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  • Male  (23)
  • Chemistry
  • American Association for the Advancement of Science (AAAS)  (23)
  • 1
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    Dosage compensation proteins targeted to X chromosomes by a determinant of hermaphrodite fate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: In many organisms, master control genes coordinately regulate sex-specific aspects of development. SDC-2 was shown to induce hermaphrodite sexual differentiation and activate X chromosome dosage compensation in Caenorhabditis elegans. To control these distinct processes, SDC-2 acts as a strong gene-specific repressor and a weaker chromosome-wide repressor. To initiate hermaphrodite development, SDC-2 associates with the promoter of the male sex-determining gene her-1 to repress its transcription. To activate dosage compensation, SDC-2 triggers assembly of a specialized protein complex exclusively on hermaphrodite X chromosomes to reduce gene expression by half. SDC-2 can localize to X chromosomes without other components of the dosage compensation complex, suggesting that SDC-2 targets dosage compensation machinery to X chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawes, H E -- Berlin, D S -- Lapidus, D M -- Nusbaum, C -- Davis, T L -- Meyer, B J -- GM30702/GM/NIGMS NIH HHS/ -- T32 GM07127/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1800-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3204, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/embryology/*genetics/physiology ; *Caenorhabditis elegans Proteins ; *DNA-Binding Proteins ; Disorders of Sex Development ; *Dosage Compensation, Genetic ; Female ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Helminth Proteins/genetics/*physiology ; Male ; Molecular Sequence Data ; Mutation ; Promoter Regions, Genetic ; Repressor Proteins/genetics/*physiology ; *Sex Determination Processes ; Transgenes ; X Chromosome/genetics/*metabolism
    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
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    Regional mu opioid receptor regulation of sensory and affective dimensions of pain (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-14
    Description: The endogenous opioid system is involved in stress responses, in the regulation of the experience of pain, and in the action of analgesic opiate drugs. We examined the function of the opioid system and mu-opioid receptors in the brains of healthy human subjects undergoing sustained pain. Sustained pain induced the regional release of endogenous opioids interacting with mu-opioid receptors in a number of cortical and subcortical brain regions. The activation of the mu-opioid receptor system was associated with reductions in the sensory and affective ratings of the pain experience, with distinct neuroanatomical involvements. These data demonstrate the central role of the mu-opioid receptors and their endogenous ligands in the regulation of sensory and affective components of the pain experience.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zubieta, J K -- Smith, Y R -- Bueller, J A -- Xu, Y -- Kilbourn, M R -- Jewett, D M -- Meyer, C R -- Koeppe, R A -- Stohler, C S -- R01 DE 12059/DE/NIDCR NIH HHS/ -- R01 DE 12743/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 2001 Jul 13;293(5528):311-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Mental Health Research Institute, Medical School, The University of Michigan, Ann Arbor, MI 48104-1687, USA. zubieta@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11452128" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amygdala/physiology ; Analgesics, Opioid/administration & dosage ; Brain/*physiology ; Brain Mapping ; Female ; Fentanyl/administration & dosage/*analogs & derivatives ; Humans ; Magnetic Resonance Imaging ; Male ; Masseter Muscle ; Opioid Peptides/physiology ; *Pain ; Pain Measurement ; Receptors, Opioid, mu/*physiology ; Thalamus/physiology ; Tomography, Emission-Computed
    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
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    Antiphase oscillation of the left and right suprachiasmatic nuclei (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-29
    Description: An unusual property of the circadian timekeeping systems of animals is rhythm "splitting," in which a single daily period of physical activity (usually measured as wheel running) dissociates into two stably coupled components about 12 hours apart; this behavior has been ascribed to a clock composed of two circadian oscillators cycling in antiphase. We analyzed gene expression in the hypothalamic circadian clock, the suprachiasmatic nucleus (SCN), of behaviorally "split" hamsters housed in constant light. The results show that the two oscillators underlying the split condition correspond to the left and right sides of the bilaterally paired SCN.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de la Iglesia, H O -- Meyer, J -- Carpino, A Jr -- Schwartz, W J -- R01 NS24542/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Oct 27;290(5492):799-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. hacho@bio.umass.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11052942" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Arginine Vasopressin/genetics/metabolism ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks/*physiology ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cricetinae ; *Gene Expression ; Helix-Loop-Helix Motifs ; In Situ Hybridization ; Light ; Male ; Mesocricetus ; Motor Activity ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Suprachiasmatic Nucleus/metabolism/*physiology ; Transcription Factors/genetics/metabolism
    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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  • 4
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    Multiple representations of pain in human cerebral cortex (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: The representation of pain in the cerebral cortex is less well understood than that of any other sensory system. However, with the use of magnetic resonance imaging and positron emission tomography in humans, it has now been demonstrated that painful heat causes significant activation of the contralateral anterior cingulate, secondary somatosensory, and primary somatosensory cortices. This contrasts with the predominant activation of primary somatosensory cortex caused by vibrotactile stimuli in similar experiments. Furthermore, the unilateral cingulate activation indicates that this forebrain area, thought to regulate emotions, contains an unexpectedly specific representation of pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Talbot, J D -- Marrett, S -- Evans, A C -- Meyer, E -- Bushnell, M C -- Duncan, G H -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1355-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de neurophysiologie comportementale, Faculte de medecine dentaire, Universite de Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2003220" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Anxiety/physiopathology ; Brain Mapping ; Cerebral Cortex/*physiology ; Functional Laterality ; Hot Temperature ; Humans ; Magnetic Resonance Imaging ; Male ; Pain/*physiopathology ; Tomography, Emission-Computed
    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
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    Assignment of a locus for familial melanoma, MLM, to chromosome 9p13-p22 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-13
    Description: Linkage analysis of ten Utah kindreds and one Texas kindred with multiple cases of cutaneous malignant melanoma (CMM) provided evidence that a locus for familial melanoma susceptibility is in the chromosomal region 9p13-p22. The genetic markers analyzed reside in a candidate region on chromosome 9p21, previously implicated by the presence of homozygous deletions in melanoma tumors and by the presence of a germline deletion in an individual with eight independent melanomas. Multipoint linkage analysis was performed between the familial melanoma susceptibility locus (MLM) and two short tandem repeat markers, D9S126 and the interferon-alpha (IFNA) gene, which reside in the region of somatic loss in melanoma tumors. An analysis incorporating a partially penetrant dominant melanoma susceptibility locus places MLM near IFNA and D9S126 with a maximum location score of 12.71. Therefore, the region frequently deleted in melanoma tumors on 9p21 presumably contains a locus that plays a critical role in predisposition to familial melanoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cannon-Albright, L A -- Goldgar, D E -- Meyer, L J -- Lewis, C M -- Anderson, D E -- Fountain, J W -- Hegi, M E -- Wiseman, R W -- Petty, E M -- Bale, A E -- CA 42014/CA/NCI NIH HHS/ -- CA 48711/CA/NCI NIH HHS/ -- RR 00064/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Nov 13;258(5085):1148-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439824" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Aged, 80 and over ; Base Sequence ; Child ; Chromosome Aberrations ; *Chromosomes, Human, Pair 9 ; Dysplastic Nevus Syndrome/genetics ; Female ; Genes, Tumor Suppressor ; Genetic Markers ; Humans ; Lod Score ; Male ; Melanoma/*genetics ; Middle Aged ; Molecular Sequence Data ; Pedigree ; Skin Neoplasms/*genetics ; Texas ; Utah
    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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  • 6
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    Defective lipolysis and altered energy metabolism in mice lacking adipose triglyceride lipase (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-06
    Description: Fat tissue is the most important energy depot in vertebrates. The release of free fatty acids (FFAs) from stored fat requires the enzymatic activity of lipases. We showed that genetic inactivation of adipose triglyceride lipase (ATGL) in mice increases adipose mass and leads to triacylglycerol deposition in multiple tissues. ATGL-deficient mice accumulated large amounts of lipid in the heart, causing cardiac dysfunction and premature death. Defective cold adaptation indicated that the enzyme provides FFAs to fuel thermogenesis. The reduced availability of ATGL-derived FFAs leads to increased glucose use, increased glucose tolerance, and increased insulin sensitivity. These results indicate that ATGL is rate limiting in the catabolism of cellular fat depots and plays an important role in energy homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haemmerle, Guenter -- Lass, Achim -- Zimmermann, Robert -- Gorkiewicz, Gregor -- Meyer, Carola -- Rozman, Jan -- Heldmaier, Gerhard -- Maier, Robert -- Theussl, Christian -- Eder, Sandra -- Kratky, Dagmar -- Wagner, Erwin F -- Klingenspor, Martin -- Hoefler, Gerald -- Zechner, Rudolf -- F 3001/Austrian Science Fund FWF/Austria -- F 3002/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 May 5;312(5774):734-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biosciences, University of Graz, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675698" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/metabolism ; Adipose Tissue/anatomy & histology/*enzymology/metabolism ; Adipose Tissue, Brown/enzymology ; Animals ; Blood Glucose/metabolism ; Carboxylic Ester Hydrolases/deficiency/genetics/*metabolism ; Cell Size ; *Energy Metabolism ; Fatty Acids, Nonesterified/blood/metabolism ; Female ; Heart Failure/pathology ; Homeostasis ; Insulin/blood ; Isoproterenol/pharmacology ; Kidney/metabolism ; Lipase/deficiency/genetics/*metabolism ; Lipids/blood ; *Lipolysis/drug effects ; Male ; Mice ; Myocardium/metabolism/pathology ; Myocytes, Cardiac/cytology/metabolism ; Oxygen Consumption ; Testis/metabolism ; Thermogenesis ; Triglycerides/*metabolism ; Ventricular Dysfunction, Left/physiopathology
    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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  • 7
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    Diminishing reciprocal fairness by disrupting the right prefrontal cortex (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: Humans restrain self-interest with moral and social values. They are the only species known to exhibit reciprocal fairness, which implies the punishment of other individuals' unfair behaviors, even if it hurts the punisher's economic self-interest. Reciprocal fairness has been demonstrated in the Ultimatum Game, where players often reject their bargaining partner's unfair offers. Despite progress in recent years, however, little is known about how the human brain limits the impact of selfish motives and implements fair behavior. Here we show that disruption of the right, but not the left, dorsolateral prefrontal cortex (DLPFC) by low-frequency repetitive transcranial magnetic stimulation substantially reduces subjects' willingness to reject their partners' intentionally unfair offers, which suggests that subjects are less able to resist the economic temptation to accept these offers. Importantly, however, subjects still judge such offers as very unfair, which indicates that the right DLPFC plays a key role in the implementation of fairness-related behaviors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knoch, Daria -- Pascual-Leone, Alvaro -- Meyer, Kaspar -- Treyer, Valerie -- Fehr, Ernst -- K24 RR018875/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):829-32. Epub 2006 Oct 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Empirical Research in Economics, University of Zurich, Blumlisalpstrasse 10, 8006 Zurich, Switzerland. dknoch@iew.unizh.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023614" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Decision Making ; Functional Laterality ; *Games, Experimental ; Humans ; Interpersonal Relations ; Judgment ; Male ; Prefrontal Cortex/*physiology ; *Social Behavior ; Transcranial Magnetic Stimulation
    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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  • 8
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    Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: New strategies for prevention and treatment of type 2 diabetes (T2D) require improved insight into disease etiology. We analyzed 386,731 common single-nucleotide polymorphisms (SNPs) in 1464 patients with T2D and 1467 matched controls, each characterized for measures of glucose metabolism, lipids, obesity, and blood pressure. With collaborators (FUSION and WTCCC/UKT2D), we identified and confirmed three loci associated with T2D-in a noncoding region near CDKN2A and CDKN2B, in an intron of IGF2BP2, and an intron of CDKAL1-and replicated associations near HHEX and in SLC30A8 found by a recent whole-genome association study. We identified and confirmed association of a SNP in an intron of glucokinase regulatory protein (GCKR) with serum triglycerides. The discovery of associated variants in unsuspected genes and outside coding regions illustrates the ability of genome-wide association studies to provide potentially important clues to the pathogenesis of common diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diabetes Genetics Initiative of Broad Institute of Harvard and MIT, Lund University, and Novartis Institutes of BioMedical Research -- Saxena, Richa -- Voight, Benjamin F -- Lyssenko, Valeriya -- Burtt, Noel P -- de Bakker, Paul I W -- Chen, Hong -- Roix, Jeffrey J -- Kathiresan, Sekar -- Hirschhorn, Joel N -- Daly, Mark J -- Hughes, Thomas E -- Groop, Leif -- Altshuler, David -- Almgren, Peter -- Florez, Jose C -- Meyer, Joanne -- Ardlie, Kristin -- Bengtsson Bostrom, Kristina -- Isomaa, Bo -- Lettre, Guillaume -- Lindblad, Ulf -- Lyon, Helen N -- Melander, Olle -- Newton-Cheh, Christopher -- Nilsson, Peter -- Orho-Melander, Marju -- Rastam, Lennart -- Speliotes, Elizabeth K -- Taskinen, Marja-Riitta -- Tuomi, Tiinamaija -- Guiducci, Candace -- Berglund, Anna -- Carlson, Joyce -- Gianniny, Lauren -- Hackett, Rachel -- Hall, Liselotte -- Holmkvist, Johan -- Laurila, Esa -- Sjogren, Marketa -- Sterner, Maria -- Surti, Aarti -- Svensson, Margareta -- Svensson, Malin -- Tewhey, Ryan -- Blumenstiel, Brendan -- Parkin, Melissa -- Defelice, Matthew -- Barry, Rachel -- Brodeur, Wendy -- Camarata, Jody -- Chia, Nancy -- Fava, Mary -- Gibbons, John -- Handsaker, Bob -- Healy, Claire -- Nguyen, Kieu -- Gates, Casey -- Sougnez, Carrie -- Gage, Diane -- Nizzari, Marcia -- Gabriel, Stacey B -- Chirn, Gung-Wei -- Ma, Qicheng -- Parikh, Hemang -- Richardson, Delwood -- Ricke, Darrell -- Purcell, Shaun -- F32 DK079466/DK/NIDDK NIH HHS/ -- F32 DK079466-01/DK/NIDDK NIH HHS/ -- K23 DK067288/DK/NIDDK NIH HHS/ -- K23 DK080145/DK/NIDDK NIH HHS/ -- K23 DK080145-01/DK/NIDDK NIH HHS/ -- K23 DK65978-04/DK/NIDDK NIH HHS/ -- K23-HL083102/HL/NHLBI NIH HHS/ -- U01 HG004171/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1331-6. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Harvard and Massachusetts Institute of Technology (MIT), Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463246" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics ; Aged ; Alleles ; Blood Glucose/analysis ; Case-Control Studies ; Chromosome Mapping ; Chromosomes, Human, Pair 9/genetics ; Diabetes Mellitus, Type 2/*genetics ; Female ; Genetic Markers ; *Genetic Predisposition to Disease ; *Genome, Human ; Genotype ; Haplotypes ; Humans ; Insulin Resistance/genetics ; Insulin-Like Growth Factor Binding Proteins/genetics ; Introns ; Male ; Meta-Analysis as Topic ; Middle Aged ; *Polymorphism, Single Nucleotide ; Quantitative Trait, Heritable ; Triglycerides/*blood
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
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    Neural mechanisms of a genome-wide supported psychosis variant (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: Schizophrenia is a devastating, highly heritable brain disorder of unknown etiology. Recently, the first common genetic variant associated on a genome-wide level with schizophrenia and possibly bipolar disorder was discovered in ZNF804A (rs1344706). We show, by using an imaging genetics approach, that healthy carriers of rs1344706 risk genotypes exhibit no changes in regional activity but pronounced gene dosage-dependent alterations in functional coupling (correlated activity) of dorsolateral prefrontal cortex (DLPFC) across hemispheres and with hippocampus, mirroring findings in patients, and abnormal coupling of amygdala. Our findings establish disturbed connectivity as a neurogenetic risk mechanism for psychosis supported by genome-wide association, show that rs1344706 or variation in linkage disequilibrium is functional in human brain, and validate the intermediate phenotype strategy in psychiatry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esslinger, Christine -- Walter, Henrik -- Kirsch, Peter -- Erk, Susanne -- Schnell, Knut -- Arnold, Claudia -- Haddad, Leila -- Mier, Daniela -- Opitz von Boberfeld, Carola -- Raab, Kyeon -- Witt, Stephanie H -- Rietschel, Marcella -- Cichon, Sven -- Meyer-Lindenberg, Andreas -- New York, N.Y. -- Science. 2009 May 1;324(5927):605. doi: 10.1126/science.1167768.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, University of Heidelberg, J5, 68159 Mannheim, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407193" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Affective Symptoms/genetics/physiopathology ; Bipolar Disorder/genetics/physiopathology ; Brain Mapping ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Hippocampus/*physiology ; Humans ; Kruppel-Like Transcription Factors/*genetics ; Magnetic Resonance Imaging ; Male ; Mental Processes ; Phenotype ; *Polymorphism, Single Nucleotide ; Prefrontal Cortex/*physiology ; Schizophrenia/*genetics/physiopathology
    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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  • 10
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    Cyclooxygenase-2 controls energy homeostasis in mice by de novo recruitment of brown adipocytes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: Obesity results from chronic energy surplus and excess lipid storage in white adipose tissue (WAT). In contrast, brown adipose tissue (BAT) efficiently burns lipids through adaptive thermogenesis. Studying mouse models, we show that cyclooxygenase (COX)-2, a rate-limiting enzyme in prostaglandin (PG) synthesis, is a downstream effector of beta-adrenergic signaling in WAT and is required for the induction of BAT in WAT depots. PG shifted the differentiation of defined mesenchymal progenitors toward a brown adipocyte phenotype. Overexpression of COX-2 in WAT induced de novo BAT recruitment in WAT, increased systemic energy expenditure, and protected mice against high-fat diet-induced obesity. Thus, COX-2 appears integral to de novo BAT recruitment, which suggests that the PG pathway regulates systemic energy homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vegiopoulos, Alexandros -- Muller-Decker, Karin -- Strzoda, Daniela -- Schmitt, Iris -- Chichelnitskiy, Evgeny -- Ostertag, Anke -- Berriel Diaz, Mauricio -- Rozman, Jan -- Hrabe de Angelis, Martin -- Nusing, Rolf M -- Meyer, Carola W -- Wahli, Walter -- Klingenspor, Martin -- Herzig, Stephan -- New York, N.Y. -- Science. 2010 May 28;328(5982):1158-61. doi: 10.1126/science.1186034. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emmy Noether and Marie Curie Research Group Molecular Metabolic Control, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448152" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes, Brown/cytology/*physiology ; Adipogenesis ; Adipose Tissue ; Adipose Tissue, Brown/cytology/*physiology ; Adipose Tissue, White/enzymology/*physiology ; Adrenergic beta-3 Receptor Agonists ; Adrenergic beta-Agonists/pharmacology ; Animals ; Body Weight ; Cyclooxygenase 2/*genetics/*metabolism ; Dietary Fats/administration & dosage ; Dioxoles/pharmacology ; *Energy Metabolism ; Female ; Gene Expression Regulation, Enzymologic ; Homeostasis ; Male ; Mesenchymal Stromal Cells/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mice, Transgenic ; Norepinephrine/metabolism ; Obesity/etiology/prevention & control ; Oxygen Consumption ; Prostaglandins/*metabolism ; Receptors, Adrenergic, beta-3/metabolism ; Signal Transduction ; *Thermogenesis
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