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  • 1
    Publication Date: 2009-10-03
    Description: Caloric restriction (CR) protects against aging and disease, but the mechanisms by which this affects mammalian life span are unclear. We show in mice that deletion of ribosomal S6 protein kinase 1 (S6K1), a component of the nutrient-responsive mTOR (mammalian target of rapamycin) signaling pathway, led to increased life span and resistance to age-related pathologies, such as bone, immune, and motor dysfunction and loss of insulin sensitivity. Deletion of S6K1 induced gene expression patterns similar to those seen in CR or with pharmacological activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK), a conserved regulator of the metabolic response to CR. Our results demonstrate that S6K1 influences healthy mammalian life-span and suggest that therapeutic manipulation of S6K1 and AMPK might mimic CR and could provide broad protection against diseases of aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selman, Colin -- Tullet, Jennifer M A -- Wieser, Daniela -- Irvine, Elaine -- Lingard, Steven J -- Choudhury, Agharul I -- Claret, Marc -- Al-Qassab, Hind -- Carmignac, Danielle -- Ramadani, Faruk -- Woods, Angela -- Robinson, Iain C A -- Schuster, Eugene -- Batterham, Rachel L -- Kozma, Sara C -- Thomas, George -- Carling, David -- Okkenhaug, Klaus -- Thornton, Janet M -- Partridge, Linda -- Gems, David -- Withers, Dominic J -- BBS/E/B/0000C236/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/E/B/0000M979/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0800339/Medical Research Council/United Kingdom -- G108/551/Medical Research Council/United Kingdom -- MC_U117531708/Medical Research Council/United Kingdom -- MC_U120027537/Medical Research Council/United Kingdom -- MC_U120097114/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Oct 2;326(5949):140-4. doi: 10.1126/science.1177221.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Healthy Ageing, Centre for Diabetes and Endocrinology, Department of Medicine, University College London, London WC1E 6JJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19797661" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; Adipose Tissue, White/metabolism ; Aging/*physiology ; Animals ; Bone Density ; Caloric Restriction ; Female ; Gene Deletion ; Gene Expression ; Gene Expression Regulation ; Insulin/metabolism ; Liver/metabolism ; Longevity/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Muscle, Skeletal/metabolism ; Protein Kinases/metabolism ; Ribosomal Protein S6 Kinases, 90-kDa/genetics/*metabolism ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; TOR Serine-Threonine Kinases ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2010-03-27
    Description: Tumor manipulation of host immunity is important for tumor survival and invasion. Many cancers secrete CCL21, a chemoattractant for various leukocytes and lymphoid tissue inducer cells, which drive lymphoid neogenesis. CCL21 expression by melanoma tumors in mice was associated with an immunotolerant microenvironment, which included the induction of lymphoid-like reticular stromal networks, an altered cytokine milieu, and the recruitment of regulatory leukocyte populations. In contrast, CCL21-deficient tumors induced antigen-specific immunity. CCL21-mediated immune tolerance was dependent on host rather than tumor expression of the CCL21 receptor, CCR7, and could protect distant, coimplanted CCL21-deficient tumors and even nonsyngeneic allografts from rejection. We suggest that by altering the tumor microenvironment, CCL21-secreting tumors shift the host immune response from immunogenic to tolerogenic, which facilitates tumor progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shields, Jacqueline D -- Kourtis, Iraklis C -- Tomei, Alice A -- Roberts, Joanna M -- Swartz, Melody A -- New York, N.Y. -- Science. 2010 May 7;328(5979):749-52. doi: 10.1126/science.1185837. Epub 2010 Mar 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; Chemokine CCL21/*metabolism ; Cytokines/metabolism ; Disease Progression ; Female ; Immune Tolerance ; Lymph Nodes/immunology ; Lymphoid Tissue/*immunology/pathology ; Melanoma, Experimental/*immunology/*pathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; RNA Interference ; Receptors, CCR7/metabolism ; Signal Transduction ; Stromal Cells/*immunology/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/immunology ; *Tumor Escape
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2011-05-28
    Description: With data from 33 nations, we illustrate the differences between cultures that are tight (have many strong norms and a low tolerance of deviant behavior) versus loose (have weak social norms and a high tolerance of deviant behavior). Tightness-looseness is part of a complex, loosely integrated multilevel system that comprises distal ecological and historical threats (e.g., high population density, resource scarcity, a history of territorial conflict, and disease and environmental threats), broad versus narrow socialization in societal institutions (e.g., autocracy, media regulations), the strength of everyday recurring situations, and micro-level psychological affordances (e.g., prevention self-guides, high regulatory strength, need for structure). This research advances knowledge that can foster cross-cultural understanding in a world of increasing global interdependence and has implications for modeling cultural change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gelfand, Michele J -- Raver, Jana L -- Nishii, Lisa -- Leslie, Lisa M -- Lun, Janetta -- Lim, Beng Chong -- Duan, Lili -- Almaliach, Assaf -- Ang, Soon -- Arnadottir, Jakobina -- Aycan, Zeynep -- Boehnke, Klaus -- Boski, Pawel -- Cabecinhas, Rosa -- Chan, Darius -- Chhokar, Jagdeep -- D'Amato, Alessia -- Ferrer, Montse -- Fischlmayr, Iris C -- Fischer, Ronald -- Fulop, Marta -- Georgas, James -- Kashima, Emiko S -- Kashima, Yoshishima -- Kim, Kibum -- Lempereur, Alain -- Marquez, Patricia -- Othman, Rozhan -- Overlaet, Bert -- Panagiotopoulou, Penny -- Peltzer, Karl -- Perez-Florizno, Lorena R -- Ponomarenko, Larisa -- Realo, Anu -- Schei, Vidar -- Schmitt, Manfred -- Smith, Peter B -- Soomro, Nazar -- Szabo, Erna -- Taveesin, Nalinee -- Toyama, Midori -- Van de Vliert, Evert -- Vohra, Naharika -- Ward, Colleen -- Yamaguchi, Susumu -- New York, N.Y. -- Science. 2011 May 27;332(6033):1100-4. doi: 10.1126/science.1197754.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Maryland, College Park, MD 20742, USA. mgelfand@psyc.umd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21617077" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Behavior ; *Cross-Cultural Comparison ; *Cultural Characteristics ; Female ; Government ; Humans ; Male ; Permissiveness ; Political Systems ; Population Density ; *Social Behavior ; *Social Conformity ; Social Control, Formal ; *Social Values ; Young Adult
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 1997-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramamoorthy, K -- Wang, F -- Chen, I C -- Safe, S -- Norris, J D -- McDonnell, D P -- Gaido, K W -- Bocchinfuso, W P -- Korach, K S -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):405-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dieldrin/metabolism/*pharmacology ; Drug Interactions ; Drug Synergism ; Estrogens, Non-Steroidal/metabolism/*pharmacology ; Female ; Humans ; Insecticides/metabolism/*pharmacology ; Mice ; Receptors, Estrogen/metabolism ; Toxaphene/metabolism/*pharmacology ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2014-10-16
    Description: Endothelial cells contribute to a subset of cardiac fibroblasts by undergoing endothelial-to-mesenchymal transition, but whether cardiac fibroblasts can adopt an endothelial cell fate and directly contribute to neovascularization after cardiac injury is not known. Here, using genetic fate map techniques, we demonstrate that cardiac fibroblasts rapidly adopt an endothelial-cell-like phenotype after acute ischaemic cardiac injury. Fibroblast-derived endothelial cells exhibit anatomical and functional characteristics of native endothelial cells. We show that the transcription factor p53 regulates such a switch in cardiac fibroblast fate. Loss of p53 in cardiac fibroblasts severely decreases the formation of fibroblast-derived endothelial cells, reduces post-infarct vascular density and worsens cardiac function. Conversely, stimulation of the p53 pathway in cardiac fibroblasts augments mesenchymal-to-endothelial transition, enhances vascularity and improves cardiac function. These observations demonstrate that mesenchymal-to-endothelial transition contributes to neovascularization of the injured heart and represents a potential therapeutic target for enhancing cardiac repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214889/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214889/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ubil, Eric -- Duan, Jinzhu -- Pillai, Indulekha C L -- Rosa-Garrido, Manuel -- Wu, Yong -- Bargiacchi, Francesca -- Lu, Yan -- Stanbouly, Seta -- Huang, Jie -- Rojas, Mauricio -- Vondriska, Thomas M -- Stefani, Enrico -- Deb, Arjun -- HL088640/HL/NHLBI NIH HHS/ -- HL105699/HL/NHLBI NIH HHS/ -- R01 HL102190/HL/NHLBI NIH HHS/ -- R01HL102190/HL/NHLBI NIH HHS/ -- T32 GM007040/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Oct 30;514(7524):585-90. doi: 10.1038/nature13839. Epub 2014 Oct 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology &Physiology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, USA. ; 1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Eli and Edythe Broad Institute of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, California 90095, USA [4] Department of Molecular, Cell and Developmental Biology, College of Letters and Sciences, University of California, Los Angeles, California 90095, USA [5] Jonsson Comprehensive Cancer Center, University of California, Los Angeles, California 90095, USA [6] Molecular Biology Institute, University of California, Los Angeles, California 90095, USA. ; 1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [4] Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA. ; Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA. ; Department of Pharmacology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, USA. ; Department of Medicine, McAllister Heart Institute, University of North Carolina, Chapel Hill, North Carolina 27599, USA. ; 1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Molecular Biology Institute, University of California, Los Angeles, California 90095, USA [4] Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [5] Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA. ; 1] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25317562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transdifferentiation ; Coronary Vessels/*cytology/*growth & development ; Endothelial Cells/*cytology ; Female ; Fibroblasts/cytology ; In Vitro Techniques ; Male ; Mesoderm/*cytology ; Mice ; Myocardial Ischemia/*pathology ; *Neovascularization, Physiologic ; Tumor Suppressor Protein p53/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
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  • 6
    Publication Date: 2013-08-13
    Description: The blood system is maintained by a small pool of haematopoietic stem cells (HSCs), which are required and sufficient for replenishing all human blood cell lineages at millions of cells per second throughout life. Megakaryocytes in the bone marrow are responsible for the continuous production of platelets in the blood, crucial for preventing bleeding--a common and life-threatening side effect of many cancer therapies--and major efforts are focused at identifying the most suitable cellular and molecular targets to enhance platelet production after bone marrow transplantation or chemotherapy. Although it has become clear that distinct HSC subsets exist that are stably biased towards the generation of lymphoid or myeloid blood cells, we are yet to learn whether other types of lineage-biased HSC exist or understand their inter-relationships and how differently lineage-biased HSCs are generated and maintained. The functional relevance of notable phenotypic and molecular similarities between megakaryocytes and bone marrow cells with an HSC cell-surface phenotype remains unclear. Here we identify and prospectively isolate a molecularly and functionally distinct mouse HSC subset primed for platelet-specific gene expression, with enhanced propensity for short- and long-term reconstitution of platelets. Maintenance of platelet-biased HSCs crucially depends on thrombopoietin, the primary extrinsic regulator of platelet development. Platelet-primed HSCs also frequently have a long-term myeloid lineage bias, can self-renew and give rise to lymphoid-biased HSCs. These findings show that HSC subtypes can be organized into a cellular hierarchy, with platelet-primed HSCs at the apex. They also demonstrate that molecular and functional priming for platelet development initiates already in a distinct HSC population. The identification of a platelet-primed HSC population should enable the rational design of therapies enhancing platelet output.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanjuan-Pla, Alejandra -- Macaulay, Iain C -- Jensen, Christina T -- Woll, Petter S -- Luis, Tiago C -- Mead, Adam -- Moore, Susan -- Carella, Cintia -- Matsuoka, Sahoko -- Bouriez Jones, Tiphaine -- Chowdhury, Onima -- Stenson, Laura -- Lutteropp, Michael -- Green, Joanna C A -- Facchini, Raffaella -- Boukarabila, Hanane -- Grover, Amit -- Gambardella, Adriana -- Thongjuea, Supat -- Carrelha, Joana -- Tarrant, Paul -- Atkinson, Deborah -- Clark, Sally-Ann -- Nerlov, Claus -- Jacobsen, Sten Eirik W -- G0701761/Medical Research Council/United Kingdom -- G0900892/Medical Research Council/United Kingdom -- G84/6443/Medical Research Council/United Kingdom -- H4RPLK0/Medical Research Council/United Kingdom -- England -- Nature. 2013 Oct 10;502(7470):232-6. doi: 10.1038/nature12495. Epub 2013 Aug 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Stem Cell Research and MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH9 16UU, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23934107" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/*cytology ; *Cell Differentiation ; Cell Lineage/genetics ; Female ; Gene Expression Regulation, Developmental ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology/metabolism ; Lymphocytes/cytology ; Male ; Mice ; Mice, Inbred C57BL
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  • 7
    Publication Date: 2014-09-19
    Description: Observations of chimpanzees (Pan troglodytes) and bonobos (Pan paniscus) provide valuable comparative data for understanding the significance of conspecific killing. Two kinds of hypothesis have been proposed. Lethal violence is sometimes concluded to be the result of adaptive strategies, such that killers ultimately gain fitness benefits by increasing their access to resources such as food or mates. Alternatively, it could be a non-adaptive result of human impacts, such as habitat change or food provisioning. To discriminate between these hypotheses we compiled information from 18 chimpanzee communities and 4 bonobo communities studied over five decades. Our data include 152 killings (n = 58 observed, 41 inferred, and 53 suspected killings) by chimpanzees in 15 communities and one suspected killing by bonobos. We found that males were the most frequent attackers (92% of participants) and victims (73%); most killings (66%) involved intercommunity attacks; and attackers greatly outnumbered their victims (median 8:1 ratio). Variation in killing rates was unrelated to measures of human impacts. Our results are compatible with previously proposed adaptive explanations for killing by chimpanzees, whereas the human impact hypothesis is not supported.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Michael L -- Boesch, Christophe -- Fruth, Barbara -- Furuichi, Takeshi -- Gilby, Ian C -- Hashimoto, Chie -- Hobaiter, Catherine L -- Hohmann, Gottfried -- Itoh, Noriko -- Koops, Kathelijne -- Lloyd, Julia N -- Matsuzawa, Tetsuro -- Mitani, John C -- Mjungu, Deus C -- Morgan, David -- Muller, Martin N -- Mundry, Roger -- Nakamura, Michio -- Pruetz, Jill -- Pusey, Anne E -- Riedel, Julia -- Sanz, Crickette -- Schel, Anne M -- Simmons, Nicole -- Waller, Michel -- Watts, David P -- White, Frances -- Wittig, Roman M -- Zuberbuhler, Klaus -- Wrangham, Richard W -- R01 AI 058715/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Sep 18;513(7518):414-7. doi: 10.1038/nature13727.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Anthropology, University of Minnesota, 395 Humphrey Center, 301 19th Avenue South, Minneapolis, Minnesota 55455, USA [2] Department of Ecology, Evolution and Behavior, University of Minnesota, 1987 Upper Buford Circle, St Paul, Minnesota 55108, USA. ; Department of Primatology, Max Planck Institute for Evolutionary Anthropology, Deutscher Platz 6, 04103 Leipzig, Germany. ; 1] Division of Neurobiology, Ludwig-Maximilians Universitaet Muenchen, Germany [2] Centre for Research and Conservation, Royal Zoological Society of Antwerp, Belgium. ; Primate Research Institute, Kyoto University, 41-2 Kanrin, Inuyama, Aichi 484-8506, Japan. ; 1] Department of Evolutionary Anthropology, Duke University, 104 Biological Sciences Building, Box 90383, Durham, North Carolina 27708-0680, USA [2] School of Human Evolution and Social Change, Arizona State University, PO Box 872402, Tempe, Arizona 85287-2402, USA. ; School of Psychology and Neuroscience, University of St Andrews, Westburn Lane, St Andrews, Fife KY16 9JP, UK. ; Wildlife Research Center, Kyoto University, 2-24 Tanaka-Sekiden-Cho, Sakyo, Kyoto, Japan. ; Division of Biological Anthropology, Department of Archaeology &Anthropology, University of Cambridge, Henry Wellcome Building, Fitzwilliam Street, Cambridge CB2 1QH, UK. ; Zoology Department, Makerere University, P.O. Box 7062, Kampala, Uganda. ; 1] Primate Research Institute, Kyoto University, 41-2 Kanrin, Inuyama, Aichi 484-8506, Japan [2] Japan Monkey Center, 26 Kanrin, Inuyama, Aichi 484-0081, Japan. ; Department of Anthropology, University of Michigan, 101 West Hall, 1085 S. University Avenue, Ann Arbor, Michigan 48109, USA. ; Gombe Stream Research Centre, The Jane Goodall Institute - Tanzania, P.O. Box 1182, Kigoma, Tanzania. ; The Lester E. Fisher Center for the Study and Conservation of Apes, Lincoln Park Zoo, Chicago, Illinois 60614, USA. ; Department of Anthropology, MSC01-1040, Anthropology 1, University of New Mexico, Albuquerque, New Mexico 87131, USA. ; Max Planck Institute for Evolutionary Anthropology, Deutscher Platz 6, 04103 Leipzig, Germany. ; Department of Anthropology, Iowa State University, 324 Curtiss, Ames, Iowa 50011, USA. ; Department of Evolutionary Anthropology, Duke University, 104 Biological Sciences Building, Box 90383, Durham, North Carolina 27708-0680, USA. ; Department of Anthropology, Washington University in St Louis, Campus Mailbox 1114, One Brookings Drive, St Louis, Missouri 63130, USA. ; University of York, Department of Psychology, Heslington, York, YO10 5DD, UK. ; Department of Anthropology, University of Oregon, Eugene, Oregon 97403, USA. ; Department of Anthropology, Yale University, 10 Sachem Street, New Haven, Connecticut 06511, USA. ; 1] School of Psychology and Neuroscience, University of St Andrews, Westburn Lane, St Andrews, Fife KY16 9JP, UK [2] Universite de Neuchatel, Institut de Biologie, Rue Emile-Argand 11, 2000 Neuchatel, Switzerland. ; Department of Human Evolutionary Biology, Harvard University, 11 Divinity Avenue Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25230664" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Aggression/*physiology/*psychology ; Animals ; Animals, Wild/physiology/psychology ; Behavior, Animal/*physiology ; Female ; Food ; *Human Activities ; Humans ; Male ; *Models, Biological ; *Pan paniscus/physiology/psychology ; *Pan troglodytes/physiology/psychology ; Population Density ; Sexual Behavior, Animal/physiology
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  • 8
    Publication Date: 1995-03-24
    Description: A process has been developed for the in situ formation of the mineral phase of bone. Inorganic calcium and phosphate sources are combined to form a paste that is surgically implanted by injection. Under physiological conditions, the material hardens in minutes concurrent with the formation of dahllite. After 12 hours, dahllite formation was nearly complete, and an ultimate compressive strength of 55 megapascals was achieved. The composition and crystal morphology of the dahllite formed are similar to those of bone. Animal studies provide evidence that the material is remodeled in vivo. A novel approach to skeletal repair is being tested in human trials for various applications; in one of the trials the new biomaterial is being percutaneously placed into acute fractures. After hardening, it serves as internal fixation to maintain proper alignment while healing occurs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Constantz, B R -- Ison, I C -- Fulmer, M T -- Poser, R D -- Smith, S T -- VanWagoner, M -- Ross, J -- Goldstein, S A -- Jupiter, J B -- Rosenthal, D I -- New York, N.Y. -- Science. 1995 Mar 24;267(5205):1796-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Norian Corporation, Cupertino, CA 95014.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7892603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apatites/*chemistry ; Bone Substitutes/*chemistry ; Calcium Carbonate/*chemistry ; Calcium Phosphates/*chemistry ; Crystallography, X-Ray ; Dogs ; Female ; Fractures, Bone/therapy ; Humans ; Microscopy, Electron ; Middle Aged ; Models, Chemical ; Osseointegration ; Rabbits ; Spectroscopy, Fourier Transform Infrared
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  • 9
    Publication Date: 2011-02-19
    Description: During pregnancy, progesterone inhibits the growth-promoting actions of estrogen in the uterus. However, the mechanism for this is not clear. The attenuation of estrogen-mediated proliferation of the uterine epithelium by progesterone is a prerequisite for successful implantation. Our study reveals that progesterone-induced expression of the basic helix-loop-helix transcription factor Hand2 in the uterine stroma suppresses the production of several fibroblast growth factors (FGFs) that act as paracrine mediators of mitogenic effects of estrogen on the epithelium. In mouse uteri lacking Hand2, continued induction of these FGFs in the stroma maintains epithelial proliferation and stimulates estrogen-induced pathways, resulting in impaired implantation. Thus, Hand2 is a critical regulator of the uterine stromal-epithelial communication that directs proper steroid regulation conducive for the establishment of pregnancy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320855/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320855/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Quanxi -- Kannan, Athilakshmi -- DeMayo, Francesco J -- Lydon, John P -- Cooke, Paul S -- Yamagishi, Hiroyuki -- Srivastava, Deepak -- Bagchi, Milan K -- Bagchi, Indrani C -- U54 HD055787-01A1/HD/NICHD NIH HHS/ -- U54HD055787/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 18;331(6019):912-6. doi: 10.1126/science.1197454.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Comparative Biosciences, University of Illinois Urbana/Champaign, Urbana, IL 61820, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21330545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/*genetics/*metabolism ; Cell Proliferation ; Embryo Implantation/*physiology ; Endometrium/drug effects/*metabolism ; Epithelial Cells/cytology/drug effects/metabolism ; Epithelium/metabolism ; Estradiol/metabolism ; Estrogen Receptor alpha/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Fibroblast Growth Factors/genetics/*metabolism ; Gene Expression Profiling ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mifepristone/pharmacology ; Mucin-1/metabolism ; Phosphorylation ; Pregnancy ; Progesterone/antagonists & inhibitors/*metabolism/pharmacology ; Receptors, Fibroblast Growth Factor/metabolism ; Receptors, Progesterone/metabolism ; *Signal Transduction ; Stromal Cells/cytology/metabolism ; Transcription, Genetic
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1992-05-22
    Description: Human immunodeficiency virus type 1 (HIV-1) transmission from infected patients to health-care workers has been well documented, but transmission from an infected health-care worker to a patient has not been reported. After identification of an acquired immunodeficiency syndrome (AIDS) patient who had no known risk factors for HIV infection but who had undergone an invasive procedure performed by a dentist with AIDS, six other patients of this dentist were found to be HIV-infected. Molecular biologic studies were conducted to complement the epidemiologic investigation. Portions of the HIV proviral envelope gene from each of the seven patients, the dentist, and 35 HIV-infected persons from the local geographic area were amplified by polymerase chain reaction and sequenced. Three separate comparative genetic analyses--genetic distance measurements, phylogenetic tree analysis, and amino acid signature pattern analysis--showed that the viruses from the dentist and five dental patients were closely related. These data, together with the epidemiologic investigation, indicated that these patients became infected with HIV while receiving care from a dentist with AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ou, C Y -- Ciesielski, C A -- Myers, G -- Bandea, C I -- Luo, C C -- Korber, B T -- Mullins, J I -- Schochetman, G -- Berkelman, R L -- Economou, A N -- New York, N.Y. -- Science. 1992 May 22;256(5060):1165-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of HIV/AIDS, Centers for Disease Control, Atlanta, GA 30333.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589796" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/blood/microbiology/*transmission ; Amino Acid Sequence ; Base Sequence ; DNA, Viral/blood/genetics/isolation & purification ; *Dentistry ; Female ; Florida ; Genetic Variation ; HIV Infections/microbiology/*transmission ; HIV-1/*genetics/isolation & purification ; Humans ; Male ; Molecular Sequence Data ; Monocytes/physiology ; Oligodeoxyribonucleotides ; *Patients ; Phylogeny ; Sequence Homology, Nucleic Acid ; Viral Envelope Proteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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