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  • 1
    Publication Date: 2001-09-05
    Description: The coagulation protease thrombin triggers fibrin formation, platelet activation, and other cellular responses at sites of tissue injury. We report a role for PAR1, a protease-activated G protein-coupled receptor for thrombin, in embryonic development. Approximately half of Par1-/- mouse embryos died at midgestation with bleeding from multiple sites. PAR1 is expressed in endothelial cells, and a PAR1 transgene driven by an endothelial-specific promoter prevented death of Par1-/- embryos. Our results suggest that the coagulation cascade and PAR1 modulate endothelial cell function in developing blood vessels and that thrombin's actions on endothelial cells-rather than on platelets, mesenchymal cells, or fibrinogen-contribute to vascular development and hemostasis in the mouse embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffin, C T -- Srinivasan, Y -- Zheng, Y W -- Huang, W -- Coughlin, S R -- HL44907/HL/NHLBI NIH HHS/ -- HL65590/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2001 Aug 31;293(5535):1666-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Institute, University of California at San Francisco (UCSF), San Francisco, California 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11533492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Coagulation ; Blood Coagulation Factors/physiology ; Blood Vessels/*embryology/metabolism ; Calcium/metabolism ; Crosses, Genetic ; *Embryonic and Fetal Development ; Endocardium/embryology/metabolism ; Endothelium, Vascular/cytology/*embryology/metabolism ; Factor V/genetics/physiology ; Female ; Fibrinogen/genetics/physiology ; Fibroblasts/metabolism ; Hemorrhage/embryology ; Hemostasis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Transgenic ; *Neovascularization, Physiologic ; Phenotype ; Prothrombin/genetics/physiology ; Receptor, PAR-1 ; Receptors, Thrombin/deficiency/genetics/*physiology ; *Signal Transduction ; Thrombin/physiology ; Thromboplastin/genetics/physiology
    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: 2001-05-12
    Description: To test the hypotheses of modern human origin in East Asia, we sampled 12,127 male individuals from 163 populations and typed for three Y chromosome biallelic markers (YAP, M89, and M130). All the individuals carried a mutation at one of the three sites. These three mutations (YAP+, M89T, and M130T) coalesce to another mutation (M168T), which originated in Africa about 35,000 to 89,000 years ago. Therefore, the data do not support even a minimal in situ hominid contribution in the origin of anatomically modern humans in East Asia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ke, Y -- Su, B -- Song, X -- Lu, D -- Chen, L -- Li, H -- Qi, C -- Marzuki, S -- Deka, R -- Underhill, P -- Xiao, C -- Shriver, M -- Lell, J -- Wallace, D -- Wells, R S -- Seielstad, M -- Oefner, P -- Zhu, D -- Jin, J -- Huang, W -- Chakraborty, R -- Chen, Z -- Jin, L -- New York, N.Y. -- Science. 2001 May 11;292(5519):1151-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, 220 Handan Road, Shanghai, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11349147" target="_blank"〉PubMed〈/a〉
    Keywords: Africa/ethnology ; Alleles ; Asia ; Female ; Gene Frequency/genetics ; Haplotypes/genetics ; Humans ; Male ; Mutation/genetics ; Pacific Islands ; *Phylogeny ; Polymorphism, Genetic/genetics ; Population Density ; Y Chromosome/*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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  • 3
    Publication Date: 2003-01-11
    Description: Atrial fibrillation (AF) is a common cardiac arrhythmia whose molecular etiology is poorly understood. We studied a family with hereditary persistent AF and identified the causative mutation (S140G) in the KCNQ1 (KvLQT1) gene on chromosome 11p15.5. The KCNQ1 gene encodes the pore-forming alpha subunit of the cardiac I(Ks) channel (KCNQ1/KCNE1), the KCNQ1/KCNE2 and the KCNQ1/KCNE3 potassium channels. Functional analysis of the S140G mutant revealed a gain-of-function effect on the KCNQ1/KCNE1 and the KCNQ1/KCNE2 currents, which contrasts with the dominant negative or loss-of-function effects of the KCNQ1 mutations previously identified in patients with long QT syndrome. Thus, the S140G mutation is likely to initiate and maintain AF by reducing action potential duration and effective refractory period in atrial myocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Yi-Han -- Xu, Shi-Jie -- Bendahhou, Said -- Wang, Xiao-Liang -- Wang, Ying -- Xu, Wen-Yuan -- Jin, Hong-Wei -- Sun, Hao -- Su, Xiao-Yan -- Zhuang, Qi-Nan -- Yang, Yi-Qing -- Li, Yue-Bin -- Liu, Yi -- Xu, Hong-Ju -- Li, Xiao-Fei -- Ma, Ning -- Mou, Chun-Ping -- Chen, Zhu -- Barhanin, Jacques -- Huang, Wei -- New York, N.Y. -- Science. 2003 Jan 10;299(5604):251-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Tongji Hospital, and Institute of Medical Genetics, Tongji University, 399 Xin Cun Road, Shanghai 200065, People's Republic of China. drchen@public7.sta.net.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522251" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Adolescent ; Adult ; Aged ; Animals ; Atrial Fibrillation/*genetics/physiopathology ; COS Cells ; Child ; China ; Chromosomes, Human, Pair 11/genetics ; Electrocardiography ; Female ; Haplotypes ; Heart Atria/physiopathology ; Heart Ventricles/physiopathology ; Humans ; KCNQ Potassium Channels ; KCNQ1 Potassium Channel ; Lod Score ; Long QT Syndrome/genetics/physiopathology ; Male ; Microsatellite Repeats ; Middle Aged ; Mutation ; *Mutation, Missense ; Myocytes, Cardiac/*physiology ; Patch-Clamp Techniques ; Pedigree ; Potassium Channels/*genetics/physiology ; *Potassium Channels, Voltage-Gated
    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
    Publication Date: 2015-12-18
    Description: T helper 17 (TH17) lymphocytes protect mucosal barriers from infections, but also contribute to multiple chronic inflammatory diseases. Their differentiation is controlled by RORgammat, a ligand-regulated nuclear receptor. Here we identify the RNA helicase DEAD-box protein 5 (DDX5) as a RORgammat partner that coordinates transcription of selective TH17 genes, and is required for TH17-mediated inflammatory pathologies. Surprisingly, the ability of DDX5 to interact with RORgammat and coactivate its targets depends on intrinsic RNA helicase activity and binding of a conserved nuclear long noncoding RNA (lncRNA), Rmrp, which is mutated in patients with cartilage-hair hypoplasia. A targeted Rmrp gene mutation in mice, corresponding to a gene mutation in cartilage-hair hypoplasia patients, altered lncRNA chromatin occupancy, and reduced the DDX5-RORgammat interaction and RORgammat target gene transcription. Elucidation of the link between Rmrp and the DDX5-RORgammat complex reveals a role for RNA helicases and lncRNAs in tissue-specific transcriptional regulation, and provides new opportunities for therapeutic intervention in TH17-dependent diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762670/" 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/PMC4762670/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Wendy -- Thomas, Benjamin -- Flynn, Ryan A -- Gavzy, Samuel J -- Wu, Lin -- Kim, Sangwon V -- Hall, Jason A -- Miraldi, Emily R -- Ng, Charles P -- Rigo, Frank W -- Meadows, Sarah -- Montoya, Nina R -- Herrera, Natalia G -- Domingos, Ana I -- Rastinejad, Fraydoon -- Myers, Richard M -- Fuller-Pace, Frances V -- Bonneau, Richard -- Chang, Howard Y -- Acuto, Oreste -- Littman, Dan R -- 1F30CA189514-01/CA/NCI NIH HHS/ -- F30 CA189514/CA/NCI NIH HHS/ -- P50 HG007735/HG/NHGRI NIH HHS/ -- P50-HG007735/HG/NHGRI NIH HHS/ -- R01 AI080885/AI/NIAID NIH HHS/ -- R01 AI121436/AI/NIAID NIH HHS/ -- R01 DK103358/DK/NIDDK NIH HHS/ -- R01 HG004361/HG/NHGRI NIH HHS/ -- R01AI080885/AI/NIAID NIH HHS/ -- R01DK103358/DK/NIDDK NIH HHS/ -- R01HG004361/HG/NHGRI NIH HHS/ -- T32 AI100853/AI/NIAID NIH HHS/ -- T32 CA009161/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Dec 24;528(7583):517-22. doi: 10.1038/nature16193. Epub 2015 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA. ; Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK. ; Center for Personal Dynamic Regulomes, Stanford University, Stanford, California 94305, USA. ; Center for Genomics and Systems Biology, Department of Biology, New York University, New York, New York 10003, USA. ; Courant Institute of Mathematical Sciences, Computer Science Department, New York University, New York, New York 10012, USA. ; Simons Center for Data Analysis, Simons Foundation, New York, New York 10010, USA. ; Isis Pharmaceuticals, Carlsbad, California 92010, USA. ; HudsonAlpha Institute for Biotechnology, Huntsville, Alabama 35806, USA. ; Instituto Gulbenkian de Ciencia, Oeiras 2780-156, Portugal. ; Integrative Metabolism Program, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida 32827, USA. ; Division of Cancer Research, University of Dundee, Dundee DD1 9SY, UK. ; Howard Hughes Medical Institute, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26675721" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/genetics/metabolism ; DEAD-box RNA Helicases/genetics/*metabolism ; Female ; Gene Expression Regulation/genetics ; Hair/abnormalities ; Hirschsprung Disease/genetics ; Humans ; Immunologic Deficiency Syndromes/genetics ; Inflammation/immunology/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mutation/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Organ Specificity ; Osteochondrodysplasias/congenital/genetics ; Protein Binding ; RNA, Long Noncoding/genetics/*metabolism ; Th17 Cells/*immunology/*metabolism ; Transcription, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-10-16
    Description: Ventral tegmental area (VTA) dopamine neurons have important roles in adaptive and pathological brain functions related to reward and motivation. However, it is unknown whether subpopulations of VTA dopamine neurons participate in distinct circuits that encode different motivational signatures, and whether inputs to the VTA differentially modulate such circuits. Here we show that, because of differences in synaptic connectivity, activation of inputs to the VTA from the laterodorsal tegmentum and the lateral habenula elicit reward and aversion in mice, respectively. Laterodorsal tegmentum neurons preferentially synapse on dopamine neurons projecting to the nucleus accumbens lateral shell, whereas lateral habenula neurons synapse primarily on dopamine neurons projecting to the medial prefrontal cortex as well as on GABAergic (gamma-aminobutyric-acid-containing) neurons in the rostromedial tegmental nucleus. These results establish that distinct VTA circuits generate reward and aversion, and thereby provide a new framework for understanding the circuit basis of adaptive and pathological motivated behaviours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493743/" 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/PMC3493743/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lammel, Stephan -- Lim, Byung Kook -- Ran, Chen -- Huang, Kee Wui -- Betley, Michael J -- Tye, Kay M -- Deisseroth, Karl -- Malenka, Robert C -- NS069375/NS/NINDS NIH HHS/ -- P50 MH086403/MH/NIMH NIH HHS/ -- England -- Nature. 2012 Nov 8;491(7423):212-7. doi: 10.1038/nature11527. Epub 2012 Oct 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 265 Campus Drive, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23064228" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning/drug effects/*physiology ; Axons/metabolism ; Dopamine/metabolism ; Dopamine Antagonists/pharmacology ; Dopaminergic Neurons/metabolism ; GABAergic Neurons/metabolism ; Habenula/cytology/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Neural Pathways/*physiology ; Receptors, Dopamine/metabolism ; *Reward ; Synapses/metabolism ; Ventral Tegmental Area/cytology/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2013-09-13
    Description: Social behaviours in species as diverse as honey bees and humans promote group survival but often come at some cost to the individual. Although reinforcement of adaptive social interactions is ostensibly required for the evolutionary persistence of these behaviours, the neural mechanisms by which social reward is encoded by the brain are largely unknown. Here we demonstrate that in mice oxytocin acts as a social reinforcement signal within the nucleus accumbens core, where it elicits a presynaptically expressed long-term depression of excitatory synaptic transmission in medium spiny neurons. Although the nucleus accumbens receives oxytocin-receptor-containing inputs from several brain regions, genetic deletion of these receptors specifically from dorsal raphe nucleus, which provides serotonergic (5-hydroxytryptamine; 5-HT) innervation to the nucleus accumbens, abolishes the reinforcing properties of social interaction. Furthermore, oxytocin-induced synaptic plasticity requires activation of nucleus accumbens 5-HT1B receptors, the blockade of which prevents social reward. These results demonstrate that the rewarding properties of social interaction in mice require the coordinated activity of oxytocin and 5-HT in the nucleus accumbens, a mechanistic insight with implications for understanding the pathogenesis of social dysfunction in neuropsychiatric disorders such as autism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4091761/" 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/PMC4091761/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dolen, Gul -- Darvishzadeh, Ayeh -- Huang, Kee Wui -- Malenka, Robert C -- NS069375/NS/NINDS NIH HHS/ -- P01 DA008227/DA/NIDA NIH HHS/ -- P30 NS069375/NS/NINDS NIH HHS/ -- R21 DA032955/DA/NIDA NIH HHS/ -- England -- Nature. 2013 Sep 12;501(7466):179-84. doi: 10.1038/nature12518.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 265 Campus Drive, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24025838" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/physiopathology ; Conditioning (Psychology) ; Female ; Gene Deletion ; Long-Term Synaptic Depression ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Neurons/metabolism ; Nucleus Accumbens/cytology/*metabolism ; Oxytocin/deficiency/genetics/*metabolism ; Presynaptic Terminals/metabolism ; Raphe Nuclei/metabolism ; Receptor, Serotonin, 5-HT1B/metabolism ; Receptors, Oxytocin/deficiency/genetics/metabolism ; *Reward ; Serotonin/*metabolism ; *Social Behavior ; Synaptic Transmission
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-23
    Description: During tactile learning there is a transformation in the way the primary somatosensory cortex integrates, represents, and distributes information from the skin. To define this transformation, the site of earliest modification has been identified in rat somatosensory cortex after a change in sensory experience. Afferent activity was manipulated by clipping all except two whiskers on one side of the snout ("whisker pairing"), and the receptive fields of neurons at different cortical depths were mapped 24 hours later. Neurons in layer IV, the target of the primary thalamic pathway, were unaltered, whereas neurons located above and below layer IV showed significant changes. These changes were similar to those that occur in layer IV after longer periods of whisker pairing. The findings support the hypothesis that the layers of cortex contribute differently to plasticity. Neurons in the supragranular and infragranular layers respond rapidly to changes in sensory experience and may contribute to subsequent modification in layer IV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diamond, M E -- Huang, W -- Ebner, F F -- NS-25907/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1885-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Sciences and Biomedical Technologies, University of Udine, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091215" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Afferent Pathways ; Animals ; Male ; *Neuronal Plasticity ; Neurons, Afferent/*physiology ; Rats ; Somatosensory Cortex/*physiology ; Thalamic Nuclei/physiology ; Vibrissae/*innervation
    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
    Publication Date: 2015-11-07
    Description: The mammalian transcription factors CLOCK and BMAL1 are essential components of the molecular clock that coordinate behavior and metabolism with the solar cycle. Genetic or environmental perturbation of circadian cycles contributes to metabolic disorders including type 2 diabetes. To study the impact of the cell-autonomous clock on pancreatic beta cell function, we examined pancreatic islets from mice with either intact or disrupted BMAL1 expression both throughout life and limited to adulthood. We found pronounced oscillation of insulin secretion that was synchronized with the expression of genes encoding secretory machinery and signaling factors that regulate insulin release. CLOCK/BMAL1 colocalized with the pancreatic transcription factor PDX1 within active enhancers distinct from those controlling rhythmic metabolic gene networks in liver. We also found that beta cell clock ablation in adult mice caused severe glucose intolerance. Thus, cell type-specific enhancers underlie the circadian control of peripheral metabolism throughout life and may help to explain its dysregulation in diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4669216/" 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/PMC4669216/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perelis, Mark -- Marcheva, Biliana -- Ramsey, Kathryn Moynihan -- Schipma, Matthew J -- Hutchison, Alan L -- Taguchi, Akihiko -- Peek, Clara Bien -- Hong, Heekyung -- Huang, Wenyu -- Omura, Chiaki -- Allred, Amanda L -- Bradfield, Christopher A -- Dinner, Aaron R -- Barish, Grant D -- Bass, Joseph -- ES05703/ES/NIEHS NIH HHS/ -- K01 DK105137/DK/NIDDK NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- P01AG011412/AG/NIA NIH HHS/ -- P60 DK020595/DK/NIDDK NIH HHS/ -- P60DK020595/DK/NIDDK NIH HHS/ -- R01 DK090625/DK/NIDDK NIH HHS/ -- R01 ES005703/ES/NIEHS NIH HHS/ -- R01DK090625/DK/NIDDK NIH HHS/ -- T32 DK007169/DK/NIDDK NIH HHS/ -- T32 GM007281/GM/NIGMS NIH HHS/ -- T32 HL007909/HL/NHLBI NIH HHS/ -- T32GM07281/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Nov 6;350(6261):aac4250. doi: 10.1126/science.aac4250.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. ; Center for Genetic Medicine, Northwestern University, Chicago, IL 60611, USA. ; Medical Scientist Training Program, University of Chicago, Chicago, IL 60637, USA. Graduate Program in the Biophysical Sciences, University of Chicago, Chicago, IL 60637, USA. James Franck Institute, University of Chicago, Chicago, IL 60637, USA. ; McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI 52705, USA. ; Graduate Program in the Biophysical Sciences, University of Chicago, Chicago, IL 60637, USA. James Franck Institute, University of Chicago, Chicago, IL 60637, USA. Department of Chemistry, University of Chicago, Chicago, IL 60637, USA. ; Department of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. j-bass@northwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26542580" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics/metabolism ; Animals ; CLOCK Proteins/metabolism ; Circadian Rhythm/*genetics ; Diabetes Mellitus, Type 2/genetics/metabolism ; Enhancer Elements, Genetic/*physiology ; Exocytosis/genetics ; *Gene Expression Regulation ; Glucose Intolerance ; Homeodomain Proteins/metabolism ; Humans ; Insulin/*secretion ; Insulin-Secreting Cells/*secretion ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Trans-Activators/metabolism ; Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2015-05-23
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4684952/" 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/PMC4684952/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Jieqi -- Wegener, Jan Eike -- Huang, Teng-Wei -- Sripathy, Smitha -- De Jesus-Cortes, Hector -- Xu, Pin -- Tran, Stephanie -- Knobbe, Whitney -- Leko, Vid -- Britt, Jeremiah -- Starwalt, Ruth -- McDaniel, Latisha -- Ward, Chris S -- Parra, Diana -- Newcomb, Benjamin -- Lao, Uyen -- Nourigat, Cynthia -- Flowers, David A -- Cullen, Sean -- Jorstad, Nikolas L -- Yang, Yue -- Glaskova, Lena -- Vingeau, Sebastien -- Kozlitina, Julia -- Yetman, Michael J -- Jankowsky, Joanna L -- Reichardt, Sybille D -- Reichardt, Holger M -- Gartner, Jutta -- Bartolomei, Marisa S -- Fang, Min -- Loeb, Keith -- Keene, C Dirk -- Bernstein, Irwin -- Goodell, Margaret -- Brat, Daniel J -- Huppke, Peter -- Neul, Jeffrey L -- Bedalov, Antonio -- Pieper, Andrew A -- P30 AI036211/AI/NIAID NIH HHS/ -- P30 CA138292/CA/NCI NIH HHS/ -- P30 ES005605/ES/NIEHS NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- R01 AG031892/AG/NIA NIH HHS/ -- R01 HD062553/HD/NICHD NIH HHS/ -- S10 RR024574/RR/NCRR NIH HHS/ -- T32 AG000183/AG/NIA NIH HHS/ -- T32 HL092332/HL/NHLBI NIH HHS/ -- U01 HL100395/HL/NHLBI NIH HHS/ -- U54 HD083092/HD/NICHD NIH HHS/ -- England -- Nature. 2015 May 21;521(7552):E1-4. doi: 10.1038/nature14444.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Pediatrics and Adolescent Medicine, Division of Pediatric Neurology, University Medical Center Gottingen, Robert-Koch-Strasse 40, 37075 Gottingen, Germany. ; 1] Jan and Dan Duncan Neurological Research Institute (Texas Children's Hospital), Baylor College of Medicine, Houston, Texas 77030, USA [2] Program in Developmental Biology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; 1] Graduate Program of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2] Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA. ; Graduate Program of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA. ; Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Jan and Dan Duncan Neurological Research Institute (Texas Children's Hospital), Baylor College of Medicine, Houston, Texas 77030, USA. ; Program in Developmental Biology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98195, USA. ; Department of Cell &Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA. ; Institute for Cellular and Molecular Immunology; University of Gottingen Medical School, Humboldtallee 34, 37073 Gottingen, Germany. ; 1] Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA [2] Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98195, USA. ; 1] Program in Developmental Biology, Baylor College of Medicine, Houston, Texas 77030, USA [2] Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030, USA [3] Center for Cell and Gene Therapy, Baylor College of Medicine, Houston, Texas 77030, USA [4] Stem Cell and Regenerative Medicine Center, Baylor College of Medicine, Houston, Texas 77030, USA [5] Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA [6] Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA. ; 1] Jan and Dan Duncan Neurological Research Institute (Texas Children's Hospital), Baylor College of Medicine, Houston, Texas 77030, USA [2] Program in Developmental Biology, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA [4] Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030, USA [5] Stem Cell and Regenerative Medicine Center, Baylor College of Medicine, Houston, Texas 77030, USA [6] Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA. ; 1] Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA [2] Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98105, USA. ; 1] Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA [2] Department of Neurology, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA [3] Veterans Affairs, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA [4] Weill Cornell Autism Research Program, Weill Cornell Medical College, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25993969" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Disease Progression ; Female ; Male ; Methyl-CpG-Binding Protein 2/*metabolism ; Microglia/*cytology/*physiology ; Rett Syndrome/*pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2016-03-05
    Description: Observing marine mammal (MM) populations continuously in time and space over the immense ocean areas they inhabit is challenging but essential for gathering an unambiguous record of their distribution, as well as understanding their behaviour and interaction with prey species. Here we use passive ocean acoustic waveguide remote sensing (POAWRS) in an important North Atlantic feeding ground to instantaneously detect, localize and classify MM vocalizations from diverse species over an approximately 100,000 km(2) region. More than eight species of vocal MMs are found to spatially converge on fish spawning areas containing massive densely populated herring shoals at night-time and diffuse herring distributions during daytime. We find the vocal MMs divide the enormous fish prey field into species-specific foraging areas with varying degrees of spatial overlap, maintained for at least two weeks of the herring spawning period. The recorded vocalization rates are diel (24 h)-dependent for all MM species, with some significantly more vocal at night and others more vocal during the day. The four key baleen whale species of the region: fin, humpback, blue and minke have vocalization rate trends that are highly correlated to trends in fish shoaling density and to each other over the diel cycle. These results reveal the temporospatial dynamics of combined multi-species MM foraging activities in the vicinity of an extensive fish prey field that forms a massive ecological hotspot, and would be unattainable with conventional methodologies. Understanding MM behaviour and distributions is essential for management of marine ecosystems and for accessing anthropogenic impacts on these protected marine species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Delin -- Garcia, Heriberto -- Huang, Wei -- Tran, Duong D -- Jain, Ankita D -- Yi, Dong Hoon -- Gong, Zheng -- Jech, J Michael -- Godo, Olav Rune -- Makris, Nicholas C -- Ratilal, Purnima -- England -- Nature. 2016 Mar 17;531(7594):366-70. doi: 10.1038/nature16960. Epub 2016 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Ocean Acoustics and Ecosystem Sensing, Northeastern University, 360 Huntington Avenue, Boston, Massachusetts 02115, USA. ; Laboratory for Undersea Remote Sensing, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA. ; Northeast Fisheries Science Center, 166 Water Street, Woods Hole, Massachusetts 02543, USA. ; Institute of Marine Research, Post Office Box 1870, Nordnes, N-5817 Bergen, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934221" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustics ; Animals ; Aquatic Organisms/*physiology ; Atlantic Ocean ; Diet/veterinary ; Ecosystem ; *Feeding Behavior ; Fishes/*physiology ; Male ; Mammals/*physiology ; *Predatory Behavior ; Time Factors ; *Vocalization, Animal ; Whales/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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