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CROSSROADS An Undergraduate Research Journal of the Monmouth University Honors School 2009 Monmouth University West Long Branch, New Jersey i Crossroads 2009 Crossroads (ISSN 1076-7166) is published annually by the Honors Program at Monmouth University. This issue of the journal is Copyrighted © 2005 by the Monmouth University Honors Program, 431 Cedar Ave., West Long Branch, New Jersey, 07764-1898 U.S.A. All rights reserved. Crossroads is printed in the United States of America. Opinions expressed in the journal are not necessarily the opinions of the Monmouth University Honors Program. The purpose of this journal is to involve students in the creative process of a journal as well as for them to gain professional experience publishing their honors theses and projects. For a free subscription, contact the Honors School Dean at: The Honors School Monmouth University 431 Cedar Avenue West Long Branch, NJ 07764-1898 U.S.A ii Crossroads 2009 TABLE OF CONTENTS EDITOR’S NOTE ............................................................................................v EDITORIAL STAFF ..................................................................................... vi ABSTRACTS [The following abstracts appear in the journal in lieu of the entire articles in order to avoid possible copyright conflicts with the professional journals in which they are being published.] IDENTIFYING ANTIAPOPTOTIC HIF-1 TARGET GENES IN RAT TESTIS (BIOLOGY) Anoop Shah......................................................................................................1 ALTERED RESPONSE TO CELLULAR STRESS UPON CONTACT INHIBITION (BIOLOGY) Marian Gaballah ..............................................................................................3 THESES COVERING SETS OF CONGRUENCE Leanne Clarke ..................................................................................................8 THEIR BELOVED BANJAR WEST AFRICA’S FORGOTTEN CONTRIBUTION TO AN AMERICAN MUSICAL TRADITION Quinn Gilly .................................................................................................... 40 iii Crossroads 2009 NARRATIVE CIRCULARITY IN CHARLOTTE BRONTË’S WORK Katelyn Mirabelli ........................................................................................ 107 THE CATHOLIC CHURCH AND THE ROAD TO ANTI-SEMITISM: A CONTROVERSIAL HISTORY FROM THE CRUSADES TO THE HOLOCAUST Nicole Stevens…………………………………………………….…….…128 INTERPRETING FORGOTTEN COLONIAL MATERIAL AT THE SALISBURY SITE Kerri Sansevere……………………………………………………….……177 iv Crossroads 2009 EDITOR’S NOTE Crossroads is an interdisciplinary, undergraduate research journal published by the Monmouth University Honors School. The contributors are Senior Honors Thesis students whose work has been chosen by the Honors Council as representing the most original, thoroughly researched, and effectively argued theses in their fields. Crossroads is made possible through the support of Monmouth University and the generosity of our benefactor Ms. Jane Freed, class of ’81. The five articles in this volume include work in the fields of: Political Science, Mathematics, English Literature, and Psychology. Deep gratitude is also due to the selfless dedication of faculty fulfilling the roles of Chief Advisor and Second Reader in the various disciplines of this year’s contributors. They spend untold hours mentoring the students through their yearlong process of research, writing, and oral defense, especially: Dr.Kevin Dooley (Political Science) for Lindsay Savage, Dr. Joseph Coyle (Mathematics) for Samantha Bourque-Trieff, Dr. Janice Stapley (Psychology) for Helene Mizrahi, and Dr. Prescott Evarts (English) for Raymond O’Meara and Karen Mintz, Additionally, we recognize the initiative and continued support of our early directors: Co-Founder, Dr. William Mitchell for his editorial assistance and his hard work and dedication to the success of all our Honor students, Dr. Saliba Sarsar, Dr. Kenneth Campbell, and Dr. Thomas Pearson. v Crossroads 2009 EDITORIAL STAFF Dr. Kevin Dooley, Dean of The Honors School Sara Iantosca, Student Editor Director of Student Standards, Advising and Services ................................................ Reenie Menditto Cover Design .......................................... Pat Cresson, Art Department Layout ................................................................................. Erin Hawk Editorial Assistant .............................................................. Erin Hawk Copy Editing……………………………………………..….Dr. Frank Fury Copy Editing………………………………………………..Dr. Neil Graves vi Crossroads 2009 Published by ............................. Monmouth University Honors School Printed.......................................... Monmouth University Copy Center vii Crossroads 2009 Thesis Abstract Identifying Antiapoptotic HIF-1 Target Genes in Rat Testis Anoop Shah Oxygen balance of the reproductive tract is essential to the health and well-being of an individual. Testicular torsion, a condition that creates oxygen imbalance in male reproductive tissues, occurs from a twisting of the spermatic cord resulting in testis ischemia (I), or a reduction in blood flow to the testis. Prolonged ischemia typically leads to hypoxia, where there is a severe deficiency in the amount of oxygen reaching the tissue. Major cellular damage occurs after reperfusion (R), or the return of blood flow to the organ, where the tissue is deemed to have undergone oxygen shock. Subsequent alterations in protein expression profiles can lead to germ cell-specific apoptosis, or the programmed cell death of sperm-producing cells. However, germ cell-nurturing Sertoli cells and sex steroid-producing Leydig cells are protected against torsion-induced apoptosis. Hypoxia-Inducible Factor-1 (HIF-1), commonly known as the master regulator of oxygen homeostasis, is a transcription factor stabilized by hypoxic conditions. Composed of an α and β subunit, HIF-1α is degraded under normoxic conditions, where there is no deficiency in oxygen levels. Under hypoxic conditions, the α and β subunits may join together to activate HIF-1. Active HIF-1 may bind to a hypoxia response element (HRE; 5’-RCGTG-3’) found in the promoter region of a target gene to initiate transcription of that gene. Potential targets of HIF-1 include genes involved in glucose metabolism, angiogenesis, cell survival, and cell death. Focusing on cell survival, we hypothesized that HIF-1 plays an important role in the protection of Leydig cells following I and I/R by activating antiapoptotic target genes in the testis. A Genomatix MatInspector search identified induced myeloid cell differentiation-1 (Mcl-1), a known antiapoptotic gene, as a potential HIF-1 target gene containing the hypoxia response element in its promoter region. Unilateral testicular torsion (720°) was surgically induced in adult, retired-breeder male Sprague-Dawley rats for periods ranging from one to six hours, immediately followed by a reperfusion period of up to four hours. Cytoplasmic and nuclear extracts were isolated from sham and torsed testes for further analysis. Results of an Active-Motif TransAM™ enzyme-linked immunosorbent assay (ELISA) quantitated HIF-1 binding to a consensus binding site from the human erythropoietin (EPO) gene promoter and demonstrated testicular HIF-1 DNA-binding activity in both sham and ischemic extracts. Immunoblotting indicated Mcl-1 presence 1 Crossroads 2009 in rat testes and unaffected steady-state levels of Mcl-1 following I and I/R (ANOVA, p<0.05). Immunohistochemical (IHC) analysis of normoxic testis tissue identified localization of Mcl-1 in rat Leydig cells. A second immunoblot of Leydig cell extracts cultured at 5% and 21% O2 respectively detected Mcl-1 in Leydig cells under hypoxic conditions and confirmed Mcl- 1 presence in Leydig cells under normoxic conditions. Patterns of Mcl-1 expression were consistent with previously obtained data of HIF-1 expression in the testis. Preliminary chromatin immunoprecipitation (ChIP) analysis demonstrated HIF-1 binding to the Mcl-1 promoter in vivo. Overall, these results supported our hypothesis that Mcl-1 is a HIF-1 target gene that may play a key role in the protection of Leydig cells following testicular torsion. Acknowledgements This work could not have been completed without the individual contributions of many people. First and foremost, I would like to thank my faculty mentor Dr. Michael A. Palladino for his guidance over the course of the last two years. I have learned a great deal from his professional approach in the laboratory, and his high expectations have contributed immensely to the success of my research. Secondly, thanks are due to the late Dr. Matthew P. Hardy from the Population Council for the Center for Biomedical Research, whose laboratory provided the cultured Leydig cell extracts. Furthermore, a large number of experiments were conducted with the help of laboratory partners Rebecca Tyson, Jaclyn Horvath, and Michael Savarese. Rebecca and Jaclyn aided with surgical procedures and performed the ChIP assay, while Michael assisted with IHC experiments. Additional thanks are directed to the second reader of this thesis, Dr. Dennis E. Rhoads, and to Dr. Brian Garvey and Reenie Menditto of the Honors School, who have been very supportive throughout the completion of the Honors curriculum. Lastly, I would like to thank the National Institute of Health (NIH) for funding this research (Grant R15-HD046451). 2 Crossroads 2009 Abstract Altered Response to Cellular Stress Upon Contact Inhibition Marian
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