DOCSLIB.ORG

2020-Abstract-Book.Pdf

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
2020-Abstract-Book.Pdf FRIDAY, APRIL 3 ABSTRACT 2020 Showcasing research, creativity, and service learning go.wisc.edu/ugsympo Welcome to our 22nd Annual Undergraduate Symposium at the University of Wisconsin-Madison. The Symposium takes a new turn this year in response to the COVID-19 pandemic whereby we celebrate the research accomplishments of our undergraduates in a virtual format. We look forward to getting back to our labs, field sites, studios and similar locations where the creativity and curiosity of our undergraduates can flourish without constraint as they build their Wisconsin Experience. Steven M. Cramer, Vice Provost for Teaching and Learning University of Wisconsin–Madison We would like to thank our major sponsors and partners: Brittingham Trust Chancellor’s and Powers-Knapp Scholarship Programs General Library System McNair Scholars Program Morgridge Center for Public Service Office of the Provost Undergraduate Academic Awards Office Undergraduate Research Scholars Program University Marketing Wisconsin Institute for Science Education and Community Engagement Wisconsin Union The Writing Center 2020 Undergraduate Symposium Organizing Committee: Hannah Bailey, Liza Chang, Steven M. Cramer, Doug DeRosa, Sarah Hagedon (coordinator), Marina Kelly, Laura Livingston, Mandy Morrow, Samantha Samreth, Amber Smith, Julie Stubbs A special thanks goes to Stephanie Diaz de Leon of The Wisconsin Union; Jay Ray and Crague Cook at College Library; DesignLab; and College Library Computer & Media Center. Cover photo by the Office of University Commications. ii HIDDEN HISTORIES AND RHETORICAL DISSONANCE IN THE PLANTATION HERITAGE SITE Heidi Weston, Michael Bernard-Donals (Mentor) My aim with this paper was to document the range of rhetorical tensions that are embodied in Plantation Heritage Sites and their preserved architecture, objects and collections, tour talks and historical interpretation. These tensions are engendered by the rhetorical needs and desires of tourism and through the uncertain admixture of Old South myths and more histori- cally accurate narratives. I argue that these rhetorical conflicts which are represented in the plantation heritage site are indicative of the friction that exists between dominant publics and subaltern counterpublics, who both view the plantation heritage site as central to their sense of self and collective identity. COLLEGE STUDENTS BEFORE CROSS CULTURAL STUDY ABROAD Kendi Aaron, Julie Larson-Guenette (Mentor) University students seeking to gain global experiences take part in study abroad programs. This research focuses on a 3-phase study investigating cultural literacy and linguistic gains among a cohort of UW-Madison students in an 11-month study abroad program in Freiburg, Germany. Data for this project consists of surveys, interviews, and writing samples taken before, during (at 4.5 months) and after the program. Dr. Julie Larson-Guenette and her colleague previously noted increased linguistic proficiency in students’ writing samples. However, the current project focuses on a subset of interview data (n=6) collected prior to the 11-month program. Data analyses explore themes present in the initial interviews that offer insight into students’ motivations for study abroad and their desire to cultivate cross-cultural awareness and linguistic development. OS AND ND ISOTOPE STRATIGRAPHY OF THE ~2.05 GA ZAONEGA FORMATION TO UNDERSTAND CHEMICAL AND PHYSICAL WEATHERING DURING THE GREAT OXIDATION EVENT Sheila Rozalia Binti Abdul Rashid, Annie Bauer (Mentor) About 2.4 billion years ago (Ga), the concentration of oxygen in Earth’s atmosphere rose dramatically, changing the nature and intensity of chemical and physical weathering until oxygen levels crashed 2.0Ga. Paleoproterozoic organic-rich shales of the Zaonega Formation in the Onega Basin, Russia, contain weathered detrital material that could provide critical infor- mation about the nature of these fluctuations in atmospheric oxygen. We performed Os and Nd isotope over 100s of meters of stratigraphy to evaluate the authigenic and detrital components in these shales. Our Os isotope results track the variation in chemical weathering input across millions of years in the Onega Basin, providing a record of the crash in oxygen levels. We use the 143Sm-147Nd isotope system to track variations in the detrital provenance throughout this interval. POSITRON EMISSION TOMOGRAPHY PROTOTYPE ASSEMBLY Paul Adu, Duncan Carlsmith (Mentor) Positron Emission Tomography (PET) is a nuclear medicine functional imaging technique for observing cell metabolism and diagnosing diseases. In the Garage Physics lab, we’re trying to assemble a pint-sized prototype of the PET scan. The system works on the principle that a radioactive tracer undergoes decay to emit a positron. The positron travels until it interacts with a nearby electron to annihilate, producing a pair of gamma photons. The gamma photons produce a scintil- lation, which is detected by a silicon photomultiplier. We use MATLAB to collect raw data. The Pint-sized PET prototype will be able to solve the problem of high operational cost associated with the existing PET scan. Moreover, it can be used to diagnose diseases from wide range of bodies: humans, pets, and lab animals. 1 THE USE OF UNNECESSARY IMAGING FOR DIAGNOSIS OF INGUINAL HERNIAS David Aguilar, Dr. Anne Lidor (Mentor) In the US, over 700,000 inguinal hernia repairs are performed each year. Inguinal hernias are usually diagnosed by a physi- cal exam. In the event where physical exams are inconclusive, imaging techniques can be used. However, some physicians order radiology studies even when a hernia is felt during the physical exam. Studies such as CT scans, ultrasounds, and MRIs are used. Unnecessary radiographic imaging can lead to adverse side-effects for the patient, increase the cost for the patient, and put an economic strain on our healthcare system. The purpose of this project is to determine how much unnecessary imagery is used. Electronic health records from the UW-Health system will be analyzed to determine the rate of usage of radiology studies in the inguinal hernia surgery population. MAPPING THE TEMPORAL: CATALOGING ECONOMIC SECTORS IN LATINO VENDOR MARKET Naga Sahiti Akondi, Edna Ledesma (Mentor) Flea markets in America generate around $300 billion in sales annually. These markets tend to be run and visited mostly by Latino in areas with a high concentration of this population. Despite this, not much attention was given to them as important places of attachment. This research studies the economic profile of these markets with a place based approach. It draws comparisons between four sample flea markets in California and Texas chosen because they are home to a high number of Latinos. The research methodology includes site observations, surveys, and key informant interviews. Some findings from this research show how Latinos feel a sense of attachment to these markets. This research aims to suggest policy measures to support Latino owned businesses. ELECTROPORATION OF GFP-MRNA INTO NK92 Adeela Ali, Christian Capitini (Mentor) Natural killer (NK) cells are a subset of lymphocytes that can kill cells in an antigen-independent manner. The human NK cell line,NK-92, when transduced with a CD19 CAR has been shown to be highly cytotoxic to cancer cells. However, conventional lentiviral approaches for CAR transfection into NK cells have the potential to cause insertional mutagenesis. Here, we attempt to transduce GFP into NK-92 cells using mRNA electroporation. This method has been shown to have higher transduction efficiency as compared to DNA-based methods. We will be testing the efficacy of electroporation as well as NK-92 cell viability post-transduction. The results from this study will help establish safer, more efficacious meth- ods of CAR transduction into NK cells for clinical purposes. GENERATION OF ENHANCED RIBOSOMES FOR OPTIMAL PROTEIN OVEREXPRESSION VIA CRISPR-CAS9-ASSISTED RECOMBINEERING Anna Allen, Silvia Cavagnero (Mentor) The accumulation of insoluble protein aggregates in overexpression conditions is a common obstacle for researchers aim- ing to study proteins and turn them into useful products. Existing methods used to prevent or counteract this problem in bacteria are largely inadequate. A promising alternative is modification of the ribosome to unlock its intrinsic ability to chaperone protein folding. This approach is made possible with the gene-editing potential of CRISPR-Cas9-assisted recombineering. Through systematic edits to the structure of the E. coli ribosome, we hope to design an idealized machine capable of both synthesizing proteins and promoting their complete, proper folding prior to release. Timely folding in this way is crucial to bypassing the aggregation pathway. 2 GEODESIGN FOR RIPARIAN VEGETATION BUFFERS TO MAINTAIN TEMPERATURES TROUT STREAMS IN A CHANGING CLIMATE Rykia Amos, David Allen Hart (Mentor) Recognized as a trout fishing haven, Wisconsin attracts tourism to its more than 10,000 miles of cold-water streams. Anthropogenic climate change threatens the long-term health of these water bodies. This project focuses on trout streams within western Dane County. The first phase involves review of observed and predicted climate trends for temperature in Wisconsin developed by the UW Center for Climatic Research, and use of the FishVis Mapper developed by the U.S Geological Survey to identify streams with cold-water species vulnerable to increasing temperatures. The second phase reviews literature about the capacity of
Load more

Recommended publications
  • Supporting Information for Proteomics DOI 10.1002/Pmic.200400942
    Supporting Information for Proteomics DOI 10.1002/pmic.200400942 Wei-Jun Qian, Jon M. Jacobs, David G. Camp II, Matthew E. Monroe, Ronald J. Moore, Marina A. Gritsenko, Steve E. Calvano, Stephen F. Lowry, Wenzhong Xiao, Lyle L. Moldawer, Ronald W. Davis, Ronald G. Tompkins and Richard D. Smith Comparative proteome analyses of human plasma following in vivo lipopolysaccharide administration using multidimensional separations coupled with tandem mass spectrometry ã 2004 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.proteomics-journal.de Supplemental Table 1: List of 804 identified plasma proteins. Note: Reference IDs correspond to either SwissProt, NCBI, or PIR database entries. For each protein, one representive peptide sequence and the peptide charge_state, SEQUEST Xcorr, and Delcn are listed. The number of different peptides identifying each specific protein is also indicated. To facilitate comparison of protein abundances between the untreated and treated samples, the numbers of peptide hit, the protein abundance ratio (treated/untreated) calculated from peptide peak area ratios, and the standard deviation of peptide peak area ratios for each protein are also listed. No abundance ratio is shown if the protein has no common peptide identified in the two samples. Whether the same protein ID was reported in reference 16 and reference 27 (195 proteins observed from two different sources) is also indicated. Reference Description # of different Representitive peptide Charge_state Xcorr DelCn peptides Peptide Hits Peptide Protein Standard
    [Show full text]
  • Signal Transduction in L-DOPA-Induced Dyskinesia: from Receptor Sensitization to Abnormal… Et Al
    Journal of Neural Transmission https://doi.org/10.1007/s00702-018-1847-7 NEUROLOGY AND PRECLINICAL NEUROLOGICAL STUDIES - REVIEW ARTICLE Signal transduction in L‑DOPA‑induced dyskinesia: from receptor sensitization to abnormal gene expression Giada Spigolon1 · Gilberto Fisone1 Received: 1 November 2017 / Accepted: 23 January 2018 © The Author(s) 2018. This article is an open access publication Abstract A large number of signaling abnormalities have been implicated in the emergence and expression of L-DOPA-induced dyskinesia (LID). The primary cause for many of these changes is the development of sensitization at dopamine receptors located on striatal projection neurons (SPN). This initial priming, which is particularly evident at the level of dopamine D1 receptors (D1R), can be viewed as a homeostatic response to dopamine depletion and is further exacerbated by chronic administration of L-DOPA, through a variety of mechanisms afecting various components of the G-protein-coupled receptor machinery. Sensitization of dopamine receptors in combination with pulsatile administration of L-DOPA leads to intermit- tent and coordinated hyperactivation of signal transduction cascades, ultimately resulting in long-term modifcations of gene expression and protein synthesis. A detailed mapping of these pathological changes and of their involvement in LID has been produced during the last decade. According to this emerging picture, activation of sensitized D1R results in the stimulation of cAMP-dependent protein kinase and of the dopamine- and cAMP-regulated phosphoprotein of 32 kDa. This, in turn, activates the extracellular signal-regulated kinases 1 and 2 (ERK), leading to chromatin remodeling and aberrant gene transcription. Dysregulated ERK results also in the stimulation of the mammalian target of rapamycin complex 1, which promotes protein synthesis.
    [Show full text]
  • Spatial Distribution of Leading Pacemaker Sites in the Normal, Intact Rat Sinoa
    Supplementary Material Supplementary Figure 1: Spatial distribution of leading pacemaker sites in the normal, intact rat sinoatrial 5 nodes (SAN) plotted along a normalized y-axis between the superior vena cava (SVC) and inferior vena 6 cava (IVC) and a scaled x-axis in millimeters (n = 8). Colors correspond to treatment condition (black: 7 baseline, blue: 100 µM Acetylcholine (ACh), red: 500 nM Isoproterenol (ISO)). 1 Supplementary Figure 2: Spatial distribution of leading pacemaker sites before and after surgical 3 separation of the rat SAN (n = 5). Top: Intact SAN preparations with leading pacemaker sites plotted during 4 baseline conditions. Bottom: Surgically cut SAN preparations with leading pacemaker sites plotted during 5 baseline conditions (black) and exposure to pharmacological stimulation (blue: 100 µM ACh, red: 500 nM 6 ISO). 2 a &DUGLDFIoQChDQQHOV .FQM FOXVWHU &DFQDG &DFQDK *MD &DFQJ .FQLS .FQG .FQK .FQM &DFQDF &DFQE .FQM í $WSD .FQD .FQM í .FQN &DVT 5\U .FQM &DFQJ &DFQDG ,WSU 6FQD &DFQDG .FQQ &DFQDJ &DFQDG .FQD .FQT 6FQD 3OQ 6FQD +FQ *MD ,WSU 6FQE +FQ *MG .FQN .FQQ .FQN .FQD .FQE .FQQ +FQ &DFQDD &DFQE &DOP .FQM .FQD .FQN .FQG .FQN &DOP 6FQD .FQD 6FQE 6FQD 6FQD ,WSU +FQ 6FQD 5\U 6FQD 6FQE 6FQD .FQQ .FQH 6FQD &DFQE 6FQE .FQM FOXVWHU V6$1 L6$1 5$ /$ 3 b &DUGLDFReFHSWRUV $GUDF FOXVWHU $GUDD &DY &KUQE &KUP &KJD 0\O 3GHG &KUQD $GUE $GUDG &KUQE 5JV í 9LS $GUDE 7SP í 5JV 7QQF 3GHE 0\K $GUE *QDL $QN $GUDD $QN $QN &KUP $GUDE $NDS $WSE 5DPS &KUP 0\O &KUQD 6UF &KUQH $GUE &KUQD FOXVWHU V6$1 L6$1 5$ /$ 4 c 1HXURQDOPURWHLQV
    [Show full text]
  • Supp Table 6.Pdf
    Supplementary Table 6. Processes associated to the 2037 SCL candidate target genes ID Symbol Entrez Gene Name Process NM_178114 AMIGO2 adhesion molecule with Ig-like domain 2 adhesion NM_033474 ARVCF armadillo repeat gene deletes in velocardiofacial syndrome adhesion NM_027060 BTBD9 BTB (POZ) domain containing 9 adhesion NM_001039149 CD226 CD226 molecule adhesion NM_010581 CD47 CD47 molecule adhesion NM_023370 CDH23 cadherin-like 23 adhesion NM_207298 CERCAM cerebral endothelial cell adhesion molecule adhesion NM_021719 CLDN15 claudin 15 adhesion NM_009902 CLDN3 claudin 3 adhesion NM_008779 CNTN3 contactin 3 (plasmacytoma associated) adhesion NM_015734 COL5A1 collagen, type V, alpha 1 adhesion NM_007803 CTTN cortactin adhesion NM_009142 CX3CL1 chemokine (C-X3-C motif) ligand 1 adhesion NM_031174 DSCAM Down syndrome cell adhesion molecule adhesion NM_145158 EMILIN2 elastin microfibril interfacer 2 adhesion NM_001081286 FAT1 FAT tumor suppressor homolog 1 (Drosophila) adhesion NM_001080814 FAT3 FAT tumor suppressor homolog 3 (Drosophila) adhesion NM_153795 FERMT3 fermitin family homolog 3 (Drosophila) adhesion NM_010494 ICAM2 intercellular adhesion molecule 2 adhesion NM_023892 ICAM4 (includes EG:3386) intercellular adhesion molecule 4 (Landsteiner-Wiener blood group)adhesion NM_001001979 MEGF10 multiple EGF-like-domains 10 adhesion NM_172522 MEGF11 multiple EGF-like-domains 11 adhesion NM_010739 MUC13 mucin 13, cell surface associated adhesion NM_013610 NINJ1 ninjurin 1 adhesion NM_016718 NINJ2 ninjurin 2 adhesion NM_172932 NLGN3 neuroligin
    [Show full text]
  • Egfr Activates a Taz-Driven Oncogenic Program in Glioblastoma
    EGFR ACTIVATES A TAZ-DRIVEN ONCOGENIC PROGRAM IN GLIOBLASTOMA by Minling Gao A thesis submitted to Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland March 2020 ©2020 Minling Gao All rights reserved Abstract Hyperactivated EGFR signaling is associated with about 45% of Glioblastoma (GBM), the most aggressive and lethal primary brain tumor in humans. However, the oncogenic transcriptional events driven by EGFR are still incompletely understood. We studied the role of the transcription factor TAZ to better understand master transcriptional regulators in mediating the EGFR signaling pathway in GBM. The transcriptional coactivator with PDZ- binding motif (TAZ) and its paralog gene, the Yes-associated protein (YAP) are two transcriptional co-activators that play important roles in multiple cancer types and are regulated in a context-dependent manner by various upstream signaling pathways, e.g. the Hippo, WNT and GPCR signaling. In GBM cells, TAZ functions as an oncogene that drives mesenchymal transition and radioresistance. This thesis intends to broaden our understanding of EGFR signaling and TAZ regulation in GBM. In patient-derived GBM cell models, EGF induced TAZ and its known gene targets through EGFR and downstream tyrosine kinases (ERK1/2 and STAT3). In GBM cells with EGFRvIII, an EGF-independent and constitutively active mutation, TAZ showed EGF- independent hyperactivation when compared to EGFRvIII-negative cells. These results revealed a novel EGFR-TAZ signaling axis in GBM cells. The second contribution of this thesis is that we performed next-generation sequencing to establish the first genome-wide map of EGF-induced TAZ target genes.
    [Show full text]
  • Systematic Elucidation of Neuron-Astrocyte Interaction in Models of Amyotrophic Lateral Sclerosis Using Multi-Modal Integrated Bioinformatics Workflow
    ARTICLE https://doi.org/10.1038/s41467-020-19177-y OPEN Systematic elucidation of neuron-astrocyte interaction in models of amyotrophic lateral sclerosis using multi-modal integrated bioinformatics workflow Vartika Mishra et al.# 1234567890():,; Cell-to-cell communications are critical determinants of pathophysiological phenotypes, but methodologies for their systematic elucidation are lacking. Herein, we propose an approach for the Systematic Elucidation and Assessment of Regulatory Cell-to-cell Interaction Net- works (SEARCHIN) to identify ligand-mediated interactions between distinct cellular com- partments. To test this approach, we selected a model of amyotrophic lateral sclerosis (ALS), in which astrocytes expressing mutant superoxide dismutase-1 (mutSOD1) kill wild-type motor neurons (MNs) by an unknown mechanism. Our integrative analysis that combines proteomics and regulatory network analysis infers the interaction between astrocyte-released amyloid precursor protein (APP) and death receptor-6 (DR6) on MNs as the top predicted ligand-receptor pair. The inferred deleterious role of APP and DR6 is confirmed in vitro in models of ALS. Moreover, the DR6 knockdown in MNs of transgenic mutSOD1 mice attenuates the ALS-like phenotype. Our results support the usefulness of integrative, systems biology approach to gain insights into complex neurobiological disease processes as in ALS and posit that the proposed methodology is not restricted to this biological context and could be used in a variety of other non-cell-autonomous communication
    [Show full text]
  • Genetic Loci Associated with Heart Rate Variability and Their Effects on Cardiac Disease Risk
    UC San Diego UC San Diego Previously Published Works Title Genetic loci associated with heart rate variability and their effects on cardiac disease risk. Permalink https://escholarship.org/uc/item/0xj2x119 Journal Nature communications, 8(1) ISSN 2041-1723 Authors Nolte, Ilja M Munoz, M Loretto Tragante, Vinicius et al. Publication Date 2017-06-14 DOI 10.1038/ncomms15805 License https://creativecommons.org/licenses/by-nc-nd/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California ARTICLE Received 9 Mar 2017 | Accepted 8 May 2017 | Published 14 Jun 2017 DOI: 10.1038/ncomms15805 OPEN Genetic loci associated with heart rate variability and their effects on cardiac disease risk Ilja M. Nolte et al.# Reduced cardiac vagal control reflected in low heart rate variability (HRV) is associated with greater risks for cardiac morbidity and mortality. In two-stage meta-analyses of genome-wide association studies for three HRV traits in up to 53,174 individuals of European ancestry, we detect 17 genome-wide significant SNPs in eight loci. HRV SNPs tag non-synonymous SNPs (in NDUFA11 and KIAA1755), expression quantitative trait loci (eQTLs) (influencing GNG11, RGS6 and NEO1), or are located in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4). Genetic risk scores account for 0.9 to 2.6% of the HRV variance. Significant genetic correlation is found for HRV with heart rate ( À 0.74orgo À 0.55) and blood pressure ( À 0.35orgo À 0.20). These findings provide clinically relevant biological insight into heritable variation in vagal heart rhythm regulation, with a key role for genetic variants (GNG11, RGS6) that influence G-protein heterotrimer action in GIRK-channel induced pacemaker membrane hyperpolarization.
    [Show full text]
  • The Human Regulator of G-Protein Signaling Protein 6 Gene (RGS6) Maps Between Markers WI-5202 and D14S277 on Chromosome 14Q24.3
    138J Hum Genet (1999) 44:138–140 © Jpn Soc Hum Genet and Springer-Verlag 1999 BRIEF REPORT—GENE MAPPING Naohiko Seki · Atsushi Hattori · Akiko Hayashi Sumie Kozuma · Tada-aki Hori · Toshiyuki Saito The human regulator of G-protein signaling protein 6 gene (RGS6) maps between markers WI-5202 and D14S277 on chromosome 14q24.3 Received: September 14, 1998 / Accepted: November 1, 1998 Abstract The recently discovered regulators of G-protein proteins by activating the intrinsic GTPase activity of the α signaling proteins, termed the RGS family, have been subunits (for reviews, see Dohlman and Thorner 1997; shown to modulate the functioning of G-proteins by activat- Koelle 1997; Neer 1997). ing the intrinsic guanosine triphosphatase (GTPase) activity At present, full or partial sequences of the mRNAs for of the α subunits. Here, we report the chromosomal loca- numerous putative RGS proteins have been identified in tion and tissue expression of the human regulator of RGS6 mammalian species (De Vries et al. 1995; Chen et al. 1996; gene. The messenger RNA was ubiquitously expressed in Druey et al. 1996; Koelle and Horvitz, 1996; Siderovski et al. various tissues. Polymerase chain reaction (PCR)-based 1996; Gold et al. 1997; Snow et al. 1997; 1998; Seki et al. analysis with a human/rodent monochromosomal hybrid 1998a). The cDNA sequence of human RGS6 has recently panel and a radiation hybrid panel indicated that the gene been registered with the public database (accession number was mapped between genetic markers WI-5202 and AF073920). We are attempting to carry out systematic chro- D14S277 on chromosome 14q24.3 region.
    [Show full text]
  • Temporal Deregulation of Genes and Micrornas in Neurons During Prion-Induced Neurodegeneration
    Temporal Deregulation of Genes and MicroRNAs in Neurons during Prion-Induced Neurodegeneration By ANNA MAJER A Thesis Submitted to the Faculty of Graduate Studies In Partial Fulfillment of the Requirements for the Degree of DOCTOR OF PHILOSOPHY Department of Medical Microbiology College of Medicine, Faculty of Health Sciences University of Manitoba Winnipeg, Manitoba © Anna Majer, October 2015 TABLE OF CONTENTS ABSTRACT .................................................................................................................................... 8 ACKNOWLEDGMENTS ............................................................................................................ 10 ABBREVIATIONS ...................................................................................................................... 12 LIST OF FIGURES ...................................................................................................................... 15 LIST OF TABLES ........................................................................................................................ 19 1.0 INTRODUCTION .................................................................................................................. 20 1.1 Common Elements of Neurodegenerative Diseases ........................................................... 21 1.2 Rodent Models for Neurodegeneration ............................................................................... 22 1.3 Prion Diseases ....................................................................................................................
    [Show full text]
  • Identification of the Mirna-Target Gene Regulatory Network in Intracranial Aneurysm Based on Microarray Expression Data
    EXPERIMENTAL AND THERAPEUTIC MEDICINE 13: 3239-3248, 2017 Identification of the miRNA-target gene regulatory network in intracranial aneurysm based on microarray expression data KEZHEN WANG1*, XINMIN WANG1*, HONGZHU LV1*, CHENGZHI CUI1*, JIYONG LENG1, KAI XU2, GUOSONG YU2, JIANWEI CHEN2 and PEIYU CONG1 1Department of Neurosurgery, Dalian Municipal Central Hospital Affiliated to Dalian Medical University, Dalian, Liaoning 116033; 2Dalian Medical University Graduate School, Dalian Medical University, Dalian, Liaoning 116044, P.R. China Received December 10, 2015; Accepted January 26, 2017 DOI: 10.3892/etm.2017.4378 Abstract. Intracranial aneurysm (IA) remains one of the neurological conditions with a prevalence of 2-3% in the general most devastating neurological conditions. However, the population (1). Unruptured IAs are typically asymptomatic; pathophysiology of IA formation and rupture still remains however, in the event that IAs rupture, this process results in unclear. The purpose of the present study was to identify the hemorrhage to the subarachnoid space, which is a devastating crucial microRNA (miRNA/miR) and genes involved in IAs condition that has been indicated to have a mortality rate of and elucidate the mechanisms underlying the development of 30-40, and 50% of survivors are left disabled (2). IAs. In the present study, novel miRNA regulation activities Previous research on the etiology of IAs indicated that in IAs were investigated through the integration of public the formation of IAs is assumed to be caused by diverse gene expression data of miRNA and mRNA using the Gene environmental and genetic factors, such as cigarette smoking, Expression Omnibus database, combined with bioinformatics excessive alcohol consumption, hypertension, female gender prediction.
    [Show full text]
  • Genetic Loci Associated with Heart Rate Variability and Their Effects on Cardiac Disease Risk
    ARTICLE Received 9 Mar 2017 | Accepted 8 May 2017 | Published 14 Jun 2017 DOI: 10.1038/ncomms15805 OPEN Genetic loci associated with heart rate variability and their effects on cardiac disease risk Ilja M. Nolte et al.# Reduced cardiac vagal control reflected in low heart rate variability (HRV) is associated with greater risks for cardiac morbidity and mortality. In two-stage meta-analyses of genome-wide association studies for three HRV traits in up to 53,174 individuals of European ancestry, we detect 17 genome-wide significant SNPs in eight loci. HRV SNPs tag non-synonymous SNPs (in NDUFA11 and KIAA1755), expression quantitative trait loci (eQTLs) (influencing GNG11, RGS6 and NEO1), or are located in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4). Genetic risk scores account for 0.9 to 2.6% of the HRV variance. Significant genetic correlation is found for HRV with heart rate ( À 0.74orgo À 0.55) and blood pressure ( À 0.35orgo À 0.20). These findings provide clinically relevant biological insight into heritable variation in vagal heart rhythm regulation, with a key role for genetic variants (GNG11, RGS6) that influence G-protein heterotrimer action in GIRK-channel induced pacemaker membrane hyperpolarization. Correspondence and requests for materials should be addressed to I.M.N. (email: [email protected]) or to H.S. (email: [email protected]) or to E.J.C.d.G. (email: [email protected]). #A full list of authors and their affiliations appears at the end of the paper. NATURE COMMUNICATIONS | 8:15805 | DOI: 10.1038/ncomms15805 | www.nature.com/naturecommunications 1 ARTICLE NATURE COMMUNICATIONS | DOI: 10.1038/ncomms15805 eart rate variability (HRV) is a physiological variation in 23 single-nucleotide polymorphism (SNPs) in 14 loci that were cardiac cycle duration.
    [Show full text]
  • G-PROTEIN COUPLED RECEPTOR MEDIATED SIGNALING PATHWAYS in CHEMORESISTANT MELANOMA and OVARIAN CANCER by MOLLY KOERTEL ALTMAN
    G-PROTEIN COUPLED RECEPTOR MEDIATED SIGNALING PATHWAYS IN CHEMORESISTANT MELANOMA AND OVARIAN CANCER by MOLLY KOERTEL ALTMAN (Under the Direction of MANDI M. MURPH) ABSTRACT Cellular signaling pathways are involved in numerous physiological processes such as reproduction, growth, and the development of cancer and chemoresistance. G- protein coupled receptors (GPCRs) are master regulators of many signaling pathways as they are expressed in numerous tissues types throughout the body. GPCRs are being investigated in cancer development particularly through their roles in angiogenesis, metastasis, and inflammation-associated cancer. Growth factors that bind and activate GPCRs to mediate signaling pathways involved in growth and survival include lysophosphatidic acid (LPA). In our studies, both in vitro and in vivo methods were used to test the importance of several signaling pathways in chemoresistant cancer cell survival and tumor biology. In our studies, we found that specific Regulators of G-protein signaling (RGS) proteins are involved in modulating growth and survival pathways in ovarian cancer. Specifically, we showed that silencing of RGS10 and RGS17 proteins increases viability of ovarian cancer cells, and we further examined the role of modulating RGS10 expression on cell differentiation, proliferation, and survival pathways. We also showed that the inhibition of autotaxin the enzyme that produces LPA is a potential therapeutic target for melanoma and how LPA mediated receptor pathways can be manipulated to overcome chemoresistance in cancer. Our most valuable observation was that our novel compounds were able to reduce tumor progression in vivo in a primary xenograft model of melanoma in correlation with a reduction in markers of angiogenesis. Our data serves to help better understand signaling pathways involved in the development of chemoresistance.
    [Show full text]