2021 Undergraduate Research Symposium Program
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Innate Pro–B-Cell Progenitors Protect Against Type 1 Diabetes By
Innate pro–B-cell progenitors protect against type 1 PNAS PLUS diabetes by regulating autoimmune effector T cells Ruddy Montandona,b,1, Sarantis Korniotisa,b,1, Esther Layseca-Espinosaa,b,2, Christophe Grasa,b, Jérôme Mégretc, Sophie Ezinea,d, Michel Dya,b, and Flora Zavalaa,b,3 aFaculté de Médecine Site Necker, Université Paris Descartes, bCentre National de la Recherche Scientifique Unité Mixte de Recherche 8147, 75015 Paris, France; cInstitut Fédératif de Recherche 94 Necker-Enfants Malades, 75015 Paris, France; and dInstitut National de la Santé et de la Recherche Médicale U1020, 75015 Paris, France Edited by Simon Fillatreau, Deutsches Rheuma-Forschungszentrum, Berlin, Germany, and accepted by the Editorial Board May 6, 2013 (received for review December 24, 2012) Diverse hematopoietic progenitors, including myeloid populations emergence of regulatory B cells (Bregs), along with acquired-type arising in inflammatory and tumoral conditions and multipotent stimulation, such as B-cell receptor (BCR) engagement concomi- cells, mobilized by hematopoietic growth factors or emerging during tant or not with CD40 activation (10, 11). Such induced regulatory parasitic infections, display tolerogenic properties. Innate immune B-cell functions are believed to be more robust than those ex- stimuli confer regulatory functions to various mature B-cell subsets pressed by naive and resting B cells, which can nevertheless tolerize but immature B-cell progenitors endowed with suppressive proper- naive T cells and induce regulatory T cells (Tregs) (12, 13). ties per se or after differentiating into more mature regulatory Bregs are a heterogeneous lymphocyte subset present among all B cells remain to be characterized. Herein we provide evidence for major B-cell populations (14–17). -
Cayuga and Store Building 69 Fall Christy Mary A., Home with Christy
SENECA FALLS VILLAGE. 267 E. Casey Mary Miss, home with her father Thomas, 13 Chapin CASEY MATTHEW R., b 1855, (Casey & Seaman), bds 40 State Richard b r- Casey A., 1862, w Elizabeth, meat cutter, h 51 Bridge b about Casey Richard, 1829 in Ireland, retired, res. 40 State Casey Richard H., b 1875, machinist, bds 84 W. Bayard,owns interest in house T. Casey Theresa Miss, dressmaker, bds 13 Chapin Casey Thomas b 1844 in Ireland, w Mary, machinist, owns h and 1 13 Chapin Casey Thomas D., b 1877, son of Thomas, clerk 62 Fall, home 13 Chapin CASEY & SEAMAN, (Matthew R. Casey & Dr. Frank G. Seaman), drugs, school and blank books, 75 Fall Cassidy Ellen, widow of John, laundress, r h 91 Bridge Castner Seymour H., b 1863 in Penn Yan, N. Y., w Eva S., pattern maker, carpenter and builder, r h 306 Fall Chamberlain Harrison, b 1837, w Ophelia G., director Ex change National Bank, prop.'r The National Yeast Co., owns the Seneca Woolen Mills, under lease to Mr. Hugh Sheridan, also two planing mills and malt and grain houses on East Fall St., also farm 96 on r 43 ; also farm 80 on r 28, occupied by Stephen Rogers ; w owns res. 30 Cayuga and store building 69 Fall Chase Jesse M. Dr., b 1865 in Ledyard, Cayuga Co., w Susie H., veterinary surgeon, graduate of Ontario Veterinary College of Toronto, infirmary and sale stable, horse trainer, agt for Groton carriages, r h Baird blk, State Chatham Hattie S. Miss, school teacher, bds 37 Chapel Chatham Sarah A., widow of Jonathan S., resident, r h 37 Chapel Christopher Claude R., b 1870, letter carrier, home 32 Miller Christopher Columbus, b 1845, w Martha J., master mechanic Goulds Mfg Co., owns res. -
Anti-Cd49a / Integrin Alpha 1 Antibody (ARG57529)
Product datasheet [email protected] ARG57529 Package: 50 μg anti-CD49a / Integrin alpha 1 antibody Store at: -20°C Summary Product Description Goat Polyclonal antibody recognizes CD49a / Integrin alpha 1 Tested Reactivity Hu Tested Application WB Host Goat Clonality Polyclonal Isotype IgG Target Name CD49a / Integrin alpha 1 Antigen Species Human Immunogen Synthetic peptide around the internal region of Human CD49a / Integrin alpha 1. (C-DKHDFQDSVRIT) Conjugation Un-conjugated Alternate Names VLA-1; CD49a; Integrin alpha-1; Laminin and collagen receptor; VLA1; CD antigen CD49a; CD49 antigen- like family member A Application Instructions Application table Application Dilution WB 0.3 - 1 µg/ml Application Note WB: Recommend incubate at RT for 1h. * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist. Calculated Mw 131 kDa (NP_852478.1) Observed Size 150 kDa (glycosylated form) Properties Form Liquid Purification Ammonium sulphate precipitation followed by affinity purification with immunogen. Buffer Tris saline (pH 7.3), 0.02% Sodium azide and 0.5% BSA. Preservative 0.02% Sodium azide Stabilizer 0.5% BSA Concentration 0.5 mg/ml Storage instruction For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C or below. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use. www.arigobio.com 1/2 Note For laboratory research only, not for drug, diagnostic or other use. Bioinformation Gene Symbol ITGA1 Gene Full Name integrin, alpha 1 Background This gene encodes the alpha 1 subunit of integrin receptors. -
Laminin-Binding Integrin A7,1: Functional Characterization and Expression in Normal and Malignant Melanocytes
CELL REGULATION, Vol. 2, 805-817, October 1991 Laminin-binding integrin a7,1: functional characterization and expression in normal and malignant melanocytes Randall H. Kramer,*t$ Mai P. Vu,* increased attachment to laminin exhibit much Yao-Fen Cheng,* Daniel M. Ramos,* higher metastatic potential in lung colonization Rupert Timpl,§ and Nahid Waleh 11 assays (reviewed in Liotta et aL, 1986). Fur- *Departments of Stomatology and Anatomy thermore, the presence of intact laminin will en- and the tCardiovascular Research Institute hance lung colonization (Barsky et aL., 1984). University of California These results and others strongly suggest that San Francisco, California 94143 melanoma cells interact with laminin-rich base- §Max-Planck-lnstitut fur Biochemie ment membrane and that this interaction facil- Martinsried, Germany itates their vascular arrest and colonization of IISRI International distant sites. Menlo Park, California 94025 During tissue invasion, metastatic melanoma cells interact with different types of extracellular matrix, including the interstitium and basement A novel integrin, a,#,, that specifically binds with membranes. It is expected, then, that these high affinity to laminin has been identified on mel- malignant cells will express surface adhesion anoma cells. This complex was purified from both receptors with diverse ligand specificities human and murine melanoma cells by laminin-af- (Ruoslahti and Giancotti, 1989). The integrin finity chromatography, and the a7 subunit was re- family of adhesion receptors consists of a large covered after gel electrophoresis. N-terminal amino number of heterodimer receptors that appear acid sequence analysis of the a7 subunit from both to mediate many of the cell-extracellular matrix human and mouse cells verifies that this integrin interactions for melanoma and other cell types is distinct from other a chains in the #I family, al- (Hynes, 1987; Ruoslahti and Pierschbacher, though strikingly similar to the as subunit. -
Integrin and Gene Network Analysis Reveals That ITGA5 and ITGB1 Are Prognostic in Non-Small-Cell Lung Cancer
Journal name: OncoTargets and Therapy Article Designation: Original Research Year: 2016 Volume: 9 OncoTargets and Therapy Dovepress Running head verso: Zheng et al Running head recto: ITGA5 and ITGB1 are prognostic in NSCLC open access to scientific and medical research DOI: http://dx.doi.org/10.2147/OTT.S91796 Open Access Full Text Article ORIGINAL RESEARCH Integrin and gene network analysis reveals that ITGA5 and ITGB1 are prognostic in non-small-cell lung cancer Weiqi Zheng Background: Integrin expression has been identified as a prognostic factor in non-small-cell Caihui Jiang lung cancer (NSCLC). This study was aimed at determining the predictive ability of integrins Ruifeng Li and associated genes identified within the molecular network. Patients and methods: A total of 959 patients with NSCLC from The Cancer Genome Atlas Department of Radiation Oncology, Guangqian Hospital, Quanzhou, Fujian, cohorts were enrolled in this study. The expression profile of integrins and related genes were People’s Republic of China obtained from The Cancer Genome Atlas RNAseq database. Clinicopathological characteristics, including age, sex, smoking history, stage, histological subtype, neoadjuvant therapy, radiation therapy, and overall survival (OS), were collected. Cox proportional hazards regression models as well as Kaplan–Meier curves were used to assess the relative factors. Results: In the univariate Cox regression model, ITGA1, ITGA5, ITGA6, ITGB1, ITGB4, and ITGA11 were predictive of NSCLC prognosis. After adjusting for clinical factors, ITGA5 (odds ratio =1.17, 95% confidence interval: 1.05–1.31) andITGB1 (odds ratio =1.31, 95% confidence interval: 1.10–1.55) remained statistically significant. In the gene cluster network analysis, PLAUR, ILK, SPP1, PXN, and CD9, all associated with ITGA5 and ITGB1, were identified as independent predictive factors of OS in NSCLC. -
Inflammatory Lesion Macrophage Exit from a Peripheral 1 Integrin
Published March 18, 2013, doi:10.4049/jimmunol.1202097 The Journal of Immunology a1b1 Integrin-Mediated Adhesion Inhibits Macrophage Exit from a Peripheral Inflammatory Lesion Henry M. Becker,*,†,‡ Jacob Rullo,*,† Mian Chen,* Magar Ghazarian,* Sungho Bak,* Haiyan Xiao,* John B. Hay,‡ and Myron I. Cybulsky*,† Integrins are adhesion molecules critical for the recruitment of leukocytes from blood into peripheral tissues. However, whether integrins are also involved in leukocyte exit from peripheral tissues via afferent lymphatics to the draining lymph node remains poorly understood. In this article, we show that adhesion by the collagen IV–binding integrin a1b1 unexpectedly inhibited macrophage exit from inflamed skin. We monitored macrophages exiting mouse footpads using a newly developed in situ pulse labeling technique. Blockade of a1b1 integrin or genetic deletion (Itga12/2) increased macrophage exit efficiency. Chemotaxis assays through collagen IV showed more efficient migration of Itga12/2 macrophages relative to wild type. Given that macro- phages are key orchestrators of inflammation, a1b1 integrin adhesion may represent a mechanism for regulating inflammatory responses by controlling macrophage exit or persistence in inflamed tissues. The Journal of Immunology, 2013, 190: 000–000. he extent and duration of leukocyte accumulation at the The family of integrins associated with the b1 subunit (CD29) site of tissue inflammation can have a profound effect on includes several that bind ECM molecules, and some of these are T the course of inflammation, -
Cardiac Fibrosis: Key Role of Integrins in Cardiac Homeostasis and Remodeling
cells Review Cardiac Fibrosis: Key Role of Integrins in Cardiac Homeostasis and Remodeling Patrick B. Meagher 1,2, Xavier Alexander Lee 1,2 , Joseph Lee 1,2 , Aylin Visram 1,2, Mark K. Friedberg 2,3,4 and Kim A. Connelly 1,2,3,* 1 Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, ON M5B 1W8, Canada; [email protected] (P.B.M.); [email protected] (X.A.L.); [email protected] (J.L.); [email protected] (A.V.) 2 Department of Physiology, University of Toronto, Toronto, ON M5S 1A8, Canada; [email protected] 3 Institute of Medical Science, University of Toronto, Toronto, ON M5S 1A8, Canada 4 Labatt Family Heart Center and Department of Paediatrics, Hospital for Sick Children, Toronto, ON M5G 1X8, Canada * Correspondence: [email protected]; Tel.: +141-686-45201 Abstract: Cardiac fibrosis is a common finding that is associated with the progression of heart failure (HF) and impacts all chambers of the heart. Despite intense research, the treatment of HF has primarily focused upon strategies to prevent cardiomyocyte remodeling, and there are no targeted antifibrotic strategies available to reverse cardiac fibrosis. Cardiac fibrosis is defined as an accumulation of extracellular matrix (ECM) proteins which stiffen the myocardium resulting in the deterioration cardiac function. This occurs in response to a wide range of mechanical and biochemical signals. Integrins are transmembrane cell adhesion receptors, that integrate signaling Citation: Meagher, P.B.; Lee, X.A.; between cardiac fibroblasts and cardiomyocytes with the ECM by the communication of mechanical Lee, J.; Visram, A.; Friedberg, M.K.; stress signals. -
Keeney Update VOL III, Number 4 Roscoe C
Keeney Update VOL III, Number 4 Roscoe C. Keeney, Jr. SEPT 1986 FAMILY OF BLUFORD KEENEY (850-191), TEXAS CO., MO ABNER KEENEY OF MISSOURI (father of Bluford) THE CYCLONE OF 1879 The terrifying tornado which Carl Carlson and seven others witnessed on their arrival at Randolph (see page 45) was chronicled in the Manhattan Nationalist of Friday, June 8, 1879. PRAYER FOR GENEALOGISTS By Curtis Woods TERRIBLE CYCLONES Lord, help me dig into the past And sift the sands of time On Friday last, a portion of Kansas and Missouri was devastated by That I might find the roots that made a terrific cyclone (or cyclones. A large number of people were This family tree of mine. killed or injured, and a great amount of property destroyed. S. M. Lord, help me trace the ancient roads On which my father’s trod Fox, of this city, visited Irving, in Marshall Co. immediately after And led them through so many lands the disaster and returned along the track of the destroyer to Fancy To find our present sod. Creek, in the northern most part of Riley Co., and has kindly Lord, help me find an ancient book furnished us the following account: Or dusty manuscript - That's safely hidden now away In some forgotten crypt; The storm, after passing the town, crossed the Blue River. It lifted Lord, let it bridge gap that haunts the long iron bridge from its piers and carried the twisted and My soul when I can't find shapeless mass some thirty feet up the river. -
Changes in Gene Expression in Cyclosporine A-Treated Gingival
CHANGES IN GENE EXPRESSION IN CYCLOSPORINE A TREATED GINGIVAL FIBROBLASTS by Jeffrey S. Wallis A thesis submitted to the Faculty of the University of Delaware in partial fulfillment of the requirements for the degree of Master of Science in Biological Sciences Summer 2005 Copyright 2005 Jeffrey S. Wallis All rights reserved UMI Number: 1428256 Copyright 2005 by Wallis, Jeffrey S. All rights reserved. UMI Microform 1428256 Copyright 2005 by ProQuest Information and Learning Company. All rights reserved. This microform edition is protected against unauthorized copying under Title 17, United States Code. ProQuest Information and Learning Company 300 North Zeeb Road P.O. Box 1346 Ann Arbor, MI 48106-1346 Changes in Gene Expression In Cyclosporine A Treated Gingival Fibroblasts by Jeffrey S. Wallis Approved: ______________________________________________________ Mary C. Farach-Carson, Ph.D. Professor in charge of thesis on behalf of the Advisory Committee Approved: ______________________________________________________ Daniel D. Carson, Ph.D. Chair of the Department of Biological Sciences Approved: ______________________________________________________ Thomas Apple, Ph.D. Dean of the College of Arts and Sciences Approved: ______________________________________________________ Conrado M. Gempesaw II, Ph.D. Vice Provost for Academic and International Programs DEDICATION I would like to give very special thanks to my advisor Dr. Cindy Farach-Carson for being an incredible mentor and teacher. Over the past 3 years I have been fortunate to have been given the opportunity to explore a subject of great personal interest in an environment that has allowed me to grow both as a scientist and a person. Her knowledge and patience is an inspiration to all those around her. I would not be the individual I am today nor would my life be headed in its current direction if it were not for her and I will be forever grateful for everything she has taught me. -
Ancestors of Donald Richard Young Sr
Ancestors of Donald Richard Young Sr Generation 1 1. Donald Richard Young Sr, son of Newton Richard Begnal-Young-Eaton and June Elsie Wilson, was born on 11 Sep 1947 in Glendale, Los Angeles Co., CA. He married Susan Ann Keller on 9 Mar 1969 in Torrance, Los Angeles Co., CA. She was born on 7 Aug 1951 in Berks Co., PA (Shoemakersville or Reading). He married Deborah Carol Asbury on 30 Jul 1974 in Yuma, AZ. She was born on 21 Mar 1954 in Yuma, Yuma Co., AZ (maybe 1 Mar 1954). Notes for Susan Ann Keller: may have been born as a Shope, adopted as Keller or visa verse. Or Schoepp, Schoep, Schopp, Shoup Generation 2 2. Newton Richard Begnal-Young-Eaton, son of Clifford Franklin Begnal Young Eaton and Thelma Ferne Perry, was born on 16 Jul 1924 in San Francisco, San Francisco Co., CA (Richard Newton Young after 1929). He died on 3 Jan 1995 in Harbor City, Los Angeles Co., CA (Cremation). He married June Elsie Wilson on 9 Sep 1946 in Pasadena, Los Angeles Co., CA (filed 12 Sep 1946). 3. June Elsie Wilson, daughter of Earle Kenneth Wilson and Antoinette Victoria Blaschko, was born on 29 Jul 1926 in New Haven, New Haven Co., CT. She died on 6 Dec 2012 in San Diego Co., CA (10:05 PM - Neptune Society ashes at sea). Notes for Newton Richard Begnal-Young-Eaton: SS# 567-20-6910 Service Number SN 19100597 The following added 11 Apr 2018 to https://www.ancestry.com/family-tree/person/tree/116281431/person/130155703152/story Newton Richard Begnal 1924-1995: is my Father b. -
Integrins Synergise to Induce Expression of the MRTF-A–SRF Target
© 2016. Published by The Company of Biologists Ltd | Journal of Cell Science (2016) 129, 1391-1403 doi:10.1242/jcs.177592 RESEARCH ARTICLE Integrins synergise to induce expression of the MRTF-A–SRF target gene ISG15 for promoting cancer cell invasion Michaela-Rosemarie Hermann1,*, Madis Jakobson1,*, Georgina P. Colo1,*, Emanuel Rognoni1, Maili Jakobson1, Christian Kupatt2, Guido Posern3 and Reinhard Fässler1,‡ ABSTRACT characteristic shape and initiate migration, and are to a large Integrin-mediated activation of small GTPases induces the extent triggered by the activation of Rho family GTPases and actin- polymerisation of G-actin into various actin structures and the binding proteins (Danen et al., 2002). Long-term effects of integrin release of the transcriptional co-activator MRTF from G-actin. Here signalling result from changes in gene expression, which regulate we report that pan-integrin-null fibroblasts seeded on fibronectin and numerous cellular processes including proliferation and differentiation expressing β1- and/or αV-class integrin contained different G-actin (Legate et al., 2009). Integrin-dependent regulation of gene pools, nuclear MRTF-A (also known as MKL1 or MAL) levels and expression is primarily thought to arise from cross talk with MRTF-A–SRF activities. The nuclear MRTF-A levels and activities growth factor receptors that increase the activity of mitogen- were highest in cells expressing both integrin classes, lower in cells activated protein (MAP) kinase pathways. A recent study, however, expressing β1 integrins -
PBDE) Levels with Biomarkers of Placental Development and Disease During Mid-Gestation Julia R
Varshavsky et al. Environmental Health (2020) 19:61 https://doi.org/10.1186/s12940-020-00617-7 RESEARCH Open Access Association of polybrominated diphenyl ether (PBDE) levels with biomarkers of placental development and disease during mid-gestation Julia R. Varshavsky1*† , Joshua F. Robinson1,2†, Yan Zhou2, Kenisha A. Puckett2, Elaine Kwan2, Sirirak Buarpung2, Rayyan Aburajab2, Stephanie L. Gaw2,3, Saunak Sen4, Sabrina Crispo Smith5, Julie Frankenfield5, June-Soo Park5, Susan J. Fisher2 and Tracey J. Woodruff1 Abstract Background: Polybrominated diphenyl ether (PBDE) exposures have been associated with adverse pregnancy outcomes. A hypothesized mechanism is via alterations in placental development and function. However, we lack biomarkers that can be used as early indicators of maternal/fetal response to PBDE exposures and/or perturbations in placental development or function. Methods: To evaluate the relationship between PBDE levels and placental biomarkers during mid-gestation of human pregnancy (n = 62), we immunolocalized three molecules that play key roles in cytotrophoblast (CTB) differentiation and interstitial/endovascular uterine invasion—integrin alpha-1 (ITGA1), vascular endothelial-cadherin (CDH5), and metalloproteinase-1 (MMP1)–and assessed three morphological parameters as potential indicators of pathological alterations using H&E-stained tissues–leukocyte infiltration, fibrinoid deposition, and CTB endovascular invasion. We evaluated associations between placental PBDE levels and of biomarkers of placental development and disease using censored Kendall’s tau correlation and linear regression methods. Results: PBDEs were detected in all placental samples. We observed substantial variation in antigen expression and morphological endpoints across placental regions. We observed an association between PBDE concentrations and immunoreactivity of endovascular CTB staining with anti-ITGA1 (inverse) or interstitial CTBs staining with anti-CDH5 (positive).