Biomed Benchmark - Honors THesis abstracts      

NEWSLETTER OF HONORS RESEARCH PROJECT ABSTRACTS

DIVISION OF BIOLOGY AND MEDICINE

BROWN UNIVERSITY  2002-2003


 

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Reproductive Trade-Offs Associated with the Innate Immune Response in Drosophila melanogaster

 

By: Melissa Zerofsky

Sponsor:  Marc Tatar

Department of Ecology and Evolutionary Biology

 

Consideration of energetic trade-offs is important in the study of senescence.  An organism that allocates fewer resources to reproduction in favor of somatic maintenance will age less rapidly.  Therefore, upregulation of one system incurs a cost in another system.  Innate immunity is thought to play a role in senescence, but the nature of this role is not well understood.  An interesting question is whether induction of the innate immune response is negatively correlated with other physiological functions.

It has been shown that induction of the innate immune response in insects is costly.  Using transgenic and mutant strains of Drosophila melanogaster in the imd/Relish immune pathway, I tested the effects of the humoral branch of the innate immune response on fecundity in Drosophila females.  I demonstrated that induction of antimicrobial peptides in Drosophila is negatively correlated with fecundity.  This is the first demonstration of reproductive trade-offs with humoral immunity in Drosophila.

 

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Non-Invasive polarized light microscopy quantitatively distinguishes the multilaminar structure of the zona pellucida of living human eggs and embryos.

 

By: Cory Pelletier

Sponsor:  David Keefe

Department of Obstetrics - Gynecology

 

We quantitively described the thickness and architecture of the zona pellucida of living human eggs and cleavage stage embryos, non-invasively with the Polscope; a digital polarizing light microscope.  Patients involved in this study were undergoing fresh, non-donar infertility treatment that underwent egg aspiration, fertilization by ICSI or traditional IVF and cleavage stage embryo (day 3) transfer.  The Polscope imaged the zona of eggs prior to ICSL and in cleavage stage embryos prior to transfer.  Thickness and

 

retardance of three zona layers were measured using Spindle View Image Analysis System, from eight quadrants.  Mean and variance in thickness and retardance were calculated for individual eggs and embryos, between eggs and embryos of a cohort and across the sample patient population.  We found that Cleavage stage (day 3) embryos have thinner zona (15.2+/-2.9mm) than both mature (20.4 +/- 2mm) and mature (19.5+/-2.2mm) eggs.  The zona of embryos is thinner, primarily due to thinning of the outer layer.  The thicker the zona layer the greater itŐs retardance.  Considerable variation exists in the thickness and retardance of zona layers around individual eggs and embryos and between members of a cohort.  The zona of eggs and embryos from different patients differ in thickness, retardance and variation.  In conclusion, thickness and organization of zonae pellucidae of human eggs and embryos varies considerably and can be quantitatively imaged using the Polscope.

 

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CD4-Independent Mechanisms of HIV-1 infection in Glial Cells and B-Cells

 

By: Leigh Baxt

Sponsor: Dr. Walter Atwood and Dr. Peter Shank

Department of Molecular, Microbiology & Immunology

 

The specific aim of our research was to investigate the possible role of syndecans as co-receptors of HIV-1 infection of B-Cells and plial cells.  Syndecans are a type of heparan sulfate molecule present on the surface of most cells.  They have been shown by Saphire et al. to function as receptors of HIV-1 infection of macrophages. We investigated the expression of syndecans on B-cells and glial cells.  We found that of the four syndecans, only syndecans 1 and 4 are present in high amounts on B-cells and glial cells.  In addition we have shown that pseudotyped HIV-1 viruses are able to infect a variety of cell types including Hos CD4/CCR5 cells, SVG-CD4/CXCR4 cells, and SVG-A cells.  Finally we have shown that incubation of these cells with monoclonal antibodies to syndecan molecules 1 and 4 on the cell surface is able to eliminate infection by the VSV-G envelope-containing pseudotype virus in both SVG cell lines.  Incubation with these Abs is also able to abrogate infection by the NL4-3 envelope-containing psuedotype virus in all three cell types.

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Temporal Changes of Vascular Endothelial Growth Factor Expression Following Traumatic Brain Injury

 

By: Wendy Chang

Sponsor:  Joanna Szmydynger-Chodobska                                 

Department of Clinical Neuroscience

 

Cerebral edema formation continues to be one of the major clinical problems in the management of patients with traumatic brain injury (TBI).  However, the arsenal of effective treatments for cerebral edema is very limited and the efficacy in reducing intracranial pressure is less than satisfactory.  Therefore, it is important to identify the molecular and cellular mechanisms responsible for progressive swelling of the brain, and to develop new and effective therapies for the victims of brain trauma. 

Vascular endothelial growth factor (VEGF) has been identified as one possible player in the development and progression of edema.  VEGF has been postulated to increase blood-brain barrier (BBB) permeability to low molecular weight markers and macromolecules by altering tight junction proteins.  This investigation analyzed the time course of VEGF changes at a protein level in rat brains after TBI.

           Using immunohistochemistry and Western blot analysis we demonstrated that after brain injury, the expression of VEGF increased steadily in the injured ipsilateral cortex.  The peak of VEGF expression post-TBI occurred on the fourth day.  However, the levels of VEGF remained elevated up to 14 days after injury.  No change in VEGF levels in the contralateral hemisphere was observed.  This time course of increased VEGF expression corresponded to the late opening of the BBB and to the subsequent development of edema after TBI.

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Investigation of the Expression of C/EP‰ in Antipsychotic-Injected Mice

 

By: Shawn Bachan

Sponsor: John Marshall

Department of Molecular Pharmacology, Physiology & Biotechnology

 

            Abnormalities in the temporal lobe make it a prime target for schizophrenic research because it houses the hippocampus, which is the center for learning and memory.  The hippocampus communicates with higher areas of cortex such as the prefrontal cortex (PFC) in the integration of information, and both cerebral areas are components of the mesolimbic and mesocortical tracts of the dopaminergic system.  Through various studies, it has been shown that typical antipsychotic drugs such as haloperidol, act as D2 dopaminergic receptors and modulate the expression of immediate early genes (IEGs) and downstream transcription factors such as cAMP response element binding protein (CREB).  CCAAT enhancer binding protein beta (C/EBPb) is a transcription factor that has roles in such processes as learning and memory, hepatocyte differeniation, and neuronal differentiation. C/EBPb has been shown to be involved in the CREB-dependent gene cascade activated in long-term memory.  As a result, like CREB, it is a possible intracellular target of antipsychotic drug therapy.

                  [This] research project aims to determine whether haloperidolŐs action on the D2 receptor modulates the expression of C/EBPb in the mouse hippocampus and cortex.  This was accomplished by immunohistochemical analyses of brain sections in haloperidol treated and vehicle treated mice at three different time points (t = 2hrs, 8 hrs, and 24 hrs).

 

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The Effects of Parental Involvement on the Behavior of Students in the Classroom

 

By: Diana Comarato

Sponsor: Robert Shaw

Associate Dean of the College

 

Much research exists on the amazing impact parental involvement can have on a childŐs achievement in school.  Furthermore, there is a great body of research that focuses upon a childŐs emotional, social, and behavioral development as a product of parentŐs influence.  Why, then, is there a lack of research focusing on the behavior of children in the classroom, already viewed as a key indicator of a childŐs development, and the impact parental involvement has on that behavior?  If parents have such a strong influence on the overall development, wherein lies the body of research promoting parental involvement as a method of improving overall behavioral health of a child in the classroom as opposed to solely improving academic achievement?

Educational progress and achievement should not be weighted to be any less important than it currently is, but rather the void which exists on the impact of parental involvement regarding childrenŐs behavior in the classroom needs to be filled.  The research undertaken by this project attempts to take the first step towards linking increased overall child development.

In this child development study, the focus is placed upon the degree of involvement parents/guardians have in their childŐs educational development; with a hypothesis that the less involved parents are in their childŐs school life and environment, the more misbehavior that will appear among these children in a classroom setting.

With past research in mind, the results of this new observational study performed show a general trend for students with lower parental involvement to have higher misbehavior in the classroom.  Due to the fact that child development, easily measured through behavior in school, is the result of so many compounding factors, the research presented thoroughly examines issues such as family background, social context variables, ethnicity, maternal employment status, and socioeconomic status.

                 

Until this connection between parental involvement and childrenŐs behavior in the classroom is strengthened, tactics to better parental involvement in the school systems may affect achievement, but will blindly ignore behavior and thus key components of child development will not be targeted.  This project refocuses the lens of parental involvement, centering it more around itŐs impact on behavioral development.  Undoubtedly, child development entails academic success, and therefore should be made the priority, even in hopes of bettering achievement.  Intervention methods must work from the top down, for only through improved overall development can a child truly be expected to succeed.

 

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The Role of gbb in the Drosophila ŇStem Cell NicheÓ

 

By: Melissa Duan

Sponsor: Kristi Wharton

Department of Molecular, Cellular Biology Biochemistry

 

                  Previous studies have demonstrated defects in reproductive processes in Drosophila melanogaster mutant for glass boat bottom (gbb).  In this paper, we characterize the defects associated with these mutants, which include a disruption in ovary morphology, the number of ovarioles, and stem cell proliferation.  We also characterize the stem cell and fat body phenotypes in larval gonads.  Antibody labeling experiments reveal a reduction in stem cell proliferation in both larval gonads and adult ovarioles.  While the phenotypes exhibited by gbb mutants.  Thus the reduction in fecundity as well as the other patterning defects characterized in the gbb mutants is not accompanied by an increase in lifespan, but rather serves to weaken the flies.

 

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Ability of Dendritic Cells to Activate Natural Killer Cells:  An In Vitro Study in the MCMV System

 

By: Tanya Hamilton

Sponsor: Christine Biron

Department of Molecular, Microbiology & Immunology

 

                  Natural killer cells are essential for host defense during the acute stages of murine cytomegalovirus (MCMV).  Dendritic cells (DC) produce the cytokines, specifically IFN-a/b and IL-12, necessary for NK cell activation in vivo during MCMV infection and mature plasmacytoid dendritic cells (PDC) are able to rapidly activate NK cells in vitro.  In this study, I further investigate the ability of DC to activated NK cells, and the role of cytokines and cell-cell contacts in this activation, by using a coculture system.  DC that matured during MCMV challenge were able to activate NK cells as measured by induction of IFN-g production and NK cell cytotoxicity, however, na•ve DC were not.  IFN-a/b produced by the DC were critical for inducing NK cell cytotoxicity in the 129 background, but were unimportant in the IFN-g response.  In contrast, at high DC concentrations, IL-12 seems to play a role in the IFN-g production in C57BI/6.  However, at low DC concentrations, IL-12 seems to play a role in the IFN-g response suggesting the possibility of different activation pathways functioning at different concentrations of DC.  When contact between DC and NK cells was prevented with cells from 129 mice the DC were still able to activate the NK cells.  In contrast, in cells from C57BI/6 mice, prevention of DC and NK cell contact abrogated the activation of NK cells.  These results indicated the presence of two pathways, one cytokine-mediated and one cell-cell contact-mediated, through which DC can activate NK cells with the cytokine-mediated pathway dominating the 129 mice and the cell-cell contact-mediated pathway dominating in the C57BI/6 mice in this system.

 

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IL-12 production by Dendritic Cells at the site of infection with Toxoplasma  gandii.

 

By: Sandy Wong

Sponsor: George Yap

Department of Molecular, Microbiology & Immunology

 

            Protective immunity towards Toxoplasma gondii infection require both innate and adaptive immune responses.  At the site of infection, antigen-presenting cells (APCs) such as dendritic cells (DCs) phagocytose the parasite, process the parasitic antigens, and present them on their cell surface coupled to MHC molecules.  These MHC plus antigen complexes prime nave T cells to proliferate into effector cells that could exert microbicidal activities.  In order to initiate adaptive immunity through T cell activation, DCs must travel from inflammatory sites to secondary lymphoid organs where the na•ve T cells reside.  DC migration is mediated not only by the upregulation of adhesion molecules that together facilitate tissue-specific homing.

                  Using FACs analyses and cell surface staining, we have begun to characterize the immune response profiles of dendritic cells in the spleen, the blood and the peritoneum on day 4.5 or 5 after intraperitoneal toxoplasma infection.  On day 4.5 a population of CDIIc+MHC IIlow immature DCs (imDCs) appear prominently in the peritoneum but not in the blood yet later on day 5, a small population of imDCs could be identified in the blood.  Further analysis revealed that a majority of the imDCs in the peritoneum seem to be of myeloid (CD11b+B220^CD8a^CD4^) not plasmacytoid nor lymphoid pehnotype.  Of these myeloid imDCs, subpopulations with distinct lymphoid organ homing potential exist in the peritoneum as well as the blood.

                  Since dendritic cells are able to produce IL-12, an important cytokine in TH1 activation, we investigated IL-12 production by intracellular staining.  Our experiments showed that only a minority of the CD11c+ dendritic cells from infected mice spontaneously produced IL-12 production and that most IL-12 producers in the peritoneum are MHC IIhigh.  From these results, we propose a hypothetical schema for monocyte to myeloid DC transition, differentiation and trafficking.

 

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RNA Interference of HIV-1 Replication

 

By: Wayne Chung

Sponsor: Bharat Ramratnam, MD

Department of Medicine

 

                  RNA interference (RNAi) is the sequence specific degradation of messenger RNA induced by homologous short, interfering (si) RNA.  The purpose of this study is to investigate the effectiveness of siRNA mediated suppression of HIV-1 replication.  We chose the first exon of the HIV-1 transactivator protein tat as the target of our siRNA.  We first determined the potency of RNAi inhibition by transient transfection of 293T cells with synthetic siRNA.  Next, we designed a molecular construct with a short hairpin (sh) RNA expression cassette to allow intracellular synthesis of siRNA.  Finally, we generated permanent cell lines that stably expressed the shRNA.  Inhibition by transient transfection was 91% compared to controls.  The recombinant adeno-associated virus (AAV) construct, AAV-tat, reduced viral replication in 293T cells by 85%.  Stable siRNA expression was achieved in H9 cells, subsequently reducing HIV-1 replication by 96%.  These results show that the introduction of an engineered expression cassette and the stable expression of siRNA can lead to long term inhibition of HIV-1 replication, and forms the basis for further research in RNA interference as a viable therapy against HIV-1.

 

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Respiratory physiology of ParkinsonŐs disease during exercise using a magnetometer.

 

By: Duncan A. Friedman

Sponsor: Carol Garber

Department of Medicine

 

                  Study Objectives:  Respiratory dysfunction is a known cause of death in ParkinsonŐs disease.  This study sought to determine if there are any differences in respiration between patients with mild to moderate PD and age and gender matched control subjects.

                  Subjects:  Twelve patients with clinically diagnosed PD (Hoehn-Yahr Stage I-III) with a mean age of 64.11 years were compared to eleven healthy participants with a mean age of 67.11 years.

                  Methods:  Participants engaged in three levels of submaximal exercise (0W, 20W, and 30W) for 5 minutes.  Data were recorded using an Epri 4-Lead Magnetometer attached at specific positions on the thorax.  These data reflected measures at resting, 0W, 20W, 30W and recovery levels of exercise.  Data were processed and analyzed statistically.

                  Results:  No significant difference existed between groups in the 5 breathing measures examined (VT, VC, Frq, VT/VC, and VE/MVV).  General trends were observed in each of these measures.  PD patients had consistently higher VT means and consistently lower Frq means.  VE plots were very similar between groups.  VE/MVV means were higher at each level of exercise for PD patients.

                  Conclusion:  PD patients in the early stages of the disease maintain a similar minute ventilation as control counterparts.  This achieved through a relative increase in breathing frequency in an effort to compensate for decreased tidal volume.  Patients might exhibit these differences due to lack of subcortical control over respiratory control areas in the brain stem.  Although no measure achieved significance, further research might confirm the general trends seen by this study and demonstrate a significant difference in between PD patients and matched controls.

 

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Molecular Mechanisms of Parathyroid Hormone (PTH) Binding

 

By: Kimberly J. Hyde

Sponsor: Dale Mierke

Department of Molecular Pharmacology, Physiology & Biotechnology

 

The parathyroid hormone (PTH) plays an essential role in the regulation of calcium ion homeostasis in the blood.  The importance of this ion in diseases such as osteoporosis and hyperparathyroidism has brought about the need to have a complete understanding of how this hormone binds to its preceptor (PTH1).  Once the precise intermolecular interactions that are responsible for the activation and suppression of this hormone system are know, it will be possible to design pharmaceutical agents that can mimic or antagonize the action of PTH, leading to a number of therapeutic solutions for the diseases that are affected by the parathyroid hormone and its receptors.  The existing model of the receptor-ligand complex for PTH is by no means complete.  New photoaffinity cross-links have been developed that play an important role in the understanding how the ligand binds to the receptor.  Here, we have incorporated this new information and performed molecular dynamics (MD) simulations on the ligand-receoptor complex to determine the molecular mechanism of PTH binding.  The starting structure for these studies originated from experimental data, including a series of photoaffinity labeling experiments, structure predictions based on homology analysis with proteins of known structures, and spectroscopic structural studies of PTH (1-34) and extracellular domains of PTH1.  The N-terminus of PTH is located on the extracellular side in the center of the seven transmembrane helix core of the receptor.  Ser1, Ile5, Met8, and His9 have side chains that project towards the core of the receptor while Ser3, Leu7, and Leu11 have side chains that project towards the extracellular matrix (ECM).  The C-terminus of PTH (1-34) interacts with the N-terminal and EC1 domains of PTH.  The hydrophobic face of the C-terminal alpha helix of PTH (1-34) (residues Vsl21, Leu24, Leu28, Val31) interacts with N-terminal domain of PTH1.  Electrostatic interactions also occur between Arg20/E177 and Lys26/E254.  Further studies are needed to supplement this model.  This model provides further insight into the molecular mechanism of ligand binding and receptor activation, which may eventually allow for rational design of drug candidates to regulate this important hormone system.

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Respiration and Locomotion of the Painted Turtle

 

By: Rebecca Kessler

Sponsor: Donald Jackson

Department of Molecular Pharmacology, Physiology & Biotechnology

 

                  Reptile anatomoy is such that their hypaxial musculature is shared between their locomotor and respiratory systems.  This may limit the capacity of the animals to breathe and move simultaneously.  Chelonians, however, possess unique anatomical characteristics that may uncouple the antagonistic functions of the hypaxial musculature such that they can maintain proper ventilation while swimming.  This hyposthesis was tested by measuring tidal volume (VT), oxygen consumption (V02) and carbon dioxide production (V02 ) in the semi-aquatic painted turtle, Chysemys picta, both at rest and while swimming at 13.5, 20, and 26 cm/s in aquatic flume.  Both VT and V02  increased significantly from resting values of 17.3 + 2.6 ml kg-1  and 0.69 + 0.07 ml 02 min-1 kg-1, respectively, compared to those at 20 cm/s (20.1 + 2.1 ml kg-1 and 1.86 + 0.26 ml 02 min-1 kg-1, respectively).  V02 was also significantly elevated from resting at 26 cm/s (1.92 + 0.67 ml 02  min-1 kg-1).  Instantaneous frequency (f1) remained constant, while the respiratory quotient (RQ) showed a statistically insignificant decreasing trend.  Alveolar ventilation (VA) showed an insignificant increase, while air convection requirement (VE/VCO2) remained relatively unchanged.  These data suggested that painted turtles can effectively ventilate their lungs during increased levels of exercise.

 

 

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Encapsulated Cell Therapy for Removal of Uremic Toxins: Uric Acid

 

By: Jan Markus Bruder

Sponsor: Michael Lysaght

Department of Molecular Pharmacology, Physiology & Biotechnology

 

This thesis will be limited to reporting the findings on uric acid; the results however were obtained in conjunction with similar studies conducted for the degradation of urea and creatinine and have to be viewed as part of the framework of this larger project.

           Existing treatment options for end-stage-renal-disease (ESRD) remain unsatisfactory; dialysis is attended by a 20% annual mortality rate and a low quality of life while donor organs are available for less than 2% of the patient population.  Accordingly, we have been investigating a novel treatment protocol utilizing encapsulated cell therapy to clear three major uremic toxins: urea, creatinine, and uric acid.  Genetically modified bacteria that contain plasmids carrying the genes for the enzymes urease, uricase and creatininase may provide patients with an alternative treatment to supplement dialysis.  In one therapy format, capsules containing these modified strains could be given orally and reduce the level of uremic toxins during their passage through the GI system.

           Previously, we have reported that a genetically  modified and encapsulated strain of E. coli DH5 (containing the urease plasmid pkAU17 from Klebsiella aerogens Đ generously provided by Scott Mulrooney) effectively degrades urea in-vitro with kinetics and mass removal rates which appear realistic for therapeutic application.  As will be shown in this paper, in our hands at least, genetically modified E. coli DH5 cells had no effect on uric acid levels, a finding that contradicts previous reports in the literature. 

           More recently, we have evaluated the capacity of free and encapsulated bacteria as well as enzymes (including uricase) to degrade uric acid in vitro as well as in vivo.

 

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Conservation Under the Citizen Suit Provision of the Endangered Species Act, 1998-2003.

 

By: Carter Romansky

Sponsor: Sharon Swartz

Department of Ecology & Evolutionary Biology

 

                  Section 11 of the Endangered Species Act gives private citizens the power to bring suit against the government when they feel that regulatory agencies are not performing their duties to the extent mandated by the Act.  Because of administrative disfavor for the Act and limited funding from Congress, the implementation of the ESA has largely fallen out of the hands of the Fish and Wildlife Service and increasingly into the hands of the courts.  This mode of enforcement has important implications for the way the Act operates in this country and for the potential survival of endangered species in North America.  In this study I have examined the practical record of the entire federal court system over the last five years with respect to enforcement of the Endangered Species Act.  I found that fish are the most often litigated type of species, that river systems are the most often litigated type of habitat, and that agriculture is the most often litigated type of human activity.  ESA citizen suits occur almost exclusively in the western half of the United States, especially on federal lands in the Sonoran Desert, throughout California, and in the Columbia and Snake River Valleys of the Pacific Northwest.  The appearance of the ESA in courts, then, appears to be just another front in the perennial struggle for the control of water rights in the West and indicates a fundamental shift in the way that this law is administered in this country.  Further, all the date taken together indicate that the ESA becomes less effective as habitats become more degraded (the exact opposite of what should happen if we hope to have an effective means for protecting species and habitat in this country), that court mandated activities do not provide an adequate platform from which to launch a nationally coherent policy to protect threatened and endangered species, and that the protection of overall biodiversity through the Act is secondary to the protection of the basic functional integrity of ecosystems.

 

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The Effect of Monoclonal Antibody b E11 Treatment on the Function of CD98 Heterodimer: Growth Inhibition via Inhibition of Amino Acid Transport

 

By: Andy Su

Sponsor: Nancy Thompson

Department of Medicine

 

                  Despite recent advances in the study of cancer, medical treatments of cancer remain imperfect due to an incomplete understanding of the processes that permit, facilitate and otherwise contribute to the abnormal growth and proliferation of cells that lead to cancer.  Traditionally, most researchers have focused their studies on how DNA damage and mutation disrupt the machineries regulating cell cycle.  While many tumor phenotypes display the malfunctioning of cell cycle control, altered expression of genes that are not involved in the regulation of cell cycle also contribute to cancer phenotypes.  We are interested in expanding the knowledge base in such type of gene product and in investigating the role of amino acid transporters in cancer progression. 

                  We study the role of CD98 activation molecule and associated amino acid transporter LAT1 (L-amino acid transporter 1) in cancer growth.  LAT1, which is a 40kDa light chain, forms the CD98 heterodimer when associated with the CD98hc, an 80kDa glycoprotein (Mannion et al., 1998).  We have previously observed that LAT1 increases system L amino acid transport in mouse hepatocytes, and these cells showed a growth of advantage in limiting conditions (Campbell et al., 2001).  Due to these and other observations, we hypothesize that the alteration of LAT1 expression confers a growth or survival advantage by increasing amino acid transport activity when amino acid availability is limited.

                  The goal of my Honors Thesis Project is to assess the relationship between amino acid transport and CD98 function in cell growth.  The study examines the relationship between amino acid transport mediated by CD98 and tumor growth and proliferation over an observation period while cancer cell lines were treated with blocking antibodies to CD98hc provided by Dr. Ira Herman (Papetti and Herman, 2001).  The b  E11 antibody, a monoclonal antibody specific to the CD98hc, inhibited the growth of several cancer cell lines in a dose dependent manner in vitro (Papetti and Herman, 2001).  However, their study did not address whether the b E11 antibody had any affect on amino acid transport activities and if any causal link could be established between growth inhibition and a change in amino acid transport activities.  To investigate whether the growth inhibition is a consequence of decreased amino acid transport mediated by b E11 blockade of CD98, the activities of amino acid transport and cell proliferation of cancer cell lines treated with b E11 or non-immune IgG1 K over several days were compared.  Current data suggests that there is a statistically significant decrease in amino acid transport level due to b E11 treatment, but it remains uncertain if the growth inhibition can be attributed to the decrease in transport activity.

 

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Novel Mechanisms for the Reduction of Hepatitis B Virus e Antigen Expression

 

By: Genie Bang

Sponsor: Shuping Tong

Department of Medicine

 

            Background:  Hepatitis B virus (HBV) expresses a secreted protein called HBeAg that is not essential for viral replication but may not promote persistent viral infection.  On the other hand, the host immune response against HBeAg helps clear HBV infected cells.  Thus, rise of anti-HBe antibody in HBV patients is usually associated with emergence of viral variants that express low HBeAg or no HBeAg at all.  So far only two types of HBeAg variants have been well characterized: core promoter mutants (with reduced transcription of HBeAg mRNA) and precore mutants (with nonsense mutation in the HBeAg coding sequence).  The generation of mature HBeAg requires removal of the N-terminal signal paptide, C-terminal basic sequence, and formation of disulfide bond between two cysteine residues (cys-7 and cys61).  Naturally occurring mutations have been found in anti-HBe patients at precore codon 17, encoding the Đ3 residue of the signal preptide cleavage site.  This mutation was proposed to impair cleavage and hence reduce HBeAg formation.  Mutation of either of the two cysteine residues was found to greatly impair HBeAg secretion and/or antigenicity, but whether such mutations will impair viral replication has not been studied.

                  Aims:  We wished to determine 1. whether the naturally occurring codon 17 mutation indeed impaired HBeAg expression, and whether it affected viral replication capacity; 2. whether mutations affecting the two cysteines affect viral replication.

                  Methods:  Site-directed mutants were generated, converted to tandem dimer, and transfected to human hepatoma cells.  HBeAg expression was measured and normalized against HBsAg, which should not be affected by the mutations.  Viral DNA replication was detected by Southern blots.

                  Results:  The codon 17 mutation did not impair HBeAg expression, but greatly reduced viral DNA replication.  A precore codon 29 mutation, which often accompanies codon 17 mutation in patients, was found to restore the replication capacity of the codon 17 mutant.  It did not affect the HBeAg expression level.  Mutation of the cys-7 impaired HBeAg expression as anticipated, but also abolished viral DNA replication.  This is consistent with the importance of the position occupying the loop of encapsidation signal, a structure essential for viral replication.  Mutation of Cys61 to ser or arg, while abolished HBeAg expression, was tolerated for viral replication.  However, a cys to arg change at this position abolished viral particle secretion. 

                  Conclusion:  1.  Contrary to prediction, precore codon 17 mutation did not impair HBeAg expression.  2.  The co-variation at codon 29 is required to maintain high replication capacity of codon 17 mutant.  3.  Đ7 cys mutant is replication defective and hence unlikely viral survival mechanism under anti-HBe.  4.  Cys61 mutation will abolish HBeAg expression, retain viral replication, and maintain or disrupt viral secretion depending on the exact nature of the substitution.

 

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Bat Flight Kinenatics and Ecological Correlations.

 

By: Daniel VanMeter

Sponsor: Sharon Swartz

Department of Ecology & Evolutionary Biology

 

                  The dynamic flight patterns of aerial animals far exceed the capabilities of many modern aircraft.  Understanding bat flight and the role of dynamically varying camber will aid in achieving the greatest amount of lift with the least cost in modern airfoils.  The goals of this experiment were first to demonstrate the relationship between camber and lift, and second, to investigate camber variation over the wing beat cycle at different wind speeds.  Camber increases drag at higher speeds, and so it is expected that camber will decrease with increasing speed.  In this experiment, flight videos of the bat Miniopterus australis in a wind tunnel were entered into the PEAK Motus system and a series of points critical to estimating wing camber and lift were digitized.  A series of segmental distances and a vector angle were used to estimate wing camber and lift.  Lift, as estimated by vertical acceleration, and camber were positively related over time.  This relationship was not perfect, however, with a change in camber sometimes offset from the change in lift.  Vertical acceleration, and camber were positively related over time.  This relationship was not perfect, however, with a change in camber sometimes offset from the change in lift.  Vertical acceleration always decreased during the downstroke from a positive value to a negative value.  Vertical acceleration during the upstroke returned to a positive value.  Adjusted camber, however, did not show such a clear trend.  The lack of a perfect correlation between camber and lift could be the result of other mechanisms of lift generation such as wing flapping.  At higher speeds camber remained relatively constant, but at the slowest speed, camber increased significantly during the downstroke.  Further data will illustrate whether trends in this study can be applied to other bat species or even other individuals.  Computer flow models could directly investigate how camber affects flow, and could be better put into context through integration with studies of other flight characteristics, such as angle of attack.

 

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An Evaluation of Astrogliosis and Synaptic Alterations in Temporal Cortex Tissue of Patients Diagnosed with Mesial Temporal Sclerosis

 

By: Krister Jones

Sponsor: Edward Stopa, M.D.

Department of Pathology & Laboratory Medicine

 

                  The most common neuronal cell dysfunction observed in patients with temporal lobe epilepsy is mesial temporal (AmmonŐs horn) sclerosis.  Synchronous hyperactivity in the hippocampus of patients diagnosed with mesial temporal sclerosis has been shown to cause neuronal cell loss, decreased synaptic density, and increased mossy fiber sprouting within the affected hippocampus (Proper et al., 2000).  In the present study, temporal cortex tissue removed through partial temporal lobectomy of patients suffering from pharmaco-resistant temporal lobe epilepsy was evaluated using synaptophysin, glial fibrillary acidic protein (GFAP), and GAP-43 immunoreactivity.  The degree of immunoreactivity was quantitatively measured using computerized image analysis.  Results indicate that while levels of GFAP in temporal cortex are similarly elevated to those found in hippocampus with mesial temporal sclerosis in temporal cortex, there may not be the widespread degeneration of synapses seen in the hippocampus of patients with this disease.  This finding may lead to further determination of the mechanisms by which the epileptic seizure is either caused or spread in the hippocampus and subsequently affects larger brain regions.

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Costs of Resistance Associated with Genetically Engineerd Cold Tolerance in Arabidopsis thaliana.

 

By: Matthew W. Jackson

Sponsor: Johanna Schmitt

Department of Ecology & Evolutionary Biology

 

            Traditionally researchers investigated costs of resistance to disease, herbivores, and herbicides in plants instead of environmental stresses.  Much of this research focuses on the costs and benefits of constitutive expression versus inductive expression in resistance pathways.  Using Arabidopsis thaliana (Brassicaceae), a primarily selfing winter annual found in temperate regions throughout the Northern Hemisphere, I used genetically engineered Arabidopsis thaliana that, in each line, constitutively overexpress an individual CBF gene to investigate the costs of resistance to cold tolerance across variable environments.  A drop in temperature induces an endogenous cold-acclimation pathway controlled by a family of transcriptional activators, the CBF gene family.  Consisting of three genes (CBF1, 2 and 3), this family activates a cascading reaction of cold-tolerance genes that prepare the pant to survive in cold environments.  I investigated the effects of cold-acclimation temperatures 4űC, and cold-shock temperatures, -6 to 8űC, on the fitness of engineered and non-engineered with a two-by-two factorial design.  Plants with cold-shock exposure produced too few fruits for analysis; however, interesting effects on lifespan occurred.  For plants without cold-shock exposure, engineered plants showed no difference in fitness across no cold-acclimation and cold-acclimation environments, unlike the control plants.  CBF2, 3 showed significant costs of resistance in all environments; however, CBF1 showed no cost of resistance in a no cold-acclimation environment, and it yielded significantly greater fitness than the controls in a cold-acclimation environment.  Interestingly, theCBF1 gene showed no cost of resistance in a normal, no cold-acclimation environment and a clear fitness benefit in a cold-acclimation environment.

 

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Slinity Fluctuations and Competitive Dynamics in Salt Marsh Bacterial Communities

 

By: Lexi Weintraub

Sponsor: Jennifer Hughes

Department of Ecology & Evolutionary Biology

 

            Theory predicts that environmental variability can play a significant role in determining community structure.  I examine the effects of salinity fluctuations on the competitive dynamics of salt marsh bacterial communities.  I measured the maximum growth rates of 6 strains of bacteria isolated from a fresh and a brackish marsh at multiple salinities and incorporated these data into a model.  The model generated predictions about the effects of salinity fluctuations on dynamics of competition between strains.

                  Maximum growth rate measurements suggested that salinity plays a role in structuring marsh bacterial communities.  Strains isolated from the fresh marsh had relatively higher growth rates at low salinities, while strains from the brackish marsh specialized at salinities approximately equal to the site from which they were isolated.  The model was unable to predict the results of fluctuations.  The data suggest that multiple interactions occurred between strains.

                  Fluctuations affected competitive dynamics in all cases, and generated an overall increase in community evenness in all competitions.  These results support the hypothesis that environmental variability influences community structure and promotes diversity.

 

 

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Comparison of 2 Methods of Fabrication of Poly (fumaric-co-sebacic) Anhydride Microspheres for Oral Delivery of Insulin

 

By: Emily Bubbers             

Sponsor: Edith Mathiowitz

Department of Molecular Pharmacology, Physiology & Biotechnology

 

            Poly (fumaric-co-sebacic) anhydride (P(FA:SA)) is used to encapsulate insulin for oral delivery to Type diabetics.  The purpose of this study is to reduce the size of P(FA:SA) microspheres to less than 2 µm in diameter in order to increase the number of microspheres absorbed by the small intestine.  Reducing the size of the spheres allows the microspheres to traverse into the blood stream either via the PeyerŐs patches, paracellularly or transcellularly.  As the microsphere degrades, carboxyl groups are formed on the surface, which bind with the glycoproteins in the intestinal lumen, increasing the residence time in the gastrointestinal tract.

Insulin loaded microspheres were fabricated using the phase inversion nanoencapsulation (PIN) method, either with or without the PIN apparatus.  A surfactant was also added to those microspheres made without the PIN apparatus.  The spheres were characterized using scanning electron microscopy (SEM) and Coulter Small Volume Particle sizing.  Insulin release profiles were obtained via in vitro release studies.  In vivo studies were performed on diabetic rats to test the ability of the microspheres to maintain blood glucose levels in the presence of food.  Microspheres fabricated with surfactant demonstrate the smallest mean diameter by volume, deliver more insulin to the body and maintain blood glucose levels for prolonged periods of time.  These microspheres can be an effective method of controlled delivery of insulin.  An oral delivery system for insulin will negate the need for daily injections of insulin and provide a more constant level of insulin in the blood stream, rather then bursts from subcutaneous injections. 

 

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Design of a Novel Immunoisolated Islet Delivery Device Utilizing Microfabrication, Polymer and Cellular Technology

 

By: Peter A. Rachlin           

Sponsor: Jeffrey Morgan

Department of Molecular Pharmacology, Physiology & Biotechnology

 

            Transplantation of islets of Langerhans is a potential treatment of Type I diabetes that aims to restore normal glucose homeostasis. Microencapsulation of islets could enable transplantation in the absence of immunosuppression, which would be beneficial as the side effects associated with immunosuppression outweigh the potential benefits of islet transplantation.  However, cell-encapsulating technology is not without challenges, including problems concerning the geometrical characteristics of the implant device, the tissue density and spatial arrangement of the encapsulated cells, and the islet cellsŐ oxygen availability.  Housing and maintaining approximately 700,000 islets in a practical implant remains as one of the major hurdles to overcome in making implantable immunoisolation devices a clinical reality.  The aim of this study is to pursue these engineering challenges and design a novel immunoisolated islet delivery device as an alternative to current therapy using microfabrication techniques and polymer and cellular technology.  Porous and topographically complex polyurethane membranes and alginate hydrogels were manufactured utilizing a soft lithography approach.  SU-8 polymer-coated silicon wafers were employed as master chips, providing a surface array of hexagons 50 µm to 200 µm deep, with radii from 25 to 300 µm on centers from 75 to 900 µm.  A battery of negative replicates of these wafers was produced using polydimethylsiloxane silicone elastomer (PDMS).  Solutions of polyurethane and alginate were polymerized on the PDMS templates to yield membranes and hydrogels, respectively.  Both the polyurethane membranes and the alginate hydrogels successfully replicated the complex surface topography of the various PDMS stamps.  These two products were subsequently envisioned to function as three-dimensional scaffolds for tissue-engineered materials, specifically an islet delivery device.  Polyurethane scaffolds were loaded with fluorescent beads approximating the size of islets and immunoisolated with a coating of alginate hydrogel.  With the concept proven to be viable, isolated rat islets were successfully loaded into a polyurethane scaffoldŐs hexagonal wells with precise and predetermined dimensions and then the scaffold was immunoisolated with a coating of alginate.  The islets remained functional and entirely contained in the polyurethane-alginate housing.  Microfabrication technology appears to be an integral component in the effort to make a reality the possibility of replacing damaged or diseased organs with artificial tissues engineered from a combination of living cells and biocompatible scaffolds.  The development of photolithography to pattern biological molecules onto surfaces, novel tools to move silicon-based fabrication to polymer-based constructs and the move from two-dimensional to three-dimensional fabrication each provide essential tools in the development of in vitro systems to study the control of cells through their environment, the production of scaffolds to support tissue architecture, and the fabrication of living hybrids of cells and scaffolds that demonstrate the incremental steps toward reconstruction of tissue function.

 

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Metabolic Cross-Feeding in Two-Species Bacterial Communities

 

By: Ian T. Carroll                 

Sponsor: Jennifer Hughes

Department of Ecology & Evolutionary Biology

 

            Metabolic cross-feeding between bacteria occurs in natural assemblages and artificial communities, including cultures of closely related Escherichia coli strains.  Laboratory communities with cross-feeding relationships support coexistence in cultures supplied with a single limiting nutrient for which response competition generates testable predictions about community structure.  The rate of supply of the limiting resource is predicted to determine whether competitive exclusion or coexistance occurs.  For increasing rates of nutrient supply, the population sizes are predicted to equilibrate at a common ratio.  Results from experimental manipulations of two independently derived pairs of cross-feeding E. coli grown in chemostat culture qualitatively agree with model predictions.

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Exploring Cytokines and Innate Immune Kinetics in the Epidermis; Development of a Non-Invasive Luminescence Based Assay to Quantify Bacterial Load

 

By: Roxanne J. Wadia        

Sponsor: Jeffrey Morgan