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The Rise and Fall of the Bovine Corpus Luteum
University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Spring 5-6-2017 The Rise and Fall of the Bovine Corpus Luteum Heather Talbott University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Biochemistry Commons, Molecular Biology Commons, and the Obstetrics and Gynecology Commons Recommended Citation Talbott, Heather, "The Rise and Fall of the Bovine Corpus Luteum" (2017). Theses & Dissertations. 207. https://digitalcommons.unmc.edu/etd/207 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. THE RISE AND FALL OF THE BOVINE CORPUS LUTEUM by Heather Talbott A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Biochemistry and Molecular Biology Graduate Program Under the Supervision of Professor John S. Davis University of Nebraska Medical Center Omaha, Nebraska May, 2017 Supervisory Committee: Carol A. Casey, Ph.D. Andrea S. Cupp, Ph.D. Parmender P. Mehta, Ph.D. Justin L. Mott, Ph.D. i ACKNOWLEDGEMENTS This dissertation was supported by the Agriculture and Food Research Initiative from the USDA National Institute of Food and Agriculture (NIFA) Pre-doctoral award; University of Nebraska Medical Center Graduate Student Assistantship; University of Nebraska Medical Center Exceptional Incoming Graduate Student Award; the VA Nebraska-Western Iowa Health Care System Department of Veterans Affairs; and The Olson Center for Women’s Health, Department of Obstetrics and Gynecology, Nebraska Medical Center. -
(12) Patent Application Publication (10) Pub. No.: US 2015/0086513 A1 Savkovic Et Al
US 20150.086513A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2015/0086513 A1 Savkovic et al. (43) Pub. Date: Mar. 26, 2015 (54) METHOD FOR DERIVING MELANOCYTES (30) Foreign Application Priority Data FROM THE HAIR FOLLCLE OUTER ROOT SHEATH AND PREPARATION FOR A. 36. 3. E. - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - E.6 GRAFTNG l9. U. 414 ) . Publication Classification (71) Applicant: UNIVERSITAT LEIPZIG, Leipzig (DE) (51) Int. Cl. A6L27/38 (2006.01) (72) Inventors: Vuk Savkovic, Leipzig (DE); Christina CI2N5/071 (2006.01) Dieckmann, Leipzig (DE); (52) U.S. Cl. Jan-Christoph Simon, Leipzig (DE); CPC ......... A61L 27/3834 (2013.01); A61L 27/3895 Michaela Schulz-Siegmund, Leipzig (2013.01); C12N5/0626 (2013.01); C12N (DE); Michael Hacker, Leipzig (DE) 2506/03 (2013.01) USPC .......................................... 424/93.7:435/366 (57) ABSTRACT (73) Assignee: NIVERSITAT LEIPZIG, Leipzig The present invention relates to the field of biology and medi (DE) cine, and more specifically, to the field of stem-cell biology, involving producing or generating melanocytes from stem (21) Appl. No.: 14/354,545 cells and precursors derived from human hair root. Addition (22) PCT Filed: Oct. 29, 2012 ally, the present invention relates to the materials and method e a? 19 for producing autografts, homografts or allografts compris (86). PCT No.: PCT/EP2012/07 1418 ing melanocytes in general, as well as the materials and meth ods for producing autografts, homografts and allografts com S371 (c)(1), prising melanocytes for the treatment of diseases related to (2) Date: Apr. 25, 2014 depigmentation of the skin and for the treatment of Scars. -
Aberrant Colourations in Wild Snakes: Case Study in Neotropical Taxa and a Review of Terminology
SALAMANDRA 57(1): 124–138 Claudio Borteiro et al. SALAMANDRA 15 February 2021 ISSN 0036–3375 German Journal of Herpetology Aberrant colourations in wild snakes: case study in Neotropical taxa and a review of terminology Claudio Borteiro1, Arthur Diesel Abegg2,3, Fabrício Hirouki Oda4, Darío Cardozo5, Francisco Kolenc1, Ignacio Etchandy6, Irasema Bisaiz6, Carlos Prigioni1 & Diego Baldo5 1) Sección Herpetología, Museo Nacional de Historia Natural, Miguelete 1825, Montevideo 11800, Uruguay 2) Instituto Butantan, Laboratório Especial de Coleções Zoológicas, Avenida Vital Brasil, 1500, Butantã, CEP 05503-900 São Paulo, SP, Brazil 3) Universidade de São Paulo, Instituto de Biociências, Departamento de Zoologia, Programa de Pós-Graduação em Zoologia, Travessa 14, Rua do Matão, 321, Cidade Universitária, 05508-090, São Paulo, SP, Brazil 4) Universidade Regional do Cariri, Departamento de Química Biológica, Programa de Pós-graduação em Bioprospecção Molecular, Rua Coronel Antônio Luiz 1161, Pimenta, Crato, Ceará 63105-000, CE, Brazil 5) Laboratorio de Genética Evolutiva, Instituto de Biología Subtropical (CONICET-UNaM), Facultad de Ciencias Exactas Químicas y Naturales, Universidad Nacional de Misiones, Felix de Azara 1552, CP 3300, Posadas, Misiones, Argentina 6) Alternatus Uruguay, Ruta 37, km 1.4, Piriápolis, Uruguay Corresponding author: Claudio Borteiro, e-mail: [email protected] Manuscript received: 2 April 2020 Accepted: 18 August 2020 by Arne Schulze Abstract. The criteria used by previous authors to define colour aberrancies of snakes, particularly albinism, are varied and terms have widely been used ambiguously. The aim of this work was to review genetically based aberrant colour morphs of wild Neotropical snakes and associated terminology. We compiled a total of 115 cases of conspicuous defective expressions of pigmentations in snakes, including melanin (black/brown colour), xanthins (yellow), and erythrins (red), which in- volved 47 species of Aniliidae, Boidae, Colubridae, Elapidae, Leptotyphlopidae, Typhlopidae, and Viperidae. -
Human Impacts on Geyser Basins
volume 17 • number 1 • 2009 Human Impacts on Geyser Basins The “Crystal” Salamanders of Yellowstone Presence of White-tailed Jackrabbits Nature Notes: Wolves and Tigers Geyser Basins with no Documented Impacts Valley of Geysers, Umnak (Russia) Island Geyser Basins Impacted by Energy Development Geyser Basins Impacted by Tourism Iceland Iceland Beowawe, ~61 ~27 Nevada ~30 0 Yellowstone ~220 Steamboat Springs, Nevada ~21 0 ~55 El Tatio, Chile North Island, New Zealand North Island, New Zealand Geysers existing in 1950 Geyser basins with documented negative effects of tourism Geysers remaining after geothermal energy development Impacts to geyser basins from human activities. At least half of the major geyser basins of the world have been altered by geothermal energy development or tourism. Courtesy of Steingisser, 2008. Yellowstone in a Global Context N THIS ISSUE of Yellowstone Science, Alethea Steingis- claimed they had been extirpated from the park. As they have ser and Andrew Marcus in “Human Impacts on Geyser since the park’s establishment, jackrabbits continue to persist IBasins” document the global distribution of geysers, their in the park in a small range characterized by arid, lower eleva- destruction at the hands of humans, and the tremendous tion sagebrush-grassland habitats. With so many species in the importance of Yellowstone National Park in preserving these world on the edge of survival, the confirmation of the jackrab- rare and ephemeral features. We hope this article will promote bit’s persistence is welcome. further documentation, research, and protection efforts for The Nature Note continues to consider Yellowstone with geyser basins around the world. Documentation of their exis- a broader perspective. -
An Albino Mutant of the Japanese Rat Snake (Elaphe Climacophora) Carries a Nonsense Mutation in the Tyrosinase Gene
Genes Genet. Syst. (2018) 93, p. 163–167Albino mutation in the Japanese rat snake 163 An albino mutant of the Japanese rat snake (Elaphe climacophora) carries a nonsense mutation in the tyrosinase gene Shuzo Iwanishi1, Shohei Zaitsu1, Hiroki Shibata2 and Eiji Nitasaka3* 1Graduate School of Systems Life Sciences, Kyushu University, 744 Motooka, Fukuoka 819-0395, Japan 2Division of Genomics, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Fukuoka 812-8582, Japan 3Department of Biological Science, Faculty of Science, Kyushu University, 744 Motooka, Fukuoka 819-0395, Japan (Received 16 April 2018, accepted 19 May 2018; J-STAGE Advance published date: 30 August 2018) The Japanese rat snake (Elaphe climacophora) is a common species in Japan and is widely distributed across the Japanese islands. An albino mutant of the Japanese rat snake (“pet trade” albino) has been bred and traded by hobbyists for around two decades because of its remarkable light-yellowish coloration with red eyes, attributable to a lack of melanin. Another albino Japanese rat snake mutant found in a natural population of the Japanese rat snake at high frequency in Iwakuni City, Yamaguchi Prefecture is known as “Iwakuni no Shirohebi”. It has been conserved by the government as a natural monument. The Iwakuni albino also lacks melanin, having light-yellowish body coloration and red eyes. Albino mutants of several organisms have been studied, and mutation of the tyrosinase gene (TYR) is responsible for this phenotype. By determining the sequence of the TYR coding region of the pet trade albino, we identified a nonsense mutation in the second exon. -
Index to the NLM Classification 2011
National Library of Medicine Classification 2011 Index Disease see Tyrosinemias 1-8 5,12-diHETE see Leukotriene B4 1,2-Benzopyrones see Coumarins 5,12-HETE see Leukotriene B4 1,2-Dibromoethane see Ethylene Dibromide 5-HT see Serotonin 1,8-Dihydroxy-9-anthrone see Anthralin 5-HT Antagonists see Serotonin Antagonists 1-Oxacephalosporin see Moxalactam 5-Hydroxytryptamine see Serotonin 1-Propanol 5-Hydroxytryptamine Antagonists see Serotonin Organic chemistry QD 305.A4 Antagonists Pharmacology QV 82 6-Mercaptopurine QV 269 1-Sar-8-Ala Angiotensin II see Saralasin 7S RNA see RNA, Small Nuclear 1-Sarcosine-8-Alanine Angiotensin II see Saralasin 8-Hydroxyquinoline see Oxyquinoline 13-cis-Retinoic Acid see Isotretinoin 8-Methoxypsoralen see Methoxsalen 15th Century History see History, 15th Century 8-Quinolinol see Oxyquinoline 16th Century History see History, 16th Century 17 beta-Estradiol see Estradiol 17-Ketosteroids WK 755 A 17-Oxosteroids see 17-Ketosteroids A Fibers see Nerve Fibers, Myelinated 17th Century History see History, 17th Century Aardvarks see Xenarthra 18th Century History see History, 18th Century Abate see Temefos 19th Century History see History, 19th Century Abattoirs WA 707 2',3'-Cyclic-Nucleotide Phosphodiesterases QU 136 Abbreviations 2,4-D see 2,4-Dichlorophenoxyacetic Acid Chemistry QD 7 2,4-Dichlorophenoxyacetic Acid General P 365-365.5 Organic chemistry QD 341.A2 Library symbols (U.S.) Z 881 2',5'-Oligoadenylate Polymerase see Medical W 13 2',5'-Oligoadenylate Synthetase By specialties (Form number 13 in any NLM -
Generalized Hypertrichosis
Letters to the Editor case of female. Ambras syndrome is a type of universal Generalized hypertrichosis affecting the vellus hair, where there is uniform overgrowth of hair over the face and external hypertrichosis ear with or without dysmorphic facies.[3] Patients with Gingival fi bromaatosis also have generalized hypertrichosis Sir, especially on the face.[4] Congenital hypertrichosis can A 4-year-old girl born out of non-consanguinous marriage occur due to fetal alcohol syndrome and fetal hydentoin presented with generalized increase in body hair noticed syndrome.[5] Prepubertal hypertrichosis is seen in otherwise since birth. None of the other family members were healthy infants and children. There is involvement of affected. Hair was pigmented and soft suggesting vellus hair. face back and extremities Distribution of hair shows an There was generalized increase in body hair predominantly inverted fi r-tree pattern on the back. More commonly seen affecting the back of trunk arms and legs [Figures 1 and 2]. in Mediterranean and South Asian descendants.[6] There is Face was relatively spared except for fore head. Palms and soles were spared. Scalp hair was normal. Teeth and nail usually no hormonal alterations. Various genodermatosis were normal. There was no gingival hypertrophy. No other associated with hypertrichosis as the main or secondary skeletal or systemic abnormalities were detected clinically. diagnostic symptom are: Routine blood investigations were normal. Hormonal Lipoatrophy (Lawrernce Seip syndrome) study was within normal limit for her age. With this Cornelia de Lange syndrome clinical picture of generalized hypertrichosis with no other Craniofacial dysostosis associated anomalies a diagnosis of universal hypertrichosis Winchester syndrome was made. -
Cellular and Molecular Signatures in the Disease Tissue of Early
Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of -
Aberrant Plumages in Grebes Podicipedidae
André Konter Aberrant plumages in grebes Podicipedidae An analysis of albinism, leucism, brown and other aberrations in all grebe species worldwide Aberrant plumages in grebes Podicipedidae in grebes plumages Aberrant Ferrantia André Konter Travaux scientifiques du Musée national d'histoire naturelle Luxembourg www.mnhn.lu 72 2015 Ferrantia 72 2015 2015 72 Ferrantia est une revue publiée à intervalles non réguliers par le Musée national d’histoire naturelle à Luxembourg. Elle fait suite, avec la même tomaison, aux TRAVAUX SCIENTIFIQUES DU MUSÉE NATIONAL D’HISTOIRE NATURELLE DE LUXEMBOURG parus entre 1981 et 1999. Comité de rédaction: Eric Buttini Guy Colling Edmée Engel Thierry Helminger Mise en page: Romain Bei Design: Thierry Helminger Prix du volume: 15 € Rédaction: Échange: Musée national d’histoire naturelle Exchange MNHN Rédaction Ferrantia c/o Musée national d’histoire naturelle 25, rue Münster 25, rue Münster L-2160 Luxembourg L-2160 Luxembourg Tél +352 46 22 33 - 1 Tél +352 46 22 33 - 1 Fax +352 46 38 48 Fax +352 46 38 48 Internet: http://www.mnhn.lu/ferrantia/ Internet: http://www.mnhn.lu/ferrantia/exchange email: [email protected] email: [email protected] Page de couverture: 1. Great Crested Grebe, Lake IJssel, Netherlands, April 2002 (PCRcr200303303), photo A. Konter. 2. Red-necked Grebe, Tunkwa Lake, British Columbia, Canada, 2006 (PGRho200501022), photo K. T. Karlson. 3. Great Crested Grebe, Rotterdam-IJsselmonde, Netherlands, August 2006 (PCRcr200602012), photo C. van Rijswik. Citation: André Konter 2015. - Aberrant plumages in grebes Podicipedidae - An analysis of albinism, leucism, brown and other aberrations in all grebe species worldwide. Ferrantia 72, Musée national d’histoire naturelle, Luxembourg, 206 p. -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
Linking Melanism to Brain Development: Expression of a Melanism-Related Gene in Barn Owl Feather Follicles Covaries with Sleep O
Scriba et al. Frontiers in Zoology 2013, 10:42 http://www.frontiersinzoology.com/content/10/1/42 RESEARCH Open Access Linking melanism to brain development: expression of a melanism-related gene in barn owl feather follicles covaries with sleep ontogeny Madeleine F Scriba1,2†, Anne-Lyse Ducrest2†, Isabelle Henry2, Alexei L Vyssotski3, Niels C Rattenborg1*† and Alexandre Roulin2*† Abstract Background: Intra-specific variation in melanocyte pigmentation, common in the animal kingdom, has caught the eye of naturalists and biologists for centuries. In vertebrates, dark, eumelanin pigmentation is often genetically determined and associated with various behavioral and physiological traits, suggesting that the genes involved in melanism have far reaching pleiotropic effects. The mechanisms linking these traits remain poorly understood, and the potential involvement of developmental processes occurring in the brain early in life has not been investigated. We examined the ontogeny of rapid eye movement (REM) sleep, a state involved in brain development, in a wild population of barn owls (Tyto alba) exhibiting inter-individual variation in melanism and covarying traits. In addition to sleep, we measured melanistic feather spots and the expression of a gene in the feather follicles implicated in melanism (PCSK2). Results: As in mammals, REM sleep declined with age across a period of brain development in owlets. In addition, inter-individual variation in REM sleep around this developmental trajectory was predicted by variation in PCSK2 expression in the feather follicles, with individuals expressing higher levels exhibiting a more precocial pattern characterized by less REM sleep. Finally, PCSK2 expression was positively correlated with feather spotting. Conclusions: We demonstrate that the pace of brain development, as reflected in age-related changes in REM sleep, covaries with the peripheral activation of the melanocortin system. -
Review Article Mouse Homologues of Human Hereditary Disease
I Med Genet 1994;31:1-19 I Review article J Med Genet: first published as 10.1136/jmg.31.1.1 on 1 January 1994. Downloaded from Mouse homologues of human hereditary disease A G Searle, J H Edwards, J G Hall Abstract involve homologous loci. In this respect our Details are given of 214 loci known to be genetic knowledge of the laboratory mouse associated with human hereditary dis- outstrips that for all other non-human mam- ease, which have been mapped on both mals. The 829 loci recently assigned to both human and mouse chromosomes. Forty human and mouse chromosomes3 has now two of these have pathological variants in risen to 900, well above comparable figures for both species; in general the mouse vari- other laboratory or farm animals. In a previous ants are similar in their effects to the publication,4 102 loci were listed which were corresponding human ones, but excep- associated with specific human disease, had tions include the Dmd/DMD and Hprt/ mouse homologues, and had been located in HPRT mutations which cause little, if both species. The number has now more than any, harm in mice. Possible reasons for doubled (table 1A). Of particular interest are phenotypic differences are discussed. In those which have pathological variants in both most pathological variants the gene pro- the mouse and humans: these are listed in table duct seems to be absent or greatly 2. Many other pathological mutations have reduced in both species. The extensive been detected and located in the mouse; about data on conserved segments between half these appear to lie in conserved chromo- human and mouse chromosomes are somal segments.