Rutgers Science Review

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Rutgers Science Review Volume 1 Issue 1 Fall 2011

gene doping The New Face of Sports?


contents Man of Science pgs 4-5 Genetic Manipulation of an AgeOld Tradition pgs 6-8 Take a Number (Primary Care: A Dying Profession) pgs 9-10 Gerty Cori pg 11 Interview with Dr. Karl Herrup pgs 12-13 Perpetual Poetry pg 14 Relationship Between Mosquito Larvae and Parasitic Mermithid Nematodes pgs 15-17 Investigation of Binary Metal Sulfide Dielectric Thin Films in Silver Coated Hollow Glass Waveguides (HGWs) for Infrared Radiation Delivery pgs 18-27 2 | Rutgers Science Review | Fall 2011

closeup of a bacterium


About

The Rutgers Science Review (RSR) biannually publishes student-written scientific features, opinions, and research papers. RSR is supported by RUSA Allocations. For more information, including submission guidelines, visit us at thersr.com

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Lawrence Xie Dr. Steven Brill Valentina Lyau

Fall 2011 | Rutgers Science Review | 3 closeup of a broken bone


Man of

Science

by neil raju

Winning the Nobel Prize in Medicine is no small feat. Since its establishment over a century ago, the award has been reserved for the best and brightest of the medical community – individuals whose research have revolutionized the modern practice of medicine. This year’s Nobel Prize-winning team was no exception; Dr. Ralph Steinman and Dr. Zanvil Cohn both made history with their discovery of the dendritic cell and its role in adaptive immunity. Steinman and Cohn, Steinman’s postdoctoral research fellow at Rockefeller University, discovered the dendritic cell in 1973. Over the years, research has shown dendritic cells to be a vital part of human (and many other mammalian) immune systems. In his 2010 video about dendritic cells, Dr. Steinman stated that “their most distinctive feature was that the cells we had discovered had many processes . . . they’re constantly probing the environment, looking for all the challenges that the immune system has to deal with. And when they see the challenge, they have to take it into the body and teach the immune system what to do.”

Dr. Ralph Steinman (January 14, 1943 – September 30, 2011) was awarded the 2011 Nobel Prize in Medicine for his work in adaptive immunity, just days after his death from pancreatic cancer. 4 | Rutgers Science Review | Fall 2011


Features Following his discovery, Dr. Steinman continued to research adaptive immunity. His contributions both broadened scientific understanding of the human immune system and enabled the development of new therapeutic techniques. Most notably, Dr. Steinman’s research lead to the production of the immunostimulant, Sipuleucel-T, a prostate cancer vaccine marketed as Provenge by the Dendreon Corporation. This treatment has proven to be one of the few effective remedies for advanced prostate cancer. Though Steinman was awarded the 2011 Nobel Prize in Medicine for his studies on adaptive immunity and immunotherapy, this research was by no means his only scientific focus. Steinman’s colleague, Dr. Sarah Schlesinger, described him as an opponent of “mice models” (a.k.a. animal testing) and a strong believer in human clinical research. He was acclaimed for his passionate drive to make a difference in people’s lives. When he was diagnosed with stage-four pancreatic cancer several years ago, Steinman determined to become his own medical guinea pig. In the past six and a half years, he went so far as to test eight different unproven and unapproved cancer treatments on himself. In spite of his under one-percent survival probability, Steinman continued his research until he passed away on September 30th, 2011. Three days later, he was declared the first posthumous recipient of the Nobel Prize in Medicine, an award well-deserved.

Because dendritic cells capture, process, and present antigens, they provide an important means for monitoring and manipulating immune function. They were discovered by Dr. Steinman and Dr. Cohn.

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Fall 2011 | Rutgers Science Review | 5


Genetic Manipulation of an Age-Old Tradition

By Ashante’ Patterson

Traditionally, athletes train for years to become masters at what they do...

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Features Traditionally, athletes train for years to become masters at what they do. Intense physical training combined with strict dieting allow athletes to push the boundaries of human performance – but gene doping can change all of that with a simple injection.

WHat is gene doping? Gene doping is the non-therapeutic use of genes, genetic elements, or cells that have the capacity to enhance athletic performance – very much analogous to the infamous anabolic steroids of the past century. By injecting viral vectors into their bodies, athletes can introduce new “transgenes” into their genetic makeup, giving them traits that let athletes jump higher, run faster, or hit harder. The technology for this use of gene therapy, although still in its infancy, is rapidly progressing and is liable to spawn a host of ethical debates.

“If people are going to expect these great performances, these falling records, they have to expect that athletes will do anything to get there.”

regulated to ensure athletes compete at an equal level. Since the release of the Speedo LZR, the full body swimsuit used by Olympian Michael Phelps in 2008, nearly 200 world records have been broken -- which resulted in its ban in 2010 among professional level swimmers. In the same year, the NBA banned Concept 1 basketball shoes for the unfair jump height advantage they gave players. The Little League, meanwhile, banned composite baseball bats for competition at the high school level. As technology advances, gene doping too will be added to the growing list of resources needed to spar with the best. Its implementation will only become more realistic as gene therapy becomes more reliable, and scientists believe gene doping will soon become a considerable temptation for athletes, especially when it comes down to the Olympics. Dr. Dan Hamner, a former world-class track athlete and physician in New York, adds, if people are going to expect these great performances, these falling records, they have to expect that athletes will do anything to get there.”

The face of sports has already been irrevocably changed by technology, whose advancement has proceeded so quickly that equipment must be

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Features

Doping Abuse Erythropoietin (EPO), a hormone that regulates for gene doping through “gene chips,� DNA

red blood cell production, is one conceivable example of gene doping. Synthetic EPO, banned by the International Olympic Committee in 1986, allows athletes to raise their endurance by producing more red blood cells and carrying more oxygen in their blood. In 2006, EPO abuse rose to a new level when Thomas Springstein, a German athletics coach, was convicted of doping his underage athletes with the drug Repoxygen. Rather than providing external EPO, Repoxygen activates the genes that code for EPO only when one’s oxygen levels are low. As a result, the drug is undetectable by traditional doping tests and highly coveted by would-be dopers.

Many young athletes do not understand the process of gene doping, nor its potential side effects. The World Anti-Doping agency (WADA) and geneticists fear that athletes may start gene doping for the sake of winning a gold medal, without

If genetically manipulated athletes are put into the mix, could we still call it a competition? considering its safety or its ethical implications. Anti-doping authorities are developing tests 8 | Rutgers Science Review | Fall 2011

microarrays featuring a menu of genes most likely to be altered by foreign performance enhancing genes like that for EPO. To use the technology, athletes will give blood to be analyzed just as they give urine for traditional drug tests. WADA and other gene doping agencies are continually working on ways to stop gene doping and to ensure the safety of athletes. Sports have always been a platform in which people from all around the world could compete in an atmosphere of equality and fairness. If genetically manipulated athletes are put into the mix, could we still call it a competition?


Take a Number Primary Care: A Dying Profession By Vishal Patel

specialist who may see patients as cases to solve rather than patients to treat. Though occasional crises do require such specialists, primary care physicians are now in ever-greater demand. The Washington Post and Health Resources and Services Administration reports that only 37% of physicians practice primary care medicine, and as few as 8% of the nation’s medical school graduates go into family medicine. With such worrisome statistics, it is apparent there is a gaping hole in American health care with little being done to stitch it up. This vanguard of preventative medicine – the veritable quarterbacks of our healthcare team – is slowly eroding, resulting in an endless baton pass among specialists who often coordinate poorly and can offer only a narrow (albeit highly accurate and extensive within their respective fields) range of medical knowledge.

The “good ol’ days” of personable, patient-friendly doctors are slowly becoming a relic of the past. No longer can patients expect detailed discussions and comfortable chit-chat – instead they are met with impersonal receptionists and perfunctory, often inadequate physical evaluations. An hour-long wait today may amount to only a minute-long examination, and sometimes, to a second-long diagnosis of “psychological” pain. As medicine has become increasingly specialized, doctor-patient relationships have deteriorated. Our new generation of doctors is becoming geared towards fine-tuned expertise in an ultra-specific field. As a result, relationships with patients are difficult to establish for the

What’s worse for patients, however, is that without primary care, they will be subject to the reactive medicine of specialists that is often unnecessary and complicating. In fact, a 2007 Harvard Health Policy Review article noted that a higher ratio of specialists to population has been correlated with higher mortality rates, while a higher ratio of primary care physicians to population is better for health. Specialty docs are often associated with technical and expensive procedures that that are perfectly bankable for physicians that are paid fee-for-service, a system whereby physicians are compensated based on the quantity of healthcare delivered instead of its quality. Caught in a vicious healthcare loop, patients are left penniless and with no end in sight.

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Features Certainly, patients are the ultimate victims under these circumstances, but here’s the rub: doctors are caught in crisis, too. Our healthcare dilemma is part of a trickle-down effect starting with the rising cost of medical education. Becoming a doctor isn’t cheap; many medical students graduate nearly $200,000 in debt. With such steep dues, newly minted M.D.’s are not willing to sacrifice a higherpaying, faster-paced specialty practice for a career in general medicine commonly perceived to be more trouble than it’s worth. According to the American Academy of Family Physicians (AAFP), the number of general practitioners has fallen by 51.8% since 1997, and this pattern is likely to continue if wide income disparities between them and specialists persist. Primary care must be incentivized for medical students, meaning that it must pay competitively enough to make it as enticing as ROAD specialties (radiology, ophthalmology, anesthesiology, dermatology). If every American were to regularly visit a general

You don’t get paid to talk to people and tell them to stop smoking. Nobody values my time to do that. practitioner, healthcare costs might come down as much as 5.6 percent a year, saving about $67 billion. Reimbursement rates for primary care physicians must also be altered at the Medicare level. This will serve as a model for private insurance companies, which use Medicare uses as guidelines for its own rates, to quickly follow suit. However, this solution is difficult to swallow for specialists who make up a majority of the Medicare committees that decide pay rates. What this would mean for these doctors is diverting money from specialist rates towards primary care, a plan that is most unpalatable to power-wielding specialists. Funding may also be integrated in the form of scholarships and loan-payback programs for graduating medical students entering primary care, while specialty rates can be cut to divert money towards it.

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Unfortunately, specialists are reluctant to leave the salaries they have accrued through extensive training for the sake of primary care. But as Joe Gravel, a family physician and chief medical officer at the Greater Lawrence Family Health Center in Massachusetts said, “You don’t get paid to talk to people and tell them to stop smoking. Nobody values my time to do that…They’ll pay for the lung transplants, but they won’t pay to prevent 50 people from needing them.” The duties performed by primary care doctors can go beyond the scope of scientific medicine, and it is an unfortunate truth that such significant actions go unnoticed and uncompensated. To enact true healthcare reform, political bureaucracy needs to end its childish squabbling and come together to create a fiscally responsible plan reforming the stigma associated with primary care – a plan centered on the public good.


important names you might not know:

Biochemist Gerty Cori (1896-1957) Though Gerty Cori was born in the Czech Republic, the story of her scientific perseverance has a distinctively American flavor. Cori entered biochemistry at a time when women were unwelcome in the scientific community. Incredibly, she graduated medical school in 1920, married her colleague Carl Ferdinand Cori, and emigrated to the United States in 1922. The Coris conducted medical research together, but Gerty had much more difficulty finding work. She acquired a position at the Roswell Park Cancer Institute six months after her husband – but even then, the institute frowned on their collaboration. Despite this reproach, the Cori’s continued their work on carbohydrate metabolism. While working at Roswell, they published 50 papers on glucose metabolism in the human body and pioneered studies on the breakdown of glycogen. In 1929, the duo discovered what is now called the Cori Cycle, the process by which glycogen in muscle tissue decomposes to lactic acid, allowing the body to produce a range of useful chemicals. Glucose 1-phosphate, an intermediate compound within the Cori cycle was named the “Cori ester” in their honor. In 1947, Gerty Cori became the first American woman – and the third woman overall – to win a Nobel Prize for scientific study. The following year, she was awarded the Garvan-Olin Medal for distinguished work as a female American chemist. Cori was also the fourth woman in history appointed to the the National Academy of Sciences, and she was a board member of the National Science Foundation until her death.

Diagram of the Cori Cycle, also known as the lactic acid cycle.

INTERESTING fact: this us postage stamp featuring gerty cori depicts the cori ester. Unfortunately, its structure has a mistake. Can you spot it? Fall 2011 | Rutgers Science Review | 11


an INterview with :

Karl Herrup, Ph.D. Dr. Herrup is a Professor and Department Chair of Cell Biology & Neuroscience at Rutgers University. His research involves cell cycle regulation in the adult neuron. 1. Could you briefly describe the research you do at Rutgers? I work on neurodegenerative diseases such as Alzheimer’s. In that work, I’m interested in how or why the nerve cells in the brain die, which is the ultimate cause of the neurological symptoms these diseases cause. We’ve found that mature neurons must constantly suppress the cell cycle and stop themselves from entering it, or they will re-enter a cycle they can’t complete – and that leads to cell death.

How did you get involved in working with cell cycle regulation? I first got involved over 20 years ago by interacting with a researcher in Texas who had knocked out a major tumor suppressor gene in mice. What she had expected to find were rampant tumors all over the affected animals, but what she found instead was massive amounts of neuronal cell death within the

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brain and spinal cord. That led me to the connection between the ability of neurons to suppress the cell cycle and the occurrence of cell death. That was the beginning, and I’ve been working on it ever since. Is this sort of “cycling” unique to only neurons? It’s clear that’s it’s true for neurons; we’ve done a lot of work on it. But my work has made it clear to me that every property that we’ve looked at is a property of any differentiated cell. What that would mean, in theory, is that this would apply to other cell types that have gone through their final differentiation and are no longer dividing. There are certain gut or muscle cells, for example, that also do that, and although I have no proof, I would speculate that that same properties of cycling would apply to all of these cells. The general principle that once a cell fully differentiates, trying to reenter the cell cycle


Interview will lead to its death. I think this might also help explain many other types of degeneration in the body.

What are the difficulties of working with neurons?

Certainly, one of the major difficulties is that they don’t divide. Unlike skin, liver or tumor cells, you can’t just grow neurons in a petri dish and make as many of them as you want – you always have to go back to a living brain and freshly isolate them every time you want to study them. They’re also highly complex in the structural sense: they’ve got a very elaborate dendrite, which is highly branched and specialized in their cellular content. They also have a very long axon, which is specialized in a different way, on the other end of the cell. That makes for a highly polarized, structurally complicated type of cell – and you can’t just pull that cell out of the brain because you will rip it apart, as it’s so intertwined with the rest of the tissues. You can only get out the cell body, but most of the cell is lost.

Do you have any advice for undergraduates who want to pursue research? Study hard, and always keep your native curiosity alive and thriving. I like to say that some of the best scientists are 2 year olds, because one of the first questions they ask is “why” – and they can irritate their parents tremendously by going around, asking, “Why, Mommy?,” “Why, Daddy?” But in essence, a good scientist does that all day – just in a slightly in a more adult sort of way. My best advice: Stay curious.

Where do you hope to see your research go in the future? Has any clinical progress been made from your research? It would be nice if we could find a drug which could block this process early, for diseases like Parkinson’s, Alzheimer’s, and ALS. It sounds simple because you would think that with all these anticancer drugs out there, stopping cells that are dividing would very easy. But in fact, the way those anticancer drugs tend to work is to try to do exactly what the neuron does automatically, which is, to kill cells that are dividing. We just want to stop them from dividing, and virtually all the cancer drugs out there don’t attack that problem – so we’re looking for a drug usable in humans that does something a little novel.

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Art In Science Perpetual Poetry - (by Daniel Naftalovich) __________________________________________ Is an atom not a machine of perpetual electron motion? Is not the mind a perpetual machine of creativity? And our imagination a machine perpetuating endless worlds? Is not our current world in perpetual war, yet our dreams of perpetual peace. Do our hearts not perpetuate lives and love? Ambition leads to endless trials and inspiration endless motivation. Do not our heroes persist in our memories and perpetuate our hopes? Do not our science laws of conservation speak of matters of energy as in perpetual existence? I see perpetual machines sitting all around me.. It seems to me the only thing that has stopped perpetuating.. .. is our belief in possibility.

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Relationship between mosquito larvae and parasitic mermithid nematodes

Research papers

Jennifer Sun & Manar Sanad Center for Vector Biology, Rutgers University, New Brunswick, NJ ABSTRACT: Mermithid nematodes are roundworms which are parasitic in their developing stage and free-living as post-parasites and adults. Romanomermis iyengari and Strelkovimermis spiculatus are of special interest because they parasitize the larvae of many disease-carrying mosquito species. This study analyzed the mermithid parasite-host relationship with Culex pipiens pipiens. Different host:parasite ratios were used to examine the effect of parasite load on mosquito heart rate, parasite infection times, and nematode host preference. There was an inverse relationship between parasite load and mosquito heart rate. Conversely, parasite load and infection time were positively correlated. The study also showed that nematode preference for previously infected hosts averages 23.67±16.71% for both species at all parasite loads. Overall, our research indicated that parasite load affects the ability of mermithids to survive through several generations; therefore, parasite load should be optimized to increase the effectiveness of in vivo nematode production for biological control purposes. droplet of distilled water containing 1 larva was placed Introduction in a tissue-culture well (35 mm diam). The appropriate quantities of nematodes were individually added to Mermithid nematodes are threadlike roundworms the droplet. Mosquito heart rate was recorded before which are parasitic in their developing stage and free- and after penetration by recording the pulsation of the living as post-parasites and adults. Eventually, mass- tubular dorsal aorta. The time taken for each nematode produced mermithids may supplement insecticides to penetrate the host’s cuticle was recorded. Infected for mosquito control. Romanomermis iyengari and larvae were reared in 17 ml of distilled water for 24 Strelkovimermis spiculatus were of special interest h before a fresh larva and an additional pre-parasite because of their ability to parasitize the larvae of many were added to the well. Mosquitoes were then fed daily medically important mosquito species, including Culex and water replaced alternate days. After 6 to 7 d, the spp. (Chandrahas & Rajagoplan, 1979; Achinelly et al., mosquitoes were placed into individual wells to observe 2004). The goal of the study was to optimize infection emergence among the pairs. rates by understanding R. iyengari and S. spiculatus Mosquito heart rate, parasite infection times, and behavior and their use of host cues for infection. This nematode host preference were recorded. The data was study may help increase the effectiveness of in vivo analyzed using ANOVA (P£ 0.05). nematode production. Results and Discussion Materials and Methods The most important effect of nematode infection Cultures of the eggs of R. iyengari and S. was a decrease in host heart rate (Fig. 1) (Shamseldean spiculatus, stored in sand, were utilized. The mosquito & Platzer, 1989). By subjecting individual larvae Culex pipiens pipiens from our laboratory colony was to penetration by 15 nematodes, we found that each used as the host. All species were maintained using additional nematode contributed to reducing the larval standard techniques (Petersen & Willis, 1972; Micieli, heart rate. While the post-infection heart rate averaged Marti, & Garcia, 2002). Sand containing nematode eggs 28.87±3.02 beats/min for parasite loads of 1 and 3 for was flooded with distilled water for 5 and 24 h prior S. spiculatus, heart rate averaged 47.98±3.02 beats/ to experimentation for R. iyengari and S. spiculatus, min for parasite loads of 5 and greater. Meanwhile, R. respectively. All experiments were conducted at 26oC. iyengari depreciated heart rate on average 21.88±1.87 Each assay involved 10 replicates of each beats/min up to a parasite load of 5; at higher host:parasite ratio (1:0, 1:1, 1:3, 1:5, 1:10, or 1:15) concentrations, heart rate dropped by 40.6±1.87 beats/ per species. The experiment was repeated 3 times. A min. Interspecies variation in the affect on host heart Fall 2011 | Rutgers Science Review | 15


rate may account for the highest incidence of parasitism reported by Achinelly & Camino (2005): 3 S. spiculatus or 5 R. iyengari per host. We conclude that this inverse relationship between parasite load and host heart rate attributes for a parasite load regulation mechanism in the nematodes to prevent premature host fatality.

Fig. 2: Time to infection. a = P≤0.05 for R. iyengari, b = P≤0.05 for S. spiculatus.

Fig. 1: Effect of parasite load on host heart rate. Individually adding 15 nematodes to the same host also caused later parasites to increase the time taken to attach to and penetrate the larva (Fig. 2). Later worms were observed to perform several laps around the droplet of water before displaying characteristics of the initiation of penetration. This behavior could account for the direct relationship between infection time for successive nematodes and parasite load. While both species of nematodes displayed an increase in time taken by successive nematodes to penetrate the host, R. iyengari differed from S. spiculatus in a few aspects. Most importantly, the infection time for the 15 nematodes of R. iyengari returned an r2 value of 0.1016, indicating the relationship among the points is not linear. By contrast, the relationship between the infection times for the 15 S. spiculatus was nearly linear (r2=0.8314). This relationship is an indication of the nature of these species regarding their patterns of swimming. Thus, we conclude that S. spiculatus has a more uniform swimming pattern than R. iyengari.

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In addition, all of the infection times for successive R. iyengari were significantly different from that of the first nematode; on the contrary, S. spiculatus infection times did not differ from the control until the eleventh parasite. Understanding that the first R. iyengari took the longest time to penetrate its host, R. iyengari may use a technique for infection where the first nematode paralyzes the host to facilitate the identification of the larva by successive nematodes. Meanwhile, S. spiculatus did not vary significantly in infection times until the eleventh nematode; therefore, this species may display a mechanism which to further parasitism of the host. These experiments indicate that randomness is not the reason for nematode penetration of mosquito larvae. To determine whether the infection times for successive nematodes increased because of a preference for uninfected hosts, we observed the host preference of a nematode when in the presence of both an infected and a fresh larva. We compared the host preference of these nematodes among various parasite loads. Figure 3 displays the percentage of these nematodes which parasitized previously infected mosquito larvae. Nematode preference for such hosts averaged 23.67Âą16.71% for both species at all parasite loads; thus, these nematodes target fresh hosts approximately 70% of the time.


Acknowledgement This study was supported in part by Rutgers University and the Aresty Research Center for Undergraduates. References

Fig. 3: Nematode preference for previously infected mosquito larvae. Therefore, the increased infection time for successive nematodes may be due to a defense mechanism whereby the parasites avoid infected larvae to limit premature host fatality. However, host immobilization may also be a technique utilized to ensure appropriate parasite load. This study showed that host immobilization is an important step in the mermithid infection process because it increased the probability of host detection and penetration by successive nematodes; intensity of parasitism is a result of parasitoid-induced behaviors in the hosts (Shamseldean & Platzer, 1989). The study confirmed the heart rate decrease predicted by Shamseldean & Platzer (1989), indicating a necessity to optimize parasite load in order to moderate premature host fatality. Interspecies variation affects each species’ infectious properties. Our study shows that R. iyengari is highly evolved to regulate the homeostatic heart rate of its host to increase the probability of successive nematodes finding a host. This mechanism is attributable to the species’ irregular swimming speed. On the contrary, S. spiculatus is better adapted to find fresh hosts to prevent premature host fatality. This characteristic is a result of factors such as the nematodes’ timing mechanism for transitioning into and out of a quiescent state (Ghosh & Emmons, 2008). The observed increase in infection times for nematodes at high parasite loads reflects the self-regulating nature of either species; if more nematodes were to enter one mosquito larvae, the parasites would kill off their hosts. Our research indicated that parasite load affects the ability of mermithid nematodes to survive and reproduce; therefore, parasite load should be optimized to increase the effectiveness of in vivo nematode production and biological control.

Achinelly, M.F., & Camino, N.B. (2005). Evaluation of the mosquitoes Aedes aegypti and Culex pipiens (Diptera: Culicidae) as alternative hosts for laboratory mass-rearing of Strelkovimermis spiculatus (Nematoda: Mermithidae). Nematology, 7, 281-284. Achinelly, M.F., Micieli, M.V., Marti, G.A., & Garcia, J.J. (2004). Susceptibility of neotropical mosquito larvae (Diptera: Culicidae) and non-target aquatic organisms to the Entomoparasitic nematode Strelkovimermis spiculatus Poinar & Camino, 1986 (Nematoda: Mermithidae). Nematology, 6, 299302. Chandrahas, R.K., & Rajagopalan, P.K. (1979). Mosquito breeding and the natural parasitism of larvae by a fungus Coelomomyces and mermithid nematode Romanomermis in paddy fields in Pondicherry. Indian Journal of Medical Research, 69, 63-70. Ghosh, R., & Emmons, S.W. (2008). Episodic swimming behavior in the nematode C. elegans. The Journal of Experimental Biology, 211, 3703-3711. Micieli, M.V., Marti, G., & Garcia, J.J. (2002). Laboratory evaluation of Mesocyclops annulatus (Wierzejski, 1892) (Copepoda: Cyclopidea) as a predator of containerbreeding mosquitoes in Argentina. Memórias do Instituto Oswaldo Cruz, 97, 835-838. Petersen, J.J., & Willis, O.R. (1972). Procedures for the mass rearing of a mermithid parasite of mosquitoes. Mosquito News, 33, 1-12. Shamseldean, M.M., & Platzer, E.G. (1989). Romanomermis culicivorax: Penetration of larval mosquitoes. Journal of Invertebrate Pathology, 54, 191-199.

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Research papers INVESTIGATION OF BINARY METAL SULFIDE DIELECTRIC THIN FILMS IN SILVER COATED HOLLOW GLASS WAVEGUIDES (HGWS) FOR INFRARED RADIATION DELIVERY

Carlos M. Bledt1, Daniel V. Kopp1, and James A. Harrington1 1 Rutgers, the State University of New Jersey Department of Materials Science & Engineering Piscataway, NJ 08854 USA ABSTRACT Hollow glass waveguides (HGWs) are an attractive alternative to traditional photonic bandgap fibers and other infrared fibers for use in various applications involving optimal transmission in the Long Wavelength Infrared (LWIR) region due to their inherent broadband transmission and easily customizable properties. The use of II-VI and IV-VI binary metal chalcogenide thin films in silver coated silica Hollow Glass Waveguides deposited via dynamic liquid phase deposition (DLPD) for infrared spectroscopy and laser delivery has allowed for maximal signal throughput with high laser power thresholds while simultaneously retaining superior single-mode like TEM00 properties. The methodology for the aqueous chemical deposition of metal chalcogenide thin films in silver coated silica hollow waveguides including cadmium sulfide (CdS) and lead sulfide (PbS) is presented in this study along with their optical response as determined primarily through Fourier Transform Infrared (FTIR) spectroscopy and infrared (CO2) laser analysis. INTRODUCTION Dielectric coated hollow glass waveguides (HGWs) are capable of low-loss, broadband delivery of electromagnetic radiation at infrared wavelengths typically ranging from 1.0 – 15.0 ¾m. In comparison to other types of available infrared fibers HGWs have the advantages of having no end reflections, high laser power throughput threshold, high chemical and mechanical stability, and low beam divergence.[1] Furthermore, HGWs can be engineered for maximum broadband transmission at desired wavelength ranges through simple control of fabrication methodology variables. The physical structure of HGWs consists of a high-purity silica capillary tube of fixed diameter with a protective polyimide or UV-acrylate outer coating. The optically functional structure is created through the deposition of a reflective film and subsequent dielectric thin film(s) on the inner surface of the silica capillary deposited from component containing aqueous solutions. HGW bore sizes can furthermore be chosen with the desired application(s) in mind, such as the necessity for low order mode propagation or high radiation intensity throughput. Figure 1 depicts a representative general diagram of an HGW.

Figure 1. Representative cross-sectional diagram of an HGW

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Losses in HGWs depend on a number of factors including bore size, applied bending radius, thin film materials used, coupling efficiency, and propagating modes.[1] The key in developing low-loss HGWs lies in the manipulation of the fabrication methodology so as to deposit high-quality dielectric films with proper thickness for maximum transmission at desired wavelength ranges as necessary. Traditionally, HGWs have incorporated silver iodide (AgI) as a dielectric film due to the ability to fabricate high-quality AgI thin films in HGWs through mass transport driven subtractive iodization of the pre-deposited silver film.[1] Alternatively, research in the development of HGWs has focused on the use of other IR transparent dielectric materials as functional thin films. Of such possible materials, the II-VI and IV-VI metal chalcogenides such as cadmium sulfide (CdS) and lead sulfide (PbS) are of particular interest due to several factors, including their high optical transparency at IR wavelengths, the vast range of refractive indices covered by these materials, and their ability to be deposited via similar electroless chemical deposition methods. Of particular interest is the use of chalcogenide thin films in multilayer dielectric HGW designs, in which metal chalcogenide films of materials with alternating low and high refractive indices are deposited to form a periodic alternating dielectric constant resulting in a low-loss, omnidirectional reflecting 1-D photonic bandgap structure.[2] EXPERIMENTAL METHODOLOGY The successful fabrication of high-quality metal chalcogenide thin films via electroless deposition from aqueous solutions relies on the simultaneous controlled release of reactive metallic ion species and free chalcogenide ions in solution. Metal chalcogenide thin films are deposited in HGWs through such electroless deposition methods via dynamic liquid phase deposition (DLPD), which is an adaption of chemical bath deposition (CBD) where the reactive solution is continuously pumped by a peristaltic pump through the pre-silver coated HGW silica capillary tube. As such, volumetric fluid flow rate poses an additional processing variable in DLPD which along with the main governing variables of component concentrations, complexing agents used, temperature, and solution pH found in CBD deposition of metal chalcogenide thin films directly influence the quality and growth rate of the films. Figure 2 shows the general DLPD processing setup involving the simultaneous pumping of unreacted constituent component solutions at equal rates through the pre-silver coated HGW.

Figure 2. General DLPD procedure setup for fabricating HGWs

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In comparison to CBD methods, DLPD has the advantage that substantially thicker films can be deposited due to the fact that the continuous flow of unreacted solutions prevents the precursor depletion and film saturation witnessed in CBD film growth methods. Deposition of Reflective Silver Thin Films Initial fabrication of HGWs involves the deposition of a highly reflective silver film on the inner surface of the silica capillary via DLPD methodology. The silver deposition procedure is preceded by a short sensitization step, in which the inner silica surface is ‘activated’ by pumping an acidic 1.60 mM tin (II) chloride solution. The sensitization procedure allows the subsequent silver film deposition procedure time to be considerably shortened due to the initial rapid reduction of complex silver ions by surface adhered tin (II) ions which effectively reduces the initiation time for the formation of the silver film. This in turn allows the total silver film deposition time to be shortened, thus reducing surface roughness seen with prolonged silver film deposition times which has been shown to increase scattering losses.[3] The silver thin film deposition procedure involves the simultaneous flow of an alkaline ammonia complexed 14.4 mM silver (I) nitrate at a pH of 11.0 – 11.4 solution and a 3.11 mM dextrose reducing solution. Reduction of the soluble silver (I) diammine cation by the aldehyde functional group containing dextrose in solution results in the deposition of the metallic silver film on the inner capillary silica surface. The deposited silver film must be thicker than the penetration depth of the wavelength for which the HGW will be used while at the same time being sufficiently thick to function as a suitable substrate for the deposition of subsequent metal chalcogenide dielectric thin films. In practice the thickness of the deposited silver film varies from 100 – 300 nm as necessary, corresponding to silver deposition times ranging from 2 – 15 minutes. All deposition procedures were carried out utilizing a standardized peristaltic pump speed which gave a steady volumetric flow rate of 17.35 mL/min and carried out under ambient conditions at 25 °C. Deposition of Dielectric Cadmium Sulfide Thin Films The successful deposition of high quality CdS thin films in HGWs requires careful control of the fabrication methodology variables, particularly component concentrations, solution pH, and volumetric fluid flow rate. The CdS deposition procedure involves simultaneous flow of an alkaline ammonia complexed cadmium ion solution and a thiourea solution as a sulfide ion source. The reaction mechanism involved in the CdS deposition procedure involves the successful complexing of a cadmium (II) nitrate solution through addition of excess ammonium hydroxide, thus creating a stable ammonia complexed cadmium ion solution to allow for controlled availability of cadmium ion species in solution. Simultaneous controlled release of sulfide ions in solution is likewise essential, with the controlled hydrolysis of dissolved thiourea in alkaline medium determining the availability of reactive sulfide ions in solution. The reaction mechanisms involved in the deposition of CdS from alkaline ammonia complexed ion and thiourea containing solutions has been discussed by several authors in the literature.[4,5,6] Primarily, two competing simultaneous deposition mechanisms have been proposed with the corresponding chemical reactions involved in the formation of CdS being presented in Equations 1 – 4.[4,6] SC(NH� )� + 2OH� ⇄ S�� + CN� H� + 2H� O (1)

Cd�� + 4NH� ⇄ Cd(NH� )� Cd(NH� )�

��

��

(2)

+ 2OH� + site → �Cd(OH)� ���� + 4NH� (3a)

20 | Rutgers Science Review | Fall 2011


�Cd(OH)� ���� + S�� → CdS(�) + 2OH� (3b)

Cd(NH� )�

��

+ S�� → CdS(�) + 4NH� (4)

The two competing mechanisms involved in the deposition of CdS films shown by Equation 3 and Equation 4 show the dilemma involved between depositing high quality CdS films of considerable thicknesses and reducing the prolonged deposition times involved in the fabrication of these films. Equation 3 shows the proposed heterogeneous ion by ion CdS film deposition mechanism in which intermediate cadmium (II) hydroxide is adsorbed on the substrate surface and is subsequently transformed to well adhering high quality CdS thin films.[4,6,7] Equation 4 shows the proposed competing homogeneous cluster by cluster CdS film deposition mechanism in which colloidal CdS particles agglomerate on the substrate to form low quality, high surface roughness, porous CdS films. While the heterogeneous deposition mechanism is preferred for the deposition of high quality CdS thin films, this reaction mechanism is much slower and can be inconvenient as the sole CdS film deposition mechanism for CdS thin films of thicknesses greater than 300 nm. The homogeneous deposition mechanism suggested by Equation 4 results in much faster film growth rates but at the expense of decreased film uniformity and quality.[5] The necessity of depositing high quality CdS films in HGWs of thicknesses greater than 300 nm while at the same time limiting the deposition procedure time suggests a careful balance between the competing heterogeneous and homogeneous deposition mechanisms must be found. Optimization of the CdS film deposition procedure involved utilizing equivalent parts of a 14.98 mM cadmium (II) nitrate, 2.0 M ammonium hydroxide solution and a 150 mM thiourea solution at a pH of 11.45 – 11.65. The experimental determination of the CdS film growth kinetics in HGWs involved fabrication of several samples coated at different deposition times ranging from 150 to 360 minutes in fixed 30 minute intervals. Deposition of Dielectric Lead Sulfide Thin Films The successful deposition of high quality PbS thin films in HGWs likewise requires careful control of several fabrication methodology variables such as component concentrations, solution pH, and volumetric fluid flow rate. Thiourea was again used as a sulfide ion source, with the complexing agent of choice for the free lead (II) ions being hydroxide ions introduced as a sodium hydroxide solution in place of ammonium hydroxide in the case of CdS deposition. The addition of excess sodium hydroxide to a solution of lead (II) cations results in the formation of plumbite complex ions. Complexing the lead (II) ions in this manner allows for controlled release of available lead (II) reactive species in solution, preventing spontaneous settling of PbS particles from solution and allowing for the controlled deposition of high-quality PbS thin films. The proposed PbS thin film deposition mechanism is presented in Equations 5 – 7.[4,6]

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It is important to note that in the case of PbS thin films, heterogeneous deposition mechanisms have been widely regarded as being predominant over homogeneous deposition mechanisms at high pH values.[4] This fact allows for the rapid deposition of high quality PbS films at substantially higher thicknesses than those currently achievable for CdS films. Optimization of the PbS film deposition procedure involved utilizing equivalent parts of a 5.43 mM lead (II) nitrate, 56.3 mM sodium hydroxide solution and a 54.4 mM thiourea solution at a pH of 12.05 – 12.15. The experimental determination of the PbS film growth kinetics in HGWs involved fabrication of several samples coated at different deposition times ranging from 15 to 135 minutes in fixed 15 minute intervals. RESULTS FTIR Spectroscopic Analysis Initial analysis of the fabricated CdS and PbS coated HGW samples involved FTIR spectroscopic analysis of each of the individual segments processed for the various deposition times. FTIR analysis was carried out using a Bruker Tensor 37 FTIR spectrometer in conjunction with a Teledyne Judson cryogenic MCT/A detector. The FTIR beam path was diverted and focused into the input end of the 15 cm long coated 700 µm ID HGW sample using a right angle silver coated parabolic mirror. The output FTIR signal from the HGW sample segment was collected using the MCT/A detector, thus making possible the qualitative and quantitative analysis of the spectral response of the various fabricated metal chalcogenide coated samples. The spectral response for each of the 16 samples was measured in this manner and the IR spectral response from λ = 2.0 – 15.0 µm for select samples is shown in Figure 3 for both metal chalcogenide deposition procedures. a)

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b)

Figure 3. Spectra of a) CdS (180, 240, 300 min) and b) PbS (45, 75, 105 min) coated HGW samples The FTIR spectra for all samples show the definitive thin film interference peaks due to the deposited chalcogenide thin films. As expected, the interference peaks shift towards longer wavelengths with increasing deposition times due to increasing film thicknesses. For the deposition times studied, all deposited films PbS films were of high-quality as depicted by the well-defined interference peaks and narrow nature of the first interference peak. The CdS films were likewise seen to be of high optical quality for most of the studied deposition times yet considerable non-uniformity was seen in film deposition times longer than 360 minutes. It is proposed that the non-uniformity of thicker CdS films may be due to increasing surface roughness with time as a result of prolonged homogenous thin film formation.[8] Thin Film Deposition Kinetics The thicknesses of the deposited films can be calculated from the spectral data by taking into account the centroid wavelength of the 1st interference peak (λp) as well as the refractive index, n, of the dielectric material using Miyagi’s formula (Equation 8) based on thin film optics theory.[2] d���� =

λ�

4√n� − 1

(8)

The film thickness for the CdS (n=2.27)[9] and PbS (n=4.00)[9] deposition procedures as a function of time shown in Figure 4 and was determined by calculating the film thicknesses at each of the corresponding deposition times from the centroid wavelength of the first interference peak for each of the obtained spectral responses.

Fall 2011 | Rutgers Science Review | 23


a)Â

b)Â

Figure 4. Growth kinetics for DLPD deposited a) CdS and b) PbS films in HGWs As expected, both the CdS and PbS deposition kinetics data show a strongly linear film growth rate in this region past the non-linear film nucleation region. Utilizing the aforementioned CdS and PbS solution precursor concentrations and fixed pH for each of the solutions, film growths of 1.86 nm/min and 3.46 nm/min were obtained for CdS and PbS films respectively. Furthermore, the deposition times involved in depositing thin films of such thicknesses are acceptable and film thickness control is high. As previously mentioned this is due to the fact that no depletion of precursor species occurs in DLPD as it does in CBD film deposition as unreacted solution is continuously pumped through the specimens. This processing methodology not only allows for a continuously linear film growth rate, but also

24 | Rutgers Science Review | Fall 2011


allows for much more thicker films to be deposited due to the non-existence of precursor depletion and saturation which limit the film thicknesses achievable by CBD methods. Infrared Transmission Properties Final analysis of CdS and PbS coated HGWs involved the fabrication of CdS and PbS coated 1.5 m long HGWs with targeted dielectric film thicknesses of approximately 500 nm and 350 nm for CdS and PbS thin films respectively. These samples were fabricated using the methodology outlined in the experimental procedure section with deposition times of 300 minutes (CdS) and 95 minutes (PbS) as determined necessary to obtained these film thicknesses from the growth rate kinetics analysis. These specific film thicknesses were chosen due to the fact that thicker dielectric films are necessary for maximum transmission at longer wavelengths as well as for the fact that good uniformity was maintained at these deposition times as determined from the preceding spectral analysis. The spectral optical response of these samples was taken with the FTIR spectrometer to determine the quality of the deposited CdS and PbS films and is shown in Figure 5.

Figure 5. FTIR spectra of Ag/CdS HGW (t = 300 min) and Ag/PbS HGW (t = 95 min) The spectra of the fabricated samples again shows high quality CdS and PbS films with calculated thicknesses of 497 nm and 378 nm respectively. The transmissive properties of the fabricated samples were analyzed using a Synrad I-series CO2 15 Watt max. laser emitting at a wavelength of 位 = 10.6 碌m. The samples were properly aligned in the beam path for optimal coupling efficiency using a zinc selenide lens with a focal length of 7.5 inches. The transmitted power for each sample was measured under no applied bending as well as applied bending radii of 2.5, 2.0, 1.5, 1.0, 0.75, and 0.5 m using an Ophir Vega power meter. The length of sample under bending was kept constant at 80 cm for all bending measurements. The losses in dB/m were calculated using a cutback methodology to reduce the possibility of experimental error

Fall 2011 | Rutgers Science Review | 25


due to coupling inefficiencies. The mathematical equation for determining the loss is a derivation of the Beer-Lambert law and is given in Equation 9.

where L is the length in meters of the entire sample, s is the length of the cutback segment, Pin is the measured power out of the cutback segment, and Pout is the measured power out of the entire sample length. Utilizing this methodology, the loss of the samples as a function of curvature was determined and presented in Figure 6. a)Â

b)Â

Figure 6. Bending losses for 1.5 m long a) CdS and b) PbS coated HGWs

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The losses were overall higher for the Ag/PbS waveguide than for the Ag/ CdS waveguide as would be expected from theory due to the higher refractive index of PbS relative to CdS. Furthermore, the loss increase upon applied bending shows the expected linear 1/R dependency and it is evident the bending loss increase of the Ag/PbS waveguide is higher than that for the Ag/CdS waveguide at mPbS = 0.124 vs. mCdS = 0.045 respectively. Overall, both metal chalcogenide films were proven to be successful in substantially reducing the loss in comparison to Ag only coated HGWs with typical straight losses of approximately 3.0 dB/m. CONCLUSION The successful deposition of high-quality cadmium sulfide and lead sulfide in HGWs via DLPD deposition methodology has been demonstrated in this study. The reaction mechanisms involved in the deposition of these metal chalcogenide thin films have been reviewed in order to gain an understanding of the processes involved to allow for the deposition of high-quality optical thin films and achieve the necessary film thickness deposition control needed to design both single layer as well as multilayer dielectric coated low-loss HGWs. The film growth kinetics at the deposition parameters presented show relatively rapid linear film growth in comparison to traditional CBD CdS and PbS methods. Spectral analysis resulting from the film deposition kinetics study shows optical grade CdS thin films up to thicknesses of approximately 600 nm and optical grade PbS thin films upwards of thicknesses of 600 nm via the aforementioned processing methodology. Infrared attenuation measurements carried out on the fabricated samples show both metal chalcogenide films are effective at substantially reducing losses in HGWs when compared to Ag only coated waveguides. Furthermore, the losses in Ag/CdS HGWs were shown to be less than those in Ag/PbS HGWs with a higher loss increase upon applied bending in Ag/PbS HGWs than in Ag/CdS HGWs. REFERENCES 1

Harrington, J. A., Infrared Fiber Optics and Their Applications, (SPIE Press, Bellingham, WA, 2004). Miyagi, M. and Kawakami, S. "Design theory of dielectric-coated circular metallic waveguides for infrared transmission," IEEE Journal of Lightwave Technology. LT-2, 116-126 (1984). 3 Rabii, C. D., Gibson, D. J., and Harrington, J. A., “Processing and characterization of silver films used to fabricate hollow glass waveguides,” Appl. Opt. 38, 4486-4493 (1999). 4 Chaparro, A. M., “Thermodynamic analysis of the deposition of zinc oxide and chalcogenides from aqueous solutions,” Chem. Mater., 17 (16), 4118-4124 (2005) 5 Guillen, C., Martinez, M. A, Herrero, J., “Accurate control of thin film CdS growth process by adjusting the chemical bath deposition parameters,” Thin Solid Films, 335, 37 – 42 (1998). 6 Niesen, T. P., De Guire, M. R., “Review: Deposition of Ceramic Thin Films at Low Temperatures from Aqueous Solutions.” Journal of Electroceramics, 6, 169 – 207 (201). 7 R. S Mane and C. D Lokhande, “Chemical deposition method for metal chalcogenide thin films,” Mat. Chem. Phys. 65, 1-31 (2000). 8 Gopal, V., Harrington, J. A., “Deposition and characterization of metal sulfide dielectric coatings for hollow glass waveguides,” Optics Express, 11, 24 (2003). 9 Palik, E. D. and Ghosh, G., Handbook of optical constants of solids, (Academic, London, 1998). 2

* cmbledt@eden.rutgers.edu; Phone 862-485-9289; irfibers.rutgers.edu

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