more advancements must be made, both in the calculations of the likelihood of rejection, and in
the
safety
hematopoietic
of stem
the cell
procedure
itself,
transplantation
before can
be
considered a viable and efficacious treatment for sicklecell disease. CobbResearchLab.com/TheBackbone
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Potential Treatments for Sickle-Cell
adults with sickle cell disease". Annals of Internal Medicine 148 (12): 939–55. doi:10.7326/0003-4819-14812-200806170-00221. PMC 3256736. PMID 18458272 5.
Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Section 10.2, Hemoglobin Transports Oxygen Efficiently by Binding Oxygen Cooperatively.
6.
Rodgers GP, Dover GJ, Uyesaka N, Noguchi CT, Schechter AN, Nienhuis AW (January 1993). "Augmentation by erythropoietin of the fetal-hemoglobin response to hydroxyurea in sickle cell disease". The New England Journal of Medicine 328 (2): 73–80. doi:10.1056/ NEJM199301143280201. PMID 7677965.
7.
Charache S, Terrin ML, Moore RD et al. (May 1995). "Effect of hydroxyurea on the frequency of painful crises in sickle cell anemia. Investigators of the Multicenter Study of Hydroxyurea in Sickle Cell Anemia". The New England Journal of Medicine 332 (20): 1317–22. doi:10.1056/NEJM199505183322001. PMID 7715639
8.
Pawliuk R, Westerman KA, Fabry ME, Payen E, Tighe R, Bouhassira EE, Acharya SA, Ellis J, London IM, Eaves CJ, Humphries RK, Beuzard Y, Nagel RL, Leboulch P (2001). "Correction of Sickle Cell Disease in Transgenic Mouse Models by Gene Therapy". Science 294 (5550): 2368–71. doi:10.1126/science.1065806. PMID 11743206.
9.
Wilson, Jennifer Fisher (18 March 2002). "Murine Gene Therapy Corrects Symptoms of Sickle Cell Disease". The Scientist – Magazine of the Life Sciences. Retrieved 17 December 2014.
10. Green NS, Fabry ME, Kaptue-Noche L, Nagel RL (Oct 1993). "Senegal haplotype is associated with higher HbF than Benin and Cameroon haplotypes in African children with sickle cell anemia". Am. J. Hematol. 44 (2): 145–6. doi:10.1002/ajh.2830440214. ISSN 0361-8609. PMID 7505527. 11. St. Jude Children's Research Hospital (4 December 2008). "Gene Therapy Corrects Sickle Cell Disease In Laboratory Study". ScienceDaily. Retrieved 17 December 2014.
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Evidence for Autism in the CC
GENETICS & EPIDEMIOLOGY
Genetic Behavioral Evidence for Autism in the Cobb Collection Jayla Harvey1,2 Fatimah Jackson, Ph.D.1,2
1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
1 in 88 children in the United States are diagnosed with autism; this number has grown exponentially over the past couple of years, primarily due to raised awareness of this disorder. The definition of autism as we know it today didn’t come about until 1980. Prior to that, autism was defined as schizoid personality disorder attributed fundamentally to a lack of maternal warmth. Mental health issues, in general, in African Americans have not been extensively studied and are frequently underdiagnosed. Differential expression of mental disease likely stems from the multi-generational inhumane effects of the transatlantic slave trade, segregation, racism, and discrimination. As a result, the literature is scant on explicit descriptions of autism for the African American population. However, new scientific advances are suggesting that autism is genetically linked by clusters of DNA markers. Since African American’s rich diversity is not widely represented in either genetic or behavioral studies, this research will search for evidence of mental disease in specific individuals within the Cobb Collection try to develop a bridge between the behavioral expression of mental disease and the presence of genetic susceptibility genes for autism. This study will focus on African American adults from the District of Columbia, Maryland, and Virginia area who died in the 1930s, 40s and 50s and for whom clinical reports and other clinical and demographic clues suggest evidence of mental disease. Advanced bioinformatic approaches will be expended to identify likely autism gene clusters in the targets of study.
Introduction
Methods and Results
Hospital in Washington, D.C between the decades of
various genes that have been linked to autism over the
1930s through 1950s were institutionalized because they
past couple years. The genes have been grouped into
Many of the patients confined at St. Elizabeth’s
1
The genes that will be studied in this experiment are
were unable to function in society. This inability to
three categories: mutated genes, deleted or copied
assimilate into the general public may be a consequence
genes, or genes with methylation changes.
of an undiagnosed mental illness. Autism Spectrum
Mutated
genes
either
show
single
nucleotide
Disorders (ASD) were not characterized separately from
polymorphisms (SNPs) or frameshift mutations. The
schizophrenia at this time, therefore it is possible that
mutated genes being studied are Dopamine Receptor D2
some patients that were being held at St. Elizabeth’s
(DRD2: Gene ID1813), Protein phosphate1, regulatory
Hospital because they didn’t exhibit ‘normal’ behavior
inhibitor subunit 1B (PPP1R1B: Gene ID 84152), and
14
Latest genetic research
Neuroligin4, X-linked (NLGN4X: Gene ID57502). DRD2
shows that ASD can be shown through a connection of
encodes for the D2 subtype of a dopamine receptor
and suffered from an ASD. many mutated genes.
2
These mutations can be
which
has
roles
in
postsynaptic
neurons
and
dopamine
synthesis
and
etiologically effected by the environment the patient was
autorecpetor
subjected to. African-Americans of this time period
neurotransmission. The receptor inhibits adenylyl cyclase
would likely be more susceptible to these mutations due
activity, which catalyzes the conversion of ATP and cyclic
to the immense stressors of living in a time of
adenosine monophosphate (cAMP) and pyrophosphate.3
segregation, Jim Crow Laws, post slavery traumatic
cAMP is important because it is used in the intracellular
syndrome, and poverty.
signal transduction. In ASD, the DRD2 gene shows an
mediating
over transmission of the T allele, which causes the gene CobbResearchLab.com/TheBackbone
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to be incorrectly, negatively effecting how cells send 4
Evidence for Autism in the CC
incorporating the trust and empathy of in-groups with
signals to each other. The PPP1R1B gene encodes for
their suspicion and rejection of outsiders. In ASDs, there
DARPP-32, a bifunctional signal transduction molecule,
is reduced to no expression of the CD38 protein due the
expressed in dopaminoceptive neurons and mediates the
fact that the gene is mutated or deleted. The CADPS2
effects of D1 and D2 dopamine receptors. In ASDs, this
gene encodes for calcium binding proteins that play a
gene shows an over transmission of the C allele, which
major role in exocytosis of neurotransmitters and
can show decreased release of dopamine. Altered levels
neuropeptides into the synapse and of dense core
of the DARPP-32 molecule displays impaired reversal
vesicles in neuroendocrine cells.8
learning. Mutated DRD2 and PPP1R1B genes additively
regulates neurotrophin release from granule cells
predispose ASDs and are
only found in male
leading to regulate cell differentiation and survival during
patients. The decreased dopamine activity in the medial
cerebellar development. CADPS2 is deleted in ASD. The
5
This gene also
prefrontal cortex is also a sign of ASD. The NLGN4X gene
gene PCDH10 deals with the establishment and function
effects cell adhesion molecules localized at the CNS
of cell to cell connections in the brain at the
synapse. It is still being studied, about the exact
synapse. This is also one of the largest deletions in ASD.9
variation of this gene sequence that predisposes ASD,
The absence of this gene negatively affects the cells to
but it has been suggested that the defect in this gene
create synapses and communicate with each other.
12
negatively affects synaptogenesis. Therefore, when this gene is mutated, neurons in the CNS have trouble communicating with each other due to the fact that they are unable to create proper synapses.
Certain genes have deleted or copied sequences that
cause either a lack of or overproduction of specific proteins. The deleterious or copied genes in this study are Fragile X mental Retardation 1 (FMR1: Gene ID2332), CD38 molecule (CD38: Gene ID952), Ca2+-dependent secretion activator 2 (CADPS2), and protocadherin alpha cluster
10,
complex
locus
(PCDHA10:
Gene
ID56139). FMR1 is a very well studied gene that encodes for the Fragile X mental retardation 1 protein. In the brain, the protein may play a role in the development of 6
the connections between nerve cells at the synapse. The protein also regulates synaptic plasticity.
Synaptic
plasticity is the ability of synapse to adapt over time in response to experience.13 Synaptic plasticity plays a role in learning and memory. In Fragile X syndrome, which has features of ASD, 200+ CGG repeats causes the gene
to be unstable and in consequence to be silenced, making little to no protein. Fragile X syndrome is a precursor for Autism. The CD38 gene encodes for a transmembrane protein, CD38, which regulates oxytocin secretion. Oxytocin is described as the 窶話onding
Methylation changes on a DNA sequence alters how the gene or protein is expressed without changing the
actual sequence. The genes with epigenetic changes that may predispose autism that are being studied in this research are Nuclear Receptor Subfamily 3, group C, Member 1 (NR3C1: Gene ID2908) and Methyl CpG Binding Protein 2 (MECP2: Gene ID4204). NR3C1 gene encodes for a glucocorticoid receptor that regulates transcription factors. Glucocorticoids are involved in inflammatory responses, cellular proliferation and differentiation in target tissues. In ASD, it has been found that suppressed methylation on hippocampal DNA may be due to deprived maternal care during infancy.10 This methylation suppression at the NR3C1 gene leads to a decreased number of the glucocorticoid receptors needed to regulate transcription. The MECP2 gene encodes for the methyl-CpG binding protein 2. This gene is located on the X chromosome at Xq28; it is an Xlinked dominant mutation that is only found in females, due to the fact that it is lethal in males. MECP2 is identified with Retts Syndrome, a precursor to autism.11 De novo mutations at CpG dinucleotide causes epigenetic change of deacylation of core histones, which changes the chromatin architecture and leads to
hormone.7 It also promotes ethnocentric behavior, CobbResearchLab.com/TheBackbone
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transcriptional repression. This repression show low
Evidence for Autism in the CC
5. Joe A Hettinger, X. L. (2012). DRD2 and PPP1R1B (DARPP32) polymorphisms independently confer increased risk
levels of gene transcription.
for autism spectrum disorders and additively predict affected status in male-only affected sib-pair families.
Conclusion
Autism is a heterogeneous neuro-developmental
syndrome with a complex genetic etiology. Unifying principles among cases of autism are likely to be at the level of brain circuitry at the synapse. All of the genes in this study effect the synaptic transmission of information
in some way. The idea that ASD can be affected or caused by environmental factors is reinforced by the
Behavioral and Brain Functions. 6. U.S National Library of Medicine. (2012, August). FMR1 Gene. Retrieved from Genetics Home Reference: http:// ghr.nlm.nih.gov/gene/FMR1 7. Heon-Jin Lee, A. H. (2009). Oxytocin: the Great Facilitator of Life. Progressive Neurobiology. 8. Declan J. James, a. T. (2013). CAPS and Munc13: CATCHRs that SNARE Vesicles. Frontiers in Endocrinology, 817.
characteristic called synaptic plasticity, in which a
9. Eric M. Morrow, S.-Y. Y.-K.-S. (2008). Identifying Autism
synapse can change and adapt by either strengthening of
Loci and Genes by Tracing Recent Shared Ancestry.
weakening over time in response to increases or
Science.
decreases in activity or because of an alternation in the number
of
neurotransmitter
receptors
on
the
synapse. Conclusively, ASD is likely to be a synaptic disorder. In the future we plan to extract DNA from the selected specimen and first look for the group of genes that would have been deleted or copied, then mutated genes. Lastly, we will look for possible methylation changes on the previously highlighted genes. If a patient exhibits more than 3 mutated genetic factors then we will pull their archived records and compare their psychiatric records with genetic evidence found on their genome
and
possibly,
tentatively
change
their
psychiatric records with genetic evidence found on their genome and possibly, tentatively change their diagnoses
10.L J van der Knaap, H. R. (2014). Glucocorticoid receptor gene (NR3C1) methylation following stressful events between birth and adolescence. The TRAILS study. Translational Psychiatry.
11. Lam CW, Y. W. (2000). Spectrum of mutations in the MECP2. J Med Genet. 12.Jamain, S. (2003). Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism. Nature Genetics 34, 27-29. 13.Sarah R. Gilman, I. I. (2011). Rare De Novo Variants Associated with Autism Implicate a Large Functional Network of Genes Involved in Formation and Function of Synapses. CellPress: Neuron, 898-907.
14.(2013). The Evolution of Autism. Retrieved from The History of Autsim: http://ct-educationadvocates.com/ information/autism/the-evolution-of-autism/
to an ASD.
References 1. Barak Goodman, J. M. (Director). (2010). American Experience: The Lobotomist [Motion Picture]. 2. Geschwind, D. H. (2008). Autism: Many Genes, Common
Pathways. CellPress, 391-395. 3. NCBI. (2015, April 5). DRD2 dopamine receptor D2 [ Homo sapiens (human) ]: Gene ID 1813. Retrieved from NCBI Gene
Summary:
http://www.ncbi.nlm.nih.gov/gene?
cmd=Retrieve&dopt=full_report&list_uids=1813 4. J. Reece, N. C. (2002). Biology. San Francisco. CobbResearchLab.com/TheBackbone
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Evolution of the Pathogenesis of Schizophrenia
GENETICS & EPIDEMIOLOGY
A Review: Evolutionary Theories of the Pathogenesis of Schizophrenia Nichelle Jackson1,2
1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
Evolutionary theories suggest schizophrenia, and other psychiatric disorders, are uniquely human disorders that coevolved during evolution of the human brain. As brain size and complexity, relative to body mass increased, the energetic demand required for advancements in cognition, language, and executive function increased. Currently, a variety of techniques using rodent models and comparative genetics are used to investigate the pathophysiology and therapeutic targets of schizophrenia while simultaneously placing this disorder into an evolutionary perspective. Theories regarding the cause of schizophrenia range from geneenvironment interactions to differences in brain chemistry and structure. Much research has been done to identify the role of single gene mutations and neuronal mitochondrial dysfunction in the onset schizophrenia.
Introduction Throughout
subjected to crude forms of therapy as researchers history,
individuals
with
psychiatric
search for long-lasting antipsychotic medications.
disorders were stigmatized, dehumanized, and separated
Currently, schizophrenia is understood as a highly
from the community. During the Middle Ages, individuals
heritable and debilitating psychological disorder with a
afflicted by an illness were thought to be either
world-wide incidence of approximately 1%. Despite
possessed by demons or punished by gods. To “cure”
medical advancements, the cause of schizophrenia is still
these disorders, individuals were subjected to blood-
unknown. Many individuals afflicted with this disorder
lettings, exorcisms or burned at the stake. By the 19th
become dependent on family members and medical
century, psychiatric disorders were still not understood,
professionals and unable to live a normal life. Instead,
but illnesses were viewed as a sickness rather than an
these individuals are. The economic costs associated
evil or divine punishment. During this time, the mentally
with the symptoms of schizophrenia total an upwards of
ill were placed in asylums and prisons where they
$63 billion dollars in the United States alone.23 If the
received inhumane and insufficient care. Emil Kraepelin
suffering of patients and families is not enough
was the first to described the symptoms of schizophrenia
motivation to fund schizophrenia research, the economic
in 1896. Kraepelin used the term dementia praecox, to
burden should be.
characterize a distinct form of dementia marked by poor
Patients afflicted by schizophrenia exhibit a variety of
mental function in addition to reoccurring delusions and
positive, negative and cognitive symptoms that vary
2
hallucinations.
In 1911, Eugen Bleuler
renamed
among individuals. Positive symptoms are characterized
dementia praecox to schizophrenia (‘schizo’=split;
by psychotic behaviors not seen in healthy individuals.
‘phren’= mind) and further characterized the disorder by
Such symptoms include, hallucinations, delusions,
noting the incidence of positive and negative symptoms.
thought
Within the last century, knowledge of the neurological
blocking,
basis and associated therapies of schizophrenia have
(stereotyped movement, catatonia). Flat affect and lack
improved. Patients with schizophrenia are no longer
of pleasure in everyday life are considered negative
disorders
(disorganized
neoglisms)
and
thinking,
movement
thought disorders
symptoms because they are qualities that disappear in CobbResearchLab.com/TheBackbone
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Evolution of the Pathogenesis of Schizophrenia
individuals presented with the disorder. Finally, cognitive
connectedness coupled with decreased expression of
symptoms are characterized by a deficits in working
GABAergic interneurons. These structural changes are
19
correlated with deficits in the formation, maintenance
Symptoms of schizophrenia typically manifests during
and orchestration of synapses that disrupts normal brain
adolescence and early adulthood, between the ages of
function.
memory,
executive
functioning
and
attention.
16 and 30. Childhood onset of schizophrenia is rare, but, does occur. However, symptoms of schizophrenia do not manifest once middle age is reached. Sexual dimorphism
Genetic and Environmental Factors
Familial studies implicate a strong genetic component
of this disorder, exists as males tend to experience
to the susceptibility of schizophrenia, and several
symptoms sooner and more severely than females.
candidate genes have been identified. Disrupted-in-
Additionally, males are more likely to be diagnosed with
schzophrenia-1 (DISC1), Neuregulin (NRG1), Nuclear
schizophrenia while females are more likely to be
receptor related 1 protein (Nurr1), and Dystrobrevin
diagnosed with schizoaffective disorders.
binding protein 1 (DTNBP1) are a few of the top
Though the precise cause of schizophrenia is unknown,
candidate genes that display positive selection for genes
genetic and environmental factors have been found to
associated with schizophrenia.13,25 However, since the
play an important role in the incidence of schizophrenia.
risk of developing schizophrenia decreases as the degree
As previously mentioned, schizophrenia occurs in 1% of
of genetic relatedness decreases, and twins do not have
the general population. For second-degree relatives of
a 100% risk of developing the disorder if one twin is
individuals diagnosed with schizophrenia, the genetic
diagnosed, environmental insults have been suggested
risk is greater than 1% and for first-degree relatives, the
to exert some degree of influence on the susceptibility to
risk is around 10%. Identical twins have the highest risk
schizophrenia. Therefore, schizophrenia is theorized to
of developing schizophrenia if one twin has the disorder
be the result of genetic and environmental interactions.
19
However, since the risk of identical twins
Environmental factors such as maternal stress, social
developing schizophrenia is well below 100%, scientists
isolation, immune activation and pharmacological
believe there are environmental factors that contribute
interference have been found to mimic or exacerbate
to greater vulnerability to.
symptoms of schizophrenia when combined with
(40-65%).
Alternatively, differences in brain chemistry and structure may play a role in schizophrenia. Schizophrenia
individuals predisposed with genetic risk factors. DISC1, is among the most characterized gene
enlarged
implicated in schizophrenia. This gene was originally
ventricles, and an overall reduction in brain size
discovered in a Scottish family with a high prevalence of
especially in the hippocampus, thalamus, and frontal
schizophrenia and psychoaffective disorders including:
has
lobes.
been
21
consistently
associated
with
Neuroimaging and immunohistochemistry of
schizoaffective
disorder,
bipolar
disorder,
major
post-mortem brains of schizophrenic patients were
depression, adolescent conduct disorder and autism
marked by neurological abnormalities, particularly in the
spectrum disorders.13,18 Dysfunction of this scaffolding
hippocampus and neocortex, when compared to normal
protein is characterized by a balanced translocation
controls. Neurons in these regions were also smaller with
between chromosomes 1 and 11 that has been linked to
abnormal
synaptic
the development of psychosis. Additionally, DISC1
organization. Moreover, immunohistochemistry found a
interacts with other proteins important to functions of
marked decrease in biomarkers for GABAergic inhibitory
intracellular
dendritic
interneurons.
24
arborization
Taken
together,
and
this
disorder
is
signaling,
neurodevelopment
and
8
synaptogenesis.
characterized by a reduction in synaptic organization and CobbResearchLab.com/TheBackbone
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Evolution of the Pathogenesis of Schizophrenia
Evolutionary Perspective of Schizophrenia
outgrowth, neurotransmitter package and release, and
Human evolution is predominantly characterized by
dendritic modeling.4 Comparative genomics suggests
the transition to bipedalism and the evolution of brain
mitochondrial genes coevolved with increased metabolic
size. The evolution of brain size led to increased
processes and neuronal activity. Mitochondria adapted
cognition and executive functioning, in addition to, more
to produce more efficient means of electron transport
complex forms of language. The increase in brain size
during oxidative phosphorylation thereby increasing
was marked by increased development of the neocortex,
energy levels necessary to maintain brain function. This
with a significant increase in size and complexity of the
is thought to have coevolved with increased gene-
prefrontal cortex (PFC). Increases of the PFC led to
expression levels of genes associated with energy
advantages in emotional processing, motor control, and
metabolism and synaptic connectivity in the human
regulation of behavior in response to environmental
neocortex compared to non-human primate relatives.10
stimuli.25 One theory suggests genetic changes that
Schizophrenia is thought to be a human specific disease
caused these enhancements occurred over 50,000 years
because its clinical symptoms indicate dysfunction
ago when Homo sapiens transitioned from precursor
among genes and/or pathways involved in human brain
5
hominid species. Additionally, these enhancements may
evolution.25 In particular, changes in metabolic pathways
have occurred when H. sapiens adapted to live in bigger
have been implicated in disorders like schizophrenia that
social groups forced to forage for sustenance. In these
impact cognitive abilities.
conditions, individuals evolved to cooperate, empathize and access the emotional states of others with cognitive adaptations.
12,7
In order to perform these energetically
demanding tasks, a balance between brain size and
Methods and Materials Animal Models of Schizophrenia To study schizophrenia, researchers must study the circuitry
energy demand was established. To meet the energetic
and molecular mechanisms of human brain. However, because
demands imposed by evolution of brain size, researchers
the organ is so vital to human life, obtaining the necessary
believe species could have increased energy intake and
samples is difficult and impractical. Tissue donated from post-
production and/or reduced the amount of energy used by other bodily functions. In order to obtain the energy necessary to maintain basal function, the brain depends on oxidative phosphorylation. At rest, the human brain uses approximately 20% of total body oxygen consumption. This can be compared to apes that use 13% and other
mortem
patients
has
led
to
several
advances
in
neuroanatomical differences observed in the disorder, but physiological information cannot be obtained from dead tissue. Additionally, studying post-mortem brains does not provide insight needed to determine whether structural changes are the cause or result of the disorder. Instead, animal models are used because basic brain circuitry and molecular mechanisms are conserved among many species throughout
vertebrate mammals that need 2-8%, but are considered
evolution.27 Traditionally, gene mutations identified from
to be less intelligent.16 The amount of total body oxygen
patient samples have been isolated and then genetically
consumed only increases when performing energetically
modified in mice. Mice exhibit validity if (1) there is a mutation
demanding tasks. Glucose metabolism is an important source of energy within neuronal mitochondria that are needed for oxidative phosphorylation and intracellular Ca2+ regulation to maintain homeostasis. Moreover, mitochondria that move within neurons are essential for processes that contribute to neurogenesis and neural plasticity including: neuronal differentiation, neurite CobbResearchLab.com/TheBackbone
in the gene that has been supported by human literature, (2) physical or behavioral phenotypes associated with the disorder are displayed, and (3) mice exhibit similar phenotypic response to therapy seen in humans. Despite construct validity, caution must be used when interpreting results because differences between human and rodent brains exist. Therefore, some results may not translate to humans, which may explain why some mouse therapies fail in preliminary
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The Backbone stages of clinical trials.
Comparative Genomics A second strategy for investigating human evolution of the brain and psychiatric disorders is the hypothesisgenerating approach. Collecting data for comparative genomics, neuroanatomical features and behaviors in human and non-human primates provides a library of information on the evolution of the human brain. As access to the fossils of archaic humans such as Neanderthals and Denisovans increases, their genome should be sequenced and included in comparative analysis. Behavioral and some neuroanatomical features unique to humans can be analyzed by visually observing physical differences between species. However, nextgeneration sequencing techniques including, Illumina, RNA-seq, chromatin immunoprecipitation coupled DNA sequencing (ChIP-seq) and de novo genome assembly can be used to identify specific genes and mutations unique to human evolution. Genomic sequences can be added to and/or downloaded from the genome-wide association study (GWAS) to examine SNPs from
schizophrenia meta-analysis. GWAS allows for the comparison highly conserved sequences within and across species as well as an indication of genetic expression levels. Once identified, the behavior of human cells and “humanized animals� can be analyzed and modified in order to target and develop novel treatments for schizophrenia.
Results
Gene-Environment Models of Schizophrenia Animal models have led to novel discoveries in the pathophysiology and potential therapeutic targets of schizophrenia. Transgenic DISC1 rodent models have been created that express phenotypic symptoms of schizophrenia seen in humans. DISC1 mice exhibit negative symptoms including depression (as measured by increased immobility in forced swim tests, as well as, tail suspension tests) and anxiety (measured by reductions in time spent in the open arms of elevated
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Evolution of the Pathogenesis of Schizophrenia
plus mazes).9.13 Pre-pulse inhibition and startle assays
measured cognitive deficits in sensorimotor gating while deficits in spatial and working memory were exhibited by delayed matching to position/non-matching to position tasks.9,14 [Li et al., 2007] Finally, positive symptoms were noted by the hyperactive ambulation of males in the open field assay.9 Phenotypes presented by DISC1 mutant mice were highly dependent on the strain of mice used, translocation site of the mutation and the sex of the animal. Immunohistochemistry of brains from post-mortem
schizophrenic patients has indicated a reduction in biomarkers, parvalbumin (PV) in GABAergic inhibitory neurons in regions of the hippocampus, anterior cingulate cortex, and the PFC.11,24,26 Other GABAergic interneuron biomarkers, like calretinin (CR) exhibit similar expression levels in schizophrenic and control humans and animals. This is significant because though comprising roughly 15% of neurons in the cortex, PV GABAergic interneurons serve an essential role in the maintenance and orchestration of normal brain function. The maturation process of these neurons is not well understood, but, accumulating evidence suggests Nmethyl-D-aspartate
receptor
(NMDAR)
signaling
influences the maturation of GABAergic interneurons. Environmental stress was also found to influence the pathogenesis of schizophrenia by
disrupting the
homeostatic physiological stress response modulated by the hypothalamic-pituitary-adrenal (HPA) axis to increase production
of
glucocorticoids.3 The
increase
in
glucocorticoid levels led to increased sensitivity to stress as well as deficits in brain maturation. Due to this,
individuals in stressful environments are prone to the development of a variety of mental disorders including schizophrenia and depression. Previous studies have examined
environmental
insults
of
psychological,
immune and pharmacological stressors in the form of maternal separation, social isolation, social defeat, viral infections and drug abuse. Restraint stress was shown to impair working memory in rodents.8 The stress of social isolation has been linked to deficits in sensorimotor Winter 2015•Spring2016
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Evolution of the Pathogenesis of Schizophrenia
gating, changes in the projections of dopaminergic
from these two hits synergistically combine to manifest
neurons, as well as, increases in despair and locomotor
symptoms of schizophrenia in adulthood.
20
activity. Finally, mice injected with viral constructs that induce innate immune responses, showed deficits in short-term
memory,
dependent
object
learning,
recognition,
social
context-
interaction
and
immunoreactivity of parvalbumin interneurons in the PFC.11 Independently both genetics and the environment can increase susceptibility to psychiatric disorders like schizophrenia. However, those with the greatest risk of
being diagnosed with schizophrenia are individuals exposed to genetic and/or environmental insults during prenatal development and adolescence. Animal models showed
that
predisposed
when DISC1
combined mice,
with
animals
genetically faced
with
environmental stressors during adolescence exhibited greater deficits in executive functioning, working memory, and increased movement disorders compared to wild-type, or DISC1/no stress cohorts.
20
Epigenetic experiments lend support to the ‘twohit’ model of schizophrenia. The first ‘hit’ occurs during the perinatal period when the embryo is exposed to genetic or environmental insults, which makes children more vulnerable to psychiatric disorders. Prenatal exogenous and endogenous environmental factors part of the ‘first hit’ include: maternal malnutrition, repeated psychological stress, exposure to infection, obstetric complications, gut microbiota and changes in prenatal endocrine
function.
These
factors,
along
with
schizophrenic candidate genes, primes the brain for neuropathological
disorders
by
(1)
increasing
neuroinflammation, (2) degenerating axons, myelin and oligodendrocytes, in addition to, (3) altering brain connectivity and morphology.
21,6
During adolescence, a
second round of environmental insults (exposure to stress, drugs, trauma and infection) unmasks the endophenotypic traits associated with schizophrenia by activating the inflammatory, oxidative and nitrosative stress pathways, mitochondrial dysfunction, apoptosis and progressive brain changes. Together, the impacts CobbResearchLab.com/TheBackbone
Coevolution of schizophrenia with the evolution of increased brain size and complexity not a human specific trait Humans, ten species of non-human primates, thirtyone non-primate eutherian mammals, two marsupials and one monotreme were used for the identification of schizophrenia related orthologues. Of the forty-two eutherian mammals, two marsupial and one monotreme genomes analyzed from the gene-disease associations compared by the Genetic Associated Database (GAD), several orthologues associated with psychiatric disorders were found.22 Orthologues were found for schizophrenia genes, as well as, genes associated with autism, ADHD, bipolar disorder, depression, anxiety, addiction, eating disorders, Alzheimer’s, Parkinson’s, migraine and stroke. GAD revealed positive selection (as measured by dN/dS mutation rates) of genes associated with schizophrenia. Both human and non-human primates (particularly catarrhines) showed similar ratios of positive selection.
Interestingly, when compared to other large brained mammals, cetaceans like the bottle-nosed dolphins and killer whales, showed higher average dN/dS ratios for psychiatric disorder orthologues.22 Taken together, this data suggests genes associated with schizophrenia are not uniquely human; rather these genes were seen in closely related apes, old world monkeys and some toothed cetaceans. This information is not particularly surprising considering
since
compared
anthropoid
to
primates
other and
mammals odontocete
cetaceans show similar evolution rates to humans. Primates and cetaceans shown a greater brain to body mass ratio and greater variations in encephalization quotients indicating a relaxation of evolutionary constrains.1 Furthermore, of the 228 genes discovered to be under positive selection in dolphins, twenty-seven were found to be associated with processes of the nervous system including synaptic plasticity, human intellectual disorders and sleep.17 Additionally, increased
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Evolution of the Pathogenesis of Schizophrenia
selection was found on genes related to mitochondria
comparative genetics has led to many advancements in
expression and metabolism.
genes and pathways involved in the disorder. Future
An increase in brain mass must be compensated by an
research must continue to have a holistic approach while
increase in energetic demands. Increased energy may
investigating the pathogenesis of schizophrenia due to
come from an increase in metabolic turnover rate,
its polytypic nature. One theory of the development of
neuronal mitochondria, reallocation of energy from
schizophrenia if the two-hit model. Environmental or
other functions or a combination of events. A positive
genetic insults during natal development can prime the
correlation between brain mass and basal metabolic
brain to become more vulnerable to psychosis.
rates among primates indicates some species do
Furthermore
compensate for larger brains by increasing metabolic
exponentially if individuals that have been primed during
12
the
risk
of
pathogenesis
increases
turnover rates. When energetic demands are not met,
development are exposed to environmental stressors
deficits occur in working memory, executive functioning
during adolescence. If so, that individual is likely to
25
manifest symptoms associated with schizophrenia in
Humans with schizophrenia display abnormalities in
adulthood. A second, more evolutionary theory for the
glucose tolerance and increased insulin resistance. Since
pathogenesis of schizophrenia is related to the
glucose in the brain is metabolized in the brain,
mitochondrial dysfunction in the brain. Essentially, if
abnormalities
suggests
mitochondria are not meeting the energy demands
schizophrenia may be associated with mitochondrial
associated with increased cognition in the human brain,
and language and an increase in psychosis is observed.
25
in
glucose
metabolism
Additional support stems from lower
individuals are prone to psychiatric disorders like
metabolic rates and lower blood flow in the frontal brain
schizophrenia. However, moving forward, one area of
during cognitive tasks, altered levels of glycolic enzymes
focus should be on characterizing the influence of AMPA
and byproducts in the brain, reduced number of
and NMDA receptors at the molecular level and in the
mitochondria
context of evolution due to their direct influence on
dysfunction.
in
the
striatum
and
hypoplastic
mitochondria in oligodendrocytes in the caudate nucleus
learning and memory.
and PFC of schizophrenic individuals compared to healthy controls. From these results, it becomes clear how mitochondrial dysfunction can lead to deficits in neurotransmission
and
synaptic
plasticity
References 1.
which
Boddy AM, McGowen MR, Sherwood CC, Grossman LI, Goodman M, & Wildman DE. 2012. Comparative analysis
increases the susceptibility to biological (oxidative) and
of encephalization in mammals reveals relaxed constraints
environmental stress.
on anthropoid primate and cetacean brain scaling. J. Evol
Discussion
Biol. 25: 981–994. 2.
Psychology Today. https://www.psychologytoday.com/
Historically, individuals suffering from schizophrenia
and other psychiatric disorders were stigmatized, dehumanized and shunned by the general population.
blog/hide-and-seek/201209/brief-history-schizophrenia 3.
interactions in psychiatric disorders. Front Behav Neurosci
evolved. With this change in perspective came novel
7: 1-13. 4.
behavioral and physiological disruptions associated with schizophrenia. Though the root of schizophrenia has not been found, use of patient samples, animal models and CobbResearchLab.com/TheBackbone
Cash-Padgett T, & Jaaro-Peled H. 2013. DISC1 mouse models as a tool to decipher gene-environment
Fortunately, the way society viewed schizophrenia has concepts and methods to identify the neuroanatomical,
Burton N. 2012. A brief history of schizophrenia.
Cheng A, Hou Y, & Mattson MP. 2010. Mitochondria and neuroplasticity. ASN NEURO 2(5): e00045.
5.
Crow TJ. 2000. Schizophrenia as the price that Homo sapiens pays for language: a resolution of the central
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The Backbone paradox in the origin of the species. Brain Res Rev 31 (2): 6.
118-129.
central nervous system to body metabolism in vertebrates: its constancy and functional basis. Am J Physiol 241: R203–
programming of schizophrenia: select mechanisms.
R212. genome provides evidence for adaptive evolution of
intergroup relations through upregulated in-group
nervous system genes and a molecular rate slowdown. P
empathy, cooperation, conformity, and defense. Biol
Roy Soc B-Biol Sci 279(1743): 3643–3651. 18. Millar JK, Wilson-Annan JC, Anderson S, Christie S, Taylor
Gamo NJ, Duque A, Paspalas CD, Kata A, Fine R, Boven L,
MS, Semple CA, Devon RS, St Clair DM, Muir WJ, Blackwood
Bryan , Lo T, Anighoro K, Bermudez L, Peng K, Annor A, Raja
DH, & Porteous DJ. 2000. Disruption of two novel genes by a
A, Mansson E, Taylor SR, Patel K, Simen AA, & Arnsten AFT.
translocation co-segregating with schizophrenia. Hum Mil
2013. Role of disrupted in schizophrenia 1 (DISC1) in stressinduced prefrontal cognitive dysfunction. Transl Psychiat 3: 9.
17. McGowen MR, Grossman LI, & Wildman DE. 2012. Dolphin
De Dreu CKW & Kret ME. 2015. Oxytocin conditions
Psychiat 15: 1-9. 8.
16. Mink JW, Blumenschine RJ, & Adams DB (1981) Ratio of
Debnath M, Venkatasubramanian G, & Berk M. 2015. Fetal Neurosci Biobehav R 49: 90-104.
7.
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Genet 22:1415-23. 19. National Institute of Mental Health. What is Schizophrenia?
1-7.
http://www.nimh.nih.gov/health/topics/schizophrenia/
Gomez-Sintes R, Kvajo M, Gogos JA, & Lucas JJ. 2014. Mice
index.shtml
with a naturally occurring DISC1 mutation display a broad
20. Niwa M, Jaaro-Peled H, Tankou S, Seshardi S, Hikida T,
spectrum of behaviors associated to psychiatric disorders.
Matsumoto Y, Cascella NG, Kano S, Ozaki N, Nabeshima T, &
Front Behav Neurosci 8: 1-12.
Sawa A. 2013. Adolescent stress-induced epigenetic control
10. Grossman LI, Wildman DE, Schmidt TR, & Goodman M. 2004. Accelerated evolution of the electron transport chain in anthropoid primates. Trends Genet 20(11): 578-585. 11. Ibi D, Nagai T, Koike H, Kitahara Y, Mizoguchi H, Niwa M, Jaaro-Peled H, Nitta A, Yoneda Y, Nabeshima T, Sawa A, &
Yamada K. 2010. Combined effect of neonatal
of dopaminergic neurons via glucocorticoids. Science 339: 335-339. 21. Roberston GS, Hori SE, & Powell KJ. 2006. Schizophrenia: an integrative approach to modelling a complex disorder. J Psych Neurosci 31(3): 157-67.
22. Ogawa LM & Vallender EJ. 2014. Evolutionary conservation
Immune activation and mutant DISC1 on phenotypic
in genes underlying human psychiatric disorders. Frontiers
changes in adulthood. Behav Brain
in Human Neuroscience 8: 1-10.
Res 206: 32-37. 12. Isler K, & van Schaik CP. 2006. Metabolic costs of brain size evolution. Biol Letters 2(4), 557–560. 13. Kivimae S, Martin PM, Ruan Y, Heberlein U, Rubenstein JLR,
23. Wu EQ, Birnbaum HG, Shi L, Ball DE, Kessler RC, Moulis M, & Aggarwal J. 2005. The economic burden of schizophrenia in the United States in 2002. J Clin Psychiatry 66: 1122-29. 24. Lewis DA, Hashimoto T, & Volk DW. 2005. Cortical inhibitory
& Cheyette BNR. 2011. Abnormal behavior in mice mutant
neurons and schizophrenia. Nat Rev Neuroscience 6: 312-
for the Disc1 binding partner, Dixdc1. Transl
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Psychiatry 1: 1-5. 14. Kvajo M, McKellar H, Arguello PA, Drew LJ, Moore H,
MacDermott AB, Karayiorgou M, & Gogos JA. 2008. A
25. Goncalves VF, Andreazza AC, & Kennedy JL. 2015. Mitochondrial dysfunction in schizophrenia: an evolutionary
perspective. Hum Genet 134(1):13-21.
mutation in mouse Disc1 that models a schizophrenia risk
26. Brisch R, Bielau H, Saniotis A, Wolf R, Bogerts B, Krell D,
allele leads to specific alterations in neuronal architecture
Steiner J, Braun K, Krzyzanowska M, Jankowski Z, Kaliszan
and cognition. PNAS 105: 7076-81.
M, Bernstein HG, & Gos T. 2015. Calretinin and parvalbumin
15. Li W, Zhou Y, Jentsch JD, Brown RAM, Tian X, Ehninger D,
in schizophrenia and affective disorders: a mini-review, a
Hennah W, Peltoneon L, Lonnqvist J, Huttunen MO, Kaprio J,
perspective on the evolutionary role of calretinin in
Trachtenberg JT, Silva AJ, & Cannon TD. 2007.
schizophrenia, and a preliminary post-mortem study of
Specific developmental disruption of disrupted-in-
calretinin in the septal nuclei. Front Cell Neurosci (9): 393.
schizophrenia-1 function results in Schizophrenia-related phenotypes in mice. PNAS 104: 18280-85.
CobbResearchLab.com/TheBackbone
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Mental Disorders Across Geographical Spaces
GENETICS & EPIDEMIOLOGY
How might the genetic identification of mental disorders vary across geographical spaces, cross culturally and through time? Sedera Moore1,2
1W.
Montague Cobb Research Laboratory, Howard University
Genetics are used to link and identify a variety of functions that occur in the body. Moreover, genetics can be utilized to analyze ailments, such as the various mental disorders that people suffer from daily. While the diagnosis of mental disorders is not a rare
concept, there are dissimilarities in the causes of people being diagnosed. However, before discussing variations in the genetic identification of mental disorders, it is important to have an understanding of what mental disorders are. This paper will introduce the concept of mental disorders and provide several examples in regards to the variation of mental disorders across geographical spaces, cross culturally, and through time relating to genetic identification, exposed environment, and specific ethnic groups.
Introduction Mental disorders are illnesses that stem from a malfunction in the brain. For the purpose of simplification, we will first view the term mental disorder as two separate entities. The word “mental” relates to the mind and one’s intellectual activity.
The term “disorder” conveys the presence of an irregularity or disturbance. Combining these separate definitions, a mental disorder is an irregularity or disturbance. How might the genetic identification of mental disorders vary across geographical spaces, cross culturally and through time? Mental disorders are not uniformly dispersed across the globe. The magnitude of people diagnosed with mental disorders varies across geographical spaces, cross culturally, and throughout generations. A prime example of this variation in the genetic identification of mental disorders can be seen in in an article titled, “The role of the genetic variation in the causation of mental illness: an evolution-informed framework.
Genetic Variation: An Evolution-Informed Network According to this article, mental illness usually begins to emerge early in the reproductive age and is linked to a considerable amount of procreative disadvantages. In theory, these procreative disadvantages observed by mental illnesses should lead to these disorders having strong negative selection pressures. On the contrary, mental disorders appear to be a
CobbResearchLab.com/TheBackbone
common diagnosis; specifically in twin studies which show a strong correlation between the disease’s etiology and its genetic contribution. This article discussed a proposed hypothesis for identifying mental illness, suggesting that the genetic contribution to mental illness results from geneenvironment interactions and rare genetic variants.
Depression and Gene-environment Interactions An example where mental disorders may be contributed with certain environmental influences can be seen with depression. Depression is a mental health condition that underlies a mood disorder causing severe sadness and affecting a person’s normal daily functionings.
Recent
discoveries show that individuals with one or two short alleles of the serotonin transporter gene promoter polymorphism (5-
HTTLPR) have an increased susceptibility to depression when encountering stressful life events.15 These results appeared when the 5-HTTLPR gene, stress, and depression were observed simultaneously over a course of 5 years prior to the onset of the depression. Depression severity displayed episodes at an average duration of 24 months and were associated with loss, threat, and humiliation. Overall, the outcome of this study revealed that the depression most likely stems from life events that occurred after the onset of the disorder.
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Increased Life Expectancy and Alzheimer’s Disease Throughout time, life expectancy has increased globally. According to the National Institute on Aging, “The dramatic increase in average life expectancy during the 20th century ranks as one of society’s greatest achievements. Although most babies born in 1900 did not live past age 50, life expectancy at birth now exceeds 83 years in Japan—the current leader—and is at least 81 years in several other countries. Less developed regions of the world have experienced a steady increase in life expectancy since World War II, although not all regions have shared in these
improvements. One notable exception is the fall in life expectancy in many parts of Africa because of deaths caused by the HIV/AIDS epidemic. The most dramatic and rapid gains have occurred in East Asia, where life expectancy at birth increased from less than 45 years in 1950 to more than 74 years today.” There is possibly a positive correlation between an increase in some mental disorders and higher life expectancies. As humans continue to live longer, they can be affected by different mental disorders later on in life. This is seen in people with Alzheimer’s disease. Alzheimer’s disease is a degenerative
brain’s neurons.
The targeted age group for Alzheimer’s
disease begins around age 65. A study done at Duke University determined that there has been approximately a fourfold increase in the rate of people being diagnosed with Alzheimer’s: escalating from 35/1000 in 1991 to a striking 135/1000 in 1999. When isolating this data by racial group and gender, the Alzheimer’s disease rate increased by a factor of 4.7 in African American women in comparison to a factor of 2.3 for White women. There is currently an estimated 5.1 million people living with Alzheimer’s disease in the United States for 2015. Due to an increase in life expectancy through time, this disease is expected to triple in its effect rising from 5.1 million to an anticipated 13.8 million by 2025.
Racial Health Disparities and Schizophrenia
Mental Disorders Across Geographical Spaces
counterparts. Schizophrenia is a severe brain disorder in which
people interpret reality abnormally. Moreover, schizophrenia may result in some combination of hallucinations, delusions, and extremely disordered thinking and behavior. A Child Health and Development Study examined the schizophrenia health disparity through study subjects conceived from black and white women from a common area. These women were enrolled during pregnancy at the Alameda County Kaiser Permanente Medical Care Plan clinics over the course of 6 years (1959-1966). During this time frame, there were 19,044 live births and of these live births 12,094 progeny were selected to be observed in the study. These offspring were charted for 16 years (1981-1997) with the purpose of addressing if African Americans have higher rates of schizophrenia than whites. In addition, the study looked into whether this expected risk increase is arbitrated by the socioeconomic status (SES) background of the offspring. The title of this study was “Race and risk of schizophrenia in a US birth cohort: another example of health disparity?” An analytic sample of 2,128 African American women and 4,508 White women were used for the data comparison. The fathers of these children were mainly the same race as the mothers (98% for African Americans and 92% for Whites). The remaining offspring were excluded from data analysis for
reasons including; death, adoption, loss to follow up, and exclusion of sibling information. Thus, the resultant sample consisted of 6,636 women; approximately 68% White and 32% African American. From this sample 62 cases of schizophrenia spectrum disorder (SSD) were diagnosed; 32 African Americans (22 men and 10 women) and 30 Whites (20 men and 10 women). Moreover, the study states that “The proportion of SSD cases diagnosed with schizophrenia was higher among African Americans (23/32) than among whites (15/30). Within diagnostic categories, the mean age at index treatment was similar for African American and white cases
(22.5 and 23.9 years for schizophrenia, 26.3 and 26.8 years for other SSDs, respectively).” When comparing these two groups, variation is present in the magnitude of people affected by this mental disorder by
Similar to Alzheimer’s disease, variations are seen in the
race. Additionally, the socioeconomic status background of
diagnosis of mental illness when looking at a correlation
these diagnosed groups were observed. There was minimal
between race and the mental disorder schizophrenia.
correlation seen between in the higher percentage of African
Specifically, certain health disparities are observed between
American’s diagnosed with schizophrenia in comparison to
blacks and whites, in terms of schizophrenia, and studies show
whites and socioeconomic status. Prior to factoring in
that blacks are more likely to be diagnosed than their white
socioeconomic status (SES) African Americans were 3-fold
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Mental Disorders Across Geographical Spaces
more likely to get schizophrenia than whites; however,
CACNA1C gene is highly expressed in the brain. When tested
succeeding the SES factorization, African Americans were 2-
for genetic variation, it was proposed that the representative
fold more times as likely. Based on this information,
SNP (the rs2159100 for rs1006737) plays a role in the
socioeconomic status may partially coincide with race when
magnitude at which the CACNA1C gene is expressed.
observing increased risks of schizophrenia.
According to the results, “carriers of the risk-associated genotype (AA) had highest expression, with heterozygotes
Genetic Identification of the Five Spectrum Disorders
(GA) having intermediate expression and the common allele carriers (GG) having the lowest expression (P = .002 for linear
Furthermore, another study that looked into the genetic identification of mental disorders focused on five specific mental disorders; autism spectrum disorder, attention deficithyperactivity disorder, bipolar disorder, major depressive
disorder, and schizophrenia. This study analyzed singlenucleotide polymorphism (SNP) data for 61,220 people of European ancestry; 33,332 cases and 27,888 controls, for the purpose of characterizing the allelic contribution of each disorder. Significant data was observed on a number of loci theoretically linked to schizophrenia and bipolar disorder in previous studies. The loci were located near MIR137 (microRNA 137), TCF4 (transcription factor 4), the MHC region on chromosome 6, and SYNE1 (spectrin repeat containing, nuclear envelope 1). Based on results from polygenic risk scores the loci showed cross disorder associations; particularly
between adult-onset disorders. Moreover, Genome Wide Association Studies (GWAS) produced data that linked 4 SNPs to bipolar disorder (rs937l601, rs10994397, rs4765914, and rs12576775) and 10 SNPs to schizophrenia (rs2021722, rs1625579, rs12966547, rs7914558, rs11191580, rs7004633, rs10503253, rs17662626, and rs17512836). Additionally, a meta-analysis done for the five disorders revealed results for regions at a genome-wide significance threshold (p<5×10−8). The SNPs on chromosome 3 (rs2535629) and chromosome 10 (rs11191454 and rs2799573) showed that these SNPs had a supported effect for all five of the disorders (autism spectrum disorder, attention deficithyperactivity disorder, bipolar disorder, major depressive disorder,
and
schizophrenia).
The
meta-analysis
for
chromosome 12 revealed the rs1024582 SNP specific to bipolar disorder and schizophrenia.
Bipolar and Schizophrenia Disorder CANA1C Gene Likewise, a different study looked into a bipolar and schizophrenia disorder risk gene CACNA1C: where the
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regression analysis).” Additionally, there was dissimilarity in the CACNA1C gene expression in terms of race/ethnicity. This was the case for whites and African Americans. The study concluded that this variation is possibly a result of a difference in minor allele frequency (26% for whites and 45%, for African Americans). The risk associated alleles are associate with increased levels of CACNA1C mRNA. Furthermore, the study shows that calcium channel defects may add to the genetic cause of bipolar disorder and schizophrenia by changing the functional activity of the brain’s electrical systems. This data corresponds to the COMT, GRM3, BDNF, and DISC1 genes that have been associated with neural circuitry diagnosis and pattern effects. The article states that, “Investigations of the N-back working memory task have shown that patients with schizophrenia and their healthy siblings have increased prefrontal cortical activity for a given
level of performance, suggesting that inefficiency in this circuitry is heritable and a good intermediate phenotype related to genetic risk for schizophrenia. Analogous studies have been performed among patients with bipolar disorder using neuroimaging tasks that target mood circuitry in the temporal lobe. Other studies have targeted serotonin signaling genes and have found that healthy subjects who are carriers of the short allele of the serotonin transporter, the target of drugs that treat the mood symptoms of bipolar disorder, have higher ratings of anxiety and depression, and have greater activation of the limbic circuitry, similar to this data.”
These results indicate that there is a genetic factor in the diagnosis of schizophrenia and bipolar disorder. Not only did the patients already diagnosed with schizophrenia have increased prefrontal cortical activity, so did their undiagnosed healthy siblings. The association of this increased prefrontal cortical activity between the patients and their siblings shows that schizophrenia may be linked to a hereditary source. Moreover, healthy people that carried the short allele of the serotonin transporter (target of drugs that treat bipolar disorder) showed increased levels of anxiety and depression.
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Mental Disorders Across Geographical Spaces
This is indicative of the short serotonin transporter allele
physical interaction was found between G72 and D-amino-acid
playing a role in bipolar disorder. Bipolar disorder displays
oxidase (DAO). DAO is expressed in the human brain, where it
symptoms of high anxiety and depression levels. Linking this to
oxidizes D-serine, a potent activator of NMDA glutamate
short allele builds a connection to the genetic identification of
receptor. Co-incubation of G72 and DAO in vitro revealed a
the bipolar disorder.
functional interaction with G72 enhancing the activity of DAO.
Bipolar and Schizophrenia Disorder at several Genes Another study looked into the genes responsible for schizophrenia and bipolar to attribute them as implications of psychiatric disease studies. The NRG1 gene has been linked to schizophrenia following multiple studies that provided
evidence supporting this association. These studies include; a systematic study of 8p21-22 and a multi-marker haplotype at the 5’ end of the NRG1 gene. The binding protein dysbindin (DTNBP1) has also been implicated as being associated with schizophrenia, however, studies of dysbindin in association with bipolar disorder have not displayed significant results. According to the article researchers, “found no significant associations in bi-polar disorder as a whole but found modestly significant evidence for association in the subset of bipolar cases with predominantly psychotic episodes of mood disturbance with a similar pattern of findings to that seen by
this group in schizophrenia. His finding suggests that variation in dysbindin confers risk to psychosis rather than to mood disorders per se, although replication is required.” The results from the binding protein dysbindin shows the variation in the genetic identification of mental disorders. Dysbindin marks significant outcomes in terms of the mental disorder schizophrenia however, it this is not the case for bipolar disorder. This may be a consequence of different mechanisms attributing to the mental disorders. Similarly, the G72(DAOA)/G30 locus, which is best associated with bipolar disorder, shows specific variants connected to the disorder. Previous studies of the G72(DAOA)/ G30 locus were performed by association mapping in the linkage region on chromosome 13q22-34. Similar results were observed between French Canadian and Russian populations at two genes; the G72 (D-amino acid oxidase activator) and the G30 gene (DAOA antisense RNA 1). According to the study, “They found associations in French Canadian and Russian populations in markers around two novel genes, G72 and G30, which are overlapping but transcribed in opposite directions. G72 is a primate-specific gene expressed in the caudate and amygdala. Using yeast two-hybrid analysis, evidence for
CobbResearchLab.com/TheBackbone
Consequently,G72 has now been named D-amino-acid oxidase activator
(DAOA)
Associations
between
DAOA
and
schizophrenia have subsequently been reported in samples from Germany, China, Ashkenazi Jews, and both the United States and South Africa, as well as a small sample of very early onset psychosis subjects from the United States. There is no consensus concerning the specific risk alleles or haplotypes across studies.” Likewise, this study also looked at the effects of the DISC1 gene in schizophrenia. This gene was associated with broad phenotypic results in connection to bipolar disorder, schizophrenia, and recurrent depression. In a balanced chromosomal translocation (1;11)(q42;q14.3), two DISC1 genes were disturbed (the DISC1 and the DISC2 gene) at chromosome 1. The article states that, “A small pedigree has recently been reported in which a 4bp deletion in exon 12 of DISC1 cosegregates with schizophrenia and schizoaffective disorder.” The final gene discussed in this article was the brain derived neurotrophic factor gene (BDNF) in association with
mood disorders; specifically bipolar disorder. It states in the text, “Only one frequent, non-conservative polymorphism in the human BDNF gene has been identified, a single nucleotide polymorphism (SNP) at nucleotide 196 within the 5’ pro-BDNF sequence that causes an amino acid substitution of valine to methionine at codon 66 (Val66Met) and may have a functionally relevant effect by modifying the processing and trafficking of BDNF.” Three positive results were recorded in a family based association study in conjunction with the BDNF gene. The family was Caucasian of European-American origin and consisted of two bipolar adults and one small onset child.
Each family member displayed an over-transmission of the Val66Met allele. According to these results, this variant may attribute to the susceptibility of bipolar disorder in certain individuals.
Variant Genetic Identification of OCD Correspondingly, another study looked into the genetic identification of obsessive compulsive disorder (OCD). OCD is a mental health disorder categorized by unreasonable thoughts and fears (obsessions) that lead to repetitive behaviors
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4.
"Living Longer." National Institute on Aging. US. Department of Health and Human Services, Oct. 2011. Web. 18 Apr. 2015. <http://www.nia.nih.gov/research/ publication/global-health-and-aging/living-longer>.
5.
"Alzheimer's Disease & Dementia | Alzheimer's Association." Alzheimer's Disease & Dementia | Alzheimer's Association. N.p., n.d. Web. 27 Apr. 2015.
6.
Taylor, Donald H., Jr., Frank A. Sloan, and Murali Doraiswamy. "Marked Increase in Alzheimer's Disease Identified in Medicare Claims Records Between 1991 and 1999." Marked Increase in Alzheimer's Disease Identified in Medicare Claims Records Between 1991 and 1999. The Geneological Society of America3, 3 Sept. 2003. Web. 26 Apr. 2015
7.
"Latest Alzheimer's Facts and Figures." Latest Facts & Figures Report. Alzheimer's Association, 17 Sept. 2013. Web. 26 Apr. 2015.
8.
"Schizophrenia." Definition. Mayo Clinic, 24 Jan. 2014. Web. 22 Apr. 2015. <http://www.mayoclinic.org/diseasesconditions/schizophrenia/basics/definition/con20021077>.
9.
Bresnahan, M., M. D. Begg, A. Brown, C. Schaefer, N. Sohler, B. Insel, L. Vella, and E. Susser. "Race and Risk of Schizophrenia in a US Birth Cohort: Another Example of Health Disparity?" International Journal of Epidemiology 36.4 (2007): 751-58. Web. 26 Apr. 2015.
daily functioning. The goal of this study was to “determine the role of genetic variation of SLC1A1 in OCD in a large casecontrol study and to better understand how SLC1A1 variation affects functionality.” This experiment consisted of 987 people; 325 obsessive compulsive disorder subjects and 662 ethnically and sex-matched controls. Significant results were observed in association of 3 genetic markers (rs3087879, rs301430, and rs7858819) in obsessive compulsive disorder using haplotype analysis. A haplotype labeled “H4” was nearly twice more common in OCD cases than in the control cases; the H4 OCD cases had a haplotype frequency of 9.4% compared to the controls haplotype frequency of 5.1%. Also, the rs393331 SNP was associated with an OCD-hoarding subphenotype as assessed by 2 independent, validated scales. This correlates with SLC1A1 gene expression and shows the association of the quantative trait loci with obsessivecompulsive disorder.
Conclusion There is evident variation in the genetic identification of mental disorders across geographical spaces, cross culturally, and through time. Studies have shown that an abnormal production of certain genes are recognized as a possibly cause of increasing a person’s susceptibility to some mental disorders. Additionally, studies have presented variation in the racial/ethnic groups affected by a mental illness. Specifically, multiple studies have recognized African Americans as a primary victims of schizophrenia. Moreover, the exposed environment of individuals have been linked to their predisposition to mental illness. Hopefully, future studies can further target the mechanisms causing mental disorders and acquire prevention techniques.
References 1.
Uher, R. "The Role of Genetic Variation in the Causation of Mental Illness: An Evolution-informed Framework." Molecular Psychiatry 14.12 (2009): 1072-082. 25 Aug. 2009. Web. 19 Apr. 2015.
2.
"Depression." NAMI: National Alliance on Mental Illness. N.p., n.d. Web. 25 Apr. 2015.
3.
Monroe, Scott M., and Mark W. Reid. "Gene-Environment Interactions in Depression Research: Genetic Polymorphisms and Life-Stress Polyprocedures." Psychological Science 19.10 (2008): 947-48. Web. 25 Apr. 2015.
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Mental Disorders Across Geographical Spaces
10. "Identification of Risk Loci with Shared Effects on Five Major Psychiatric Disorders: A Genome-wide Analysis." The Lancet 381.9875 (2013): 1371-379. Web. 25 Apr. 2015. 11. Bigos, K. L., V. S. Mattay, J. H. Callicott, R. E. Straub, R. Vakkalanka, B. Kolachana, T. M. Hyde, B. K. Lipska, J. E. Kleinman, and D. R. Weinberger. "Genetic Variation in CACNA1C Affects Brain Circuitries Related to Mental Illness." Archives of General Psychiatry 67.9 (2010): 93945. Web. 27 Apr. 2015. 12.
Craddock, N. "Genes for Schizophrenia and Bipolar Disorder? Implications for Psychiatric Nosology." Schizophrenia Bulletin 32.1 (2005): 9-16. Web
13. "Obsessive-compulsive Disorder (OCD)." - Mayo Clinic. N.p., n.d. Web. 27 Apr. 2015. 14. Wendland, J. R., P. R. Moya, K. R. Timpano, A. P. Anavitarte, M. R. Kruse, M. G. Wheaton, R. F. RenPatterson, and D. L. Murphy. "A Haplotype Containing Quantitative Trait Loci for SLC1A1 Gene Expression and Its Association With Obsessive-Compulsive Disorder." Archives of General Psychiatry 66.4 (2009): 408-16. Web. 23 Apr. 2015. 15. Caspi, A., Sugden, K., Moffitt, T.E., Taylor, A., Craig, I.W., Harrington, H., McClay, J., Mill, J., Martin, J., Braithwaite, A., and Poulton, R. Influence of life stress
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Prevalence and Anatomical Evidence of Treponemal Infection
GENETICS & EPIDEMIOLOGY
Prevalence and Anatomical Evidence of Treponemal Infection in the Cobb Collection Nicholas Guthrie1,2
1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
Understanding the health of our ancestors can give us a viewpoint to understand present-day health conditions. The relationship of African American (AA) ancestry to infectious disease status has not been extensively studied. This study aims to characterize AA health by osteologically investigating the microbial effects of Treponema palladium (TP) bacteria on AAs who died in the greater DC metropolitan area from 1930 to 1969. The gram-negative, spiral shaped bacteria has four pathogenic subspecies; pallidum, pertenue, endemicum, and carateum, causing syphilis, yaws, endemic syphilis, and pinta, respectively. To confirm TP infection, we will use the Cobb Collection autopsy and clinical records in conjunction with scientific methods of microscopic analysis, microbial analysis, and various imaging techniques. Our expected results will yield better understanding of the pathology of TP and its contribution to AA morbidity and mortality during the era of overt racial segregation to the present day.
Introduction
with significant clinical and autopsy data including age,
The W. Montague Cobb Research Laboratory is a rare resource for research on a unique human skeletal and bioarchaeological collection. The Cobb Collection is named after the first African American biological anthropologist
and
renowned
Chair
of
Howard
University’s Anatomy Department, Dr. William Montague Cobb. His research aimed to create a less racialized perspective on human life and showed the impact race could have on the heath of a person, showing that racism in America had an impact on the health and livelihood of African Americans.1 The Cobb collection contains approximately 699 de-fleshed human cadavers that were donated and collected for scientific purposes during the
majority of the 20th century, and is unique in that it is the only skeletal collection residing at a historically black university. The Cobb Collection has undergone very little research and lends itself to novel insights about the lives and deaths of Americans living in the Washington, D.C. area. This affords this research a unique opportunity to become a reference on African Americans from the late 19th to mid- 20th Century. Approximately 83% of the Cobb Collection is African American and contains records CobbResearchLab.com/TheBackbone
sex, place of death, cause(s) of death, and morbidity.2 Health disparities for African Americans include differences in rates of cardiovascular diseases, diabetes, periodontitis and life expectancy relative to whites. In addition, populations living in poverty also exhibit health issues including asthma attacks and obesity. Since a greater percent of African-descendant people continue to live below the poverty line, a duality of risk factors exist for this population. Furthermore, previous research hints at differences in health between Africandescendant people in Africa and the United States, suggesting that variation in environment, such as slavery and poverty, affects general health.3
Treponemes (TP) are helically coiled, corkscrewshaped cell with a double membrane system. The spirochete has two flagella that originate at both ends of the organism and point inward along its length, and are contained in the periplasmic space between the inner and outer membranes, which enable motility. The pathogenic treponemes’ classification is based primarily upon the clinical manifestations of the respective diseases they cause: Treponema pallidum subsp. Winter 2015•Spring2016
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Prevalence and Anatomical Evidence of Treponemal Infection
pallidum is the causative agent of venereal syphilis; T
pallidum subsp. Pertenue causes yaws; T pallidum subsp. endemicum causes endemic syphilis; and T carateum is associated with pinta. -These microbes are generally transmitted by close non-venereal contact, with the exception of venereal syphilis. DNA hybridization shows high genetic relation between the species, but overall understanding
of
the
pathogenesis
of
human
treponematoses is limited. The inability to grow these spirochetes in vitro and limited viability in vivo requires expensive
and
laboratory
difficult
animals.
ultrastructure
continual
Also,
permits
only
their
propagation
fragile
limited
in
cellular
FIGURE 5: RENAL OSTEODYSTROPHY X-RAY24
mechanical
manipulation of the pathogen, in order to preserve its integrity and viability.7 Diagnosis of treponemal disease relies heavily on its clinical manifestation. The patient's symptoms and signs, in combination with knowledge of the epidemiological context of human treponematoses aid in a positive diagnosis. Treponemal disease manifests in three stages: primary, secondary, and tertiary. In all stages, tissue
FIGURE 1: Rothschild figure showing superior view of the cranium and lateral view of tibiae with prominent periosteal reactions and periosteal striations23
damage is caused by both localized and systemic inflammation. Primary infection produces mild, nondiagnostic lesions, secondary stage infection adds osteitis, or inflammation of the inner structures of bone
FIGURE 6: EXAMPLE OF LYTIC BONE LESION25
(though it can heal spontaneously), and tertiary infection shows distinctive skeletal lesions and osteomyelitis, an infection originating in the marrow. Neurological affects do occur but symptoms may not become apparent until years after infection, though infection of the central nervous system occurs relatively early. In the laboratory, the available diagnostic tools for detection are direct
detection of treponemes in biological specimens, through including molecular assays and serological tests is desirable.4
Methods and Procedures In order to screen the Cobb Collection for TP, the database of medical records was evaluated for TP cause of death. Three members of the collection, CC18, CC22, CC109, were then inspected for TP bone lesions using CobbResearchLab.com/TheBackbone
FIGURE 2: Rothschild figure showing lateral view of ulna and tibiae with gummatous lesions but minimal periosteal striations
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FIGURE 3: Lateral view of CC18 radius showing periosteal reactions and prominent cortical thickening and periosteal striations
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Prevalence and Anatomical Evidence of Treponemal Infection
FIGURE 5: Lateral view of CC109 radius showing a large gummatous lesion
Conclusion Through screening, TP infection was visually confirmed in the 3 subjects. While a sample size of 3 does not allow for many conclusions to be drawn about the health conditions of the time period, additional screening of the Cobb Collections can be conducted in the future. The TP infection lesions are not unique to TP infection. For example, Mycobacterium tuberculosis, the causative agent of tuberculosis, is shown to cause bone lesions in late stages of infection.5 Therefore, CC members with similar bone degradation should be screened for TP infection using DNA extraction and molecular diagnosis. FIGURE 4: Lateral view of CC22 radius showing a large gummatous lesion
methods from Rothschild et al (1994).6 All surfaces of
References 1.
COBB." The Backbone 1.1 (2015): n. pag. Web. 10 Apr.
skeletal remains were visually examined to identify all occurrences of bone alterations throughout each
Kamei, Yah. "THE LIFE OF DR. WILLIAM MONTAGUE 2015.
2.
Cross, Christopher N. "APPLYING NEXT GENERATION
skeleton and variation from normal smooth cortical
SCIENCE
surfaces was noted. Treponemal disease was specifically
LABORATORY." The Backbone 1.1 (2015): n. pag. RSS.
recognized on the basis of periosteal reaction and osteitis.
STANDARDS
IN
THE
COBB
RESEARCH
Web. 10 Apr. 2015. 3.
Gomez, M. "USING THE CONTENTS OF THE COBB RESEARCH LABORATORY TO UNDERSTAND TODAY'S HEALTH DISPARITIES." The Backbone 1.1 (2015): n. pag.
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Web. 10 Apr. 2015.
4.
Harper, K. N., Zuckerman, M. K., Harper, M. L., Kingston, J. D. and Armelagos, G. J. (2011), The origin and antiquity of syphilis revisited: An Appraisal of Old World preColumbian evidence for treponemal infection. Am. J. Phys. Anthropol., 146: 99–133. doi: 10.1002/ajpa.21613
5.
Haas, CJ. "Molecular Evidence for Different Stages of Tuberculosis in Ancient Bone Samples from
6.
Rothschild, BM. "Treponemal Disease Revisited: Skeletal Discriminators for Yaws Bejel, and Venereal Syphilis." Clinical Infectious Diseases (1994): n. pag. Web.
7.
Giazani, Lorenzo, and Sheila A. Lukehart. “The Endemic Treponematoses.” Clinical Microbiology Reviews 27.1 (2014): 89–115. PMC. Web. 11 Apr. 2015.
8.
Hungary." National Center for Biotechnology Information. U.S. National Library of Medicine, n.d. Web. 10 Apr. 2015.
9.
Radolf, Justin D. Treponema. U.S. National Library of Medicine, n.d. Web. 10 Apr. 2015.
CobbResearchLab.com/TheBackbone
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BIOHISTORIES The Story of CC18
The Backbone
Cobb Collection Short Biohistory
The Story of CC18 Theodore Meadough1,2 Jermaine E. Robertson 1,2 1Summer
Medical and Dental Education Program Scholars, W. Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University 3Department of English, University of California
Editor’s Note
This series of biographical sketches were authored by the 2015 class of the Howard University branch of AAMC’s Summer Medical Dental Education Program (SMDEP) at the W. Montague Cobb Research Laboratory. The students were assigned a Cobb Collection (CC) individual and conducted research about that individual. The papers were reviewed by The Backbone editorial team and the name of the CC individual was redacted. All other factual information was retained.
CC18 was born in South Carolina, approximately in the year of 1903. It can be speculated CC18’s birthplace was Rock Hill, South Carolina as both his parents were born there. Although slavery was abolished in 1865, during this time African Americans were faced with many obstacles. Due to being born in the South, CC18 was not only introduced to an atmosphere full of violence, but an environment that was segregated. Between the end of the nineteenth-century and early twentieth century African Americans had a difficult time establishing their presence in a predominantly White society. Blacks were terrorized for attempting to access the same resources to which Whites were privileged. Traumatizing events such as being spat on, raped, burned, and lynched were commonplace incidents that victimized Blacks in the South (Washington). Violence was not the only issue for African Americans living in the South; Jim Crow Laws, laws that were racially discriminant and disenfranchised African Americans, added more harsh treatment to their cruel circumstances. In a legal sense African Americans were “separate but equal,” however this was not their reality (Dred Scott). Opportunities and privileges were not the same for Blacks as for Whites. Jim Crow Laws embodied White privilege as they enforced racism through segregation of public schools, public transportation, and public places such as restrooms, restaurants, and drinking fountains (SandovalStrausz).Southern states were also struggling with issues such as The Great Migration and The Great Depression. The Great Migration was a time period where one and a half million African Americans relocated from the south into western and northern states in quest of equality, CobbResearchLab.com/TheBackbone
along with escaping unemployment and oppression (The Great Migration). Even though many families migrated in hopes of a decent living, the stock market crashed in October 1929 sparking The Great Depression (Romer). By this time CC18 was about twenty-five years old and experiencing the economic pressures of banks closing down, cotton prices dropping, and a low number of job opportunities. Due to South Carolina’s economy being depressed prior to The Great Depression, the stock market crashing only worsened the socioeconomic conditions of the state (The New Deal). Despite the crash, Washington, DC suburbs continued to expand which may have been the reason CC18 moved to the district in 1931 (B.3.3 Modern Period). Although it is feasible that CC18 may have relocated in desire of a better lifestyle, he was soon faced with another impediment. Even with forward progression, African Americans did not benefit from the District of Columbia’s Federal expansion (B.3.3 Modern Period). It was difficult to make ends meet and even more so for Williams because he worked as a laborer. Having to work long hours, tirelessly for low pay could have been a daily source of stress worsening his already jeopardized health. CC18 was suffering from syphilis presumably in its late stages since he would die a short time after moving to Washington, DC. Along with extensive hours, working conditions were severely hazardous for all blue-collar workers during the early 1900’s (Tomyn, Media). As a laborer, CC18 was at risk of death every minute on the job. He was regularly exposed to toxic fumes and excessive heat while working in small spaces with improper ventilation. Working in these conditions did not Winter 2015•Spring 2016
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The Backbone
aid in his overall health at all. CC18 died at the young age of 28, February 18th, 1932 in Gallinger Municipal hospital due to his syphilis infection. Syphilis is a highly contagious bacterial infection that is primarily spread by sexual contact. Syphilis may also be transmitted from mother to fetus during pregnancy, labor, or breastfeeding, resulting in congenital syphilis. Infants with congenital syphilis may have symptoms at birth, but it is not unusual for symptoms to develop later in life. Syphilis is caused by the spirochete bacterium Treponema pallidum. Even the very first sign of syphilis, designated to be a painless sore, can be easily confused for an ingrown hair, zipper cut, or any other seemingly innocuous bump. Syphilis infections in adults can be divided into different stages: primary, secondary, latent, and tertiary. The primary stage of syphilis is characterized by one or more painless ulcers, denoted as chancres, appearing at the site of infection. Chancres contain millions of syphilis bacteria and are highly contagious. On average chancres will appear three weeks after initial contact with syphilis. The usual locations for chancres are around the anus, mouth, or genital area. If left untreated, the ulcers can take anywhere between two and six weeks to heal (Syphilis). If the infection has not been treated it will progress into the secondary stage, which will occur six weeks to six months after initial exposure to syphilis. The secondary stage is known to manifest in a variety of ways, symptoms most commonly involve the skin, mucous membranes, and lymph nodes. The most visible symptom is a non-itchy rash covering the whole body, particularly the extremities, including the palms and soles. Another perceptible symptom is white patches on tongue or roof of the mouth. These rashes are akin to chancre in that they carry millions of syphilis bacteria and are highly infectious. Other, less discernible symptoms include a flu-like illness, loss of appetite, swollen glands, patchy hair loss, and chronic headaches. The latent stage of syphilis is characterized by a regression of symptoms where the infection lies dormant without causing symptoms. If no treatment is received, syphilis can remain inactive in the body for years without any signs of infection. Tertiary syphilis is the most violent form of the infection. At this stage syphilis can affect the heart and possibly the nervous system. Symptoms resultant of these affects includes difficulty coordinating muscle movements, paralysis, blindness, numbness, and dementia. In the tertiary stage of syphilis the disease can damage internal organs, which may eventually lead to one’s death (Syphilis). CobbResearchLab.com/TheBackbone
BIOHISTORIES The Story of CC18
An outbreak of syphilis occurred around the turn of twentieth century in the United States that is speculated to have infected “ten to fifteen percent of the general population” (Jabbour). Since syphilis was primarily contracted through sexual relations the stigma surrounding the topic dissuaded people from revealing their possible infection. This stigma may have caused CC18 to avoid medical care in order to avoid being permanently exiled by his community. CC18 may also been under more pressure to avoid such a label in order to protect his job as a laborer. The regressive effects of syphilis probably encouraged CC18 to go on without seeking medical care as well. Limited access to healthcare due to segregation in the 1900s was also a factor that could have deterred CC18 from getting treatment. Segregation would have also restricted CC18 from educational attainment, which in turn could have helped him be properly informed about the illness from which he was suffering. However, it’s also a possibility that he contracted congenital syphilis from his mother because he died of syphilis at 28 years old. Symptoms of congenital syphilis can be latent in an infant until adolescent years. For CC18 to have died from syphilis it had to be in its late stages meaning it resided in his body for many years. At the beginning of the 1900s, the medical establishment was relatively new and at its early stages of development as an organized profession. State licensing and certification of physicians was only emerging and as such there were many frauds in the healthcare system during this time. Syphilitics often sought the consultation of frauds or “quack” doctors, who offered baths, rubs, and hot springs as therapies for pain in order to protect their confidentiality (Jabbour). The fragile state of the healthcare system made the outbreak of syphilis difficult to contain because syphilitics did not view the institution as reliable. For example, the Tuskegee Syphilis Experiment (an experiment performed between 1932 and 1972 on four hundred black men in the late stages of syphilis) heightened African Americans skepticism towards physicians during that time. The experiment was meant to compare how syphilis affected African Americans as opposed to whites. African Americans were already experiencing a lack of quality healthcare, to be told they were being treated for “bad blood” without any knowledge they had syphilis was completely unethical. The only data collected for the Tuskegee Experiment was from the autopsies of the men (Resnik). Events such as the Tuskegee Experiment lead Blacks to be highly skeptical of the healthcare they were likely to receive if they sought out medical attention. Winter 2015•Spring 2016
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One of the major issues physicians faced was simply assessing if their patients had syphilis. Physicians were not sure how to communicate with their patients about such a sensitive topic without making their patients feel they were invading their privacy. The personal complications that the diagnosis of syphilis could potentially cause a patient were also a burden physicians had trouble handling. Despite efforts of legitimate physicians like Dr. Cobb to stress the importance of consulting professional care so a proper diagnosis could be made patients wanted to conceal their infection. In order to mitigate the fear of patients due to the stigma attached to syphilis, the American Medical Association adopted “Principles of Medical Ethics” in May 1903 to replace its “Code of Ethics” from 1847 (Jabbour). The new principles established explicit guidelines for patient confidentiality. Fritz Richard Schaudinn, a German zoologist, and Erich Hoffmann, a dermatologist discovered the syphilis causing bacteria, Treponema pallidum, in 1905. Subsequently after, in 1906 August Paul von Wassermann, a German bacteriologist, developed a complement fixation serum antibody test for syphilis known as the Wassermann reaction. In 1909, German scientist Paul Ehrlich discovered arsphenamine, which would be marketed as Salvarsan. Released in 1910, Salvarsan was the biggest advancement in managing the spread of syphilis until its cure was found in the year 1943 (John). CC18 was infected with syphilis during a time when a healthcare system was barely emerging in the United States. The relationship medical professions had with the state and public was at best tenuous because of the unsure role of physicians and the ignorance of the public. It is likely if CC18 did not have access to Salvarsan because of his unequal access to proper healthcare due to segregation. Cost may have also been a factor that discouraged CC18 because of his low pay as a laborer and “many hospitals did not have provisions for the treatment of syphilis” (Jabbour). Even if CC18 had the opportunity to receive any medical care it is very probable he refused because of the social stigma that coupled with syphilis. It is also likely that any hospital that admitted him did not have the provisions for the treatment of syphilis. A large part of the reason the syphilis outbreak was a significant challenge for medical practices was the stigma surrounding the disease due to the fact it was primarily transmitted through sexual contact. Syphilis was a disease that no one wanted to be unfortunate enough to be infected with and have to discuss with another. CobbResearchLab.com/TheBackbone
BIOHISTORIES The Story of CC18
Syphilis is now diagnosed by a blood test that is sometimes combined with an examination of lesions on the body. The human body’s immune system usually responds to syphilis by releasing antibodies that can be detected with a relatively inexpensive blood test. The antibodies produced by the body can stay in the blood for years after infection. The only limitation of a blood test is it cannot measure how long a patient has been infected with syphilis. It is highly encouraged that women receive a blood test nowadays given the risk of congenital syphilis (Syphilis). Discovered in 1928, and used as a cure for syphilis in 1943, penicillin is now widely used to treat the infection (John). A single dose of penicillin is most effective in treating early stages of syphilis, but it is still fairly effective in treating later stages of the disease. However, if the disease has progressed to the third stage when it can cause damage to the nervous system or internal organs then the effects will be incurable. As a substitute to penicillin for those who might be allergic for allergy purposes, azithromycin or doxycycline can be administered as well (Syphilis). After receiving medication routine check ups are advisable to ensure that the bacterial infection is completely eradicated. Today, if CC18 had contracted syphilis, he would have found that seeking treatment is relatively simple. CC18 would only need to search for the nearest clinic or health center that administers blood test and treatment for sexually transmitted diseases. CC18 also would not have had to deal with the pressure of being labeled an exile because much of the social stigma surrounding sexually transmitted infections has dissipated over the decades. CC18 could find solace in knowing that patient confidentiality is a much more strict policy today than it was at the beginning of the twentieth century. Many of the socioeconomic barriers impeding CC18 from seeking treatment such as his wages as a laborer or segregation are not an issue in modern day times. Treatment for sexually transmitted diseases is widely available to all from many sources for low cost. It is worth noting that there are still many disparities throughout the healthcare system in the United States today. For instance, minorities continue to be underrepresented within the medical workforce, despite the country becoming more diversified. Minorities are also less likely to have access to medical institutions for an abundance of reasons. Through research projects similar to those conducted at the Cobb Research Lab it is possible to eliminate these disparities by bringing attention to them. Despite the health disparities that exist within the United States, it is likely that if CC18 contracted syphilis today he would Winter 2015•Spring 2016
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have lived a much longer life instead of dying tragically at the young age of 28, due to improper health care.
References
“DRED SCOTT v. SANDFORD.” Dred Scott v. Sandford. Web. 08 July 2015. <http://www.oyez.org/cases/18511900/1856/1856_0/>.
BIOHISTORIES The Story of CC18 Washington, Margaret. “Obstacles Faced by African Americans.” PBS. PBS. Web. 08 July 2015. <http:// www.pbs.org/wgbh/amex/1900/filmmore/reference/ interview/washing_obstaclesfaced.html>. Wormser, Richard. “The Great Migration.” PBS. PBS. Web. 08 July 2015. <http://www.pbs.org/wnet/jimcrow/ stories_events_migration.html>.
Frith, John. “Syphilis – Its Early History and Treatment until Penicillin and the Debate on Its Origins. ”JMVH. Web. 08 July 2015. <http://jmvh.org/article/syphilis-its -early-history-and-treatment-until-penicillin-and-the-debateon-its-origins/>. “The Great Depression and the New Deal.” Choice Reviews Online 39.01 (2001). Web. 8 July 2015. Jabbour, Nicholas. “Syphilis from 1880 to 1920: A Public Health Nightmare and the First Challenge to Medical Ethics.” Syphilis from 1880 to 1920: A Public Health Nightmare and the First Challenge to Medical Ethics. Corcoran Department of History. Web. 08 July 2015. <http://www.uri.edu/artsci/com/swift/ HPR319UDD/Syphilis.html#n50>. “The Modern Period ( 1789-1999).” 1999 (2002). Web. 8 July 2015. “National Institute of Environmental Health Sciences.” Research Ethics Timeline (1932-Present). Web. 08 July 2015. <http://www.niehs.nih.gov/research/resources/bioethics/ timeline/>. Romer, Christina D. “The Great Crash and the Onset of the Great Depression.” Oxford University Press. Web. 8 July 2015. <http%3A%2F%2Fwww.jstor.org%2Fstable%2F2937892% 3Fseq%3D1%23page_scan_tab_contents>. Sandoval- Strauz, A. K. “Travelers, Strangers, and Jim Crow: Law, Public Accommodations, and Civil Rights in America.” American Society for Legal History, 2005. Web. 8 July 2015. <http%3A%2F%2Fwww.jstor.org%2Fstable%2F30042844% 3Fseq%3D1%23page_scan_tab_contents>. “Syphilis Symptoms, Causes, and Diagnosis.” WebMD. WebMD. Web. 08 July 2015. <http://www.webmd.com/sexual -conditions/guide/syphilis>. “Syphilis.” Syphilis. Web. 08 July 2015. <http:// www.niaid.nih.gov/topics/syphilis/pages/default.aspx>. Tolnay, Stewart E., and E. M. Beck. “Racial Violence and Black Migration in the American South, 1910 to 1930.” American Sociological Association. Web. 8 July 2015. <http%3A%2F% 2Fwww.jstor.org%2Fstable%2F2096147%3Fseq%3D1% 23page_scan_tab_contents>. Tomyn, Rosanne, and Demand Media. “What Were the Work Conditions in American Factories in 1900? | The Classroom | Synonym.” The Classroom. Web. 08 July 2015. <http:// classroom.synonym.com/were-work-conditions-americanfactories-1900-23383.html>.
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BIOHISTORIES The Story of CC112
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Cobb Collection Short Biohistory
The Story of CC112 Turquoisia McNabb1,2 Whitley Hatton1,3
1Summer
Medical and Dental Education Program Scholars, W. Montague Cobb Research Laboratory, Howard University 2Department of Agricultural and Life Science, University of Florida 3Departmeny of Biology, Howard University
Editor’s Note
This series of biographical sketches were authored by the 2015 class of the Howard University branch of AAMC’s Summer Medical Dental Education Program (SMDEP) at the W. Montague Cobb Research Laboratory. The students were assigned a Cobb Collection (CC) individual and conducted research about that individual. The papers were reviewed by The Backbone editorial team and the name of the CC individual was redacted. All other factual information was retained.
CC112, Negro, age 60, died from meningitis on November 18, 1934 at Gallinger Municipal Hospital. According to Sara E. Branham and Sadie A. Carlin from the National institute of Health, the first recorded outbreak of meningitis in the United States was in 1806. Meningitis since then has a periodic return to epidemic2 proportions at intervals of approximately ten years. At the National Institute of Health, meningitis showed peaks of cases in 1918, 1929, and 1936. Since there was an outbreak of meningitis from 1928 to 1934, we know now that CC112 contracted this virus during the outbreak. Looking through ancestry.com and many other websites, we found endless records going by the name of [Redacted]. Searching through, it was very difficult to narrow down to just one name because there were so many factors we had to consider. For instance, on ancestry.com, there came up 11 different people that had similar backgrounds to our person. One selection was a man that died the same year, but lived in Virginia and not D.C. Another man we looked up lived in D.C., but died earlier than our date of death. But not one of the sources on ancestry matched completely and none of these sources had died from meningitis. After finding a never ending list of [Redacted]’s, we then turned our search to the hospital and treatment of meningitis during the 1930’s. CC112 was treated at Gallinger Municipal Hospital. This hospital resided in southeast D.C. and was first built in 1846. This hospital was first an Asylum that housed the city’s indigent patients and a work house for the people convicted of minor crimes. In 1922, after placing a new building, the Asylum became more of a hospital with a smallpox hospital, quarantine station, and CobbResearchLab.com/TheBackbone
disinfectant plant. According to Jacob Fenston, who wrote “From Public Hospital to Homeless Shelter: The long History of D.C General”, he explains that hospitals during the time it was functional were for the poor, homeless, and criminals. By the 1940’s, the hospital was a filthy place swarming with flies, according to a U.S. Senator. To know who this hospital was used for, the time period our person was living in, and what he died from, we can make an educated assumption on CC112 and his life. There are two types of meningitis, viral and bacterial. Viral meningitis most often caused by enteroviruses that live in the intestines and can be spread through food, water, or contaminated objects. This kind of virus occurs mostly in kids and babies. Bacterial meningitis is a very serious illness. This is passed from one person to another through infected saliva or mucus. Streptococcus pneumoniae and Neisseria meningitides. This kind of bacteria can be located in your throat without getting sick, but can be transferred to others. Also, this kind of meningitis occurs mostly in adults. so we can assume that CC112 was diagnosed with bacterial meningitis since he was older and because bacterial meningitis is more severe than the viral infection. Although anyone can be infected with meningitis, there are many factors that can increase risk. Genetics, being male, being in crowded living conditions, exposure to insects and rodents, not having your immunizations, and not receiving vaccinations are all factors that can increase the chance of contracting meningitis. In all of these factors, we can assume that since CC112 was a Winter 2015•Spring 2016
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Negro during the early 1900’s that he was of a lower class and didn’t have great access to health care. We can also take a guess that CC112 also lived in crowded living conditions, had a greater exposure to rodents and insects, and was an older adult that didn’t receive their vaccinations. We can make an educated assumption that during this time, blacks were living in a crowded neighborhood of their own, which in the D.C. area could be infested with insects and rodents. Since CC112 was an older man who was diagnosed with meningitis, we can also assume that he didn’t receive his immunizations as well. Anacostia was a city designed in the 1900’s for the working class. The only surprising thing I found, was that most of Anacostia was for working class of whites and not blacks. This finding made me think that maybe CC112 was a more well off Negro that had a better paying job, till he couldn’t work anymore. So I can come to a safe conclusion that CC112 as he got older, moved into a more crowded area of the city, didn’t receive his immunizations due to lack of money probably from retiring. Since he was placed in Gallinger Municipal Hospital, makes an even better guess that he had become poorer as he aged. Without antibiotics and immunizations there is an eighty percent chance mortality rate. Penicillin is used for patients with meningitis. Since penicillin was discovered in 1928, it was probably only available for people who could afford it. With this knowledge, we can assume that CC112 didn’t have healthcare that could afford him to take penicillin, or penicillin wasn’t known to help treat meningitis at this time. With all these findings and factors, we can see how and why CC112 died. During his time, he wouldn’t survive, unfortunately should he have been alive today, he would have probably survived. CC112 was one of the many people in year 1934, to catch meningitis. During this era this epidemic had over 500 different strains present in multiple communities around the nation. On November 18, 1934 in the Gallinger Municipal Hospital this epidemic ended CC112’s life. The outbreak of what is now known as meningitis was very popular in the early 19th century. CC112 most likely went to Gallinger Municipal Hospital prior to his death with symptoms of a stiff neck, headache, and severe sensitivity to light. This was diagnosed with a spinal tap. Physicians would take a long needle and stick it in the back and draw fluid from around the spine. With this fluid they could tell if there was inflammation in the meninges. Symptoms for this disease varies according to CobbResearchLab.com/TheBackbone
BIOHISTORIES The Story of CC112
age (Healthline.com). Once diagnosed with meningitis he was admitted into the hospital for treatment. At this particular time there were no ground breaking vaccines available so patients were treated with penicillin (Chapter 28: a history of bacterial meningitis). The cause of meningitis in this time period were identified later in the 19th century as Streptococcus pneumoniae, Neisseria meningitis and Haemophilus influenza (Chapter 28: a history of bacterial meningitis), but these causes were only for bacterial meningitis which wasn’t discovered until the 20th century. CC112 could have had one of five meningitis diseases or another disease associated with meningitis known as meningococcal disease. Meningitis is inflammation on the meninges around the spinal cord and brain (Healthline.com). It causes fever, intense headaches, stiff neck, nausea, vomiting, drowsiness, confusion, and sensitivity to light (Healthline.com). Unlike meningococcal bacteria which specifically affects adolescents aged eleven to seventeen. Meningococcal causes an infection in the blood stream. Symptoms include: joint pain, red or purple rash that does not turn white when pressure is applied, and coming into close contact with a person with the disease (Meningitis vs Meningococcal: Difference in deadly diseases). If CC112 would have caught this disease in the 20th century his chances of living would have increased greatly. Vaccinations for meningitis debuted in the early 20th century. Vaccinations against Neisseria meningitis and Haemophilus influenzae were also created (Chapter 28: a history of bacterial meningitis). Those two diseases were the two causes of meningitis. With new research found on the disease doctors were able to narrow the strands on meningitis down to: bacterial, viral, fungal, parasitic, and noninfectious meningitis. Bacterial meningitis is very similar to Neisseria meningitis and Streptococcus pneumoniae (CDC). These medical conditions require immediate medical attention. Bacterial meningitis is usually taken care of with antibiotics because the medication kills the bacteria. These antibiotics include: ampicillin, claforan, rocephin, gentamicin, penicillin G, and vancocin (Web MD). This medications can be taken for a specific amount of time and the disease would have been cured. If CC112 was around during this era his life would have lasted a little longer. Viral meningitis is caused only by viruses like non-polio enteroviruses, arboviruses, and herpes simplex viruses (CDC). Compared to bacterial meningitis this is not that severe. People with a healthy immune system can fight Winter 2015•Spring 2016
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this virus on their own within 7 to 10 days (CDC). People at risk of catching this disease are five and under (CDC). The likeliness of CC112 having this strand is very low.
Jackson would have been one of many a survivors of such a fatal disease.
Fungal Meningitis is caused by fungi like Cryptococcus and Histoplasma and acquired by inhaling fungal spores in the environment (CDC). This strand of meningitis is rare and only caused by other fungus. People with other diseases like diabetes, cancer, and HIV are at higher risk of catching fungal meningitis (CDC). It also takes longer to cure people with these diseases because they are known for having low immune systems. The benefit of having this strand versus any other is this strand is not contagious and cannot be given to another person. Fungal meningitis can be treated with high doses of antifungal medications, usually given though IV (CDC).
References
Primary amebic meningoencephalitis (PAM), also known as parasitic meningitis is the fourth strand it is caused by parasites and less common in developed countries (CDC). These parasites usually contaminate food, water and soil. This disease is popular in places with large bodies of warm and fresh water, the diseases could also be contracted from pools that are not properly maintained. Catching parasitic meningitis is very dangerous, although there is treatment most people that get treated still die (CDC). This disease presents symptoms very similar to bacterial and viral meningitis according to centers for diseases control and prevention. Finally, there is Non-Infectious Meningitis. This form of meningitis is caused by cancers, systemic lupus erythematosus, certain drugs, head injury, and brain surgery (CDC). Its symptoms are just like the others, sensitivity to light, confusion, vomiting, and nausea (CDC). This form or meningitis is not contagious because you can only get it if you have one of the causes listed above. Since Mr. Jackson cause of death was only meningitis I think it is safe to say he did not have noninfectious meningitis either.
Lights, Verneda, and Elizabeth Boskey. "Meningitis." Healthline. August 16, 2012. Accessed July 3, 2015 Ken, Tyler. "Chapter 28: A History of Bacterial Meningitis." Pubmed.gov. 2010. Accessed July 3, 2015. Adams, Andie. "Meningitis vs Meningococcal: Difference in Deadly Diseases." Nbcsandiego.com. February 20, 2014. Accessed July 2, 2015. Bacterial Meningitis." Centers for Disease Control and Prevention. April 1, 2014. Accessed July 3, 2015. Thompson, Gregory. "Antibiotics for Bacterial Meningitis." WebMD. November 14, 2014. Accessed July 3, 2015. "Viral Meningitis." Centers for Disease Control and Prevention. November 26, 2014. Accessed July 3, 2015. "Fungal Meningitis." Centers for Disease Control and Prevention. April 1, 2014. Accessed July 4, 2015. "Parasitic Meningitis." Centers for Disease Control and Prevention. April 1, 2014. Accessed July 4, 2015. "Non-Infectious Meningitis." Centers for Disease Control and Prevention. March 15, 2012. Accessed July 3, 2015.
Since 1806, meningitis has been a fatal disease and has killed thousands of people since then. Mr. Jackson was one of the many taken by such a fatal disease. Mr. Jackson was at an extremely high risk of getting the disease because he was African American, poor and elderly living in an era when medicine was not readily available. His chances of living a longer life would have increased greatly if he was present in the millennium. New medication has been invented since 1806, which have increased the life expectancy of people with meningitis. Discrimination in health care has also decreased greatly so he would receive great care. Mr. CobbResearchLab.com/TheBackbone
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BIOHISTORIES The Story of CC312
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Cobb Collection Short Biohistory
The Story of CC312 Christine Okaro1,2 Christopher Wilson1,3
1Summer
Medical and Dental Education Program Scholars, W. Montague Cobb Research Laboratory, Howard University 2Department of Global Health Studies, Mercer University 3Department of Psychology, Washington University
Editor’s Note
This series of biographical sketches were authored by the 2015 class of the Howard University branch of AAMC’s Summer Medical Dental Education Program (SMDEP) at the W. Montague Cobb Research Laboratory. The students were assigned a Cobb Collection (CC) individual and conducted research about that individual. The papers were reviewed by The Backbone editorial team and the name of the CC individual was redacted. All other factual information was retained.
The death certificate of a fifty-nine year old woman from Arlington, Virginia, was examined to discover the relationship between her cause of death and the social, economic and healthcare disparities. The death certificate revealed that she died from lung abscess at the Gallinger Hospital, an inadequate public hospital largely serving minority populations, in Washington DC in 1943. Factors including her level of education, race and treatment options were analyzed to interpret the influence of ethnic and economic disparities on her health and access to adequate care. Due to the impact of segregation, minorities were limited regarding the type of treatment received and often died from preventable illnesses. CC312 was born in 1884 and lived in Arlington, Virginia until her death on April 11, 1943 (1920 United States Federal Census). Though CC312 resided in post-slavery Virginia, it is expected that she experienced racial tensions and division in her lifetime. The effects of the Civil War and the Reconstruction era greatly impacted Virginians. Atrocities faced by African Americans, such as the public whipping post, were abolished during the “Readjuster” government of the early 1880’s (Virginia Historical Society).
Historical and Societal Impacts
During this “Readjuster” government, Virginia worked to enfranchise Blacks by promoting voting rights. This opportunity was short-lived. The election of Governor Fitzhugh Lee in 1885 and the rise of the Confederacy stifled the progress of African Americans until the
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momentum of the Civil Rights Movement (Virginia Historical Society). Although slavery was abolished in 1863 by mandate of Abraham Lincoln’s Emancipation Proclamation, Virginian governance enacted laws and regulations that greatly oppressed the civil rights of all African Americans through rigid segregation. Due to the economic and educational restrictions on Black Americans living in Virginia, it is probable that CC312 and her husband did not receive an adequate education, which limits economic mobility. African Americans were largely treated as second-class citizens; this sentiment is reflected in the standard jobs available to them. African Americans generally worked as sharecroppers in rural areas, and menial or domestic service jobs in urban locations of Virginia (Virginia Historical Society). All aspects of life, including education, career options and living conditions were inferior to Whites. By the 1910’s and 1920’s, Virginia underwent a revival of the Klu Klux Klan and enacted the Racial Integrity Act in 1924 passed by the Virginia General Assembly (Sherman). This Act labeled all non-white individuals as “colored,” sanctioned the one-drop rule, which labels all individuals with any trace of African ancestry as “Black,” and banned interracial marriage as a mechanism for preserving the privilege and status of Whites in Virginia (Sherman). CC312 likely experienced the outcome of racial insensitivity and violence. Constant exposure to segregation and taunting is classified as a stressor, which can negatively affect health and contribute to the manifestation of predispositions. Winter 2015•Spring 2016
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BIOHISTORIES The Story of CC312
CC312 lived through pivotal moments in history that have shaped the lives of post-slavery African Americans, which ushered in legislations towards justice for all. Monumental moments, such as the ending of the Civil War, and the start of the Reconstruction era, which struggled to tackle the need for black freedom. Plessy v. Ferguson (1896), a case which sanctioned the notion that Blacks remaining “separate, but equal” from Whites was constitutional. Along with experiencing racial segregation, CC 312 may have later experienced the rise of prominent Black institutions and voices.
CC312 lived approximately twenty-seven miles away from this hospital, suggesting that this institution, based on her economic and racial background, was her primary source for medical care. At the time, receiving medical care at public institutions was exclusively for poor or minority citizens. Private physicians largely treated affluent White individuals. Consequently, segregation led to inadequate medical attention and little effort directed towards improving the services rendered by public hospitals, such as Gallinger Municipal Hospital.
The National Association for the Advancement of Colored People (NAACP) was established in 1909. From its founding the NAACP, “the nation’s largest and oldest civil rights organization,” has worked to “fight for social justice for all Americans,” especially minorities and underrepresented populations (NAACP). The outbreak of World War I in 1914 was a pivotal moment in African American history, as events such as The Great Depression (1929-1939), The New Deal (1933-1938), and The Great Migration directly affected the economic aspects of African American communities. The birth of the NAACP and a movement towards the advancement of Black and minority Americans likely influenced and empowered CC312, despite the fear induced by living in lawful segregation.
Illness and Resistance to Treatment
Analysis of Personal Life
Exploring the aspects of CC312’s personal life reveals the lifestyle and living conditions that may have led to her death. According to the 1920 Census Record, CC312 lived in Richmond Madison Ward, Richmond (Independent City), Virginia at the age of thirty-six. CC312 was married and identified as the head of household’s wife. Her husband was also born in Virginia in 1877. CC312 could both read and write, which suggests CC312 had, at the least, a basic level of education. The parents of both CC312 and her husband were born in Virginia. This establishes CC312 as a generational dweller of Virginia. Due to segregation, CC312’s access to quality health care was limited. On April 11, 1943, CC 312 died at the Gallinger Municipal Hospital. This hospital, established in 1806, was the first public hospital in Washington, D.C. From its inception, resources at this hospital were inadequate. Only the poor and minorities utilized Gallinger for treatment, which often suffered from overcrowding, low supplies of medicine, and inefficient laboratory and x-ray services (Fenston). CobbResearchLab.com/TheBackbone
The death certificate of CC312 lists her cause of death as “abscesses of the lungs”. Abscess of the lung is a bacterial infection in the lung resulting from bacterial growth in the mouth. This illness causes tissue to die, and results in pus accumulating in that space (Bartlett). The symptoms of this disease appear gradually over time and may not be diagnosed until the disease is well advanced. Common symptoms include coughing, fever, shivering, and night sweats. Chest pain and shortness of breath can also be present in some cases. In many cases, symptoms are mistaken for a common cold, which may have influenced the severity of her illness. CC312 died from this disease because she either did not receive timely, adequate medical treatment. Instead of immediately seeking medical attention, CC312 may have sought the aid of home remedies, until the illness became life threatening. Apart from the probability of CC312 neglecting the progression of her illness, it is possible that her care at Gallinger Hospital was subpar and ineffective -- leading to a worsened state of health. In the early stages of public health care, patients were not afforded advanced medical exams, equipment and treatments. The worsening the disease plaguing CC312 likely led to a complicated medical case that Gallinger Hospital was not equipped to treat. Furthermore, the severity of her disease coupled with the second-class treatment of minorities, especially African Americans during segregation, directly affects the quality of medical attention received. Another factor contributing to CC312’s lack of treatment was the attitude of minorities and poor individuals towards hospital-based medical treatment. While it is true that minorities and African Americans used public hospitals as medical resources, the marginalization of African American lives in medicine resulted in a culture of distrust. Due to events such as The Tuskegee Syphilis Experiment (1932-1972), which Winter 2015•Spring 2016
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infected African American patients with the syphilis virus, African Americans largely lost trust in America’s healthcare system. The fear of unwarranted medical exploitation often outweighed the need for hospital visits.
Early Treatment Methods
Between 1935 and 1945, the most recognized treatment for abscess of the lung involved the use of sulfonamides (Willis). Prior to this treatment, the disease was managed through the draining, posturing, conducting a bronchoscopy, or surgery. The mortality rate of abscess to the lung before 1930 was 32-34% (Willis). Although this treatment was widely accepted, the introduction of sulfonamides as a form of treatment did not significantly alter the mortality rate. However, in the late 1940’s penicillin was introduced as a method to alleviate the effects of this disease, which lead to a lower death rates and a 90-95% patient recovery rate. As the benefits of penicillin were recognized, it became the primary treatment method. It is likely that CC 312 did not receive penicillin as a form of treatment, which contributed to her death from an avoidable and treatable disease. Because CC 312 died after the discovery of penicillin method of treatment, it is unlikely that she received penicillin. This may be one of the reasons why she succumbed to the disease. CC 312’ case reiterates the disparities many African Americans were faced, due to the lack of public hospitals that provided quality medical care.
floor without offering assistance (Los Angeles Hospital to Close). This egregious conduct led to its closure. Similarly, reports of neglect and medical incidents lead to the recent closing of Gallinger Hospital in 2001 (Fenston). To withstand rising healthcare costs, The Affordable Healthcare Act (2010) extends the coverage of medical care and lowers the intended cost of services (U.S. Department of Health and Human Services). Through this health care law, disparities in the availability of health care can be eliminated. This means more individuals are able to obtain preventative treatment to manage illnesses early, which avoids unnecessary deaths from treatable diseases. Regular doctor visits, made possible by the availability of health insurance, can lead to longer, healthier lives for all patients, regardless of race, financial ability, or social class. As healthcare services have improved overtime, so has the treatment of abscess of the lungs. At present, the mortality rate for abscess of the lung is less than 10% (Bartlett). This is due to new antibiotic drug discoveries. Current treatment consists of clindamycin antibiotic therapy for four to six weeks, followed by an x-ray to assess the progress of treatment (Kamangar). This advancement is acknowledged as a more effective treatment than penicillin, the previous treatment of lung abscess. Although laws are now enacted to ensure equality in medical care, health disparities are still prevalent in minority populations.
The Story of CC312 Treating CC 312 Today
Since CC312’s death in 1943, the medical field has undergone several changes physically and technologically. As of now, patients have choices when selecting a hospital or health care provider. Despite this, health care disparities still exist, as the best medical service is available to those who can afford it. Although health insurance is meant to alleviate these disparities, these policies equate better medical care to higher premiums. Generally, poorer and minority neighborhoods are still served by hospitals that provide comparatively substandard service. Martin Luther King, Jr. Hospital in Los Angeles California is an example of an inner-city medical facility, with mainly minority patients living in close proximity. In 2007, this hospital’s poor patient care made headlines as staff ignored a minority patient who lay dying on the CobbResearchLab.com/TheBackbone
From the research provided, the circumstances of CC312’s life, which led to her premature death, can be asserted. CC312, a Black woman, lived in Arlington, Virginia during World War II and the confederacy. CC312 dismissed the early symptoms of the disease, due to the benign signs of abscess lungs: cough and fever. As the symptoms worsened, she weighed the inconvenience of leaving her home and work to travel to Washington D.C. for treatment. Due to the progression and severity of her illness, including chest pain and shortness of breath, she was eventually forced to travel a great distance to twenty-seven miles to Gallinger Hospital. Closer to her death, CC312 experienced intensified coughing accompanied by putrid smelling mucus. She had to part with her husband for the journey, due to their inability to afford transportation for the two of them. Upon arriving at Gallinger Hospital, CC312 waited for several hours to receive services, due to the Winter 2015•Spring 2016
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overcrowding patients and under-resourcing of staff. After being admitted, CC312 was placed in a crowded, under-furnished, unsanitary examination room, in which she did not receive an adequate examination. By this time, CC312 experienced intense pain and discomfort while still unsure of her illness or potential treatment methods. Because of the progression of her illness, the lack of medical supplies at Gallinger Hospital, and the misdiagnosing of her disease, CC312 did not receive adequate care. This medical oversight led to her death. If CC312 suffered from abscess lungs today, she would be prescribed the antibiotic clindamycin (Kamangar). This would have increased her chances of survival and decreased her probability of death to 1/8th of the previous treatment (Kamangar). Additionally, CC312 would have the resources to seek treatment earlier, as Medicare or the Affordable Care Act would likely cover her medical costs. Coupled with an increase in the number of hospitals, as well as affordable public transportation, CC312 would have more opportunities to seek earlier treatment. Educational opportunities for women and minorities have improved over recent years, which would have provided CC312 with economic and social advancement resulting in employment and access to companyprovided health insurance. Due to the economic advancements, medical innovations, and civil rights movements The United States has become a nation better fit to address the medical needs of individuals. If born at this time, it is highly expected that CC312 would live a healthier and longer life.
BIOHISTORIES The Story of CC312
Sherman, Richard B. “The Last Stand”: The Fight for Racial Integrity in Virginia in the 1920s.” The Journal of Southern History 54.1 (1988): 69, Web. 4 July 2015. Therapy, Surgical Care. Medscape, 18 Dec. 2014. Web. 08 July 2015. <http://emedicine.medscape.com/ article/299425-treatment#d8>. The Virginia Historical Society. “Virginia Historical Society”, New Southerners. The Virginia Historical Society,Web. 04 July 2015. <http:// www.vahistorical.org/what-you-can-see/story-virginia/ explore-story-virginia/1861-1900/new-southerners>. Willis, AT. “Anaerobic Bacteria: Role in disease.” Annals of Internal Medicine Ann Intern Med 82.6 (1975): 862. Web. 1877 Census. Richmond Madison Ward, Richmond (Independent City), Virginia, United States Richmond (Independent City) Virginia Male 43 1877 Head African American Black. 1920 United States Federal Census. Official Enumeration Date: January 1, 1920. Enumeration District: 143. Place: Richmond Madison Ward, Richmond (Independent City), Virginia, United States. Household ID: 59. Publication Number: T625. Page: 3A. Line Number: 40. Microfilm Number: 1821911. Image number: 00417.
References
Bartlett, John G. "Clinical Infectious Diseases." Oxford Journal 40.7 (2004): 923-25. Print. Fenston, Jacob. “From Public Hospital To Homeless Shelter: The Long History of D.C. General.” WAMU 88.5. Web. 01 July 2015. Kamangar, Nadar. "Lung Abscess Treatment & Management." Lung Abscess Treatment & Management: Medical Care, Antibiotic NAACP. “National Association for the Advancement of Colored People." NAACP. National Association for the Advancement of Colored People. Web. 04 July 2015. CobbResearchLab.com/TheBackbone
Winter 2015•Spring 2016
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BIOHISTORIES The Story of CC315
The Backbone
Cobb Collection Short Biohistory
The Story of CC315 James M. Byrne III1,2 Lopriela Seabrook1,3
1Summer
Medical and Dental Education Program Scholars, W. Montague Cobb Research Laboratory, Howard University 2Department of Biological Sciences, University of Maryland: Baltimore 3Department of Biology, Savannah State University
Editor’s Note
This series of biographical sketches were authored by the 2015 class of the Howard University branch of AAMC’s Summer Medical Dental Education Program (SMDEP) at the W. Montague Cobb Research Laboratory. The students were assigned a Cobb Collection (CC) individual and conducted research about that individual. The papers were reviewed by The Backbone editorial team and the name of the CC individual was redacted. All other factual information was retained.
Washington, D.C. is customarily acknowledged for upholding past executive leaders, congressional legislative initiations, and judicial upbringings of the country. For centuries, however, the prestigious province has also been the home of countless societal movements, and renewal projects. It has also served as a refugee for manifolds of migrants, including CC315 who was born in the District of Columbia in 1867. Upon her arrival, Jim Crow law manifestation and irrational segregation became the national ideals that would come to affect her for the rest of her life. CC315’s unfortunate placement in society would limit her chances of success, represent her unequally under the law, dictate her residential location, and have an influence over her chances of survival. CC315 resided at 210 F Street SW with her Virginian relative, who was born in 1892. The 1940 Census indicates that the relative was labeled as the head of the household while CC315 was his roommate and labeled as the roomer. Although the relationship of the two is mistaken for kinship, they actually shared a common law marriage. This type of marriage was established when a man and a woman lived together for a certain amount of time and declared themselves as being informally married. This is a significant fact because CC315 was originally widowed. Listings of tracts from the 1940 U.S. Census, which are geographical regions where population data is collected, shows that Holmes lived in tract 60 of Washington, D.C. Tract 60 outlines a community referred to as the Southwest Waterfront. This area borders the south CobbResearchLab.com/The Backbone
boundary of the Capitol mall, lies west of South Capitol street SW, east of 4th street SW, and north of M street SW. This area served as an affordable option of residence for the poorest Washingtonians after the Civil War. The waterfront had been strategically used as a commercial wharf but was abandoned by the military around 1865 after the war concluded. In the meantime, the area became settled by thousands of freed slaves and European immigrants who sought after the work opportunities along the waterfront. Around the 1900’s the government gained an interest in the waterfront and implemented plans to utilize the area by rebuilding old buildings and abandoned wharves, and widening streets that led to them (“Timeline”). Up until the 1950’s, the area continued to attract more settlers including African Americans who participated in the Great Migration to escape the effects of the crop destroying boll weevil and other economic factors in the rural South. Jim Crow laws, segregation, and prejudice followed blacks to the north as they became more urbanized. At least one and a half million African Americans resided in the north by the 1940’s (“The Second Great Migration”). The vastly populating community eventually created divided neighborhoods that attracted white Irish, Scottish, and German people on the west of Fourth Street SW, and blacks on the east. The row houses on and around F Street, where CC315 resided, had the cheapest rent prices that persisted well below the average cost of forty-five dollars in the 1940’s (“HCHT”). Although the majority of the community was rather poor, the scenery of the area maintained its daily Winter 2015•Spring 2016
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display of busy activities that included moderate traffic and street crossing pedestrians (Abrams). The beginnings of societal landscape shifting took place around the 1970’s when the government called for an urbanizing renewal project that would remove thousands of businesses and lead a countless number of residents into eviction (“Timeline”). This project soon modified the population into white predominance and nonetheless provided solutions for the concerns squalid neighborhoods remaining near the nation’s capital (Abrams). Large offices, expensive apartments, and other new features contradicted to poorer adjacent neighborhoods that only offered the view of tents and shacks as homes as a result of the changes (SW Heritage). After interstate 395 was built directly upon F Street Northwest during the process of renewal, CC315’s home, as she knew it, had ceased. It is important to note that CC315 lived through the Great Depression. This historical event began with the crash of the New York Stock Exchange in 1929 and lasted until about 1939. During this time period, the unemployment rate skyrocketed to around 25% (Nelson). For blacks, the unemployment rate rose above 50% (Trotter). This means that it is very probable that CC315 was exposed to extreme poverty; even more so than her white counterparts. Whites called for action stating that no black man could get a job until every white man was employed (Trotter). Though CC315 chose not to work later in her life, the economic times during the Great Depression led to many black women being employed as house maids for only $5 a week (Trotter). Around this time, many African-Americans in this time period were supporting Republican president Herbert Hoover due to his views on emancipation. Under democratic President Franklin Roosevelt, many blacks were subject to discrimination through his introduction of the New Deal program. Certain programs that were part of the New Deal eliminated around 60% of AfricanAmerican government paychecks and their benefits from social security programs (Trotter). Consequently, this led to African-Americans fighting for their rights through entities such as the NAACP. Records indicate that CC315 died from burns at age 46 on August 26, 1943 at Casualty Hospital in the District of Columbia. The Cobb Lab’s records incorrectly indicate that she died at age 79. Logically, Holmes received care from Casualty Hospital around her time of death, which was federally funded by the government for those who could not pay for healthcare treatment (Pohl). In order for skin to be burned, it must be subjected to a heat source or a chemical source that damages the skin. CobbResearchLab.com/The Backbone
BIOHISTORIES The Story of CC315
There are different degrees of burns: first, second, and third. First-degree burns indicate only the outer layer of the skin was damaged. A second-degree burn affects the outer layer of the skin, the epidermis, and the layer below it, the dermis. The most severe burn, a thirddegree burn, can result in complete destruction of the skin and even tissues below the skin such as muscle (“Burns Fact Sheet”). Most burns will cause blisters, infection, and swelling, and if they were severe enough, they can even result in anaphylactic shock, or death. The skin acts as a protective layer for the human body and also allows for regulation of body heat. Therefore, burned skin is damaged and more prone to foreign materials entering the body and causing infection (“Your Skin”). During this time burn treatment was limited and lacked effectiveness. If 50% of a person’s body was burned it was likely that the accident would result in death. Doctors commonly used refrigerated skin from cadavers as a temporary dressing for burns around the 1940’s (“Skin Grafts”). Skin grafts were first used to treat burns in 1871, however the recipient’s immune system usually ended up rejecting the foreign skin. During the time of CC315’s death, treatments for burns were rapidly changing due to the amount of soldiers in the World War II receiving burn wounds. Burns were treated by irrigating the wound with saline solution or by using Tannafax jelly, which contained some tannic acid (“WW2 Burns Survivor”). Tannic acid was the common treatments for burn wounds before the war until physicians realized it could lead to eradication of the skin. In Holmes’s case, since this was a time of racial inequality, it is likely that she did not get priority care. It is also very likely that she did not have access to the fairly new and lifesaving burn interventions. Some possible home remedies for burn injury that were probably used by those who could not afford health care included using: white vinegar to extract heat, natural honey for its pH balancing and antibiotic effects, a milk bath to soothe and heal the skin, essential oils from coconut or vitamin E to reduce scarring, and tea bags for retrieving small amounts of tannin acid (Shea). The condition of CC315’s burns is presently unknown, which makes it difficult to determine whether or not these home remedies would have been beneficial for her. However, since the burns resulted in her fate, her condition must have been relatively severe or her burns could have been painfully infected. Since there is a lack of explanation about the event of CC315’s incident, one can assume that the burns she acquired may have been the result of a house fire. While the risks of American house fires have decreased Winter 2015•Spring 2016
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BIOHISTORIES The Story of CC315
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tremendously over the past decades, studies from the Federal Emergency Management Agency (FEMA) show that socioeconomic factors such as poverty, undereducation, race, and income lead to an increased risk of fire incidents. The 1997 National Fire Data Center states that vacant and abandoned buildings serve as fire hazards in poor neighborhoods by appealing to individuals who are likely to ignite illegal materials. It also recognizes the possibility of homeless people seeking to stay warm by making fires in these places during the winters. Furthermore, the report expresses the notion that low income indicates poor quality of housing with problems regarding heating systems, inadequate electrical wiring not suitable for excessive load, and malfunctioning plumbing issues. The report then goes on to state that a household with a lower income is considered less likely to invest in fire prevention devices such as smoke detectors, which decreased the number of deaths caused by late night fires by 25% between 1980 and 1990. The risks caused by overcrowded housing in poorer facilities is then discussed to be a fire hazard due to the expected “wear and tear” of appliances and larger numbers of possible victims in need of rescue. Lastly, the factor of undereducation is linked to minorities less likely to be exposed to public fire safety education and less likely to read warning labels due to lower literacy rates (“SFIF”). The eighth grade graduate, CC315, fits into these studies because she more than likely received support from Andrew Johnson’s low income and resided in an underprivileged neighborhood. CC315 would be admitted into the Burn Center MedStar Washington Hospital if she were a victim of severe burns today. Similar to the Casualty Hospital that admitted patients who could not afford treatment, MedStar ensures to provide quality care to patients underinsured or uninsured (“About the Burn Center”). Depending on her conditions, her treatment at MedStar could consist of retaining fluids through an IV to prevent dehydration, pain relievers such as morphine and antianxiety medications, decompression for blood circulation, tube feeding for nutritional purposes, breathing assistance, skin replacement or skin reconstruction, physical therapy for burns that may cover bone joints, and trustworthy penicillin antibiotics (“Diseases and Conditions”). Penicillin had been discovered years before Holmes’s hospitalization. However, the antibiotic was not yet made onto an industrial scale (“WW2 Burns Survivor”). Therefore, if Holmes had survived her accident, she would have faced amputations of bacterial infected body limbs. CobbResearchLab.com/The Backbone
CC315’s story remains significant because there is a possibility that individuals currently living in settings similar to CC315 could die from similar influences. When taking into consideration the predicaments of those who cannot afford healthcare or a good quality of living, the scenario is destined to repeating itself. Modern society must continue to search for solutions to address these problems and provide better outcomes for people like CC315.
References
“About the Burn Center at MedStar Washington Hospital Center.” MedSeek. MedStar Health, n.d. Web. 4 Jul. 2015. Abrams, Amanda. “Southwest Waterfront: A Neighborhood Where a Change is Gonna Come.” UrbanTurf. Urban Turf LLC, 02 Dec. 2010. Web. 3 July. 2015. “Burns Fact Sheet.” National Institute of General Medical Sciences. U.S. Dept. of Health and Human Services, n.d. Web. 02 July 2015. “Diseases and Conditions: Burns.” Mayoclinic. Mayo Foundation for Medical Education and Research, n.d. Web. 4 Jul. 2015. “Historical Census of Housing Tables.” U.S. Census Bureau. Housing and Household Economic Statistics Division, 31 Oct. 2011. Web. 06 Jul. 2015. Nelson, Cary. “About the Great Depression.” The Great Depression. University of Illinois, n.d. Web. 02 July 2015. Pohl, Robert. “Lost Capitol Hill: Casualty Hospital.” The Hill Is Home. The Hill Is Home, 27 Sept. 2010. Web. 03 July 2015. Shea, Taylor. “11 Surprising Home Remedies for Burns.” Reader’s Digest. Reader’s Digest Association Inc, n.d. Web. 8 Jul. 2015. “Skin Grafts.” Brought to Life. Science Museum, n.d. Web. 02 July 2015.
Winter 2015•Spring 2016
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BIOHISTORIES The Story of CC331
The Backbone
Cobb Collection Short Biohistory
The Story of CC331 Jordan Mitchell1,2 Jordan R. Howard1,3
1Summer
Medical and Dental Education Program Scholars, W. Montague Cobb Research Laboratory, Howard University 2Department of Biology, University of Maryland: College-Park 3Department of Biological and Physical Sciences, South Carolina State University
Editor’s Note
This series of biographical sketches were authored by the 2015 class of the Howard University branch of AAMC’s Summer Medical Dental Education Program (SMDEP) at the W. Montague Cobb Research Laboratory. The students were assigned a Cobb Collection (CC) individual and conducted research about that individual. The papers were reviewed by The Backbone editorial team and the name of the CC individual was redacted. All other factual information was retained.
Born in the year 1915, CC331 was a colored female
races within the same room or serve the two races
native to the southern state of Georgia. The name of her
anywhere under the same license.” (NPS)
mother, father, and other relatives are unknown,
These laws denied African Americans from various rights
however she did have a sister whose information was
that they deserved. It was not until 1965 until these laws
documented. Times were very rough for African
were made illegal throughout the United States.
American families because discrimination against black
In addition to dealing with a racial war of segregation
communities in Georgia was prevalent. Being that CC331
and inequality, CC331 also lived during World War II.
lived in America during this time of widespread racial
Taking place between the years 1939-1945, the effects of
imbalance, she more than likely was not born to family of
World War II were emotionally and physically damaging.
wealth. As many African Americans suffered from
During this time, over 2.5 million black men registered
countless acts of segregation and prejudice between
for the draft. Aside from casualties stemming from direct
1882-1930. Over 458 blacks were deprived of their right
combat, external situations also occurred which caused
of citizenship, and denied admission to various public
distress in people’s lives. One of the most notable
settings including restaurants, hotels, and professional
external situations was the utilization of concentration
societies.
camps by the Nazi to prosecute the Jewish people. World
During this time, Jim Crow Laws provided a strong
War II affected people’s lives in a negative way because
support system for this reoccurring racial injustice
the resulting carnage and distress it created left many
preventing African Americans from establishing and
people homeless and burdened with monumental costly
developing relationships with people not of color. For
damage. Although this might not have affected CC331
example, specifically in Georgia:
personally, there is a high possibility that one of her
“It was unlawful for a white person to marry anyone
family members might have served in the war. However,
except a white person…[an] officer in charge shall not
this information is unknown.
bury, or allow to be buried, any colored persons upon
Most schools in the south during this time
ground set apart or used for the burial of white persons...
period were very segregated as there were separate
[or even] all persons licensed to conduct a restaurant,
schools for both black and white students. It is also
[were only to] serve either white people exclusively or
unspecified the length of time in which CC331 lived in
colored people exclusively and shall not sell to the two
Georgia. In 1930, Georgia spent about $43 per person for
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BIOHISTORIES The Story of CC331
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a white student, but only spent $10 for a black student.
segregation during the 1940s in the south served as a
From this it can be assumed that CC331 did not get as
barrier between blacks and access to healthcare. A
great of an education as her white counterparts. CC331’s
possible reason why CC331 might have chosen to
education may also have been affected by her lower
relocate to Washington D.C. was probably because it was
cultural capital. Cultural capital refers to the relationship
the only location closest her with a hospital that openly
of one’s socialization and cultural activities. Examples of
served people of color.
aspects that can be considered as cultural capital include
For decades, African Americans “have had the worst
interest in the art of music, literature and histrionics
health care, the worst health status, and the worst
(Matthijs
CC331’s
health outcome of any racial or ethnic group in the
circumstances might not have granted her access to such
U.S” (Byrd). Most treatment was biased and unfair until
opportunities, it also might have had regressive impact
more black individuals became physicians and other
on the advancement of her education.
healthcare professionals. It was not until after 1965
and
Kraaykamp).
Because
Later in her life, CC331 and possibly her family moved
when black health care began to improve.
to Jacksonville, Florida. She lived on 1126 Duvall Street.
In the 1940s, there was a lack of various treatments
Unfortunately, racial discrimination in Florida was no less
and health. Equally prevalent in both males and females
common than in Georgia. Blacks dealt with white
and generally occurring in people twenty-five and
supremacy and racial dismay on a regular basis. In fact,
younger, diabetes mellitus ketoacidosis (DKA) is a form
Florida led the nation in the highest number of lynching
of metabolic acidosis that is the result of a lack of
per capita. Massive attacks on the black community
glucose in the body and can be identified as chronic or
occurred on November 2, 1920 and in Rosewood on
mild. When there is insufficient glucose in the body, the
January 1923. These attacks resulted in the burning
body begins burning fat, muscle, and liver cells, and
down of many African American homes. The exact date
using them as a means to obtain the necessary amount
and time in which CC331 relocated to Jacksonville,
of energy required for daily activity. Because of glucose
Florida is undetermined. No matter where she moved or
insufficiency, substances known as ketones produced by
lived, there is a strong possibility that CC331 faced
oxidation begin to develop within the body. The
hatred from people not of color simply because of her
presence of ketones leads to problems such as an
skin color.
increase in blood sugar, which can disable the kidneys
As CC331 progressed through life, she lived a life as a
from retaining extra sugar. Dehydration is the result of
transient worker, traveling around from place to place
ketones in the urine and can make urination
doing small jobs. Her skill level as it pertains to job
immoderate. This excessive urination may cause loss of
qualification is unknown. After once upon a time residing
vital body fluids and essential elements such as certain
in both Georgia and Florida, CC331 eventually made her
salts and potassium. Ketone buildup in the body can
way to Washington DC. Although there is no solidified
cause the body to become poisoned because of the
justification for her relocation to DC, it can be assumed
acidity it causes.
that this second known move might have been in search of better work opportunities.
type 1 or type 2 diabetes, but is more likely to affect
Unfortunately, on June 20th, 1944 at the age of twenty-nine,
died
of
diabetes
those who have type 1. Symptoms include low blood
mellitus
sugar, high fever, lack of insulin, confusion, lethargy, dry
ketoacidosis at Freedmen’s Hospital in Washington D.C.
skin, acetone breath, extreme thirst, frequent urination,
Freedmen’s Hospital, now known as Howard University
vomiting, abdominal pain, low blood pressure, general
Hospital was founded in 1862 by Dr. Daniel Hale
weakness, increased heart rate, difficulty of and or rapid
Williams. The enforcement of the Jim Crow laws and
breathing, increased heart rate, and loss of appetite.
CobbResearchLab.com
CC331
DKA has the potential to affect anyone with either
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BIOHISTORIES The Story of CC331
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People at risk include those who have experienced heart
treatments of disease.
attack, stroke, trauma, stress, alcohol abuse, or who
It was not until the late 1940s when insulin syringes
smoke. DKA can cause shock or even death if left
became available, which was after CC331 had died.
untreated. Although deadly, this disease can be treated,
Today, there are better treatments for diabetes and
with the proper health care. Methods of treatment are
people have better control over their sugar levels. Back
usually the introduction of sodium bicarbonate into the
then African Americans did not have healthcare or any
body, fluid replacement, or insulin administration
means of paying for treatment unless they paid for it
intravenously, which is also known as insulin therapy.
themselves. If so, it was very hard for an African
Although these treatments are beneficial, they also have
American to get medical treatment unless it was at a
side effects and potential complications such as low
hospital run by black individuals. Currently, the United
blood sugar, low potassium, both pulmonary and
States has Medicaid, which is health insurance to aid
cerebral edema, seizure and cardiorespiratory arrest.
people that are not as wealthy, such as CC331. Also,
These treatments are very beneficial because they
under the Affordable Care Act, passed on March 23,
help to prolong the lives of people with this illness, but
2010, African Americans now have better health care
prevention and self-awareness of health is better. People
coverage, quality, and financial security. Because of this
that already have diabetes are more prone to DKA.
act, there are less health care disparities and fewer
However, there are ways to help prevent individuals with
African Americans are uninsured.
type 1 or type 2 diabetes from progressing to this
Diabetes was rare among the African Americans
horrible disease. Small anatomical and physiological
population before the 1940â&#x20AC;&#x2122;s. During this decade, a
maintenance such as staying hydrated, monitoring blood
connection was made between diabetes and the long -
sugar levels, injections of an acting form of insulin,
term complication of kidney disease. In 1936 diabetes
consumption of sugar free fluids, and awareness of
was divided into groups based on insulin sensitivity, but
certain
Reliable
there was no clear distinction of the type until 1959.
examinations to help in the detection of DKA include
There may have been a possibility that even if CC331 had
arterial blood gas, potassium blood tests, amylase blood
access to treatment, there would not have been a
function tests, serum electrolytes, blood testing strips. In
solidified conclusion as to whether or not the disease
the case of Willie Mae, it is more likely that she suffered
stemmed from insulin dependent or non-insulin
from type 1 diabetes and it developed into to
dependent diabetes. She also did not have the chance to
ketoacidosis. Chest x-rays, an electrocardiogram, CT
receive aid from oral drugs that would have helped
scans of the brain, and urine analyses are also utilized to
lower her blood glucose levels due to the fact that these
check for the presence of this illness. Because of
drugs were not introduced until 1955.
infections
are
helpful
methods.
disadvantages, such as finances and racial inequality,
Today, there are thousands of new treatments and
CC331 probably did not have access to some of these
medical breakthroughs for diabetes, specifically for
methods of testing for the presence of this illness. In the
Diabetes Mellitus Ketoacidosis. If CC331 were still living
case of the CT brain scan, it had not been invented at the
today, she would be better off and most likely lived a
time.
healthier lifestyle. In America today, there are more
A lot has changed since CC331 has died, especially the
resources available for African Americans that they did
rights of African Americans and the abolishment of
not have access to in the past. If she had the proper
segregation. Although there is still racial prejudice in
treatment and was able to control her sugar and insulin
todayâ&#x20AC;&#x2122;s society, it is not as prevalent as it was during the
levels, she could have lived longer than twenty-nine.
1920s-1940s. African Americans have access to better
Also, CC331 might have been able to find better work
health care and there is more advancement in
other than being a transient worker. She would have
CobbResearchLab.com
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51 Volume 02 Issue 01 3
BIOHISTORIES The Story of CC437
The Backbone
Cobb Collection Short Biohistory
The Story of CC437 Rachel Davalos1,2 Mariela A. Martínez1,3
1Summer
Medical and Dental Education Program Scholars, W. Montague Cobb Research Laboratory, Howard University 2College of Arts and Science, Florida Gulf Coast University 3Department of Natural Sciences, University of Puerto Rico at Cayey Campus
Editor’s Note
This series of biographical sketches were authored by the 2015 class of the Howard University branch of AAMC’s Summer Medical Dental Education Program (SMDEP) at the W. Montague Cobb Research Laboratory. The students were assigned a Cobb Collection (CC) individual and conducted research about that individual. The papers were reviewed by The Backbone editorial team and the name of the CC individual was redacted. All other factual information was retained.
Understanding the society, era, economy, and political status of the people during their lifetime is an essential part of understanding someone’s history. The W. Montague Cobb Research Lab is a key component in understanding history as a result of the research being conducted. They are advancing the development of scientific, anthropological and biological knowledge. They involve a combination of these disciplines to advance their knowledge. This is achieved by obtaining a variety of cadavers, with the main objective to study the impact of the death of that particular person due to their race and social status in their society in that time frame. Research like this allows us to profoundly understand physiological, mental, economic, cultural and geographical details that affect a specific individual. Ancestry.com is a website that serves as a primary source in the recollection of data from the National Archives and the 1920 Census of a citizen named CC437. Due to the fact that the 1920 Census was the fourteenth Census conducted in the USA there are some details lacking that we would be able to find in today’s Census. They were not particularly detailed in the information like exact address or date of birth, but instead it focused on name, occupation, race, place, and literacy. During this same time period there were many changes going on in the nation, the 19th amendment was passed and even though it didn’t give the right to vote to Southern African Americans due to their legal status, it was a start. The Harlem Renaissance also began in this time, it was the explosion of art, culture, and social interest (The Harlem Renaissance). There was a large amount of change happening with the African American population. CC437 was described as a Negro female that is thought CobbResearchLab.com/TheBackbone
to be born around the 1890’s right in at the start of The Progressive Era of the United States. She was found to have lived in Maryland her whole life. Both of her parents were born in Maryland meaning that she probably had family in the area. She seemed to be stable in the sense that she didn’t have a major move or change in environment. When she moved, it was from areas that were not very far from each other. From the census of 1920 there was a lot of information given to us about CC437. In the census we found out that she was educated because they mention she could speak English as well as read and write. Her occupation in 1920 was as a laundress, where she was part of the economical and racial disadvantage, since this in that time was a common job for African-American women. Out of all of the African American women in the 1920’s approximately 1,500,000 were working gainful occupations. Specifically there were around 280,000 laundresses at this time. Agricultural jobs were more common having around 400,000 women working gainfully and then 350,000 working servantly. Typically, if one was not working in an agriculturally based job, one was either a servant or laundress. Historically, it was a poorly paid job requiring hard work and labor. Additionally, this occupation was about 75% of the work African American women did during this time period to earn a living. Many sources stated that a large amount of laundresses were employed in private homes. The overworking of many laundress’ lead to “The New Deal,” which helped those paid extremely poorly to have a standard minimum wage. This also implemented a maximum of 40 hours per weeks. These workers typically worked for 14 to 30 cents an hour (Adna Hill 110-113). CC437, in 1920, lived as what was called a “roomer”. This Winter 2015•Spring 2016
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meant different people were living in the same home with many people who were not necessarily family. She lived at the time in Maryland on a street named Cookey Court just 40 miles from the center of District of Columbia. CC437 lived with three other people with the names of Edward Alexander, Marble King, and Raymond Proctor. They each had different lives but convened together when it came to paying the rent for the house. Alexander was 38 years old at the time of the census and worked as a cement mechanic; he was the head of the house he rented. In the census they mention he could not read or write. King was 24 at the time, married, and a laundress just like CC437 and was also able to read and write. The last person, Proctor, was a 30 year old divorced driver who was able to read and write (All 1920 United States Federal Census Results). This lifestyle is one which can be interpreted as lack of economic stability or in need to be close to their jobs; therefore have to agglomerate many people in the same place in order to survive. We imagine that she lived in this home to be near her employer and get the best advantage. CC437 had died at a very young age approximately fifty- four years old. It is said to be at an early age because life expectancy in the USA in 1951 was approximately 71.4 years according to the website "Life Expectancy in the USA, 1900-98." At the time of her death she was a resident at 1876 M Street N.W. District of Columbia, USA. She had died at the Gallinger Municipal Hospital Psychopathic Ward on January 26th of 1951. We propose that she had been going in and out of the hospital since she was 28 years old since could not find any more information about her after the 1920 census because it could be possible that they didn’t take into consideration people with mental illnesses or in a mental ward during the census. The cause of death of CC437 was respiration obstruction as well as food aspiration. She died at an early age of 54. Typically, people who experience this life -threatening situation are experiencing a solid that is lodged in the trachea preventing breathing or swallowing leading to asphyxiation. Without assistance and immediate attention this situation will result in death. The close to complete obstruction of the airways would cause immediate death but other smaller items could be swallowed and stuck in your esophagus. These items stuck in your esophagus or in other parts of the digestive system could lead to infection if not extracted in time causing severe pain or even death. (Warshawsky) She was a psychiatric patient; we imagine that her mental state was highly severe and she may not have been able to ingest food or medications by herself. If she was CobbResearchLab.com/TheBackbone
BIOHISTORIES The Story of CC437
mentally capable, then it is assumed that she was neglected care when she needed assistance. The hospital where CC437 died at was commonly known as Gallinger Hospital or officially known at the time as Gallinger Municipal Hospital Psychopathic Ward. This was located in the District of Columbia. This hospital had later on changed its name to be District of Columbia General Hospital in 1953. Then, after 2001, the area where the hospital was located had changed into a health campus with a variety of clinics. They offered everything from women services to a detoxification center. This hospital had been serving people for over 200 years ever since 1806. It was originally an infirmary, later turning into an asylum. In 1922, the building where CC437 was treated was built (Historic Medical Sites in the Washington). From what we interpreted, due to the time frame the hospital was open; there was segregation between blacks and whites in the population. Due to this fact, she may have not had the best care or attention she needed at the time. The hospital may have had too many patients while lacking attentive staff, causing the patients to lack quality care. It could have been possible if there was more staff maybe this tragedy wouldn’t have happened to CC437. We were comparing CC437’s hospital Gallinger to another psychiatric institution that was in the same area at that time. It could have been possible that if CC437 had been a patient of St Elizabeth’s Hospital she may have had attention quicker and would have survived her cause of death. The hospital was known for their advanced technology since it was the first psychiatric hospital in USA, which opened in 1855. This hospital cared for thousands of patients in 1950s around the same time Mahoney was hospitalized. In fact it provided health care for mentally ill residents of the District of Columbia, U.S. Army and U.S. Navy (Historic Medical Sites in the Washington, DC Area). Patients with mental illnesses were treated very different from modern times. It was possible that CC437 had suffered electroshocks, hydrotherapy, metrazol convulsion and insulin shocks which were very popular methods in 1930s, the same time we believe that she was hospitalized. Later in the 1950’s, doctors used only artificial fever therapy and electroshock. Electroconvulsive therapy (ECT) is defined by Mayo Clinic as “a procedure in which electric currents are passed through the brain, intentionally triggering a brief seizure. ECT seems to cause changes in brain chemistry that can quickly reverse symptoms of certain mental illnesses. It often works when other treatments are unsuccessful. Much of the stigma attached to ECT is based on early Winter 2015•Spring 2016
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treatments in which high doses of electricity were administered without anesthesia, leading to memory loss, fractured bones and other serious side effects”. Patients described this as a horrible treatment that put them at risk for further physical trauma. We have concluded that if CC437 lived in modern day society she may have had a longer life than what she had experienced. With hospitals such as Psychiatric Institute of Washington with services for adults, she could have had intensive short-term care that treats disorders such as depression, schizophrenia and bipolar disorder. In modern day society there are many qualified psychiatrist that she could have gone to diagnose her mental illness and consider possible treatments. With better resources and higher staff to patient ratio, CC437 would have hand more consistent and effective treatment in this modern day. In the last several decades there have been many new changes and advancements in understanding and treating mental illness. We now have a better understanding of the brain as well as technology to see the brain like MRI. In the 1950’s the era of over the counter drugs for treatment mental illnesses was just starting and obviously the poor could not afford those medications. Many patients during that time were sent to hospitals for care and spent years there which are what we suspect happened to CC437. Besides this, many people intentionally went to these hospitals as alternatives to incarceration or homelessness. We believe due to situations like CC437’s, healthcare professionals have learned to prevent problems like respiration obstruction and food aspiration by being attentive to inhibited patients during meal times. It’s highly probable that CC437 would have received better and more urgent care now than in her time frame. It could be possible that she could have died due to neglect because of her skin color. We believe her cause of death is becoming less of an issue in modern day due to the amount of commoners who know CPR and the Heimlich maneuver.
BIOHISTORIES The Story of CC437 Web. 02 July 2015.http://www.crimeandjustice.org/ councilinfo.cfm?pID=54>. "Historic Medical Sites in the Washington, DC Area - District of Columbia General Hospital." U.S National Library of Medicine. NIH U.S. National Library of Medicine. Web. 3 July 2015. <http://www.nlm.nih.gov/hmd/medtour/dcgeneral.html>. "Life Expectancy in the USA, 1900-98." Life Expectancy in the USA, 1900-98. Web. 3 July 2015. Rosenberg, Jennifer. "The 1920s - Historical Timeline of Events." About Education. Web. 3 July 2015. "The Harlem Renaissance." PBS The Rise and Fall of Jim Crow. Educational Broadcasting Corporation, 2002. Web. 3 July 2015. <http://www.pbs.org/wnet/jimcrow/ stories_events_harlem.html>. "The Progressive Era (1890 - 1920)." The Eleanor Roosevelt Paper Project. N.p., n.d. Web. 29 June 2015. Warshawsky MD, Martin E. "Foreign Body Aspiration." Medscape : Background, Pathophysiology, Epidemiology. Medscape, 20 Nov. 2013. Web. 3 July 2015.
References
Adna Hill, Joseph. "Women in Gainful Occupations, 1870 to 1920 Pages 110-113." Google Books. United States Government Printing Office, 1929. Web. 3 July 2015. Web. Anderson, Mark, and Lynda Cannova. "50 Years of Mental Health Hope and Struggle: 1957-2007." Council on Crime and Justice. 2005. Web. 3 July 2015. < • Arnesen, E. (2007). Encyclopedia of U.S. Labor and Working-class History. New York: Taylor & Francis Group, LLC. "Electroconvulsive Therapy (ECT)." - Mayo Clinic. N.p., n.d.
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BIOHISTORIES The Story of CC459
The Backbone
Cobb Collection Short Biohistory
The Story of CC459 Jasmine Mack1,2 Ambra Palushi1,3
1Summer
Medical and Dental Education Program Scholars, W. Montague Cobb Research Laboratory, Howard University 2Department of Biological Sciences, Troy University 3Department of Family Science, University of Maryland: College Park
Editor’s Note
This series of biographical sketches were authored by the 2015 class of the Howard University branch of AAMC’s Summer Medical Dental Education Program (SMDEP) at the W. Montague Cobb Research Laboratory. The students were assigned a Cobb Collection (CC) individual and conducted research about that individual. The papers were reviewed by The Backbone editorial team and the name of the CC individual was redacted. All other factual information was retained.
CC459 was an African American female born in Washington, DC in the early 19th century (1901). CC459’s birth date and month are unknown. She resided on Northwest Street in Washington, DC. The 19th century was a time when African Americans had to adjust to their newly found freedom from slavery (Maloney, Thomas). Sadly, African Americans did not reap the full benefits of being a citizen as whites did because of the lack of progress made from the mid-1800s to the 20th century. As segregation was at its peak, there was a significant gap between people of color and whites. African Americans were disadvantaged in areas such as the job market, education system, and home ownership. Facts reveal that about 50% of black men and 35% percent of black women reported that they worked on a farm as a laborer, however, only about 33% of white men and 8% of white women reported to working on farms as well (EHnet). According to the 1939 census report, black women averaged a mean income around $331.42 compared to the average pay of a white woman, which was around $771.69, which was quite a notable difference. Compared to the 1989 census report, black women were making an average of $15,319.29, which was a dramatic increase. However, they were still ranked the lowest paid group of all. Based on Integrated Public Use Microdata Series Census 1900 and 1990, a vast number of African Americans were involved in jobs that did not require much skill because they were undereducated. A vast CobbResearchLab.com
number of African American children had not even attended school. On the other hand, the white children had more than likely attended a school and would continue their studies in college. The percentage of whites attending school almost doubled those of African Americans. African Americans also did not have the privilege of home ownership. Typically an average African American family lived and worked on a farm owned by whites. Unfortunately, only about one-fifth of African Americans owned their own homes, which was less than half the percentage of whites. As these facts show, African Americans were not treated with equality among whites. Unfortunately, CC459 developed degeneration of the spinal cord. Spinal degeneration affects the spine, brain, and nerves. CC459 received an autopsy on February 4, 1952, which confirmed that she suffered from this disease. She also suffered from encephalomalacia, which is the softening of the frontal lobe in the brain. Spinal degeneration is the result of a lack of vitamin B12 in one’s diet. Diagnosis of vitamin B12 deficiency is typically based on measurement of serum vitamins. A test known as Schilling test is used in order to test for vitamin B12 deficiency. Based on research, spinal degeneration overall lead to CC459’s encephalomalacia. Symptoms of encephalomalacia include headaches, terminal coma, blindness, severe head spinning, or lack of movement coordination. Winter 2015•Spring 2016
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We were unable to locate CC459’s information on any census reports; however, we can assume that she lived with someone else. The recession may have caused a lack of resources as well. We are uncertain if CC459 had an occupation. However, if she did work, research suggests that maybe CC459’s work life could have contributed to her illness. According to EH.net, there was a great need for cheap laborers for Northern employers. More than likely, CC459 decided to join the workforce as a laborer in order to earn an income. Although research does not include the kind of environment CC459 may have worked in, other facts suggests that CC459 could have worked in an atmosphere that requires a tremendous amount of manual labor such as lifting, bending, and twisting. Actions such as these could have caused her condition to worsen over time. These working conditions may have eventually contributed to her death. Vitamin B12 is gained by consuming foods such as beef, liver, and most dairy products. CC459’s diet may have lacked these items. This deficiency of vitamin B12 leads to the abnormal buildup of fatty acids primarily around the spinal cord, but it could also affect the brain and peripheral nerves. The buildup of fatty acids causes the areas to become softer and the areas begin to lose their stability. Some symptoms of this spinal degeneration include abnormal sensations such as tingling or burning, sleepiness/drowsiness, change in mental state, depression, and decreased vision. CC459 checked into Freedman’s Hospital in Washington, DC to receive medical attention. Freedman’s Hospital, which was controlled by the federal government, became the first hospital to provide medical care for former slaves after its founding in 1862 in Washington, DC. This hospital became a refuge for the majority of disabled, aged, and freed African Americans. Poor whites were also going to Freedman’s Hospital to receive medical attention. Unfortunately, Freedman’s Hospital’s leadership team, in the beginning, was involved in several malpractices and misconduct. These acts were very common in low-income hospitals. The malpractice cases consisted of being charged with using the hospital service for selfish gains, along the lines of neglect and even embezzlement. Despite these awful circumstances, a few doctors and nurses working in this hospital continued to help serve the poor by providing treatment whenever possible. Soon states ruled that hospital care should be provided to everyone. In 1990, CobbResearchLab.com
BIOHISTORIES The Story of CC459
there were about 40 black hospitals operating across the country. Freedman’s Hospital was relocated from 13th and R Streets in Northwest Washington, DC to Bryant and 6th Street in 1909. The older building still stands today and it is now known as the Howard University’s School of Communications. In order to preserve the history of the building, it has yet to be completely remodeled, with old hospital rooms still being located in the basement. As for the new facility, it houses 278 state-of-the-art beds, which attracted many potential administrators. One of those administrators was Dr. Charles Drew who is well known for his exceptional blood plasma research. Dr. Drew eventually gained a leadership role and he successfully ran the hospital from 1941 until 1950. The hospital’s reputation was remarkable and it continued to grow in size (Freedman’s Hospital/Howard University Hospital). CC459 most likely visited this hospital because of how close it was to her home. CC459 was likely to have passed from degeneration of the spinal cord as a result of inadequate treatment or lack thereof. Through research, it’s unclear whether CC459’s death occurred due to failure of administering treatment on the hospital's behalf, affordability on her behalf, or availability/existence of treatment options during this time period. Sadly, CC459, age 51, passed away at Freedman’s Hospital in the year 1952. Societal conditions during CC459’s life are significantly different than modern day society. Today, African Americans are able to enjoy the luxury of having opportunities to advance, such as through higher education and availability of resources. According to Fast Facts, between 2000 and 2012, the percentage of college students who were black rose from 11.7 to 14.9 percent. Due to education, African Americans are able to compete in the workforce through accomplishments such as owning businesses, teaching, working for congress, in the healthcare field, and in a variety of other employment sectors. According to the 2012 U.S. Census Bureau report, a resounding 64% of African American women worked in “white collar” and 50% of African American men held “white collar” jobs. Today, home ownership is available to all who can afford it regardless of race and gender. According to the 2012 U.S. Census Bureau report, African American home ownership has decreased from 46% to 42.5% between 2005 and 2012. This could have been contributed to the housing crisis, Winter 2015•Spring 2016
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which caused many Americans to lose their homes due to foreclosure. Unfortunately, in modern day society, all Americans do not have access to healthcare and cannot receive the treatments offered now. According to FastStats 2012 report, the percentage of African Americans under the age of 65 with health care was 17.8%. Sadly, these people could be in the similar situation as CC459. Those individuals’ fate could be the same as CC459’s if left untreated. Interpreting the facts found through research, it shows that CC459 was born in a time period where blacks were not treated as citizens, but rather foreigners. CC459 had to work in an unsafe environment with low pay in order to survive. CC459’s illness may have been the result of an accident on the job that caused severe head trauma. We can assume she continued to work in order to sustain a standard of living, which led to negative progression of her health problems. We presume that by the time she took measures to see a physician her illness was rather irreversible. More than likely, if CC459 lived today, she would have received treatment for her spinal degeneration and encephalomalacia. In present day, CC459 may have endured a better standard of living where she would be presented with educational or employment opportunities that do not require intensive manual labor. Today, there are treatment options available such as physical therapy or spinal surgery. If she were a member of society today, under good conditions, the likelihood of her developing this illness would be very low. Overall, CC459 would have been able to enjoy a less stressful life by being provided with more opportunities to advance in modern society, therefore leading her to live a healthier lifestyle and prevent her tragic illness.
References
BIOHISTORIES The Story of CC459 Encephalomalacia: Symptoms, Causes, and Treatment”. http://www.buzzle.com/articles/ encephalomalaciasymptoms-causes-and-treatment.html “Foods Highest in B12”. http://nutritiondata.self.com/foods -000116000000000000000.html “Freedmen’s Hospital/Howard University Hospital”. http:// www.blackpast.org/aah/freedmen-s-hospital-howarduniversity-hospital-1862 “Historic Medical Areas in Washington, D.C. Area.” http:// www.nlm.nih.gov/hmd/medtour/howard.html J Craniofac Surg. 2011 Nov;22(6):2374-5. doi: 10.1097/ SCS.0b013e318231e511. Maloney, Thomas. “African Americans in the Twentieth Century”. EH.Net Encyclopedia. Robert Whaples. January 14, 2002. URL http://eh.net/ encyclopedia/african-americans-in-the-twentieth-century “National Center for Education Statistics”. http:// nces.ed.gov/fastfacts/display.asp?id=98 “Spinal Degenerative Disease”. http:// neurosurgery.med.miami.edu/clinical-subspecialties/thespine-institute/spinal-degenerative-disease “Subacute combined degeneration”. http:// www.nlm.nih.gov/medlineplus/ency/article/000723.htm “U.S. Census 2012 American Community Survey.” http:// blackdemographics.com/households/housing/
“CDC/NCHS, National Health Interview Survey”. 2012. http://www.cdc.gov/nchs/data/series/sr_10/sr10_259.pdf “Census ACS 2012.” http://blackdemographics.com/ economics/employment/ “Corinna Underwood”. “Schilling Test”. http:// www.healthline.com/health/schilling-test#Overview1“
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RECENT ABSTRACTS Validation of Cobb Collection Biohistories
The Backbone
Recent Abstract from the Cobb Research Lab
Validation of Cobb Collection Biohistories Davlyn Hollie1,2 1W.
Montague Cobb Research Laboratory, Howard University 2Department of History, Howard University
The Summer Medical Dental Medical Education Program, (SMDEP) scholars from the 2015 class of the Howard University site conducted hands-on interdisciplinary bio-anthropological and biomedical research on the 19th and 20th century human skeletal and dental remains, artifacts of the Cobb Collection (CC). For publication in The Backbone, these scholars reconstructed and presented a case studies on the culture, health, lives and deaths of selected individuals in the CC. The purpose of this research is to validate the nine CC Biohistories prepared by the students of the SMDEP summer program. The cases were lightly edited , as the Social Science research group decided to confirm all subjective information before publication. The three History Majors in the W. Montague Cobb Research Lab (CRL) Social Science Committee were assigned a total of three cases. This validation of this information provides an additional experience to the SMDEP students and an opportunity for the history students to conduct primary research. Furthermore, this provides a robust framework for the completion of biohistories for the entire Cobb Collection.
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RECENT ABSTRACTS The Cobb Research Laboratory and Increasing STEM-affiliated Students
Recent Abstract from the Cobb Research Lab
How the Cobb Research Lab succeeds in increasing the number of STEM and STEM-affiliated Students Sherese Taylor1,2
1W.
Montague Cobb Research Laboratory, Howard University of Sociology and Anthropology, Howard University
2Department
While research indicates an under-representation of African Americans and women in STEM (Science, Technology, Engineering and Mathematics), programs that mediate the problem have not been significantly effective. However, minority-serving institutions have been leaders in increasing the number of minority participants in STEM fields, particularly the W. Montague Cobb Research Laboratory at Howard University. The W. Montague Cobb Research Laboratory succeeds in their recruitment efforts because of the sociological insight provided to African American undergraduate STEM majors. The research will aim to understand how this insight is used to effectively recruit African American undergraduate STEM majors. Using participant data, a longitudinal study was conducted from 2014-2016 to investigate the levels of student participation in research and learning. The data is anticipated to indicate that a combination of purely scientific thought and sociological insight, if it aligned with their identity, increases the likelihood of African American undergraduate studentsâ&#x20AC;&#x2122; participation in STEM fields and further in graduate and professional school.
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RECENT ABRACTS Investigation of the Cobb Collection, A Statistical Approach
Recent Abstract from the Cobb Research Lab
Investigation of the Cobb Collection, A Statistical Approach Nicholas Guthrie1,2
1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
Health disparities for African Americans (AA) include differences in rates of cardiovascular diseases, diabetes, periodontitis and life expectancy. In addition, populations living in poverty also exhibit health issues including asthma attacks, obesity, and because a greater percent of Afro-descendant people continue to live below the poverty line, a duality of risk factors exist for this population. The Cobb Collection (CC) is an invaluable snapshot of AA medical history in the late 19th and early 20th centuries, being the largest skeletal archive for AA’s in the United States. Archiving numerous points of medical data in a randomized fashion, the CC is a perfect candidate collection to compare pathology incident rates over the last 150 years. The data points of the CC include cause of death, place of death with a corresponding morgue number, death certificate number, age, sex, race, birthplace, maternal and paternal birthplace, address, and duration dwelling in Washington, DC. This study aims to present the patterns of these AA’s from the Washington DC Area, including migration patterns and pathology incident rates. Once completed, this data will be compared to patterns in the modern day to provide a historical background and make inferences on medical progress and health disparities over the past 150 years.
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RECENT ABSTRACTS
The Backbone
The Cobb Research Lab and SMDEP
Recent Abstract from the Cobb Research Lab
Overview of the Interface of the Cobb Research Laboratory and the Robert Wood Johnson Summer Medical and Dental Education Program (SMDEP) at Howard University Donna Grant-Mills, RDH, M.Ed., DDS1,2 1W.
Montague Cobb Research Laboratory, Howard University 2College of Dentistry, Howard University
The Summer Medical Dental Medical Education Program (SMDEP), funded by Robert Wood Johnson and hosted by Howard University Colleges of Dentistry and Medicine provides 80 academically talented premedical and pre-dental students from under-represented groups with STEM based academic enrichment, mentoring, clinical shadowing opportunities and cultural enrichment. The scholars conduct hands-on interdisciplinary bio-anthropological and biomedical research on the 19th and 20th century human skeletal and dental remains, artifacts, and publish in The Backbone, the official journal of the Cobb Research Laboratory. Scholars are trained, paired with, and work closely with peer mentors, and senior scientists to reconstruct and present case studies on the culture, health, lives and deaths of the individuals in the Cobb Collection. The scholars that complete their research objectives and case studies are presented with a certificate of meritorious research at the SMDEP Closing Ceremony. The value the collaboration is multifaceted. First, for the majority of the 2015 cohort (82.5%), it was their first formal research experience. Second, it connected the scholars to mentors in STEM and other disciplines thus providing them with team based inter-professional experience which is the new gold standard for healthcare delivery. Third, they gain more confidence in their ability to pursue future STEM based opportunities, and fourth they gained a firm understanding of importance of approaching research with cultural sensitivity and respect, by taking into account the socio- economics, history, racial climate, inequalities, and other factors faced by the individuals of the Cobb Collection. As people of color, primarily African Americans, the scholars gained a sense of ownership over and respect of their cultural legacy, and a sense of responsibility with regard to how their ancestors are treated, studied, and documented for future generations.
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RECENT ABSTRACTS
Analysis of DNA Extraction Techniques from Teeth
Recent Abstract from the Cobb Research Lab
Comparative Analysis of DNA Extraction Techniques on DNA yield from Ancient Teeth Latifa Jackson, Ph.D.1,2 Christopher Cross, M.A.,2,3 Muneer Abbas1,4 Fatimah Jackson, Ph.D.2,5 1National
Human Genome Center, Howard University Hospital Montague Cobb Research Laboratory, Howard University 3Department of Anatomy, College of Medicine, Howard University 4Department of Microbiology, College of Medicine, Howard University 5Department of Biology, Howard University 2W.
While much reporting has been done to understand ancient DNA techniques for archaic human populations, little work has been done to characterize the feasibility of extracting DNA from historical populations of humans who lived less than 200 years ago. Here we examine three methods for DNA extraction from skeletal remains using CC672, an individual from the W. Montague Cobb Skeletal Collection, who died 85 years ago. Dentine-cement powder was obtained from molar teeth. Molars were scraped free of cementum (CC), calculus (CL), and periodontal ligament (PDL). Each was isolated separately and then the remaining CC, CL, and PDL debris was combined in a mixed sample (MX). Extraction was conducted using Oragene (saliva based), Qiagen (blood and tissue), and phenol-chloroform. These techniques were implemented in parallel. Extractions were then measured for DNA concentration, confirmed for DNA quality and finally amplified to further assess DNA viability. We were able to recover DNA from all three methods in all samples. The phenol chloroform extraction yielded the largest DNA amounts (138.2-1865.6 ng/µL), next the Qiagen yielded between (12.7-13.9 ng/µL for S samples, 6.5-9.7 ng/µL for CC672 samples) and Oragene yielded intermediate DNA amounts (S5:75.5 ng/µL and MX:21.2 ng/ µL). DNA was amplified using the FOXP3 gene with 90% success. This molecular analysis suggests that conventional extraction methods for ancient DNA are robust to analysis of Cobb Collection samples. Amplification of the DNA extracted shows that human DNA was present in sufficient quality. This exciting result will be followed up with further analysis.
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RECENT ABSTRACTS
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Geospatial Assessment of CC Individuals
Recent Abstract from the Cobb Research Lab
Geospatial Assessment of Residential and Work Sites for Cobb Collection Individuals Hasan Jackson1,2 1W.
Montague Cobb Research Laboratory, Howard University of Geographical Studies, University of Maryland
2Department
Due to the history of segregation in the Washington area it is likely that the populations of certain neighborhoods were mostly uniform in terms of ethnicity. There may have also been important geographic substructure by occupation as well, resulting in significant clustering of African Americans (AAs) from the Cobb Collection (CC) individuals in the Washington DC region. Social status, occupation, education, and affluence may also have contributed to the selection of neighborhoods and worksites. Communities with lower socioeconomic status likely resided and worked in non-favorable neighborhoods with close proximity to pollutants and increased distance from major roads. The residential and work settings of 19th and 20th century CC individuals resulted in increased levels of exposure to pollutants for some neighborhoods compared with others. Spatial analyses are used to understand the chemical and physical exposure dynamics of Cobb Collection individuals in the District of Columbia metropolitan area from 1920-1960 to environmental factors that could modify the gene expression patterns in 150 individuals. Specifically, this research looks for possible signs of community segregation related to disease status, ethnic background and occupation. The residences and worksites of CC individuals are mapped and the demographic, genomic, and potentially epigenomic influences stratified horizontally across the Washington DC region. Historical maps of the District of Columbia and its surrounding areas dated to the mid-20th century will be obtained from databases of historical maps located in the National Archives as well as gathered from other peer reviewed sources. The CC has address-based residential and occupational information on each individual in the target population. These data will be used to provide a single reference location for each CC individual under study. Residences will be geocoded based upon the historical maps of the region, providing a latitudinal and longitudinal reference for each individual. The Cartesian plane of residences will be ingested into a spatially referenced database. This will allow spatial comparisons to be made for each residential point, the center for each residence (centroid) will be used, and at the level of neighborhood/ ward. Previous studies of spatial clustering in urban areas have used spatial aggregation of geocoded data points to identify area level characteristics in studies of health patterns (25-28). ArcGIS 10.2 version (ESRI, Redlands, CA) is used to perform geocoding tasks
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RECENT ABSTRACTS
Minimally Invasive Method to Extract DNA
Recent Abstract from the Cobb Research Lab
Minimally Invasive Method to extract DNA from Dentition using Cobb Collection Human Skeletal Remains Alexis Payne1,2 Christopher Cross, M.S.1,3, Latifa Jackson, Ph.D.1 John Harvey, D.D.S.4, Fatimah Jackson, Ph.D.1,2 1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University 3Department of Anatomy, Howard University 4College of Dentistry, Meharry Medical College
Teeth have been used as a source of DNA for identifying fragmented and degraded human remains. Cellular cementum is collected and analyzed for DNA sequencing. Cementum is the outside layer of the tooth that is located on the roots. The location of teeth within the jawbone makes them a great choice due to the protection the bone provides. Teeth selection for extraction is based on studies of the anatomical characteristics of teeth. Additionally, it is known that cellular cementum will be greatest on teeth with the largest root surface area, like molars, premolars and canines. The extraction process of removing cementum, however is not as widely understood. With the use of the Cobb Collectionâ&#x20AC;&#x2122;s dental remains, a new procedure for cementum extraction that grants preservation of the entire tooth has been developed. The Cobb Collection provides a unique source of 19th and 20th century African American biological histories. Cementum extraction and DNA sequencing of these individuals will support further subsample studies on raw material of human remains. The procedure also supports oral microbiome analysis to understand dietary habits and disease exposure in studied individuals. Cementum extraction through the roots is a minimally invasive. It can provide critical information that can advance clinical science. Our methodology re-engineers current clinical dental practices for research purposes by curvette removal of plaque, calculus, cementum, and remnant periodontal ligament tissue. We have successfully extracted dental-derived DNA from all of the aforementioned layers and are currently optimizing these procedures. This technique both protects and makes use of the precious material for current studies and future generations.
CobbResearchLab.com/TheBackbone
Winter 2015â&#x20AC;˘Spring2016
Volume 02 Issue 01 64 1
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RECENT ABSTRACTS Causes of African American Osteoarthritis in the Cobb Collection
Recent Abstract from the Cobb Research Lab
Trends and Causes of African American Osteoarthritis and Osteoporosis within the Cobb Collection Sierra Williams1,2 2Department
1W.
Montague Cobb Research Laboratory, Howard University of Health, Human Performance and Leisure Studies, Howard University
Like many other health problems, the misconception that African Americans should not be concerned about developing osteoporosis leads to African American women being under diagnosed and treated. Statistically, African American women have a higher bone mineral density than European American women. Bone mineral density represents the strength of the bone and the amount of calcium within the bone. Degeneration and “wear and tear” on the bones will show aging in the bones, a sign of osteoarthritis. It is a condition expected to be seen in the collection due to the lifestyles of the individuals. Within the Cobb Collection we will be looking for the presence of osteoarthritis and osteoporosis likely caused by disease, poor nutrition, inadequate physical activity, excessive thinness and being post menopausal. There are increased risks of fracture and bone strength with those suffering from osteoporosis. By observing the skeletal remains we will be able to recognize some of these conditions that may cause osteoporosis. From our observations we hope to validate the presence of bone disease in the African American females of the CC, though we anticipate the prevalence to be much lower than that of their white counterparts. This study will focus on a subset of African American and European American post-menopausal women, who from clinical and physical clues suggest evidence of bone disease. These groups will then be analyzed for statistical significance using ANOVA/t-test. We hope to shed light on the need for further research in the area of bone disease in African Americans.
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Winter 2015•Spring2016
Volume 02 Issue 01 65 1
RECENT ABSTRACTS
The Backbone
Osteoarthritis within the Cobb Collection
Recent Abstract from the Cobb Research Lab
Evidence for Arthritis and Specifically Osteoarthritis in the Cobb Collection Maimouna Traore1,2 1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
Arthritis is a chronic disease characterized as the inflammation of joints caused by the degradation of the fundamental cartilage. The symptoms associated with arthritis are severe pain, swelling and stiffness amidst the affected joints which can impede the motility of the affected individual. Consequently, arthritis has risen as the main cause of disability amongst Americans. Although there are a multitude of forms of the disease, one of the most common forms is osteoarthritis. Osteoarthritis occurs predominantly on joints that endure the pressure of weight such as the knees and hips of the human body. Naturally, the risk of acquiring osteoarthritis increases with age as the cartilage degrades over the course of several years. Currently, between 10%-20% of adults are suffering from a degree of osteoarthritis in North America alone. However, age is not the only variable with which the disease correlates. Studies analyzing knee radiographics have shown that osteoarthritis has a greater prevalence amongst African Americans, more specifically African American women. Therefore, the Cobb Research Lab intends to investigate the African American individuals of the skeletal collection for evidence of osteoarthritis. The determined severity of the disease in each case can give further insight into the identity of the individuals as it suggests age, physical health and range of motility.
CobbResearchLab.com/TheBackbone
Winter 2015â&#x20AC;˘Spring2016
Volume 02 Issue 01 66 1
The Backbone
RECENT ABSTRACTS
Bio-Historical Analysis of Cardiovascular Disease
Recent Abstract from the Cobb Research Lab
Bio-Historical Analysis of Cardiovascular Disease in the Cobb Collection Jameshisa Alexander1,2 1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
Cardiovascular disease, commonly known as heart disease, consists of multiple complications involving the cardiovascular system. People with medical conditions like diabetes and obesity and live lifestyles with, poor diet, lack of exercise and high alcohol consumption are at increased risk for cardiovascular disease. The greatest risk factors for cardiovascular disease are high blood pressure, high cholesterol and smoking. The incidence and prevalence of CVD is directly related to the incidence and prevalence of CVD risk factors. There has been an increasing prevalence of obesity from 15 to 30 percent between 1960 and 2000 and in diabetes rising from 1.8 to 5.0 percent. However, some major risk factors like high cholesterol, hypertension and smoking have decreased. The prevalence statistics show that high cholesterol has decreased from 34 to 17 percent, hypertension from 31 to 15 percent, and smoking from 39 to 26 percent. Even though the prevalence of some major risk factors have increased, the prevalence of CVD has decreased. About 610,000 deaths occur in the United States every year is caused by cardiovascular disease (CVD), making it the leading cause of death for both men and women. Cardiovascular disease is divided into four main categories: heart valve complications (regurgitation and stenosis), arrhythmia, heart attack and stroke. Atherosclerosis is the building of plaque in arteries commonly leading to heart attacks or strokes. Physicians diagnose patients with these ailments based on risk factors identified from medical history, physical exam and a variety of specific tests. These conditions are treated with medications, institution of medical devices such as pacemakers, implantable cardioverter defibrillator (ICD) or Left Ventricular Assist Devices (LVAD), procedures like heart value replacements/repairs, heart transplants, and surgery. In the Cobb Collection (CC), we have multiple cases of cardiovascular disease such as congestive heart failure, atherosclerotic heart disease, value issues and hypertrophy. Using the data collected on the individuals in the CC, we can compare the trends and of cardiovascular disease previously and presently. This allows us to examine this chronic disease from a unique historical perspective.
CobbResearchLab.com/TheBackbone
Winter 2015â&#x20AC;˘Spring2016
Volume 02 Issue 01 67 1
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RECENT ABSTRACTS
Trends of Hypertension and Cardiovascular Disease in the CC
Recent Abstract from the Cobb Research Lab
Historical Trends of Hypertension and Cardiovascular Disease within the Cobb Collection Janet Mansaray1,2 1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
Hypertension is a current health issue that greatly affects the African American community. It is linked to the cause of cardiovascular conditions such as rheumatic heart disease, arteriosclerotic heart disease, hypertensive heart disease, cerebrovascular accidents (CVA), and inflammatory heart disease (carditis). To investigate the progression of such conditions in African Americans and their evolution of treatment, we will analyze these clinical manifestations within the Cobb Collection. In the database, the number of cause of deaths for each condition found is as follows: rhuemeric-2, hypertensive-11, arteriosclerotic-23, CVA-17, inflammatory-11, general cardiovascular diease-8, and those with a condition called myocarditis-6. This is a total of 78 individuals revealing that hypertension and its related cardiovascular conditions was a problem for African Americans, as it today. 5 individuals out of the 78 were chosen for case studies and their biological histories were reconstructed. This information was then compared to modern profiles of African Americans in order to observe whether modern treatments have affected the life expectancy within people who suffer from cardiac disease. The main purpose of this study was to provide a historical prospective on cardiovascular conditions caused by hypertension in hopes of seeing why such conditions are still prevalent in African Americans.
CobbResearchLab.com/TheBackbone
Winter 2015â&#x20AC;˘Spring2016
Volume 02 Issue 01 68 1
RECENT ABSTRACTS
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Biohistory of Congestive Heart Failure in the CC
Recent Abstract from the Cobb Research Lab
The Prevalence and Biohistory of Congestive Heart Failure in the Cobb Collection Kayla Bedeau1,2 2Department
1W.
Montague Cobb Research Laboratory, Howard University of Health, Human Performance and Leisure Studies, Howard University
Congestive heart failure (CHF) is a common cause of death, affecting over 5 million people in the United States in 2013. CHF occurs when the muscle of the heart weakens, failing to provide oxygenated blood throughout the body. In the later stages, blood will pool inside of the heart, leading to complete failure. Among others, hypertension is a major risk factor for CHF. Commonly known as high blood pressure, hypertension is indicated when the systolic blood pressure and diastolic blood pressure are above 140 mmHg and 90 mmHg respectively. Hypertension continues to be a major health risk, especially in the African American (AA) community where over 40 percent of AAâ&#x20AC;&#x2122;s are affected. Because of this prevalence, the Cobb Collection (CC) is an invaluable source, being the largest collection of AA archeological material in the country. We have identified 36 individuals from the CC who have died from Congestive Heart Failure in order to analyze their medical history and lifestyles. Then, a comparison of incidents and treatments between the 1900s and modernity will create a better understanding of the impact that hypertension has on congestive heart failure, while also contributing to the sparse amount of scientific literature on the AA community.
CobbResearchLab.com/TheBackbone
Winter 2015â&#x20AC;˘Spring2016
Volume 02 Issue 01 69 1
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RECENT ABSTRACTS
Factors of Diabetes in the African American Community
Recent Abstract from the Cobb Research Lab
The Correlations between African-American Life Experiences and Type 2 Diabetes Whitney Griffith1,2
1W.
Montague Cobb Research Laboratory, Howard University 2Department of Computer Science, Howard University
The increasing prevalence of diabetes is considered problematic, as it is the seventh leading cause of death in the United States. The CDC’s 2014 National Diabetes Statistics Report states that in the US, 29.1 million people are living with diabetes out of which 13.2% (3,841,200) are African-Americans. Interestingly, this number is approximately 1.7 times more than the number of diabetic whites in the US. Diabetes is a disease that involves abnormal levels of blood glucose resulting from problems in how insulin is produced or works. There are two types of diabetes, Type 1, which is caused by the destruction of the insulinproducing cells in the pancreas and Type 2, which is a result of insulin resistance among cells. Type 2 diabetes is described as a lifestyle disease as it develops due to specific risk factors in one’s life. This research intends to show that the prevalence of Type 2 diabetes among African Americans is not due to personal life choices but that it results from the stresses society places on African Americans such as residential, economic, and educational segregation. The Cobb Collection offers a special resource of the study of African Americans from the 19th and 20th century. It is highly suited for this research as it contains African Americans who were living in a time of Jim Crow Laws. Thus, individuals in the Cobb Collection that were diagnosed with Type 2 diabetes can be identified and their lifestyles analyzed in an attempt to indicate the environmentally- caused emotional, physical and nutritional stressors that contributed to their development of Type 2 Diabetes.
CobbResearchLab.com/TheBackbone
Winter 2015•Spring2016
Volume 02 Issue 01 70 1
RECENT ABSTRACTS
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Cerebrovascular Accident within the CC
Recent Abstract from the Cobb Research Lab
Prevalence of Cerebrovascular Accident within African Americans of the Cobb Collection Natalia Christian1,2 1W.
Montague Cobb Research Laboratory, Howard University of World Languages and Culture, Howard University
2Department
In the African American community, cerebral vascular accident (or stroke) is one of the leading causes of death. Hypertension causes approximately 50% of ischemic strokes, which are caused by a development of atherosclerosis. Studies show that African-Americans have the highest rate of hypertension in the United States. Stress can significantly contribute to the development of hypertension through recurrent blood pressure elevation and stimulation of the nervous system to produce large amounts of vasoconstriction hormones that eventually lead to elevated blood pressure. Socio-economical, sociological and psychological factors coupled with familial history in the African American community contribute to the development of this fluctuation in blood pressure and nervous response. From the clinical materials available on the Cobb Collection, I will identify the individuals who reportedly died from ischemic stroke. I will use additional resources to reconstruct the biological histories of a subset of individuals with stroke and relating ailments. By performing case studies on the affected individuals in the Cobb Collection and delving into their personal lives, the causes of hypertension and eventual stroke will be identified and placed in historical context. This information will provide insight into the progression of modern day environmental circumstances and treatments that have contributed to the clinical expression of cerebrovascular accident.
CobbResearchLab.com/TheBackbone
Winter 2015â&#x20AC;˘Spring2016
Volume 02 Issue 01 71 1
RECENT ABSTRACTS
The Backbone
The Resurgence of Rickets and Scoliosis
Recent Abstract from the Cobb Research Lab
Assessment on the Resurgence of Rickets and Scoliosis on African Americans Khristian Ifill1,2 2Department
1W.
Montague Cobb Research Laboratory, Howard University of Health, Human Performance and Leisure Studies, Howard University
The purpose of this study is to identify and comprehensively assess the effects of scoliosis and rickets on the African American community. Prior studies have shown that African Americans are at greater risk of being diagnosed with scoliosis and are more susceptible to rickets as well. This increased risk factor for African Americans stems from the decreased levels of vitamin D able to be synthesized by people of darker skin complexions. By using the laboratory materials in the Cobb Research Lab, I will examine and analyze subjects reported to have passed away from rickets and scoliosis. I will also use a multitude of various resources such as scientific evidence, medical journals and the reports made by the Cobb Research Lab to reform the biological history of specific groups of affected people. By analyzing these diseases in detail, I will in turn develop a better overall level of understanding of the historical causes and treatments of scoliosis and rickets and how they matriculated over time.
CobbResearchLab.com/TheBackbone
Winter 2015â&#x20AC;˘Spring2016
Volume 02 Issue 01 72 1
The Backbone
Recent Abstracts Effects and Treatment of Alzheimer’s in African Americans
Recent Abstract from the Cobb Research Lab
Identifying the effects and treatment of Alzheimer’s disease in African Americans Youngho Jung1,2 1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
The first ever recorded case of Alzheimer’s can be credited to Dr. Alois Alzheimer, a pioneer in linking symptoms to microscopic brain changes. He describes the haunting case of Auguste D. in 1906, a patient who had profound memory loss, unfounded suspicions about her family, and other worsening psychological changes. After her death 5 years later, Dr. Alois discovered that her brain underwent dramatic shrinkage and abnormal deposits in an around the nerve cells. Early discoveries regarding the peculiar disease were initiated using the electron microscope, for example, to allow further study of the brain. Beta-amyloid, a novel cerebrovascular amyloid protein and the chief component of Alzehimer’s brain plaques and the trigger for nerve cell damage was discovered in 1984. Since then, major strides have been taken to deterimine the genes responsible for Alzheimer’s disease. In 1991, a clinical study was launched by the federal governments. This led to the new criteria and guidelines for Alzheimer’s disease diagnosis, and in turn, paved the way for the first major clinical trial for the prevention of Alzheimer’s disease. But as with much progress, there are still an estimated 5.3 million Americans with Alzheimer’s today, and more than half are African Americans. What is most surprising is that, it wasn’t until August 11, 2015, they discovered the disease occurred much differently among patients from the European and non-European communities. That convinced researchers to further investigate patients treated historically. The Cobb Collection is an excellent site. Currently, I am attempting to elucidate the clear differences on how Alzheimer’s affects the African-American community, and the mistreatment in turn to the patients that lived before our lifetime.
CobbResearchLab.com/TheBackbone
Winter 2015•Spring2016
Volume 02 Issue 01 73 1
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RECENT ABSTRACTS
Reconstructing Environmental Biohistory and Health
Recent Abstract from the Cobb Research Lab
Lead in Teeth: Reconstructing Environmental Biohistory and Health at the New York African Burial Ground Using Laser Ablation-Inductively Coupled Plasma-Mass Spectrometry (LAICP-MS) Joseph L. Jones, Ph.D.1,2 1W.
Montague Cobb Research Laboratory, Howard University of Anthropology, College of William and Mary
2Department
The study of ancestral skeletal remains continues to reveal new dimensions and important details of African diasporic biohistory. Teeth, for example, develop at known ages (through adolescence) while incorporating environmental chemical exposures associated with forced migration, diet and health. Even a single tooth crown formed over several years serves as an archive of childhood and/or adolescent living conditions; biohistories potentially formed across varied African and American settings. Here, I report on the recent analysis of enamel-lead for 44 children, women and men excavated at the 17th- and 18thcentury New York African Burial Ground in lower Manhattan. This study is the first quantitative investigation of human lead exposure in early America via laser ablation- inductively coupled plasma-mass spectrometry (LA-ICP-MS). This recently-developed microprobe methodology enables the spatial mapping of lead concentration in teeth such that age-related changes in the extent and (acute versus chronic) nature of exposure are detectable. Among the key findings, enamel-lead concentrations ranged from 0.39 μg g-1 (i.e., the instrument limit of detection or LOD) to 14.7 μg g-1, suggesting negligible (background level) exposures for some while others spent their childhoods in high-lead environments. Mean enamellead concentration for young children (5.88 μg g-1) is over five times that of adults (1.11 μg g-1), a significant difference reflecting these groups’ mostly American versus African geographic origins, respectively. These findings shed new light on lead exposure and poisoning – persistent public and global health concerns – at the origins of African America and the nation.
CobbResearchLab.com/TheBackbone
Winter 2015•Spring2016
Volume 02 Issue 01 74 1
RECENT ABSTRACTS Elemental Determination of Soil Samples
The Backbone
Recent Abstract from the Cobb Research Lab
Profile and initial elemental determination of soil samples collected from the New York African Burial Ground Remains Candice Duncan, Ph.D.1,2 1W.
Montague Cobb Research Laboratory, Howard University Human Genome Center, Howard University Hospital
2National
Soil analysis is an important tool to understand the bioanthropology of human habitation and grave locations. Analysis of metals, phosphorus and other molecules can build a portrait of the environmental conditions in which populations of interest existed. The New York African Burial Ground and the W. Montague Cobb Research Laboratory each contain numerous grave soil samples that can enhance current understandings of the daily lives of these 17th and 18th century populations. The initial determinations on the grave soil samples includes: 1. Determination of total soil mass collected. The one bag soil sample will be weighed, soil transferred into a sealed glass container and cloth bag weighed. The cloth bag will also be transferred into a sealed glass container for future chemical analysis. 2. A grab sample of X grams will be collected, and set aside in a sealed glass container, for future chemical and microbiological analysis.
3. A sieving process will be used to determine the particle size of soil composition to classify soil material (i.e. sand, silt, etc.). 4. A pictorial classification will be created to identify and separate all soil and non-soil (i.e. hair or bone) materials with the remaining sample. An EPA Method 3052 will be used for the acid digestion of the soil followed by atomic absorption (AA) spectroscopy to determine the iron, lead, copper, magnesium, zinc, calcium and silver compositions of the grave soil. These data will permit complex analytical chemistry assessments upon which we can construct a rich portrait of the environmental toxins to which these individuals were exposed and identify possible gene X environment interactions at this site.
CobbResearchLab.com/TheBackbone
Winter 2015â&#x20AC;˘Spring2016
Volume 02 Issue 01 75 1
The Backbone
RECENT ABSTRACTS
Analysis of Grave Soil Samples at the NYABG
Recent Abstract from the Cobb Research Lab
Analysis of Grave Soil Samples found in the New York African Burial Ground Keely Clinton1,2 1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
The New York African Burial Ground is the location of the greatest number of free and enslaved African burials in a common place during the 17th and 18th centuries. It is speculated that the burial ground was more than likely established by Negro frontier residents initially being called the “Negroes Burial Ground”. The burial ground was specifically found on a lot in lower Manhattan (Block 154) surrounded by Broadway to the west, Duane St. to the north, Reade St. to the south and Elm St. to the east, with important landmarks such as Crolius pottery to the northeast and Collect Pond to the east, as early maps indicate. Location must be taken into account as it determines the composition and condition of the grave soil samples. In this study we are able to observe the origin of each grave sample, their orientation in relation to each other, the depth at which the grave soil was obtained (between 6ft. and 25 ft.) and whether or not there was an individual/ partial remains/ artifacts associated with each sample. We are also able to observe the stratigraphic analysis based on differences in color and type of the soil and archaeological records. Most of the 49 grave samples are derived from the Middle Group of the African Burial Ground. The Middle Group is documented as the collection of burials located throughout the excavated site except north of the fence line during the time the burial ground was extensively used.
CobbResearchLab.com/TheBackbone
Winter 2015•Spring2016
Volume 02 Issue 01 76 1
RECENT ABSTRACTS
The Backbone
Access to Research on the ABG Materials
Recent Abstract from the Cobb Research Lab
Enhancing Public Access to Recent Research on the African Burial Ground Materials: Grave Soil and Oral Microbiome Analyses Fatimah Jackson, Ph.D.1,2 1W.
Montague Cobb Research Laboratory, Howard University 2Department of Biology, Howard University
The 17th and 18th century samples in the Cobb Research Laboratory are derived from the New York African Burial Ground remains currently housed at Howard University and on loan from the National Park Service. The NYABG is the nationâ&#x20AC;&#x2122;s earliest and largest African burial ground. These previously buried samples reflect African/African American biological diversity from the late 17th to late 18th centuries in New Amsterdam/New York City. While there are an estimated 15,000 burials, we have well-documented, archived biological remnants from approximately 250 individuals. Research on these 17th and 18th century samples hold the key to providing evidence for important processes in human evolutionary biology and biological history. For example, the grave soil studies will reveal the biological relationship between individuals in various grave sites, the molecular sex of juveniles, the extent to which deceased individuals were exposed to specific environmental toxins and certain pathogens, and their ancestry genetics. The oral microbiome studies will yield insights into the dietary patterns of individuals, their exposure to certain infectious diseases, and their contact with ingested toxins in the form of medications and drugs. The two research projects proposed will generate unique data on the life histories and background biology of NYABG individuals. By using minimally invasive research techniques, the projects will enhance preservation of the collection while providing essential knowledge which will then be disseminated to scientific professionals, NPS interpreters, and the public. The research projects will optimize student outreach and education and increase the numbers of underrepresented ethnic minority group members in science, technology, education, and mathematics research. The NYABG is already a designated visitor site for the entire freshman class each year at Howard University. Implementation of these projects and translation of the research results to make them accessible to the general public will make the NYABG even more valued and compelling site for visitation, reflection, and growth.
CobbResearchLab.com/TheBackbone
Winter 2015â&#x20AC;˘Spring2016
Volume 02 Issue 01 77 1