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  • Articles  (251)
  • Female  (251)
  • American Association for the Advancement of Science (AAAS)  (251)
  • Blackwell Publishing Ltd
  • Institute of Physics
  • 2005-2009  (251)
  • Medicine  (251)
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  • Articles  (251)
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  • 11
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    An integrated genomic analysis of human glioblastoma multiforme (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: Glioblastoma multiforme (GBM) is the most common and lethal type of brain cancer. To identify the genetic alterations in GBMs, we sequenced 20,661 protein coding genes, determined the presence of amplifications and deletions using high-density oligonucleotide arrays, and performed gene expression analyses using next-generation sequencing technologies in 22 human tumor samples. This comprehensive analysis led to the discovery of a variety of genes that were not known to be altered in GBMs. Most notably, we found recurrent mutations in the active site of isocitrate dehydrogenase 1 (IDH1) in 12% of GBM patients. Mutations in IDH1 occurred in a large fraction of young patients and in most patients with secondary GBMs and were associated with an increase in overall survival. These studies demonstrate the value of unbiased genomic analyses in the characterization of human brain cancer and identify a potentially useful genetic alteration for the classification and targeted therapy of GBMs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820389/" 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/PMC2820389/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parsons, D Williams -- Jones, Sian -- Zhang, Xiaosong -- Lin, Jimmy Cheng-Ho -- Leary, Rebecca J -- Angenendt, Philipp -- Mankoo, Parminder -- Carter, Hannah -- Siu, I-Mei -- Gallia, Gary L -- Olivi, Alessandro -- McLendon, Roger -- Rasheed, B Ahmed -- Keir, Stephen -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Busam, Dana A -- Tekleab, Hanna -- Diaz, Luis A Jr -- Hartigan, James -- Smith, Doug R -- Strausberg, Robert L -- Marie, Suely Kazue Nagahashi -- Shinjo, Sueli Mieko Oba -- Yan, Hai -- Riggins, Gregory J -- Bigner, Darell D -- Karchin, Rachel -- Papadopoulos, Nick -- Parmigiani, Giovanni -- Vogelstein, Bert -- Velculescu, Victor E -- Kinzler, Kenneth W -- 5P50-NS-20023/NS/NINDS NIH HHS/ -- CA09547/CA/NCI NIH HHS/ -- CA108786/CA/NCI NIH HHS/ -- CA11898/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- NS052507/NS/NINDS NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- P50 CA062924-160017/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-04/CA/NCI NIH HHS/ -- R01 CA140316/CA/NCI NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA043460-27/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-13/CA/NCI NIH HHS/ -- R37 CA057345-17/CA/NCI NIH HHS/ -- R37 CA057345-18/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 26;321(5897):1807-12. doi: 10.1126/science.1164382. Epub 2008 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics, and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772396" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Neoplasms/*genetics/mortality ; Female ; Gene Amplification ; Gene Dosage ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genome, Human ; Glioblastoma/*genetics/mortality ; Humans ; Isocitrate Dehydrogenase/chemistry/*genetics ; Male ; Middle Aged ; *Mutation ; Mutation, Missense ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA ; Signal Transduction ; Survival Rate
    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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  • 12
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    Ribosomal protein S6 kinase 1 signaling regulates mammalian life span (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 13
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    A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-17
    Description: Obesity is a serious international health problem that increases the risk of several common diseases. The genetic factors predisposing to obesity are poorly understood. A genome-wide search for type 2 diabetes-susceptibility genes identified a common variant in the FTO (fat mass and obesity associated) gene that predisposes to diabetes through an effect on body mass index (BMI). An additive association of the variant with BMI was replicated in 13 cohorts with 38,759 participants. The 16% of adults who are homozygous for the risk allele weighed about 3 kilograms more and had 1.67-fold increased odds of obesity when compared with those not inheriting a risk allele. This association was observed from age 7 years upward and reflects a specific increase in fat mass.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646098/" 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/PMC2646098/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frayling, Timothy M -- Timpson, Nicholas J -- Weedon, Michael N -- Zeggini, Eleftheria -- Freathy, Rachel M -- Lindgren, Cecilia M -- Perry, John R B -- Elliott, Katherine S -- Lango, Hana -- Rayner, Nigel W -- Shields, Beverley -- Harries, Lorna W -- Barrett, Jeffrey C -- Ellard, Sian -- Groves, Christopher J -- Knight, Bridget -- Patch, Ann-Marie -- Ness, Andrew R -- Ebrahim, Shah -- Lawlor, Debbie A -- Ring, Susan M -- Ben-Shlomo, Yoav -- Jarvelin, Marjo-Riitta -- Sovio, Ulla -- Bennett, Amanda J -- Melzer, David -- Ferrucci, Luigi -- Loos, Ruth J F -- Barroso, Ines -- Wareham, Nicholas J -- Karpe, Fredrik -- Owen, Katharine R -- Cardon, Lon R -- Walker, Mark -- Hitman, Graham A -- Palmer, Colin N A -- Doney, Alex S F -- Morris, Andrew D -- Smith, George Davey -- Hattersley, Andrew T -- McCarthy, Mark I -- 079557/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- G0000934/Medical Research Council/United Kingdom -- G0500070/Medical Research Council/United Kingdom -- G0600705/Medical Research Council/United Kingdom -- G9815508/Medical Research Council/United Kingdom -- MC_U106179471/Medical Research Council/United Kingdom -- MC_U106188470/Medical Research Council/United Kingdom -- Z99 AG999999/Intramural NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 May 11;316(5826):889-94. Epub 2007 Apr 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics of Complex Traits, Institute of Biomedical and Clinical Science, Peninsula Medical School, Magdalen Road, Exeter, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17434869" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Adolescent ; Adult ; Aged ; Alleles ; Birth Weight ; *Body Mass Index ; Case-Control Studies ; Child ; Cohort Studies ; Diabetes Mellitus, Type 2/*genetics ; Female ; *Genetic Predisposition to Disease ; Great Britain ; Homozygote ; Humans ; Infant, Newborn ; Male ; Middle Aged ; Obesity/*genetics ; Overweight/genetics ; *Polymorphism, Single Nucleotide
    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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  • 14
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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
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Whither or wither microbicides? (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-26
    Description: After disappointing results from all efficacy trials conducted to date, the field of microbicides research now faces substantial challenges. Poor coordination among interested parties and the choice of nonvalidated scientific targets for phase III studies have hampered progress and created mistrust about the use of microbicides as a method to prevent HIV-1 sexual transmission. Although new promising strategies are available, there will need to be serious reappraisals of how decisions are made to advance the next generations of candidates into clinical trials, and the use of appropriate animal models in this process will be critical.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835691/" 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/PMC2835691/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grant, Robert M -- Hamer, Dean -- Hope, Thomas -- Johnston, Rowena -- Lange, Joep -- Lederman, Michael M -- Lieberman, Judy -- Miller, Christopher J -- Moore, John P -- Mosier, Donald E -- Richman, Douglas D -- Schooley, Robert T -- Springer, Marty S -- Veazey, Ronald S -- Wainberg, Mark A -- U19 AI076981/AI/NIAID NIH HHS/ -- U19 AI076981-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Jul 25;321(5888):532-4. doi: 10.1126/science.1160355.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉J. David Gladstone Institutes, University of California-San Francisco, San Francisco, CA 94518, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18653884" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Intravaginal ; Animals ; Anti-HIV Agents/*administration & dosage/pharmacology/therapeutic use ; Anti-Infective Agents, Local/*administration & dosage/pharmacology/therapeutic ; use ; Clinical Trials as Topic ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Drug Therapy, Combination ; Female ; HIV Infections/drug therapy/*prevention & control/transmission ; HIV-1/*drug effects ; Humans ; Male ; Patient Compliance ; Polymers/*administration & dosage/pharmacology/therapeutic use ; Primates ; Reverse Transcriptase Inhibitors/*administration & ; dosage/pharmacology/therapeutic use ; Vaginal Diseases/drug therapy/*prevention & control
    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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  • 16
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    Disruption of the CFTR gene produces a model of cystic fibrosis in newborn pigs (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-27
    Description: Almost two decades after CFTR was identified as the gene responsible for cystic fibrosis (CF), we still lack answers to many questions about the pathogenesis of the disease, and it remains incurable. Mice with a disrupted CFTR gene have greatly facilitated CF studies, but the mutant mice do not develop the characteristic manifestations of human CF, including abnormalities of the pancreas, lung, intestine, liver, and other organs. Because pigs share many anatomical and physiological features with humans, we generated pigs with a targeted disruption of both CFTR alleles. Newborn pigs lacking CFTR exhibited defective chloride transport and developed meconium ileus, exocrine pancreatic destruction, and focal biliary cirrhosis, replicating abnormalities seen in newborn humans with CF. The pig model may provide opportunities to address persistent questions about CF pathogenesis and accelerate discovery of strategies for prevention and treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570747/" 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/PMC2570747/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogers, Christopher S -- Stoltz, David A -- Meyerholz, David K -- Ostedgaard, Lynda S -- Rokhlina, Tatiana -- Taft, Peter J -- Rogan, Mark P -- Pezzulo, Alejandro A -- Karp, Philip H -- Itani, Omar A -- Kabel, Amanda C -- Wohlford-Lenane, Christine L -- Davis, Greg J -- Hanfland, Robert A -- Smith, Tony L -- Samuel, Melissa -- Wax, David -- Murphy, Clifton N -- Rieke, August -- Whitworth, Kristin -- Uc, Aliye -- Starner, Timothy D -- Brogden, Kim A -- Shilyansky, Joel -- McCray, Paul B Jr -- Zabner, Joseph -- Prather, Randall S -- Welsh, Michael J -- AI076671/AI/NIAID NIH HHS/ -- DK54759/DK/NIDDK NIH HHS/ -- HL07638/HL/NHLBI NIH HHS/ -- HL51670/HL/NHLBI NIH HHS/ -- K08 AI076671/AI/NIAID NIH HHS/ -- K08 AI076671-01/AI/NIAID NIH HHS/ -- P01 HL051670/HL/NHLBI NIH HHS/ -- P01 HL051670-15/HL/NHLBI NIH HHS/ -- P30 DK054759/DK/NIDDK NIH HHS/ -- P30 DK054759-10/DK/NIDDK NIH HHS/ -- P30 DK054759-109004/DK/NIDDK NIH HHS/ -- R01 DK051315/DK/NIDDK NIH HHS/ -- T32 HL007638/HL/NHLBI NIH HHS/ -- T32 HL007638-23/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 26;321(5897):1837-41. doi: 10.1126/science.1163600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18818360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Chlorides/metabolism ; *Cystic Fibrosis/genetics/pathology/physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator/*genetics/metabolism ; *Disease Models, Animal ; Female ; Gallbladder/pathology ; Ileus/pathology/physiopathology ; Intestines/pathology ; Ion Transport ; Liver/pathology ; Liver Cirrhosis, Biliary/pathology ; Lung/pathology ; Male ; Pancreas, Exocrine/pathology ; Recombination, Genetic ; *Swine
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Neurokinin 1 receptor antagonism as a possible therapy for alcoholism (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-16
    Description: Alcohol dependence is a major public health challenge in need of new treatments. As alcoholism evolves, stress systems in the brain play an increasing role in motivating continued alcohol use and relapse. We investigated the role of the neurokinin 1 receptor (NK1R), a mediator of behavioral stress responses, in alcohol dependence and treatment. In preclinical studies, mice genetically deficient in NK1R showed a marked decrease in voluntary alcohol consumption and had an increased sensitivity to the sedative effects of alcohol. In a randomized controlled experimental study, we treated recently detoxified alcoholic inpatients with an NK1R antagonist (LY686017; n = 25) or placebo (n = 25). LY686017 suppressed spontaneous alcohol cravings, improved overall well-being, blunted cravings induced by a challenge procedure, and attenuated concomitant cortisol responses. Brain functional magnetic resonance imaging responses to affective stimuli likewise suggested beneficial LY686017 effects. Thus, as assessed by these surrogate markers of efficacy, NK1R antagonism warrants further investigation as a treatment in alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉George, David T -- Gilman, Jodi -- Hersh, Jacqueline -- Thorsell, Annika -- Herion, David -- Geyer, Christopher -- Peng, Xiaomei -- Kielbasa, William -- Rawlings, Robert -- Brandt, John E -- Gehlert, Donald R -- Tauscher, Johannes T -- Hunt, Stephen P -- Hommer, Daniel -- Heilig, Markus -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 14;319(5869):1536-9. doi: 10.1126/science.1153813. Epub 2008 Feb 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276852" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; *Alcohol Drinking/drug therapy ; Alcoholism/*drug therapy ; Animals ; Behavior, Addictive/drug therapy ; Brain/drug effects/physiology ; Emotions/drug effects ; Ethanol/administration & dosage/pharmacology ; Female ; Humans ; Hydrocortisone/blood ; Magnetic Resonance Imaging ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; *Neurokinin-1 Receptor Antagonists ; Pyridines/administration & dosage/pharmacology/*therapeutic use ; Receptors, Neurokinin-1/deficiency/genetics/*physiology ; Triazoles/administration & dosage/pharmacology/*therapeutic use
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Ecology. North Atlantic right whales in crisis (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kraus, Scott D -- Brown, Moira W -- Caswell, Hal -- Clark, Christopher W -- Fujiwara, Masami -- Hamilton, Philip K -- Kenney, Robert D -- Knowlton, Amy R -- Landry, Scott -- Mayo, Charles A -- McLellan, William A -- Moore, Michael J -- Nowacek, Douglas P -- Pabst, D Ann -- Read, Andrew J -- Rolland, Rosalind M -- New York, N.Y. -- Science. 2005 Jul 22;309(5734):561-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Edgerton Research Laboratory, New England Aquarium, Boston, MA 02110-3399, USA. skraus@neaq.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16040692" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atlantic Ocean ; Ecology ; *Ecosystem ; Environment ; Female ; Fisheries ; Male ; Mortality ; Population Dynamics ; Population Growth ; Public Policy ; Reproduction ; Ships ; *Whales/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 19
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    Sequence variants in SLITRK1 are associated with Tourette's syndrome (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-15
    Description: Tourette's syndrome (TS) is a genetically influenced developmental neuropsychiatric disorder characterized by chronic vocal and motor tics. We studied Slit and Trk-like 1 (SLITRK1) as a candidate gene on chromosome 13q31.1 because of its proximity to a de novo chromosomal inversion in a child with TS. Among 174 unrelated probands, we identified a frameshift mutation and two independent occurrences of the identical variant in the binding site for microRNA hsa-miR-189. These variants were absent from 3600 control chromosomes. SLITRK1 mRNA and hsa-miR-189 showed an overlapping expression pattern in brain regions previously implicated in TS. Wild-type SLITRK1, but not the frameshift mutant, enhanced dendritic growth in primary neuronal cultures. Collectively, these findings support the association of rare SLITRK1 sequence variants with TS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, Jesse F -- Kwan, Kenneth Y -- O'Roak, Brian J -- Baek, Danielle Y -- Stillman, Althea A -- Morgan, Thomas M -- Mathews, Carol A -- Pauls, David L -- Rasin, Mladen-Roko -- Gunel, Murat -- Davis, Nicole R -- Ercan-Sencicek, A Gulhan -- Guez, Danielle H -- Spertus, John A -- Leckman, James F -- Dure, Leon S 4th -- Kurlan, Roger -- Singer, Harvey S -- Gilbert, Donald L -- Farhi, Anita -- Louvi, Angeliki -- Lifton, Richard P -- Sestan, Nenad -- State, Matthew W -- K23 RR16118/RR/NCRR NIH HHS/ -- R01 NS054273/NS/NINDS NIH HHS/ -- R01 NS43520/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):317-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Child Study Center, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224024" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Adolescent ; Animals ; Attention Deficit Disorder with Hyperactivity/complications/genetics ; Brain/metabolism ; Child ; Child, Preschool ; Chromosome Inversion ; Chromosome Mapping ; *Chromosomes, Human, Pair 13 ; Dna ; DNA Mutational Analysis ; Female ; Frameshift Mutation ; Humans ; In Situ Hybridization, Fluorescence ; Male ; Membrane Proteins/*genetics ; Mice ; *Mutation ; Nerve Tissue Proteins/*genetics ; Pedigree ; Sequence Analysis, DNA ; Tourette Syndrome/complications/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 20
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    Widespread lateral gene transfer from intracellular bacteria to multicellular eukaryotes (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-01
    Description: Although common among bacteria, lateral gene transfer-the movement of genes between distantly related organisms-is thought to occur only rarely between bacteria and multicellular eukaryotes. However, the presence of endosymbionts, such as Wolbachia pipientis, within some eukaryotic germlines may facilitate bacterial gene transfers to eukaryotic host genomes. We therefore examined host genomes for evidence of gene transfer events from Wolbachia bacteria to their hosts. We found and confirmed transfers into the genomes of four insect and four nematode species that range from nearly the entire Wolbachia genome (〉1 megabase) to short (〈500 base pairs) insertions. Potential Wolbachia-to-host transfers were also detected computationally in three additional sequenced insect genomes. We also show that some of these inserted Wolbachia genes are transcribed within eukaryotic cells lacking endosymbionts. Therefore, heritable lateral gene transfer occurs into eukaryotic hosts from their prokaryote symbionts, potentially providing a mechanism for acquisition of new genes and functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunning Hotopp, Julie C -- Clark, Michael E -- Oliveira, Deodoro C S G -- Foster, Jeremy M -- Fischer, Peter -- Munoz Torres, Monica C -- Giebel, Jonathan D -- Kumar, Nikhil -- Ishmael, Nadeeza -- Wang, Shiliang -- Ingram, Jessica -- Nene, Rahul V -- Shepard, Jessica -- Tomkins, Jeffrey -- Richards, Stephen -- Spiro, David J -- Ghedin, Elodie -- Slatko, Barton E -- Tettelin, Herve -- Werren, John H -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1753-6. Epub 2007 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Research, J. Craig Venter Institute, 9712 Medical Center Drive, Rockville, MD 20850, USA. jhotopp@som.umaryland.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Crosses, Genetic ; DNA, Bacterial ; Drosophila/genetics/microbiology ; Female ; *Gene Transfer, Horizontal ; Genes, Bacterial ; In Situ Hybridization, Fluorescence ; Insects/*genetics/microbiology ; Male ; Molecular Sequence Data ; Nematoda/*genetics/microbiology ; Retroelements ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Analysis, DNA ; Symbiosis ; Wolbachia/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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