Curriculum Vitae BENITA S. KATZENELLENBOGEN Page 1 – May 5, 2020
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Exposure to Female Hormone Drugs During Pregnancy
British Journal of Cancer (1999) 80(7), 1092–1097 © 1999 Cancer Research Campaign Article no. bjoc.1998.0469 Exposure to female hormone drugs during pregnancy: effect on malformations and cancer E Hemminki, M Gissler and H Toukomaa National Research and Development Centre for Welfare and Health, Health Services Research Unit, PO Box 220, 00531 Helsinki, Finland Summary This study aimed to investigate whether the use of female sex hormone drugs during pregnancy is a risk factor for subsequent breast and other oestrogen-dependent cancers among mothers and their children and for genital malformations in the children. A retrospective cohort of 2052 hormone-drug exposed mothers, 2038 control mothers and their 4130 infants was collected from maternity centres in Helsinki from 1954 to 1963. Cancer cases were searched for in national registers through record linkage. Exposures were examined by the type of the drug (oestrogen, progestin only) and by timing (early in pregnancy, only late in pregnancy). There were no statistically significant differences between the groups with regard to mothers’ cancer, either in total or in specified hormone-dependent cancers. The total number of malformations recorded, as well as malformations of the genitals in male infants, were higher among exposed children. The number of cancers among the offspring was small and none of the differences between groups were statistically significant. The study supports the hypothesis that oestrogen or progestin drug therapy during pregnancy causes malformations among children who were exposed in utero but does not support the hypothesis that it causes cancer later in life in the mother; the power to study cancers in offspring, however, was very low. -
TE INI (19 ) United States (12 ) Patent Application Publication ( 10) Pub
US 20200187851A1TE INI (19 ) United States (12 ) Patent Application Publication ( 10) Pub . No .: US 2020/0187851 A1 Offenbacher et al. (43 ) Pub . Date : Jun . 18 , 2020 ( 54 ) PERIODONTAL DISEASE STRATIFICATION (52 ) U.S. CI. AND USES THEREOF CPC A61B 5/4552 (2013.01 ) ; G16H 20/10 ( 71) Applicant: The University of North Carolina at ( 2018.01) ; A61B 5/7275 ( 2013.01) ; A61B Chapel Hill , Chapel Hill , NC (US ) 5/7264 ( 2013.01 ) ( 72 ) Inventors: Steven Offenbacher, Chapel Hill , NC (US ) ; Thiago Morelli , Durham , NC ( 57 ) ABSTRACT (US ) ; Kevin Lee Moss, Graham , NC ( US ) ; James Douglas Beck , Chapel Described herein are methods of classifying periodontal Hill , NC (US ) patients and individual teeth . For example , disclosed is a method of diagnosing periodontal disease and / or risk of ( 21) Appl. No .: 16 /713,874 tooth loss in a subject that involves classifying teeth into one of 7 classes of periodontal disease. The method can include ( 22 ) Filed : Dec. 13 , 2019 the step of performing a dental examination on a patient and Related U.S. Application Data determining a periodontal profile class ( PPC ) . The method can further include the step of determining for each tooth a ( 60 ) Provisional application No.62 / 780,675 , filed on Dec. Tooth Profile Class ( TPC ) . The PPC and TPC can be used 17 , 2018 together to generate a composite risk score for an individual, which is referred to herein as the Index of Periodontal Risk Publication Classification ( IPR ) . In some embodiments , each stage of the disclosed (51 ) Int. Cl. PPC system is characterized by unique single nucleotide A61B 5/00 ( 2006.01 ) polymorphisms (SNPs ) associated with unique pathways , G16H 20/10 ( 2006.01 ) identifying unique druggable targets for each stage . -
New Insights for Hormone Therapy in Perimenopausal Women Neuroprotection
Chapter 12 New Insights for Hormone Therapy in Perimenopausal Women Neuroprotection Manuela Cristina Russu and Alexandra Cristina Antonescu Additional information is available at the end of the chapter http://dx.doi.org/10.5772/intechopen.74332 Abstract Perimenopause is a mandatory period in women’s life, when the medical staff may initiate hormone therapy with sex steroids for the delay of brain aging and neurodegenerative diseases, during the so-called “window of opportunity.” Animals’ models are helpful to sustain the still controversial results of human clinical observational and/or randomized controlled studies. Estrogens, progesterone, and androgens, with their nuclear and mem- brane receptors, genes, and epigenetics, with their connections to cholinergic, GABAergic, serotoninergic, and glutamatergic systems are involved in women’snormalbrainorin brain’s pathology. The sex steroids are active through direct and/or indirect mechanisms to modulate and/or to protect brain plasticity, and vessels network, fuel metabolism—glucose, ketones, ATP, to reduce insulin resistance, and inflammation of the aging brain through blood-brain barrier disruption, microglial aberrant activation, and neural cell survival/loss. Keywords: perimenopause, “window” of opportunity, neuroprotection, sex steroid hormones 1. Introduction The months/years of perimenopause represent an important moment during women’saging, when sex steroids and their receptors decline are evident in the hippocampal and cortical neu- rons, after estrogen exposure during the reproductive years. The sex steroid hormones decline is associated/acts synergic to other factors as hypertension, diabetes, hypoxia/obstructive sleep apnea, obesity, vitamin B12/folate deficiency, depression, and traumatic brain injury to promote diverse pathological mechanisms involved in brain aging, memory impairment, and AD. -
Estrogen Receptor Beta Is a Negative Regulator of Mammary Cell Proliferation Xiaozheng Song University of Vermont
University of Vermont ScholarWorks @ UVM Graduate College Dissertations and Theses Dissertations and Theses 2014 Estrogen Receptor Beta Is A Negative Regulator Of Mammary Cell Proliferation Xiaozheng Song University of Vermont Follow this and additional works at: https://scholarworks.uvm.edu/graddis Part of the Animal Sciences Commons, and the Molecular Biology Commons Recommended Citation Song, Xiaozheng, "Estrogen Receptor Beta Is A Negative Regulator Of Mammary Cell Proliferation" (2014). Graduate College Dissertations and Theses. 259. https://scholarworks.uvm.edu/graddis/259 This Dissertation is brought to you for free and open access by the Dissertations and Theses at ScholarWorks @ UVM. It has been accepted for inclusion in Graduate College Dissertations and Theses by an authorized administrator of ScholarWorks @ UVM. For more information, please contact [email protected]. ESTROGEN RECEPTOR BETA IS A NEGATIVE REGULATOR OF MAMMARY CELL PROLIFERATION A Dissertation Presented by Xiaozheng Song to The Faculty of the Graduate College of The University of Vermont In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Specializing in Animal Science October, 2014 Accepted by the Faculty of the Graduate College, The University of Vermont, in partial fulfillment of the requirements for the degree of Doctor of Philosophy, specializing in Animal Science. Dissertation Examination Committee: ____________________________________ Advisor Zhongzong Pan Ph.D. ____________________________________ Co-Advisor Andre-Denis Wright Ph.D. ____________________________________ Rona Delay, Ph.D. ____________________________________ David Kerr, Ph.D. ____________________________________ Chairperson Karen M. Lounsbury, Ph. D. ____________________________________ Dean, Graduate College Cynthia J. Forehand, Ph.D. Date: May 5, 2014 ABSTRACT The mammary gland cell growth and differentiation are under the control of both systemic hormones and locally produced growth factors. -
Diverse Signaling Pathways Modulate Nuclear Receptor Recruitment of N-Cor and SMRT Complexes (Estrogen Receptor͞tamoxifen͞corepressor Complex)
Proc. Natl. Acad. Sci. USA Vol. 95, pp. 2920–2925, March 1998 Biochemistry Diverse signaling pathways modulate nuclear receptor recruitment of N-CoR and SMRT complexes (estrogen receptorytamoxifenycorepressor complex) ROBERT M. LAVINSKY*†,KRISTEN JEPSEN*†,THORSTEN HEINZEL*, JOSEPH TORCHIA*, TINA-MARIE MULLEN‡, RACHEL SCHIFF§,ALFONSO LEON DEL-RIO*, MERCEDES RICOTE¶,SALLY NGO¶,JOSLIN GEMSCH‡, SUSAN G. HILSENBECK§,C.KENT OSBORNE§,CHRISTOPHER K. GLASS¶,MICHAEL G. ROSENFELD*, \ AND DAVID W. ROSE‡ *Howard Hughes Medical Institute, ¶Cellular and Molecular Medicine, ‡Whittier Diabetes Program, and †UCSD Graduate Program in Biology, Department and School of Medicine, University of California at San Diego, La Jolla, CA 92093-0648; and §Department of Medicine, Division of Medical Oncology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78284-7884 Contributed by Michael G. Rosenfeld, January 9, 1998 ABSTRACT Several lines of evidence indicate that the partial agonistic activity (31). Various agents that raise intra- nuclear receptor corepressor (N-CoR) complex imposes li- cellular cAMP levels or stimulate the rasyMAP kinase path- gand dependence on transcriptional activation by the retinoic way can similarly cause estrogen receptor (ER) activation in acid receptor and mediates the inhibitory effects of estrogen the presence of tamoxifen or the absence of any activating receptor antagonists, such as tamoxifen, suppressing a con- ligand (9, 32–35). In this manuscript we show that diverse stitutive N-terminal, Creb-binding proteinycoactivator com- molecular strategies regulate the association of N-CoR- or plex-dependent activation domain. Functional interactions SMRT-containing complexes with specific nuclear receptors, between specific receptors and N-CoR or SMRT corepressor including the nature of the ligand, the levels of available complexes are regulated, positively or negatively, by diverse N-CoRySMRT, and the action of diverse protein kinase- signal transduction pathways. -
Estriol Therapy for Autoimmune and Neurodegenerative Diseases and Disorders
(19) TZZ¥Z__T (11) EP 3 045 177 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 20.07.2016 Bulletin 2016/29 A61K 31/565 (2006.01) A61K 31/566 (2006.01) A61K 31/568 (2006.01) A61K 45/06 (2006.01) (2006.01) (2006.01) (21) Application number: 16000349.7 A61K 31/785 A61P 25/00 (22) Date of filing: 26.09.2006 (84) Designated Contracting States: (72) Inventor: Voskuhl, Rhonda R. AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Los Angeles, CA 90024 (US) HU IE IS IT LI LT LU LV MC NL PL PT RO SE SI SK TR (74) Representative: Müller-Boré & Partner Patentanwälte PartG mbB (30) Priority: 26.09.2005 US 720972 P Friedenheimer Brücke 21 26.07.2006 US 833527 P 80639 München (DE) (62) Document number(s) of the earlier application(s) in Remarks: accordance with Art. 76 EPC: This application was filed on 11-02-2016 as a 13005320.0 / 2 698 167 divisional application to the application mentioned 06815626.4 / 1 929 291 under INID code 62. (71) Applicant: The Regents of the University of California Oakland, CA 94607 (US) (54) ESTRIOL THERAPY FOR AUTOIMMUNE AND NEURODEGENERATIVE DISEASES AND DISORDERS (57) The present invention relates to a dosage from comprising estriol and glatiramer acetate polymer-1 for use in the treatment of multiple sclerosis (MS), as well as to a kit comprising estriol and glatiramer acetate polymer-1. EP 3 045 177 A1 Printed by Jouve, 75001 PARIS (FR) EP 3 045 177 A1 Description [0001] This invention was made with Government support under Grant No. -
STEROID RECEPTORS in HEALTH and DISEASE SERONO SYMPOSIA, USA Series Editor: James Posillico
STEROID RECEPTORS IN HEALTH AND DISEASE SERONO SYMPOSIA, USA Series Editor: James Posillico ACROMEGALY: A Century of Scientific and Clinical Progress Edited by Richard J. Robbins and Shlomo Melmed BASIC AND CLINICAL ASPECTS OF GROWTH HORMONE Edited by Barry B. Bercu THE PRIMATE OVARY Edited by Richard L. Stouffer SOMATOSTATIN: Basic and Clinical Status Edited by Seymour Reichlin STEROID RECEPTORS IN HEALTH AND DISEASE Edited by Virinder K. Moudgil A Continuation Order Plan is available for this series. A continuation order will bring delivery of each new volume immediately upon publication. Volumes are billed only upon actual shipment. For further infor mation please contact the publisher. STEROID RECEPTORS IN HEALTH AND DISEASE Edited by Virinder K. Moudgil Oakland University Rochester, Michigan PLENUM PRESS • NEW YORK AND LONDON library of Congress Cataloging in Publication Data Meadow Brook Conference on Steroid Receptors in Health and Disease (tst(tst:: t987 : Rochester, Mich .) Ste roid receptors in health and disease / edited by Virinder K. Moudgil. p. cm . "Proc" Proceedingseedings of the Meadow Brook Conference on Steroid Receptors in Health and Disease, spon sored by Serono Symposia. USA and Oakland University. held September 20-23, 19871987.. in Rochester. Michigan ··-T.p. verso. Includes bibliographies and indexes. IS8N 978-1-4684-5543-4 IS8N 978-1-4684-5541-0 (eBook) 00110.1007/978-1-4684-5541-0 I . Steroid hormones-Receptors-Congresses. 1. Moudgil, V.V. K.K. (Virinder K.), 1945- . 11. Sereno Symposia, USA. III.Ill. Oakland Universityly. IV. Title. [oNlM[oNlM:: tt. Receptors , Sleroid-congresses. W3 ME3781st 1987s / WK 150 M482 1987sJ1987sj oP571.7.M42 1987 512 '. -
Effects of Diethylstilbestrol, Norethindrone, and Mestranol on Selected Microbes
Loyola University Chicago Loyola eCommons Master's Theses Theses and Dissertations 1974 Effects of Diethylstilbestrol, Norethindrone, and Mestranol on Selected Microbes John N. Haan Loyola University Chicago Follow this and additional works at: https://ecommons.luc.edu/luc_theses Part of the Physiology Commons Recommended Citation Haan, John N., "Effects of Diethylstilbestrol, Norethindrone, and Mestranol on Selected Microbes" (1974). Master's Theses. 2756. https://ecommons.luc.edu/luc_theses/2756 This Thesis is brought to you for free and open access by the Theses and Dissertations at Loyola eCommons. It has been accepted for inclusion in Master's Theses by an authorized administrator of Loyola eCommons. For more information, please contact [email protected]. This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License. Copyright © 1974 John N. Haan EFFECTS OF DIETHYLSTILBESTROL, NORETHINDRONE, AND MESTRANOL ON SELECTED MICROBES by John N. Haan A Thesis Submitted to the Faculty of the Graduate School of Loyola University of Chicago in Partial Fulfillment of the Requirements for the Degree of Master of Science November 1974 TABLE OF CONTENTS ,.' I. Introduction and Review of the Literature ................... 1 'II. Materials and Methods....................................... 7 III. Results· ..................................................... 13 A. Effects of Ethanol on the Microbes Studied .............. 13 1. Growth Studies ...................................... 13 B. Effects of Norethindrone -
Studies on Squamous Metaplasia in Rat Bladder II . Effects of Estradiol and Estradiol Plus Hexestrol*T
Studies on Squamous Metaplasia in Rat Bladder II . Effects of Estradiol and Estradiol plus Hexestrol*t A. ANGRIST, P. CAPURRO, AND B. MOUMGIS (Department of Pathology, Albert Einstein College of Medicine of Yeshiva University, New York 61, N.Y.) SUMMARY The effects of estrogens were studied with and without foreign body (rough glass beads and paraffin pellets) on the metaplasia of the bladder of rats on stock main tenance diet and on a vitamin A-deficient diet. Estradiol increased the degree of metaplasia in the bladder of rats when combined with vitamin A deficiency and/or foreign body stimulation. Estradiol affected bladder epithelium already made squamous more effectively than it did the normal transitional uroepithelium. A high dose of hexestrol, when added to estradiol, showed no enhance ment of the degree of metaplasi.a by estradiol benzoate in the bladder of the rat. The combination of vitamin A deficiency, foreign body in situ, and estrogenadminis tration was an effective means of obtaining keratinizing squamous metaplasia in the urinary bladder for studies of its developmental and reversal changes. In a previous presentation (4) the relation of The animals were divided into the following different forms of foreign-body irritation and of groups (the number of rats surviving with tissue vitamin A deficiency to squamous metaplasia in for study and the total number in each group mi the bladders of rats was reported. It is also known tinily are given following each group): that estrogens will cause squamous metaplasia. I. Stock diet + estradiol (6 survivals/lI rats) The metaplasia following estrogen administration II. -
Diethylstilbestrol Lignant Cervical and Vaginal Tumors (Polyps, Squamous-Cell Papilloma, and Myosarcoma) in Female Hamsters, and Benign and Malignant Tes CAS No
Report on Carcinogens, Fourteenth Edition For Table of Contents, see home page: http://ntp.niehs.nih.gov/go/roc Diethylstilbestrol lignant cervical and vaginal tumors (polyps, squamouscell papilloma, and myosarcoma) in female hamsters, and benign and malignant tes CAS No. 56-53-1 ticular tumors (granuloma, adenoma, and leiomyosarcoma) in male hamsters. Prenatal exposure also caused uterine cancer (adenocarci Known to be a human carcinogen noma) in female mice and hamsters, benign ovarian tumors (cystad First listed in the First Annual Report on Carcinogens (1980) enoma and granulosacell tumors) in female mice, and benign lung Also known as DES, diethylstilboestrol, or stilboestrol tumors (papillary adenoma) in mice of both sexes. Prenatal expo sure did not cause tumors in monkeys observed for up to six years CH 3 after birth. Mice developed cervical and vaginal tumors after receiv H2C ing a single subcutaneous injection of diethylstilbestrol on the first C OH day of life, and male rats developed cancer of the reproductive tract HO C (squamouscell carcinoma) after receiving daily subcutaneous injec CH2 tions for the first month of life. Diethylstilbestrol also caused cancer in experimental animals ex H3C Carcinogenicity posed as adults. When administered orally, diethylstilbestrol caused cancer of the mammary gland (carcinoma and adenocarcinoma) in Diethylstilbestrol is known to be a human carcinogen based on suffi mice of both sexes and benign mammarygland tumors (fibroade cient evidence of carcinogenicity from studies in humans. noma) in rats of both sexes. In addition, cancer of the cervix and uterus (adenocarcinoma), vagina (squamouscell carcinoma), and Cancer Studies in Humans bone (osteosarcoma) occurred in mice, and benign and malignant The strongest evidence for carcinogenicity comes from epidemiolog pituitarygland and liver tumors (hepatocellular tumors and heman ical studies of women exposed to diethylstilbestrol in utero (“diethyl gioendothelioma) occurred in rats. -
Workshop 1.4 Nature of the Ligand-Binding Pocket
Pure Appl. Chem., Vol. 75, Nos. 11–12, pp. 2397–2403, 2003. © 2003 IUPAC Workshop 1.4 Nature of the ligand-binding pocket of estrogen receptor a and b: The search for subtype- selective ligands and implications for the prediction of estrogenic activity* John A. Katzenellenbogen‡, Rajeev Muthyala, and Benita S. Katzenellenbogen Departments of Chemistry, Molecular and Integrative Physiology, University of Illinois, Urbana, 61801 IL, USA Abstract: The ligand-binding pockets of estrogen receptor alpha and beta (ERα and ERβ) ap- pear to have subpockets of different size and flexibility. To find ligands that will discriminate between the two ER subtypes on the basis of affinity or efficacy, we have prepared com- pounds of varying size, shape, and structure. We have evaluated the binding affinity of these compounds and their potency and efficacy as transcriptional activators through ERα and ERβ. In this manner, we have identified a number of ligands that show pronounced ER sub- type selectivity. These studies also highlight the eclectic structure–activity relationships of estrogens and the challenges inherent in developing computational methods for the predic- tion of estrogenic activity. INTRODUCTION The actions of estrogens are mediated by the estrogen receptor (ER), an intracellular protein that func- tions as a ligand-regulated transcription factor [1]. There are two subtypes of the estrogen receptor, ER α and ERβ; these subtypes have different tissue distributions and are thought to regulate different estro- gen responses [2]. Therefore, ligands that are selective in activating or inhibiting these two subtypes could have a desirable pattern of pharmacological activity that might be useful in regulating fertility, in treating menopausal symptoms, and in preventing and treating breast cancer [1]. -
Transcription Factors Underlying the Development and Endocrine Functions of the Placenta † † † JAMES C
Transcription Factors Underlying the Development and Endocrine Functions of the Placenta † † † JAMES C. CROSS,* LYNN ANSON-CARTWRIGHT, AND IAN C. SCOTT *Department of Biochemistry & Molecular Biology, University of Calgary Faculty of Medicine, Calgary, Alberta T2N 4N1 Canada; †Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5 Canada ABSTRACT The placenta has been the subject of extensive basic research efforts in two distinct fields. The developmental biology of placenta has been studied because it is the first organ to develop during embryogenesis and because a number of different gene mutations in mice result in embryonic lethality due to placental defects. The trophoblast cell lineage is relatively simple such that only two major, terminally differentiated cell types appear: an “invasive trophoblast” cell subtype such as extravillous cytotrophoblast cells in humans and trophoblast giant cells in mice, and a “transport trophoblast” cell subtype that is a syncytium (syncytiotrophoblast) in humans and mice. These two cell types also have been the focus of endocrinologists because they are the source of major placental hormones. Understanding the transcriptional regulation of placental hormone genes has given insights into the control of specificity of gene expression. Because most placental hormones are produced by very specific trophoblast cell subtypes, the transcriptional details promise to give insights into cell-subtype specification. The fields of developmental biology and molecular endocrinology appear to be meeting on this common ground with the recent discovery of key transcription factors. Specifically, the basic helix-loop-helix (bHLH) transcription factor Hand1 is essential for differen- tiation of trophoblast giant cells in mice and also regulates the promoter for the giant cell-specific hormone, placental lactogen I gene (Pl1).