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  • Articles  (281)
  • Mice  (159)
  • Female  (143)
  • 2015-2019
  • 2010-2014  (281)
  • 2012  (281)
  • Science. 335(6064): 104-8. doi: 10.1126/science.1211600.  (1)
  • Science. 335(6064): 29. doi: 10.1126/science.335.6064.29.  (1)
  • Science. 335(6064): 49. doi: 10.1126/science.1217940.  (1)
  • Science. 335(6064): 52. doi: 10.1126/science.1215579.  (1)
  • Science. 335(6064): 79-82. doi: 10.1126/science.1211451.  (1)
  • Science. 335(6064): 93-6. doi: 10.1126/science.1214115.  (1)
  • Science. 335(6065): 165-6; author reply 166-8. doi: 10.1126/science.335.6065.165-b.  (1)
  • Science. 335(6065): 165; author reply 166-8. doi: 10.1126/science.335.6065.165-a.  (1)
  • Science. 335(6065): 166; author reply 166-8. doi: 10.1126/science.335.6065.166-a.  (1)
  • Science. 335(6065): 166; author reply 166-8. doi: 10.1126/science.335.6065.166-b.  (1)
  • Science. 335(6065): 211-4. doi: 10.1126/science.1210270.  (1)
  • Science. 335(6065): 225-8. doi: 10.1126/science.1214400.  (1)
  • Science. 335(6065): 229-32. doi: 10.1126/science.1214448.  (1)
  • Science. 335(6066): 281. doi: 10.1126/science.335.6066.281.  (1)
  • Science. 335(6066): 282-3. doi: 10.1126/science.335.6066.282.  (1)
  • Science. 335(6066): 292-3. doi: 10.1126/science.1217451.  (1)
  • Science. 335(6066): 293-4. doi: 10.1126/science.1217819.  (1)
  • Science. 335(6066): 332-5. doi: 10.1126/science.1215930.  (1)
  • Science. 335(6066): 335-8. doi: 10.1126/science.1212443.  (1)
  • Science. 335(6066): 338-41. doi: 10.1126/science.1213230.  (1)
  • 25
  • Medicine  (281)
Collection
  • Articles  (281)
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  • 2015-2019
  • 2010-2014  (281)
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  • 1
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    Mice lacking a Myc enhancer that includes human SNP rs6983267 are resistant to intestinal tumors (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-03
    Description: Multiple cancer-associated single-nucleotide polymorphisms (SNPs) have been mapped to conserved sequences within a 500-kilobase region upstream of the MYC oncogene on human chromosome 8q24. These SNPs may affect cancer development through altered regulation of MYC expression, but this hypothesis has been difficult to confirm. We generated mice deficient in Myc-335, a putative MYC regulatory element that contains rs6983267, a SNP accounting for more human cancer-related morbidity than any other genetic variant or mutation. In Myc-335 null mice, Myc transcripts were expressed in the intestinal crypts in a pattern similar to that in wild-type mice but at modestly reduced levels. The mutant mice displayed no overt phenotype but were markedly resistant to intestinal tumorigenesis induced by the APCmin mutation. These results establish that a cancer-associated SNP identified in human genome-wide association studies has a functional effect in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sur, Inderpreet Kaur -- Hallikas, Outi -- Vaharautio, Anna -- Yan, Jian -- Turunen, Mikko -- Enge, Martin -- Taipale, Minna -- Karhu, Auli -- Aaltonen, Lauri A -- Taipale, Jussi -- New York, N.Y. -- Science. 2012 Dec 7;338(6112):1360-3. doi: 10.1126/science.1228606. Epub 2012 Nov 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Science for Life Center, Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23118011" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/genetics/pathology ; Animals ; Cell Transformation, Neoplastic/*genetics ; Colon/metabolism/pathology ; Enhancer Elements, Genetic/*genetics ; Humans ; Ileum/metabolism/pathology ; Intestinal Neoplasms/*genetics/pathology ; Mice ; Mice, Mutant Strains ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins c-myc/*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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  • 2
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    Behavior. Origins of cumulative culture (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurzban, Robert -- Barrett, H Clark -- New York, N.Y. -- Science. 2012 Mar 2;335(6072):1056-7. doi: 10.1126/science.1219232.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Pennsylvania, Philadelphia, PA 19104, USA. kurzban@psych.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22383839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cultural Evolution ; Female ; Humans ; *Mental Processes ; *Problem Solving ; *Social Behavior
    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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    Economics. Implications of scarcity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zwane, Alix Peterson -- New York, N.Y. -- Science. 2012 Nov 2;338(6107):617-8. doi: 10.1126/science.1230292.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bill & Melinda Gates Foundation, Seattle, WA 98109, USA. alix.zwane@gatesfoundation.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23118174" target="_blank"〉PubMed〈/a〉
    Keywords: *Attention ; *Decision Making ; Female ; Humans ; Male ; Poverty/*psychology ; *Socioeconomic Factors
    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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    Trim28 is required for epigenetic stability during mouse oocyte to embryo transition (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-24
    Description: Phenotypic variability in genetic disease is usually attributed to genetic background variation or environmental influence. Here, we show that deletion of a single gene, Trim28 (Kap1 or Tif1beta), from the maternal germ line alone, on an otherwise identical genetic background, results in severe phenotypic and epigenetic variability that leads to embryonic lethality. We identify early and minute epigenetic variations in blastomeres of the preimplantation embryo of these animals, suggesting that the embryonic lethality may result from the misregulation of genomic imprinting in mice lacking maternal Trim28. Our results reveal the long-range effects of a maternal gene deletion on epigenetic memory and illustrate the delicate equilibrium of maternal and zygotic factors during nuclear reprogramming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Messerschmidt, Daniel M -- de Vries, Wilhelmine -- Ito, Mitsuteru -- Solter, Davor -- Ferguson-Smith, Anne -- Knowles, Barbara B -- 079249/Wellcome Trust/United Kingdom -- 095606/Wellcome Trust/United Kingdom -- MR/J001597/1/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1499-502. doi: 10.1126/science.1216154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Development Group, Institute of Medical Biology, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; DNA Methylation ; Down-Regulation ; *Embryo Loss ; Embryo, Mammalian/*physiology ; Embryonic Development ; *Epigenesis, Genetic ; Female ; Gene Expression Regulation, Developmental ; *Genomic Imprinting ; Insulin-Like Growth Factor II/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/*genetics/*physiology ; Oligonucleotide Array Sequence Analysis ; Oocytes/*physiology ; Phenotype ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/*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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  • 5
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    Ancestral developmental potential facilitates parallel evolution in ants (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-10
    Description: Complex worker caste systems have contributed to the evolutionary success of advanced ant societies; however, little is known about the developmental processes underlying their origin and evolution. We combined hormonal manipulation, gene expression, and phylogenetic analyses with field observations to understand how novel worker subcastes evolve. We uncovered an ancestral developmental potential to produce a "supersoldier" subcaste that has been actualized at least two times independently in the hyperdiverse ant genus Pheidole. This potential has been retained and can be environmentally induced throughout the genus. Therefore, the retention and induction of this potential have facilitated the parallel evolution of supersoldiers through a process known as genetic accommodation. The recurrent induction of ancestral developmental potential may facilitate the adaptive and parallel evolution of phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajakumar, Rajendhran -- San Mauro, Diego -- Dijkstra, Michiel B -- Huang, Ming H -- Wheeler, Diana E -- Hiou-Tim, Francois -- Khila, Abderrahman -- Cournoyea, Michael -- Abouheif, Ehab -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):79-82. doi: 10.1126/science.1211451.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, McGill University, 1205 Avenue Dr. Penfield, Montreal, Quebec, Canada, H3A 1B1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ants/*genetics/growth & development/physiology ; *Biological Evolution ; Environment ; Female ; Genes, Insect ; Larva/growth & development ; Male ; Methoprene/pharmacology ; Molecular Sequence Data ; Phenotype ; Phylogeny ; Selection, Genetic ; Social Behavior ; Wings, Animal/growth & development
    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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    MARF1 regulates essential oogenic processes in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-24
    Description: Development of fertilization-competent oocytes depends on integrated processes controlling meiosis, cytoplasmic development, and maintenance of genomic integrity. We show that meiosis arrest female 1 (MARF1) is required for these processes in mammalian oocytes. Mutations of Marf1 cause female infertility characterized by up-regulation of a cohort of transcripts, increased retrotransposon expression, defective cytoplasmic maturation, and meiotic arrest. Up-regulation of protein phosphatase 2 catalytic subunit (PPP2CB) is key to the meiotic arrest phenotype. Moreover, Iap and Line1 retrotransposon messenger RNAs are also up-regulated, and, concomitantly, DNA double-strand breaks are elevated in mutant oocytes. Therefore MARF1, by suppressing levels of specific transcripts, is an essential regulator of important oogenic processes leading to female fertility and the development of healthy offspring.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612990/" 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/PMC3612990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, You-Qiang -- Sugiura, Koji -- Sun, Fengyun -- Pendola, Janice K -- Cox, Gregory A -- Handel, Mary Ann -- Schimenti, John C -- Eppig, John J -- CA34196/CA/NCI NIH HHS/ -- HD42137/HD/NICHD NIH HHS/ -- P01 HD042137/HD/NICHD NIH HHS/ -- P30 CA034196/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1496-9. doi: 10.1126/science.1214680.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Jackson Laboratory, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442484" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Cycle Proteins/chemistry/genetics/*metabolism ; DNA Breaks, Double-Stranded ; Embryonic Development ; Female ; *Fertility ; Meiosis ; Mice ; Molecular Sequence Data ; Mutation ; Oocytes/*physiology ; *Oogenesis ; Phenotype ; Protein Phosphatase 2/genetics/metabolism ; Protein Structure, Tertiary ; RNA, Messenger/genetics/metabolism ; Retroelements ; Transcription, Genetic ; Transcriptome ; Up-Regulation
    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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  • 7
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    Paying for tissue: the case of WI-38 (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayflick, Leonard -- New York, N.Y. -- Science. 2012 Sep 14;337(6100):1292. doi: 10.1126/science.337.6100.1292-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22984048" target="_blank"〉PubMed〈/a〉
    Keywords: *Ethics, Research ; Female ; Humans ; Male ; *Patient Rights ; *Tissue Donors
    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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    The ancient drug salicylate directly activates AMP-activated protein kinase (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-21
    Description: Salicylate, a plant product, has been in medicinal use since ancient times. More recently, it has been replaced by synthetic derivatives such as aspirin and salsalate, both of which are rapidly broken down to salicylate in vivo. At concentrations reached in plasma after administration of salsalate or of aspirin at high doses, salicylate activates adenosine monophosphate-activated protein kinase (AMPK), a central regulator of cell growth and metabolism. Salicylate binds at the same site as the synthetic activator A-769662 to cause allosteric activation and inhibition of dephosphorylation of the activating phosphorylation site, threonine-172. In AMPK knockout mice, effects of salicylate to increase fat utilization and to lower plasma fatty acids in vivo were lost. Our results suggest that AMPK activation could explain some beneficial effects of salsalate and aspirin in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399766/" 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/PMC3399766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hawley, Simon A -- Fullerton, Morgan D -- Ross, Fiona A -- Schertzer, Jonathan D -- Chevtzoff, Cyrille -- Walker, Katherine J -- Peggie, Mark W -- Zibrova, Darya -- Green, Kevin A -- Mustard, Kirsty J -- Kemp, Bruce E -- Sakamoto, Kei -- Steinberg, Gregory R -- Hardie, D Grahame -- 080982/Wellcome Trust/United Kingdom -- 097726/Wellcome Trust/United Kingdom -- MC_U127088492/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 May 18;336(6083):918-22. doi: 10.1126/science.1215327. Epub 2012 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517326" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/genetics/*metabolism ; Amino Acid Substitution ; Animals ; Aspirin/pharmacology ; Binding Sites ; Carbohydrate Metabolism/drug effects ; Cell Line ; Enzyme Activation ; Enzyme Activators/pharmacology ; HEK293 Cells ; Humans ; Lipid Metabolism/drug effects ; Liver/drug effects/metabolism ; Mice ; Mice, Knockout ; Mutation ; Oxygen Consumption/drug effects ; Phosphorylation ; Pyrones/pharmacology ; Rats ; Salicylates/blood/*metabolism/*pharmacology ; Thiophenes/pharmacology
    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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  • 9
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    Airborne transmission of influenza A/H5N1 virus between ferrets (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: Highly pathogenic avian influenza A/H5N1 virus can cause morbidity and mortality in humans but thus far has not acquired the ability to be transmitted by aerosol or respiratory droplet ("airborne transmission") between humans. To address the concern that the virus could acquire this ability under natural conditions, we genetically modified A/H5N1 virus by site-directed mutagenesis and subsequent serial passage in ferrets. The genetically modified A/H5N1 virus acquired mutations during passage in ferrets, ultimately becoming airborne transmissible in ferrets. None of the recipient ferrets died after airborne infection with the mutant A/H5N1 viruses. Four amino acid substitutions in the host receptor-binding protein hemagglutinin, and one in the polymerase complex protein basic polymerase 2, were consistently present in airborne-transmitted viruses. The transmissible viruses were sensitive to the antiviral drug oseltamivir and reacted well with antisera raised against H5 influenza vaccine strains. Thus, avian A/H5N1 influenza viruses can acquire the capacity for airborne transmission between mammals without recombination in an intermediate host and therefore constitute a risk for human pandemic influenza.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herfst, Sander -- Schrauwen, Eefje J A -- Linster, Martin -- Chutinimitkul, Salin -- de Wit, Emmie -- Munster, Vincent J -- Sorrell, Erin M -- Bestebroer, Theo M -- Burke, David F -- Smith, Derek J -- Rimmelzwaan, Guus F -- Osterhaus, Albert D M E -- Fouchier, Ron A M -- DP1-OD000490-01/OD/NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1534-41. doi: 10.1126/science.1213362.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology, Erasmus Medical Center, Rotterdam, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723413" target="_blank"〉PubMed〈/a〉
    Keywords: Air Microbiology ; Amino Acid Substitution ; Animals ; Antiviral Agents/pharmacology ; Containment of Biohazards ; Disease Models, Animal ; Female ; *Ferrets ; Hemagglutinin Glycoproteins, Influenza ; Virus/chemistry/genetics/immunology/metabolism ; Humans ; Immune Sera ; Influenza A Virus, H5N1 Subtype/drug effects/*genetics/*pathogenicity/physiology ; Influenza in Birds/epidemiology/virology ; Influenza, Human/epidemiology/transmission/*virology ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Mutation ; Orthomyxoviridae Infections/transmission/*virology ; Oseltamivir/pharmacology ; Pandemics ; Poultry ; RNA Replicase/chemistry/genetics ; Reassortant Viruses/pathogenicity ; Receptors, Virus/metabolism ; Respiratory System/*virology ; Reverse Genetics ; Serial Passage ; Sialic Acids/metabolism ; Viral Proteins/chemistry/genetics ; Virulence ; Virus Replication ; Virus Shedding
    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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    Elfn1 regulates target-specific release probability at CA1-interneuron synapses (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-09
    Description: Although synaptic transmission may be unidirectional, the establishment of synaptic connections with specific properties can involve bidirectional signaling. Pyramidal neurons in the hippocampus form functionally distinct synapses onto two types of interneurons. Excitatory synapses onto oriens-lacunosum moleculare (O-LM) interneurons are facilitating and have a low release probability, whereas synapses onto parvalbumin interneurons are depressing and have a high release probability. Here, we show that the extracellular leucine-rich repeat fibronectin containing 1 (Elfn1) protein is selectively expressed by O-LM interneurons and regulates presynaptic release probability to direct the formation of highly facilitating pyramidal-O-LM synapses. Thus, postsynaptic expression of Elfn1 in O-LM interneurons regulates presynaptic release probability, which confers target-specific synaptic properties to pyramidal cell axons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sylwestrak, Emily L -- Ghosh, Anirvan -- R01 NS067216/NS/NINDS NIH HHS/ -- R01NS067216/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 26;338(6106):536-40. doi: 10.1126/science.1222482. Epub 2012 Oct 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093-0366, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23042292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/metabolism ; CA1 Region, Hippocampal/*metabolism ; Cells, Cultured ; Gene Knockdown Techniques ; Green Fluorescent Proteins/genetics/metabolism ; HEK293 Cells ; Humans ; Interneurons/*metabolism ; Mice ; Nerve Tissue Proteins/genetics/*metabolism ; RNA, Small Interfering/metabolism ; Rats ; Rats, Inbred LEC ; Synapses/genetics/*metabolism ; Synaptic Transmission
    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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  • 11
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    Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: Rapamycin, an inhibitor of mechanistic target of rapamycin complex 1 (mTORC1), extends the life spans of yeast, flies, and mice. Calorie restriction, which increases life span and insulin sensitivity, is proposed to function by inhibition of mTORC1, yet paradoxically, chronic administration of rapamycin substantially impairs glucose tolerance and insulin action. We demonstrate that rapamycin disrupted a second mTOR complex, mTORC2, in vivo and that mTORC2 was required for the insulin-mediated suppression of hepatic gluconeogenesis. Further, decreased mTORC1 signaling was sufficient to extend life span independently from changes in glucose homeostasis, as female mice heterozygous for both mTOR and mLST8 exhibited decreased mTORC1 activity and extended life span but had normal glucose tolerance and insulin sensitivity. Thus, mTORC2 disruption is an important mediator of the effects of rapamycin in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324089/" 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/PMC3324089/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamming, Dudley W -- Ye, Lan -- Katajisto, Pekka -- Goncalves, Marcus D -- Saitoh, Maki -- Stevens, Deanna M -- Davis, James G -- Salmon, Adam B -- Richardson, Arlan -- Ahima, Rexford S -- Guertin, David A -- Sabatini, David M -- Baur, Joseph A -- 1F32AG032833-01A1/AG/NIA NIH HHS/ -- CA129105/CA/NCI NIH HHS/ -- F32 AG032833/AG/NIA NIH HHS/ -- P30DK19525/DK/NIDDK NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-05/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1638-43. doi: 10.1126/science.1215135.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461615" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, White/metabolism ; Animals ; Carrier Proteins/genetics/metabolism ; Female ; Gluconeogenesis ; Glucose/metabolism ; Glucose Clamp Technique ; Homeostasis ; Insulin/administration & dosage/blood ; *Insulin Resistance ; Liver/metabolism ; *Longevity ; Male ; Mice ; Mice, Inbred C57BL ; Multiprotein Complexes ; Muscle, Skeletal/metabolism ; Phosphorylation ; Proteins/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sirolimus/*pharmacology ; TOR Serine-Threonine Kinases/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    A logic-gated nanorobot for targeted transport of molecular payloads (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-22
    Description: We describe an autonomous DNA nanorobot capable of transporting molecular payloads to cells, sensing cell surface inputs for conditional, triggered activation, and reconfiguring its structure for payload delivery. The device can be loaded with a variety of materials in a highly organized fashion and is controlled by an aptamer-encoded logic gate, enabling it to respond to a wide array of cues. We implemented several different logical AND gates and demonstrate their efficacy in selective regulation of nanorobot function. As a proof of principle, nanorobots loaded with combinations of antibody fragments were used in two different types of cell-signaling stimulation in tissue culture. Our prototype could inspire new designs with different selectivities and biologically active payloads for cell-targeting tasks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Douglas, Shawn M -- Bachelet, Ido -- Church, George M -- New York, N.Y. -- Science. 2012 Feb 17;335(6070):831-4. doi: 10.1126/science.1214081.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wyss Institute for Biologically Inspired Engineering, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22344439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/immunology ; Antigens, Differentiation, Myelomonocytic/immunology ; Cell Line, Tumor ; *DNA/chemistry ; Histocompatibility Antigens Class I/immunology ; Humans ; Immunoglobulin Fragments/immunology ; Metal Nanoparticles ; Mice ; Molecular Conformation ; *Nanostructures ; *Robotics ; Sialic Acid Binding Ig-like Lectin 3 ; *Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Alzheimer's research. Stopping Alzheimer's before it starts (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2012 Aug 17;337(6096):790-2. doi: 10.1126/science.337.6096.790.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22903991" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Age of Onset ; Alzheimer Disease/diagnosis/*genetics/*prevention & control ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized/therapeutic use ; Apolipoprotein E4/genetics ; Child ; *Clinical Trials as Topic ; DNA Mutational Analysis ; Female ; *Genetic Predisposition to Disease ; Heterozygote Detection ; Humans ; Information Services ; Male ; Pedigree ; Primary Prevention/*methods ; Risk
    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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  • 14
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    A single progenitor population switches behavior to maintain and repair esophageal epithelium (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-24
    Description: Diseases of the esophageal epithelium (EE), such as reflux esophagitis and cancer, are rising in incidence. Despite this, the cellular behaviors underlying EE homeostasis and repair remain controversial. Here, we show that in mice, EE is maintained by a single population of cells that divide stochastically to generate proliferating and differentiating daughters with equal probability. In response to challenge with all-trans retinoic acid (atRA), the balance of daughter cell fate is unaltered, but the rate of cell division increases. However, after wounding, cells reversibly switch to producing an excess of proliferating daughters until the wound has closed. Such fate-switching enables a single progenitor population to both maintain and repair tissue without the need for a "reserve" slow-cycling stem cell pool.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527005/" 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/PMC3527005/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doupe, David P -- Alcolea, Maria P -- Roshan, Amit -- Zhang, Gen -- Klein, Allon M -- Simons, Benjamin D -- Jones, Philip H -- 079249/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- G0601740/Medical Research Council/United Kingdom -- G0700600/1/National Centre for the Replacement, Refinement and Reduction of Animals in Research/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- MC_U105370181/Medical Research Council/United Kingdom -- U.1053.00.010(70181)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1091-3. doi: 10.1126/science.1218835. Epub 2012 Jul 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Cancer Cell Unit, Hutchison-MRC Research Centre, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22821983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Doxycycline/pharmacology ; Epithelial Cells/*physiology ; Epithelium/drug effects/metabolism/*physiology ; Esophagus/*cytology/*physiology ; Green Fluorescent Proteins/biosynthesis ; Histones/biosynthesis ; Mice ; Mice, Inbred C57BL ; Recombinant Fusion Proteins/biosynthesis ; *Regeneration ; Stem Cells/metabolism/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Locally synchronized synaptic inputs (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-24
    Description: Synaptic inputs on dendrites are nonlinearly converted to action potential outputs, yet the spatiotemporal patterns of dendritic activation remain to be elucidated at single-synapse resolution. In rodents, we optically imaged synaptic activities from hundreds of dendritic spines in hippocampal and neocortical pyramidal neurons ex vivo and in vivo. Adjacent spines were frequently synchronized in spontaneously active networks, thereby forming dendritic foci that received locally convergent inputs from presynaptic cell assemblies. This precise subcellular geometry manifested itself during N-methyl-D-aspartate receptor-dependent circuit remodeling. Thus, clustered synaptic plasticity is innately programmed to compartmentalize correlated inputs along dendrites and may reify nonlinear synaptic integration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, Naoya -- Kitamura, Kazuo -- Matsuo, Naoki -- Mayford, Mark -- Kano, Masanobu -- Matsuki, Norio -- Ikegaya, Yuji -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):353-6. doi: 10.1126/science.1210362.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267814" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; CA3 Region, Hippocampal/cytology/physiology ; Calcium/metabolism ; Dendritic Spines/*physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nerve Net/*physiology ; Neuronal Plasticity ; Organ Culture Techniques ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Somatosensory Cortex/cytology/physiology ; Synapses/*physiology
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  • 16
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    Neuroscience. Revitalizing remyelination--the answer is circulating (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Redmond, Stephanie A -- Chan, Jonah R -- R01 NS062796/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):161-2. doi: 10.1126/science.1221689.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499927" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Demyelinating Diseases/*physiopathology/therapy ; Macrophages/*physiology ; Mice ; Myelin Sheath/*physiology ; Oligodendroglia/*physiology ; Parabiosis ; Phagocytosis ; Spinal Cord Diseases/*physiopathology/therapy
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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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    Psychology. Tapping into the wisdom of the crowd--with confidence (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hertwig, Ralph -- New York, N.Y. -- Science. 2012 Apr 20;336(6079):303-4. doi: 10.1126/science.1221403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Basel, Missionsstrasse 60-64, CH-4055 Basel, Switzerland. ralph.hertwig@unibas.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517847" target="_blank"〉PubMed〈/a〉
    Keywords: *Decision Making ; Female ; *Group Processes ; Humans ; *Interpersonal Relations ; Male
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  • 18
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    Identification and functional expression of the mitochondrial pyruvate carrier (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-26
    Description: The transport of pyruvate, the end product of glycolysis, into mitochondria is an essential process that provides the organelle with a major oxidative fuel. Although the existence of a specific mitochondrial pyruvate carrier (MPC) has been anticipated, its molecular identity remained unknown. We report that MPC is a heterocomplex formed by two members of a family of previously uncharacterized membrane proteins that are conserved from yeast to mammals. Members of the MPC family were found in the inner mitochondrial membrane, and yeast mutants lacking MPC proteins showed severe defects in mitochondrial pyruvate uptake. Coexpression of mouse MPC1 and MPC2 in Lactococcus lactis promoted transport of pyruvate across the membrane. These observations firmly establish these proteins as essential components of the MPC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herzig, Sebastien -- Raemy, Etienne -- Montessuit, Sylvie -- Veuthey, Jean-Luc -- Zamboni, Nicola -- Westermann, Benedikt -- Kunji, Edmund R S -- Martinou, Jean-Claude -- MC_U105663139/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Jul 6;337(6090):93-6. doi: 10.1126/science.1218530. Epub 2012 May 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Geneva, Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628554" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anion Transport Proteins/chemistry/genetics/*metabolism ; Biological Transport ; Biosynthetic Pathways ; Culture Media ; Lactococcus lactis/genetics/metabolism ; Leucine/metabolism ; Mice ; Mitochondria/*metabolism ; Mitochondrial Membrane Transport Proteins/chemistry/genetics/*metabolism ; Mitochondrial Membranes/*metabolism ; Molecular Sequence Data ; Proprotein Convertase 1/chemistry/genetics/*metabolism ; Proprotein Convertase 2 ; Pyruvic Acid/*metabolism ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/genetics/growth & development/metabolism ; Saccharomyces cerevisiae Proteins/chemistry/genetics/*metabolism ; Thioctic Acid/biosynthesis/metabolism ; Valine/metabolism
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  • 19
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    Neuropathology. Blast injuries linked to neurodegeneration in veterans (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2012 May 18;336(6083):790-1. doi: 10.1126/science.336.6083.790.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22605724" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Axons/pathology ; Blast Injuries/metabolism/*pathology ; Brain/*pathology ; Brain Chemistry ; Brain Injury, Chronic/metabolism/*pathology ; Humans ; Male ; Mice ; Middle Aged ; *Military Personnel ; *Veterans ; Young Adult ; tau Proteins/analysis
    Print ISSN: 0036-8075
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  • 20
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    Bateman in nature: predation on offspring reduces the potential for sexual selection (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-10
    Description: Sexual selection is driven by competition for mates, and the advantage of a competitor is determined by the number of offspring it produces. Early experiments by Angus Bateman characterized this interaction, and the quantitative relationship between a male's number of mates and number of offspring is known as the Bateman slope. Sexual dimorphism, one of the most obvious results of sexual selection, largely requires a positive Bateman relationship, and the slope provides an estimate of the potential for sexual selection. However, natural selection from the environment can also influence male success, as can random effects, and some have argued for inclusion of the latter in calculations of mate success. Data from pronghorn (Antilocapra americana) reveal the presence of a positive Bateman slope in each year of a 10-year study. We found no evidence that random effects skewed male mating success; however, substantial yearly variation in the Bateman slope due to predation on fawns was evident. These results support the validity of the Bateman relationship, yet they also demonstrate that environmental or extrinsic influences can limit the potential for sexual selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Byers, John -- Dunn, Stacey -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):802-4. doi: 10.1126/science.1224660.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Idaho, Moscow, ID 83844-3051, USA. jbyers@uidaho.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23139332" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antelopes/*physiology ; Biological Evolution ; Coyotes ; Female ; Linear Models ; Male ; *Mating Preference, Animal ; Montana ; *Predatory Behavior ; Reproduction ; Selection, Genetic ; Sex Characteristics ; Sex Ratio ; *Sexual Behavior, Animal
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  • 21
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    Highly conserved protective epitopes on influenza B viruses (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-11
    Description: Identification of broadly neutralizing antibodies against influenza A viruses has raised hopes for the development of monoclonal antibody-based immunotherapy and "universal" vaccines for influenza. However, a substantial part of the annual flu burden is caused by two cocirculating, antigenically distinct lineages of influenza B viruses. Here, we report human monoclonal antibodies, CR8033, CR8071, and CR9114, that protect mice against lethal challenge from both lineages. Antibodies CR8033 and CR8071 recognize distinct conserved epitopes in the head region of the influenza B hemagglutinin (HA), whereas CR9114 binds a conserved epitope in the HA stem and protects against lethal challenge with influenza A and B viruses. These antibodies may inform on development of monoclonal antibody-based treatments and a universal flu vaccine for all influenza A and B viruses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3538841/" 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/PMC3538841/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dreyfus, Cyrille -- Laursen, Nick S -- Kwaks, Ted -- Zuijdgeest, David -- Khayat, Reza -- Ekiert, Damian C -- Lee, Jeong Hyun -- Metlagel, Zoltan -- Bujny, Miriam V -- Jongeneelen, Mandy -- van der Vlugt, Remko -- Lamrani, Mohammed -- Korse, Hans J W M -- Geelen, Eric -- Sahin, Ozcan -- Sieuwerts, Martijn -- Brakenhoff, Just P J -- Vogels, Ronald -- Li, Olive T W -- Poon, Leo L M -- Peiris, Malik -- Koudstaal, Wouter -- Ward, Andrew B -- Wilson, Ian A -- Goudsmit, Jaap -- Friesen, Robert H E -- GM080209/GM/NIGMS NIH HHS/ -- P41RR001209/RR/NCRR NIH HHS/ -- RR017573/RR/NCRR NIH HHS/ -- T32 GM080209/GM/NIGMS NIH HHS/ -- U54 GM094586/GM/NIGMS NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 14;337(6100):1343-8. doi: 10.1126/science.1222908. Epub 2012 Aug 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22878502" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/chemistry/*immunology ; Antibodies, Neutralizing/chemistry/immunology ; Conserved Sequence ; Hemagglutinin Glycoproteins, Influenza Virus/*immunology ; Humans ; Immunodominant Epitopes/chemistry/*immunology ; Influenza B virus/*immunology ; Influenza Vaccines/*immunology ; Mice ; Molecular Sequence Data ; Neutralization Tests ; Orthomyxoviridae Infections/*prevention & control ; Protein Conformation
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  • 22
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    Cancer research. Cancer prevention with a diabetes pill? (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, Gary -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):29. doi: 10.1126/science.335.6064.29.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223788" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; Animals ; Anticarcinogenic Agents/*therapeutic use ; Blood Glucose/metabolism ; Clinical Trials as Topic ; Diabetes Mellitus, Type 2/drug therapy ; Humans ; Hypoglycemic Agents/pharmacology/*therapeutic use ; Insulin/blood/metabolism ; Metformin/pharmacology/*therapeutic use ; Mice ; Neoplasms/epidemiology/*prevention & control ; Protein-Serine-Threonine Kinases/metabolism ; Somatomedins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 23
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    Interleukin-22 drives endogenous thymic regeneration in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-03
    Description: Endogenous thymic regeneration is a crucial function that allows for renewal of immune competence after stress, infection, or immunodepletion. However, the mechanisms governing this regeneration remain poorly understood. We detail such a mechanism, centered on interleukin-22 (IL-22) and triggered by the depletion of CD4(+)CD8(+) double-positive thymocytes. Intrathymic levels of IL-22 were increased after thymic insult, and thymic recovery was impaired in IL-22-deficient mice. IL-22, which signaled through thymic epithelial cells and promoted their proliferation and survival, was up-regulated by radio-resistant RORgamma(t)(+)CCR6(+)NKp46(-) lymphoid tissue inducer cells after thymic injury in an IL-23-dependent manner. Administration of IL-22 enhanced thymic recovery after total body irradiation. These studies reveal mechanisms of endogenous thymic repair and offer innovative regenerative strategies for improving immune competence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616391/" 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/PMC3616391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudakov, Jarrod A -- Hanash, Alan M -- Jenq, Robert R -- Young, Lauren F -- Ghosh, Arnab -- Singer, Natalie V -- West, Mallory L -- Smith, Odette M -- Holland, Amanda M -- Tsai, Jennifer J -- Boyd, Richard L -- van den Brink, Marcel R M -- AI080455/AI/NIAID NIH HHS/ -- CA107096/CA/NCI NIH HHS/ -- HL069929/HL/NHLBI NIH HHS/ -- HL095075/HL/NHLBI NIH HHS/ -- R01 AI080455/AI/NIAID NIH HHS/ -- R01 CA107096/CA/NCI NIH HHS/ -- R01 HL069929/HL/NHLBI NIH HHS/ -- R01 HL095075/HL/NHLBI NIH HHS/ -- T32 CA009207/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 6;336(6077):91-5. doi: 10.1126/science.1218004. Epub 2012 Mar 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. dudakovj@mskcc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22383805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Proliferation ; Cell Survival ; Dendritic Cells/physiology ; Epithelial Cells/cytology/physiology ; Interleukin-23/metabolism ; Interleukins/administration & dosage/deficiency/genetics/*metabolism ; Lymphocytes/cytology/physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics/metabolism ; Radiation Dosage ; Receptors, Interleukin/metabolism ; Recombinant Proteins/administration & dosage ; *Regeneration ; Signal Transduction ; Thymocytes/*physiology ; Thymus Gland/cytology/immunology/*physiology/radiation effects ; Up-Regulation ; Whole-Body Irradiation
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    Identification of small molecule activators of cryptochrome (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: Impairment of the circadian clock has been associated with numerous disorders, including metabolic disease. Although small molecules that modulate clock function might offer therapeutic approaches to such diseases, only a few compounds have been identified that selectively target core clock proteins. From an unbiased cell-based circadian phenotypic screen, we identified KL001, a small molecule that specifically interacts with cryptochrome (CRY). KL001 prevented ubiquitin-dependent degradation of CRY, resulting in lengthening of the circadian period. In combination with mathematical modeling, our studies using KL001 revealed that CRY1 and CRY2 share a similar functional role in the period regulation. Furthermore, KL001-mediated CRY stabilization inhibited glucagon-induced gluconeogenesis in primary hepatocytes. KL001 thus provides a tool to study the regulation of CRY-dependent physiology and aid development of clock-based therapeutics of diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3589997/" 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/PMC3589997/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirota, Tsuyoshi -- Lee, Jae Wook -- St John, Peter C -- Sawa, Mariko -- Iwaisako, Keiko -- Noguchi, Takako -- Pongsawakul, Pagkapol Y -- Sonntag, Tim -- Welsh, David K -- Brenner, David A -- Doyle, Francis J 3rd -- Schultz, Peter G -- Kay, Steve A -- GM074868/GM/NIGMS NIH HHS/ -- GM085764/GM/NIGMS NIH HHS/ -- GM096873/GM/NIGMS NIH HHS/ -- MH051573/MH/NIMH NIH HHS/ -- MH082945/MH/NIMH NIH HHS/ -- P50 GM085764/GM/NIGMS NIH HHS/ -- R01 GM041804/GM/NIGMS NIH HHS/ -- R01 GM074868/GM/NIGMS NIH HHS/ -- R01 GM096873/GM/NIGMS NIH HHS/ -- R01 MH051573/MH/NIMH NIH HHS/ -- R01 MH082945/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1094-7. doi: 10.1126/science.1223710. Epub 2012 Jul 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798407" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Carbazoles/chemistry/isolation & purification/*pharmacology ; Cell Line, Tumor ; Circadian Clocks/*drug effects ; Cryptochromes/*agonists/metabolism ; Gluconeogenesis/drug effects/genetics ; Glucose-6-Phosphatase/genetics ; HEK293 Cells ; Hepatocytes/drug effects/metabolism ; Humans ; Liver/cytology/drug effects/metabolism ; Mice ; Molecular Sequence Data ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; Protein Stability/drug effects ; Proteolysis/drug effects ; *Small Molecule Libraries ; Sulfonamides/chemistry/isolation & purification/*pharmacology
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    Airn transcriptional overlap, but not its lncRNA products, induces imprinted Igf2r silencing (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-15
    Description: Mammalian imprinted genes often cluster with long noncoding (lnc) RNAs. Three lncRNAs that induce parental-specific silencing show hallmarks indicating that their transcription is more important than their product. To test whether Airn transcription or product silences the Igf2r gene, we shortened the endogenous lncRNA to different lengths. The results excluded a role for spliced and unspliced Airn lncRNA products and for Airn nuclear size and location in silencing Igf2r. Instead, silencing only required Airn transcriptional overlap of the Igf2r promoter, which interferes with RNA polymerase II recruitment in the absence of repressive chromatin. Such a repressor function for lncRNA transcriptional overlap reveals a gene silencing mechanism that may be widespread in the mammalian genome, given the abundance of lncRNA transcripts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Latos, Paulina A -- Pauler, Florian M -- Koerner, Martha V -- Senergin, H Basak -- Hudson, Quanah J -- Stocsits, Roman R -- Allhoff, Wolfgang -- Stricker, Stefan H -- Klement, Ruth M -- Warczok, Katarzyna E -- Aumayr, Karin -- Pasierbek, Pawel -- Barlow, Denise P -- New York, N.Y. -- Science. 2012 Dec 14;338(6113):1469-72. doi: 10.1126/science.1228110.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, 1090 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23239737" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Cells, Cultured ; *Gene Silencing ; *Genomic Imprinting ; Mice ; Multigene Family ; Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; RNA, Long Noncoding/genetics/*metabolism ; Receptor, IGF Type 2/*genetics ; *Transcription, Genetic
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    Physiology. COX-2 inhibitors and cardiovascular risk (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cannon, Christopher P -- Cannon, Paul J -- New York, N.Y. -- Science. 2012 Jun 15;336(6087):1386-7. doi: 10.1126/science.1224398.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Thrombolysis in Myocardial Infarction Study Group, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA. cpcannon@partners.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22700906" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiovascular Diseases/chemically induced ; Cyclooxygenase 2/genetics/*metabolism ; Cyclooxygenase 2 Inhibitors/*adverse effects/pharmacology ; Endothelial Cells/*enzymology ; Epoprostenol/metabolism ; Genetic Engineering ; Humans ; Hypertension/*chemically induced ; Mice ; Muscle, Smooth, Vascular/*enzymology ; Risk Factors ; Thrombosis/*chemically induced
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    Activation-induced B cell fates are selected by intracellular stochastic competition (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-10
    Description: In response to stimulation, B lymphocytes pursue a large number of distinct fates important for immune regulation. Whether each cell's fate is determined by external direction, internal stochastic processes, or directed asymmetric division is unknown. Measurement of times to isotype switch, to develop into a plasmablast, and to divide or to die for thousands of cells indicated that each fate is pursued autonomously and stochastically. As a consequence of competition between these processes, censorship of alternative outcomes predicts intricate correlations that are observed in the data. Stochastic competition can explain how the allocation of a proportion of B cells to each cell fate is achieved. The B cell may exemplify how other complex cell differentiation systems are controlled.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, Ken R -- Wellard, Cameron J -- Markham, John F -- Zhou, Jie H S -- Holmberg, Ross -- Hawkins, Edwin D -- Hasbold, Jhagvaral -- Dowling, Mark R -- Hodgkin, Philip D -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):338-41. doi: 10.1126/science.1213230. Epub 2012 Jan 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hamilton Institute, National University of Ireland, Maynooth, Ireland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology/*immunology ; Cell Death ; Cell Differentiation ; Cell Division ; Female ; Immunoglobulin Class Switching ; *Lymphocyte Activation ; Mice ; Models, Immunological ; Stochastic Processes
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    The biology of genomes. Single-cell sequencing tackles basic and biomedical questions (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2012 May 25;336(6084):976-7. doi: 10.1126/science.336.6084.976.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628633" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/genetics ; Cell Line, Tumor ; Female ; Genes, Neoplasm ; *Genome, Human ; Humans ; Lab-On-A-Chip Devices ; Male ; Mutation ; Recombination, Genetic ; Sequence Analysis, DNA/*methods ; *Single-Cell Analysis ; Spermatozoa
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  • 29
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    Evolution and functional impact of rare coding variation from deep sequencing of human exomes (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-19
    Description: As a first step toward understanding how rare variants contribute to risk for complex diseases, we sequenced 15,585 human protein-coding genes to an average median depth of 111x in 2440 individuals of European (n = 1351) and African (n = 1088) ancestry. We identified over 500,000 single-nucleotide variants (SNVs), the majority of which were rare (86% with a minor allele frequency less than 0.5%), previously unknown (82%), and population-specific (82%). On average, 2.3% of the 13,595 SNVs each person carried were predicted to affect protein function of ~313 genes per genome, and ~95.7% of SNVs predicted to be functionally important were rare. This excess of rare functional variants is due to the combined effects of explosive, recent accelerated population growth and weak purifying selection. Furthermore, we show that large sample sizes will be required to associate rare variants with complex traits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708544/" 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/PMC3708544/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tennessen, Jacob A -- Bigham, Abigail W -- O'Connor, Timothy D -- Fu, Wenqing -- Kenny, Eimear E -- Gravel, Simon -- McGee, Sean -- Do, Ron -- Liu, Xiaoming -- Jun, Goo -- Kang, Hyun Min -- Jordan, Daniel -- Leal, Suzanne M -- Gabriel, Stacey -- Rieder, Mark J -- Abecasis, Goncalo -- Altshuler, David -- Nickerson, Deborah A -- Boerwinkle, Eric -- Sunyaev, Shamil -- Bustamante, Carlos D -- Bamshad, Michael J -- Akey, Joshua M -- Broad GO -- Seattle GO -- NHLBI Exome Sequencing Project -- R01 HG003229/HG/NHGRI NIH HHS/ -- RC2 HL-102923/HL/NHLBI NIH HHS/ -- RC2 HL-102924/HL/NHLBI NIH HHS/ -- RC2 HL-102925/HL/NHLBI NIH HHS/ -- RC2 HL-102926/HL/NHLBI NIH HHS/ -- RC2 HL-103010/HL/NHLBI NIH HHS/ -- RC2 HL102926/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 6;337(6090):64-9. doi: 10.1126/science.1219240. Epub 2012 May 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22604720" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/*genetics ; Disease/genetics ; European Continental Ancestry Group/*genetics ; *Evolution, Molecular ; *Exome ; Female ; Gene Frequency ; Genetic Association Studies ; Genetic Predisposition to Disease ; *Genetic Variation ; *Genome, Human ; *High-Throughput Nucleotide Sequencing ; Humans ; Male ; *Polymorphism, Single Nucleotide ; Population Growth ; Selection, Genetic
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    Cell biology. FGF21 takes a fat bite (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-15
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616235/" 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/PMC3616235/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Canto, Carles -- Auwerx, Johan -- 231138/European Research Council/International -- New York, N.Y. -- Science. 2012 May 11;336(6082):675-6. doi: 10.1126/science.1222646.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nestle Institute of Health Sciences, Ecole Polytechnique Federale de Lausanne Campus, Quartier de l'Innovation, Batiment G, CH-1015 Lausanne, Switzerland. carlos.cantoalvarez@rd.nestle.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582248" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/*metabolism ; Animals ; Fasting/metabolism ; Fibroblast Growth Factors/blood/*metabolism/pharmacology ; Humans ; Metabolic Syndrome X/metabolism ; Mice ; Overweight/metabolism ; PPAR gamma/metabolism ; Signal Transduction ; *Thermogenesis ; Trans-Activators/metabolism ; Transcription Factors
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    Ecological context influences epidemic size and parasite-driven evolution (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: The occurrence and magnitude of disease outbreaks can strongly influence host evolution. In particular, when hosts face a resistance-fecundity trade-off, they might evolve increased resistance to infection during larger epidemics but increased susceptibility during smaller ones. We tested this theoretical prediction by using a zooplankton-yeast host-parasite system in which ecological factors determine epidemic size. Lakes with high productivity and low predation pressure had large yeast epidemics; during these outbreaks, hosts became more resistant to infection. However, with low productivity and high predation, epidemics remained small and hosts evolved increased susceptibility. Thus, by modulating disease outbreaks, ecological context (productivity and predation) shaped host evolution during epidemics. Consequently, anthropogenic alteration of productivity and predation might strongly influence both ecological and evolutionary outcomes of disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, Meghan A -- Ochs, Jessica Housley -- Penczykowski, Rachel M -- Civitello, David J -- Klausmeier, Christopher A -- Hall, Spencer R -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1636-8. doi: 10.1126/science.1215429.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biology, Georgia Institute of Technology, Atlanta, GA 30332-0230, USA. duffy@gatech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Daphnia/*microbiology/*physiology ; *Ecosystem ; Female ; Fishes ; *Host-Pathogen Interactions ; Indiana ; *Lakes ; Male ; Metschnikowia/*pathogenicity ; Models, Biological ; Population Dynamics ; Predatory Behavior ; Reproduction ; Zooplankton/microbiology/physiology
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    A Bruce effect in wild geladas (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-01
    Description: Female rodents are known to terminate pregnancies after exposure to unfamiliar males ("Bruce effect"). Although laboratory support abounds, direct evidence for a Bruce effect under natural conditions is lacking. Here, we report a strong Bruce effect in a wild primate, the gelada (Theropithecus gelada). Female geladas terminate 80% of pregnancies in the weeks after a dominant male is replaced. Further, data on interbirth intervals suggest that pregnancy termination offers fitness benefits for females whose offspring would otherwise be susceptible to infanticide. Taken together, data support the hypothesis that the Bruce effect can be an adaptive strategy for females.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Eila K -- Lu, Amy -- Bergman, Thore J -- Beehner, Jacinta C -- New York, N.Y. -- Science. 2012 Mar 9;335(6073):1222-5. doi: 10.1126/science.1213600. Epub 2012 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Michigan, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22362878" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Wild ; *Behavior, Animal ; Birth Rate ; Estrogens/analysis ; Ethiopia ; Feces/chemistry ; Female ; *Genetic Fitness ; Gestational Age ; Male ; Pregnancy ; Pregnancy Outcome ; *Pregnancy, Animal ; Sexual Behavior, Animal ; Social Behavior ; *Social Dominance ; *Theropithecus/physiology/psychology
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    Asymmetric segregation of polarized antigen on B cell division shapes presentation capacity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-28
    Description: During the activation of humoral immune responses, B cells acquire antigen for subsequent presentation to cognate T cells. Here we show that after mouse B cells accumulate antigen, it is maintained in a polarized distribution for extended periods in vivo. Using high-throughput imaging flow cytometry, we observed that this polarization is preserved during B cell division, promoting asymmetric antigen segregation among progeny. Antigen inheritance correlates with the ability of progeny to activate T cells: Daughter cells receiving larger antigen stores exhibit a prolonged capacity to present antigen, which renders them more effective in competing for T cell help. The generation of progeny with differential capacities for antigen presentation may have implications for somatic hypermutation and class switching during affinity maturation and as B cells commit to effector cell fates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thaunat, Olivier -- Granja, Aitor G -- Barral, Patricia -- Filby, Andrew -- Montaner, Beatriz -- Collinson, Lucy -- Martinez-Martin, Nuria -- Harwood, Naomi E -- Bruckbauer, Andreas -- Batista, Facundo D -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 27;335(6067):475-9. doi: 10.1126/science.1214100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22282815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigens/*analysis/*immunology ; B-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Proliferation ; Cells, Cultured ; Coculture Techniques ; Computer Simulation ; Flow Cytometry ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Immunological ; Muramidase/analysis/immunology ; T-Lymphocytes/*immunology
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    Polio campaign. Closing a deadly refuge (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Leslie -- New York, N.Y. -- Science. 2012 Aug 3;337(6094):520-1. doi: 10.1126/science.337.6094.520.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859467" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Disease Eradication/*trends ; Female ; *Homicide ; Humans ; Male ; Mass Vaccination/*trends ; Pakistan/epidemiology ; Patient Education as Topic ; Poliomyelitis/*epidemiology/*prevention & control ; Violence
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    Animal domestication. In search of the wild chicken (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, Andrew -- New York, N.Y. -- Science. 2012 Nov 23;338(6110):1020-4. doi: 10.1126/science.338.6110.1020.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23180839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Domestic/*genetics ; *Breeding ; Chickens/*genetics ; Extinction, Biological ; Female ; Influenza in Birds/genetics ; Male
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    Polio campaign. Fighting polio in Pakistan (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Leslie -- New York, N.Y. -- Science. 2012 Aug 3;337(6094):517-21. doi: 10.1126/science.337.6094.517.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859466" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Disease Eradication/*methods/*trends ; Female ; Humans ; Male ; Mass Vaccination/*methods/*trends ; Pakistan/epidemiology ; Poliomyelitis/*epidemiology/*prevention & control ; World Health Organization
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    The motherhood effect (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2012 May 18;336(6083):802. doi: 10.1126/science.336.6083.802-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22605734" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Mobility ; Female ; Humans ; Male ; *Mathematics ; *Mothers ; *Science ; *Women, Working
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    Wnt/beta-catenin signaling regulates telomerase in stem cells and cancer cells (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: Telomerase activity controls telomere length and plays a pivotal role in stem cells, aging, and cancer. Here, we report a molecular link between Wnt/beta-catenin signaling and the expression of the telomerase subunit Tert. beta-Catenin-deficient mouse embryonic stem (ES) cells have short telomeres; conversely, ES cell expressing an activated form of beta-catenin (beta-cat(DeltaEx3/+)) have long telomeres. We show that beta-catenin regulates Tert expression through the interaction with Klf4, a core component of the pluripotency transcriptional network. beta-Catenin binds to the Tert promoter in a mouse intestinal tumor model and in human carcinoma cells. We uncover a previously unknown link between the stem cell and oncogenic potential whereby beta-catenin regulates Tert expression, and thereby telomere length, which could be critical in human regenerative therapy and cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmeyer, Katrin -- Raggioli, Angelo -- Rudloff, Stefan -- Anton, Roman -- Hierholzer, Andreas -- Del Valle, Ignacio -- Hein, Kerstin -- Vogt, Riana -- Kemler, Rolf -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1549-54. doi: 10.1126/science.1218370.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723415" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*metabolism ; Animals ; Cell Line, Tumor ; Embryonic Stem Cells/*metabolism ; HEK293 Cells ; Humans ; Kruppel-Like Transcription Factors/metabolism ; Mice ; Neoplasms/genetics/*metabolism ; Promoter Regions, Genetic ; RNA, Messenger/genetics/metabolism ; Telomerase/*genetics/metabolism ; Telomere/metabolism/ultrastructure ; Telomere Homeostasis ; Transcription Initiation Site ; Wnt Proteins/metabolism ; *Wnt Signaling Pathway ; beta Catenin/genetics/*metabolism
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    Synaptic dysfunction in depression: potential therapeutic targets (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-09
    Description: Basic and clinical studies demonstrate that depression is associated with reduced size of brain regions that regulate mood and cognition, including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these areas. Antidepressants can block or reverse these neuronal deficits, although typical antidepressants have limited efficacy and delayed response times of weeks to months. A notable recent discovery shows that ketamine, a N-methyl-D-aspartate receptor antagonist, produces rapid (within hours) antidepressant responses in patients who are resistant to typical antidepressants. Basic studies show that ketamine rapidly induces synaptogenesis and reverses the synaptic deficits caused by chronic stress. These findings highlight the central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424898/" 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/PMC4424898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duman, Ronald S -- Aghajanian, George K -- R01 MH093897/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 5;338(6103):68-72. doi: 10.1126/science.1222939.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT 06508, USA. ronald.duman@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23042884" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antidepressive Agents/*administration & dosage ; Atrophy/pathology ; Behavior/drug effects ; Depressive Disorder, Major/*drug therapy/pathology/*physiopathology ; Homeostasis/drug effects ; Humans ; Mice ; Neurons/pathology ; Stress, Psychological/pathology/physiopathology ; Synapses/*drug effects/pathology/*physiology
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    Segregation of axonal and somatic activity during fast network oscillations (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-16
    Description: In central neurons, information flows from the dendritic surface toward the axon terminals. We found that during in vitro gamma oscillations, ectopic action potentials are generated at high frequency in the distal axon of pyramidal cells (PCs) but do not invade the soma. At the same time, axo-axonic cells (AACs) discharged at a high rate and tonically inhibited the axon initial segment, which can be instrumental in preventing ectopic action potential back-propagation. We found that activation of a single AAC substantially lowered soma invasion by antidromic action potential in postsynaptic PCs. In contrast, activation of soma-inhibiting basket cells had no significant impact. These results demonstrate that AACs can separate axonal from somatic activity and maintain the functional polarization of cortical PCs during network oscillations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dugladze, Tamar -- Schmitz, Dietmar -- Whittington, Miles A -- Vida, Imre -- Gloveli, Tengis -- New York, N.Y. -- Science. 2012 Jun 15;336(6087):1458-61. doi: 10.1126/science.1222017.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurophysiology, Charite-Universitatsmedizin Berlin, Chariteplatz 1, 10117 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22700932" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Axons/*physiology ; CA3 Region, Hippocampal/cytology/*physiology ; Electric Stimulation ; GABA-A Receptor Antagonists/pharmacology ; In Vitro Techniques ; Interneurons/*physiology ; Mice ; Nerve Net/*physiology ; Neural Inhibition ; Patch-Clamp Techniques ; Presynaptic Terminals/physiology ; Pyramidal Cells/*physiology ; Pyridazines/pharmacology ; Receptors, GABA-A/metabolism ; Synapses/physiology ; gamma-Aminobutyric Acid/pharmacology
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    HIV/AIDS in America. Introduction (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Leslie -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):167. doi: 10.1126/science.337.6091.167.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798592" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*epidemiology ; *Epidemics ; Female ; HIV Infections/diagnosis/*epidemiology ; Humans ; Male ; United States/epidemiology
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    Wnt5a potentiates TGF-beta signaling to promote colonic crypt regeneration after tissue injury (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-08
    Description: Reestablishing homeostasis after tissue damage depends on the proper organization of stem cells and their progeny, though the repair mechanisms are unclear. The mammalian intestinal epithelium is well suited to approach this problem, as it is composed of well-delineated units called crypts of Lieberkuhn. We found that Wnt5a, a noncanonical Wnt ligand, was required for crypt regeneration after injury in mice. Unlike controls, Wnt5a-deficient mice maintained an expanded population of proliferative epithelial cells in the wound. We used an in vitro system to enrich for intestinal epithelial stem cells to discover that Wnt5a inhibited proliferation of these cells. Surprisingly, the effects of Wnt5a were mediated by activation of transforming growth factor-beta (TGF-beta) signaling. These findings suggest a Wnt5a-dependent mechanism for forming new crypt units to reestablish homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3706630/" 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/PMC3706630/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyoshi, Hiroyuki -- Ajima, Rieko -- Luo, Christine T -- Yamaguchi, Terry P -- Stappenbeck, Thaddeus S -- 5T35DK074375/DK/NIDDK NIH HHS/ -- DK90251/DK/NIDDK NIH HHS/ -- P30-DK52574/DK/NIDDK NIH HHS/ -- R01 DK071619/DK/NIDDK NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 5;338(6103):108-13. doi: 10.1126/science.1223821. Epub 2012 Sep 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22956684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement/drug effects/physiology ; Cell Proliferation/drug effects ; Cells, Cultured ; Colon/embryology/*injuries/*physiology ; Culture Media, Conditioned/pharmacology ; Homeostasis/drug effects/physiology ; Intestinal Mucosa/embryology/injuries/physiology ; Ligands ; Mesoderm/cytology/embryology ; Mice ; Mice, Knockout ; Receptor Tyrosine Kinase-like Orphan Receptors/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Stem Cells/cytology/drug effects/physiology ; Tamoxifen/pharmacology ; Transforming Growth Factor beta/*metabolism ; Wnt Proteins/genetics/pharmacology/*physiology ; Wound Healing/drug effects/*physiology
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    Pheromonal induction of spatial learning in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-15
    Description: Many mammals use scent marking for sexual and competitive advertisement, but little is known about the mechanism by which scents are used to locate mates and competitors. We show that darcin, an involatile protein sex pheromone in male mouse urine, can rapidly condition preference for its remembered location among females and competitor males so that animals prefer to spend time in the site even when scent is absent. Learned spatial preference is conditioned through contact with darcin in a single trial and remembered for approximately 14 days. This pheromone-induced learning allows animals to relocate sites of particular social relevance and provides proof that pheromones such as darcin can be highly potent stimuli for social learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Sarah A -- Davidson, Amanda J -- McLean, Lynn -- Beynon, Robert J -- Hurst, Jane L -- BB/J002631/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC503897/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Dec 14;338(6113):1462-5. doi: 10.1126/science.1225638.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Behaviour and Evolution Group, Institute of Integrative Biology, University of Liverpool, Leahurst Campus, Neston CH64 7TE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23239735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Competitive Behavior/drug effects/*physiology ; Conditioning (Psychology)/drug effects/physiology ; Female ; Male ; Maze Learning/drug effects/*physiology ; Mice ; Mice, Inbred C57BL ; Proteins/pharmacology/*physiology ; Sex Attractants/pharmacology/*physiology/urine ; Smell/drug effects/physiology ; Spatial Behavior/drug effects/*physiology
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    Cuckoos combat socially transmitted defenses of reed warbler hosts with a plumage polymorphism (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-04
    Description: In predator-prey and host-parasite interactions, an individual's ability to combat an opponent often improves with experience--for example, by learning to identify enemy signals. Although learning occurs through individual experience, individuals can also assess threats from social information. Such recognition could promote the evolution of polymorphisms if socially transmitted defenses depend on enemy morph frequency. This would allow rare variants to evade detection. Female brood parasitic common cuckoos, Cuculus canorus, are either gray or rufous. The gray morph is a Batesian mimic whose hawk-like appearance deters host attack. Hosts reject this disguise through social learning, increasing their own defenses when they witness neighbors mobbing a cuckoo. Our experiments reveal that social learning is specific to the cuckoo morph that neighbors mob. Therefore, while neighbors alert hosts to local cuckoo activity, frequency-dependent social information selects for a cuckoo plumage polymorphism to thwart host detection. Our results suggest that selection for mimicry and polymorphisms comes not only from personal experience but also from social learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thorogood, Rose -- Davies, Nicholas B -- New York, N.Y. -- Science. 2012 Aug 3;337(6094):578-80. doi: 10.1126/science.1220759.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Cambridge, Cambridge CB2 3EJ, UK. rt303@cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859487" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Feathers/*anatomy & histology ; Female ; Learning ; *Nesting Behavior ; *Pigmentation ; *Social Behavior ; Songbirds/*anatomy & histology
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    Civilization's double-edged sword (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, Andrew -- New York, N.Y. -- Science. 2012 May 18;336(6083):832-3. doi: 10.1126/science.336.6083.832.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22605753" target="_blank"〉PubMed〈/a〉
    Keywords: Archaeology ; Cambodia ; Civilization/*history ; Female ; History, Ancient ; Homicide/history ; Humans ; Male ; Syria ; Thailand ; Violence/*history ; *Warfare ; Weapons
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    Cancer. Taking a back door to target Myc (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evan, Gerard -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):293-4. doi: 10.1126/science.1217819.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK. gie20@cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*genetics ; *Cell Transformation, Neoplastic ; Female ; *Genes, myc ; Humans ; Proto-Oncogene Proteins c-myc/*metabolism ; *Transcription, Genetic ; Ubiquitin-Activating Enzymes/*genetics
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    Gap junctions compensate for sublinear dendritic integration in an inhibitory network (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-10
    Description: Electrically coupled inhibitory interneurons dynamically control network excitability, yet little is known about how chemical and electrical synapses regulate their activity. Using two-photon glutamate uncaging and dendritic patch-clamp recordings, we found that the dendrites of cerebellar Golgi interneurons acted as passive cables. They conferred distance-dependent sublinear synaptic integration and weakened distal excitatory inputs. Gap junctions were present at a higher density on distal dendrites and contributed substantially to membrane conductance. Depolarization of one Golgi cell increased firing in its neighbors, and inclusion of dendritic gap junctions in interneuron network models enabled distal excitatory synapses to drive network activity more effectively. Our results suggest that dendritic gap junctions counteract sublinear dendritic integration by enabling excitatory synaptic charge to spread into the dendrites of neighboring inhibitory interneurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587282/" 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/PMC3587282/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vervaeke, Koen -- Lorincz, Andrea -- Nusser, Zoltan -- Silver, R Angus -- 064413/Wellcome Trust/United Kingdom -- 090197/Wellcome Trust/United Kingdom -- 095667/Wellcome Trust/United Kingdom -- 293681/European Research Council/International -- 294667/European Research Council/International -- BB/F005490/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- F005490/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0400598/Medical Research Council/United Kingdom -- G0400598(71261)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1624-8. doi: 10.1126/science.1215101. Epub 2012 Mar 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Physiology and Pharmacology, University College London, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22403180" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Cerebellar Cortex/cytology ; Computer Simulation ; Dendrites/*physiology/*ultrastructure ; Electrical Synapses/*physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; Interneurons/*physiology ; Ion Channels/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Neurological ; Nerve Net/*physiology/ultrastructure ; *Neural Inhibition ; Patch-Clamp Techniques ; Synapses/physiology ; Synaptic Transmission
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    Psychology. Bird-brained illusionists (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Barton L -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):292-3. doi: 10.1126/science.1217451.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Psychology, University of Sydney, Sydney, NSW 2006, Australia. barta@psych.usyd.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Male ; *Mating Preference, Animal ; *Optical Illusions ; Passeriformes/*physiology ; *Sexual Behavior, Animal
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    Economics. Ready, steady, compete (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Villeval, Marie Claire -- New York, N.Y. -- Science. 2012 Feb 3;335(6068):544-5. doi: 10.1126/science.1218000.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Lyon, 69007 Lyon, France. villeval@gate.cnrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22301308" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; Male ; *Policy ; *Task Performance and Analysis ; *Women
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Microbiology. Animal behavior and the microbiome (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ezenwa, Vanessa O -- Gerardo, Nicole M -- Inouye, David W -- Medina, Monica -- Xavier, Joao B -- New York, N.Y. -- Science. 2012 Oct 12;338(6104):198-9. doi: 10.1126/science.1227412.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Odum School of Ecology and Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23066064" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles gambiae/microbiology ; Anxiety/microbiology ; Bacteria/genetics ; Bacterial Adhesion/genetics ; Bacterial Secretion Systems/genetics ; *Behavior, Animal ; Decapodiformes/microbiology ; Drosophila melanogaster/microbiology ; Gastrointestinal Tract/microbiology ; Heteroptera/microbiology ; Host-Pathogen Interactions ; Humans ; Iguanas/microbiology ; Metagenome/*genetics/*physiology ; Mice ; Sexual Behavior, Animal ; Stress, Psychological/microbiology ; *Symbiosis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Extremely long-lived nuclear pore proteins in the rat brain (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-04
    Description: To combat the functional decline of the proteome, cells use the process of protein turnover to replace potentially impaired polypeptides with new functional copies. We found that extremely long-lived proteins (ELLPs) did not turn over in postmitotic cells of the rat central nervous system. These ELLPs were associated with chromatin and the nuclear pore complex, the central transport channels that mediate all molecular trafficking in and out of the nucleus. The longevity of these proteins would be expected to expose them to potentially harmful metabolites, putting them at risk of accumulating damage over extended periods of time. Thus, it is possible that failure to maintain proper levels and functional integrity of ELLPs in nonproliferative cells might contribute to age-related deterioration in cell and tissue function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296478/" 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/PMC3296478/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savas, Jeffrey N -- Toyama, Brandon H -- Xu, Tao -- Yates, John R 3rd -- Hetzer, Martin W -- F32 AG039127/AG/NIA NIH HHS/ -- F32 AG039127-01A1/AG/NIA NIH HHS/ -- F32AG039127/AG/NIA NIH HHS/ -- HHSN268201000035C/PHS HHS/ -- P01 AG031097/AG/NIA NIH HHS/ -- P01 AG031097-03/AG/NIA NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- P30 CA014195-35/CA/NCI NIH HHS/ -- P41 RR011823/RR/NCRR NIH HHS/ -- P41 RR011823-14/RR/NCRR NIH HHS/ -- R01 MH067880/MH/NIMH NIH HHS/ -- R01 MH067880-08/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2012 Feb 24;335(6071):942. doi: 10.1126/science.1217421. Epub 2012 Feb 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Physiology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22300851" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/*metabolism ; Cell Aging ; Chromatin/metabolism ; Female ; Half-Life ; Liver/metabolism ; Mitosis ; Nuclear Pore/*metabolism ; Nuclear Pore Complex Proteins/*metabolism ; Proteome/metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors
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    A global perspective on HIV/AIDS (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saxena, Shailendra K -- Tiwari, Sneham -- Nair, Madhavan P N -- New York, N.Y. -- Science. 2012 Aug 17;337(6096):798. doi: 10.1126/science.337.6096.798.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22903995" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*epidemiology ; *Epidemics ; Female ; HIV Infections/*epidemiology ; Humans ; Male
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The structures of COPI-coated vesicles reveal alternate coatomer conformations and interactions (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-26
    Description: Transport between compartments of eukaryotic cells is mediated by coated vesicles. The archetypal protein coats COPI, COPII, and clathrin are conserved from yeast to human. Structural studies of COPII and clathrin coats assembled in vitro without membranes suggest that coat components assemble regular cages with the same set of interactions between components. Detailed three-dimensional structures of coated membrane vesicles have not been obtained. Here, we solved the structures of individual COPI-coated membrane vesicles by cryoelectron tomography and subtomogram averaging of in vitro reconstituted budding reactions. The coat protein complex, coatomer, was observed to adopt alternative conformations to change the number of other coatomers with which it interacts and to form vesicles with variable sizes and shapes. This represents a fundamentally different basis for vesicle coat assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faini, Marco -- Prinz, Simone -- Beck, Rainer -- Schorb, Martin -- Riches, James D -- Bacia, Kirsten -- Brugger, Britta -- Wieland, Felix T -- Briggs, John A G -- New York, N.Y. -- Science. 2012 Jun 15;336(6087):1451-4. doi: 10.1126/science.1221443. Epub 2012 May 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Structural and Computational Biology Unit, European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COP-Coated Vesicles/*chemistry/*ultrastructure ; Coat Protein Complex I/*chemistry ; Coatomer Protein/*chemistry ; Cryoelectron Microscopy ; Electron Microscope Tomography ; Image Processing, Computer-Assisted ; Mice ; Models, Molecular ; Protein Conformation
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    GSK3-TIP60-ULK1 signaling pathway links growth factor deprivation to autophagy (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-28
    Description: In metazoans, cells depend on extracellular growth factors for energy homeostasis. We found that glycogen synthase kinase-3 (GSK3), when deinhibited by default in cells deprived of growth factors, activates acetyltransferase TIP60 through phosphorylating TIP60-Ser(86), which directly acetylates and stimulates the protein kinase ULK1, which is required for autophagy. Cells engineered to express TIP60(S86A) that cannot be phosphorylated by GSK3 could not undergo serum deprivation-induced autophagy. An acetylation-defective mutant of ULK1 failed to rescue autophagy in ULK1(-/-) mouse embryonic fibroblasts. Cells used signaling from GSK3 to TIP60 and ULK1 to regulate autophagy when deprived of serum but not glucose. These findings uncover an activating pathway that integrates protein phosphorylation and acetylation to connect growth factor deprivation to autophagy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Shu-Yong -- Li, Terytty Yang -- Liu, Qing -- Zhang, Cixiong -- Li, Xiaotong -- Chen, Yan -- Zhang, Shi-Meng -- Lian, Guili -- Liu, Qi -- Ruan, Ka -- Wang, Zhen -- Zhang, Chen-Song -- Chien, Kun-Yi -- Wu, Jiawei -- Li, Qinxi -- Han, Jiahuai -- Lin, Sheng-Cai -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):477-81. doi: 10.1126/science.1217032.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Fujian, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cell Line ; Cell Line, Tumor ; Culture Media ; Culture Media, Serum-Free ; Glucose/metabolism ; Glycogen Synthase Kinase 3/genetics/*metabolism ; HEK293 Cells ; Histone Acetyltransferases/genetics/*metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/genetics/*metabolism ; Mice ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Rats ; *Signal Transduction ; Trans-Activators/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Tumor necrosis factor signaling requires iRhom2 to promote trafficking and activation of TACE (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-17
    Description: The cytokine tumor necrosis factor (TNF) is the primary trigger of inflammation. Like many extracellular signaling proteins, TNF is synthesized as a transmembrane protein; the active signal is its ectodomain, which is shed from cells after cleavage by an ADAM family metalloprotease, ADAM17 (TNFalpha-converting enzyme, TACE). We report that iRhom2 (RHBDF2), a proteolytically inactive member of the rhomboid family, is required for TNF release in mice. iRhom2 binds TACE and promotes its exit from the endoplasmic reticulum. The failure of TACE to exit the endoplasmic reticulum in the absence of iRhom2 prevents the furin-mediated maturation and trafficking of TACE to the cell surface, the site of TNF cleavage. Given the role of TNF in autoimmune and inflammatory diseases, iRhom2 may represent an attractive therapeutic target.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3272371/" 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/PMC3272371/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adrain, Colin -- Zettl, Markus -- Christova, Yonka -- Taylor, Neil -- Freeman, Matthew -- MC_U105178780/Medical Research Council/United Kingdom -- U.1051.01.009(78780)/Medical Research Council/United Kingdom -- U105178780/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):225-8. doi: 10.1126/science.1214400.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246777" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/*metabolism ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; Enzyme Activation ; Furin/metabolism ; Humans ; Lipopolysaccharides/immunology ; Macrophages/metabolism ; Mice ; Mice, Knockout ; Protein Binding ; Protein Transport ; *Signal Transduction ; Tumor Necrosis Factor-alpha/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Crystal structure of the heterodimeric CLOCK:BMAL1 transcriptional activator complex (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-02
    Description: The circadian clock in mammals is driven by an autoregulatory transcriptional feedback mechanism that takes approximately 24 hours to complete. A key component of this mechanism is a heterodimeric transcriptional activator consisting of two basic helix-loop-helix PER-ARNT-SIM (bHLH-PAS) domain protein subunits, CLOCK and BMAL1. Here, we report the crystal structure of a complex containing the mouse CLOCK:BMAL1 bHLH-PAS domains at 2.3 A resolution. The structure reveals an unusual asymmetric heterodimer with the three domains in each of the two subunits--bHLH, PAS-A, and PAS-B--tightly intertwined and involved in dimerization interactions, resulting in three distinct protein interfaces. Mutations that perturb the observed heterodimer interfaces affect the stability and activity of the CLOCK:BMAL1 complex as well as the periodicity of the circadian oscillator. The structure of the CLOCK:BMAL1 complex is a starting point for understanding at an atomic level the mechanism driving the mammalian circadian clock.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694778/" 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/PMC3694778/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Nian -- Chelliah, Yogarany -- Shan, Yongli -- Taylor, Clinton A -- Yoo, Seung-Hee -- Partch, Carrie -- Green, Carla B -- Zhang, Hong -- Takahashi, Joseph S -- R01 GM081875/GM/NIGMS NIH HHS/ -- R01 GM090247/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):189-94. doi: 10.1126/science.1222804. Epub 2012 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22653727" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/*chemistry/genetics/metabolism ; Amino Acid Sequence ; Animals ; CLOCK Proteins/*chemistry/genetics/metabolism ; Cells, Cultured ; *Circadian Rhythm ; Crystallography, X-Ray ; DNA/metabolism ; HEK293 Cells ; Helix-Loop-Helix Motifs ; Humans ; Mice ; Models, Molecular ; Molecular Sequence Data ; Mutant Proteins/chemistry/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Multimerization ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Subunits/chemistry/metabolism ; Static Electricity ; *Transcriptional Activation
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    Reproductive biology. Potential egg stem cells reignite debate (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2012 Mar 2;335(6072):1029-30. doi: 10.1126/science.335.6072.1029.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22383817" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology ; Animals ; Cell Proliferation ; Cell Separation ; Female ; Humans ; Mice ; Oocytes/*cytology ; *Oogenesis ; Oogonia/*cytology ; Ovary/cytology
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    An overlapping protein-coding region in influenza A virus segment 3 modulates the host response (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-30
    Description: Influenza A virus (IAV) infection leads to variable and imperfectly understood pathogenicity. We report that segment 3 of the virus contains a second open reading frame ("X-ORF"), accessed via ribosomal frameshifting. The frameshift product, termed PA-X, comprises the endonuclease domain of the viral PA protein with a C-terminal domain encoded by the X-ORF and functions to repress cellular gene expression. PA-X also modulates IAV virulence in a mouse infection model, acting to decrease pathogenicity. Loss of PA-X expression leads to changes in the kinetics of the global host response, which notably includes increases in inflammatory, apoptotic, and T lymphocyte-signaling pathways. Thus, we have identified a previously unknown IAV protein that modulates the host response to infection, a finding with important implications for understanding IAV pathogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552242/" 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/PMC3552242/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jagger, B W -- Wise, H M -- Kash, J C -- Walters, K-A -- Wills, N M -- Xiao, Y-L -- Dunfee, R L -- Schwartzman, L M -- Ozinsky, A -- Bell, G L -- Dalton, R M -- Lo, A -- Efstathiou, S -- Atkins, J F -- Firth, A E -- Taubenberger, J K -- Digard, P -- 073126/Wellcome Trust/United Kingdom -- 088789/Wellcome Trust/United Kingdom -- G0700815/Medical Research Council/United Kingdom -- G0700815(82260)/Medical Research Council/United Kingdom -- G9800943/Medical Research Council/United Kingdom -- MR/J002232/1/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):199-204. doi: 10.1126/science.1222213. Epub 2012 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745253" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Codon ; Conserved Sequence ; Female ; *Frameshifting, Ribosomal ; Gene Expression Regulation ; Genome, Viral ; HEK293 Cells ; Humans ; Influenza A Virus, H1N1 Subtype/*genetics/growth & development/pathogenicity ; Influenza A virus/*genetics/metabolism ; Lung/pathology/virology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutation ; *Open Reading Frames ; Orthomyxoviridae Infections/genetics/immunology/pathology/*virology ; Protein Interaction Domains and Motifs ; Proteome ; RNA Replicase/chemistry/*genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Viral/genetics/metabolism ; Reassortant Viruses/genetics ; Repressor Proteins/chemistry/*genetics/*metabolism ; Viral Nonstructural Proteins/chemistry/*genetics/*metabolism ; Viral Proteins/biosynthesis/chemistry/*genetics/*metabolism ; Virus Replication
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    Cell biology. Rapamycin paradox resolved (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Katherine J -- Kennedy, Brian K -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1578-9. doi: 10.1126/science.1221365.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Buck Institute for Research on Aging, Novato, CA 94945, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; *Insulin Resistance ; *Longevity ; Male ; Sirolimus/*pharmacology
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    The group self (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-19
    Description: Although people often tend to consider themselves and others as unique individuals, there are many situations in which they think, feel, and act primarily as group members. This can bring out the best in them, as when they are inspired to help fellow citizens in need, or the worst, as when they show hostility against others simply because they represent another religious or ethnic group. Understanding when and why the group self becomes more important than the individual self, and how this affects people's thoughts, feelings, and behaviors, can help to prevent and redirect unwelcome aspects of human behavior by addressing them at the appropriate level of self.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ellemers, Naomi -- New York, N.Y. -- Science. 2012 May 18;336(6083):848-52. doi: 10.1126/science.1220987.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Psychological Research, Department of Social and Organizational Psychology, Leiden University, Post Office Box 9555, 2300 RB Leiden, Netherlands. Ellemers@fsw.leidenuniv.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22605760" target="_blank"〉PubMed〈/a〉
    Keywords: *Behavior ; Brain/physiology ; Female ; Humans ; Male ; *Self Concept ; Social Behavior ; *Social Identification
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    Regional astrocyte allocation regulates CNS synaptogenesis and repair (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-30
    Description: Astrocytes, the most abundant cell population in the central nervous system (CNS), are essential for normal neurological function. We show that astrocytes are allocated to spatial domains in mouse spinal cord and brain in accordance with their embryonic sites of origin in the ventricular zone. These domains remain stable throughout life without evidence of secondary tangential migration, even after acute CNS injury. Domain-specific depletion of astrocytes in ventral spinal cord resulted in abnormal motor neuron synaptogenesis, which was not rescued by immigration of astrocytes from adjoining regions. Our findings demonstrate that region-restricted astrocyte allocation is a general CNS phenomenon and reveal intrinsic limitations of the astroglial response to injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059181/" 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/PMC4059181/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Hui-Hsin -- Li, Huiliang -- Fuentealba, Luis C -- Molofsky, Anna V -- Taveira-Marques, Raquel -- Zhuang, Helin -- Tenney, April -- Murnen, Alice T -- Fancy, Stephen P J -- Merkle, Florian -- Kessaris, Nicoletta -- Alvarez-Buylla, Arturo -- Richardson, William D -- Rowitch, David H -- G0501173/Medical Research Council/United Kingdom -- G0800575/Medical Research Council/United Kingdom -- R01 NS028478/NS/NINDS NIH HHS/ -- R37 HD032116/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jul 20;337(6092):358-62. doi: 10.1126/science.1222381. Epub 2012 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745251" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*physiology ; Bacterial Proteins/metabolism ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Brain/abnormalities/*cytology/physiology ; Brain Injuries/physiopathology ; *Cell Movement ; Green Fluorescent Proteins ; Homeodomain Proteins/metabolism ; Integrases/genetics ; Luminescent Proteins/metabolism ; Mice ; Mice, Transgenic ; Motor Neurons/*physiology ; Nerve Tissue Proteins/genetics ; Proteins/metabolism ; RNA, Untranslated ; Spinal Cord/abnormalities/*cytology/physiology ; Spinal Cord Injuries/physiopathology ; Synapses/*physiology ; Transcription Factors/metabolism ; Transcription, Genetic
    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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    Research ethics. Paying patients for their tissue: the legacy of Henrietta Lacks (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-07
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4256075/" 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/PMC4256075/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Truog, Robert D -- Kesselheim, Aaron S -- Joffe, Steven -- 1 UL1 RR025758-01/RR/NCRR NIH HHS/ -- K08HS18465-01/HS/AHRQ HHS/ -- UL1 RR025758/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 6;337(6090):37-8. doi: 10.1126/science.1216888.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital Boston, Boston, MA 02115, USA. robert.truog@childrens.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22767914" target="_blank"〉PubMed〈/a〉
    Keywords: Economics ; *Ethics, Research ; Female ; Humans ; Informed Consent ; Male ; *Patient Rights ; Policy ; *Tissue Donors
    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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    Body cues, not facial expressions, discriminate between intense positive and negative emotions (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-01
    Description: The distinction between positive and negative emotions is fundamental in emotion models. Intriguingly, neurobiological work suggests shared mechanisms across positive and negative emotions. We tested whether similar overlap occurs in real-life facial expressions. During peak intensities of emotion, positive and negative situations were successfully discriminated from isolated bodies but not faces. Nevertheless, viewers perceived illusory positivity or negativity in the nondiagnostic faces when seen with bodies. To reveal the underlying mechanisms, we created compounds of intense negative faces combined with positive bodies, and vice versa. Perceived affect and mimicry of the faces shifted systematically as a function of their contextual body emotion. These findings challenge standard models of emotion expression and highlight the role of the body in expressing and perceiving emotions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aviezer, Hillel -- Trope, Yaacov -- Todorov, Alexander -- New York, N.Y. -- Science. 2012 Nov 30;338(6111):1225-9. doi: 10.1126/science.1224313.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Princeton University, Princeton, NJ 08540, USA. haviezer@mail.huji.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23197536" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; *Cues ; Emotions/*physiology ; *Facial Expression ; Female ; Humans ; Illusions ; *Kinesics ; Male ; *Perception ; Young Adult
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Natural SIV hosts: showing AIDS the door (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-10
    Description: Many species of African nonhuman primates are naturally infected with simian immunodeficiency viruses (SIVs) in the wild and in captivity. In contrast to HIV-infected humans, these natural SIV hosts typically do not develop AIDS, despite chronic infection with a highly replicating virus. In this Review, we discuss the most recent advances on the mechanisms of protection from disease progression in natural SIV hosts, with emphasis on how they differ from pathogenic HIV/SIV infections of humans and rhesus macaques. These mechanisms include: (i) resolution of immune activation after acute infection, (ii) restricted pattern of target cell infection, and (iii) protection from mother-to-infant transmission. We highlight the areas that should be pursued in future studies, focusing on potential applications for the treatment and prevention of HIV infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822437/" 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/PMC3822437/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chahroudi, Ann -- Bosinger, Steven E -- Vanderford, Thomas H -- Paiardini, Mirko -- Silvestri, Guido -- P51-RR00165/RR/NCRR NIH HHS/ -- R01 AI066998/AI/NIAID NIH HHS/ -- R01 AI084836/AI/NIAID NIH HHS/ -- R01-AI066998/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2012 Mar 9;335(6073):1188-93. doi: 10.1126/science.1217550.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22403383" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; CD4-Positive T-Lymphocytes/immunology/virology ; Cercocebus atys ; Cercopithecus aethiops ; Disease Progression ; Female ; HIV Infections/immunology/transmission/virology ; Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Infectious Disease Transmission, Vertical ; Simian Acquired Immunodeficiency Syndrome/*immunology/transmission/*virology ; *Simian Immunodeficiency Virus/immunology/pathogenicity/physiology ; T-Lymphocyte Subsets/immunology/virology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Task force's prevention advice proves hard to swallow. Interview by Eliot Marshall (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moyer, Virginia -- New York, N.Y. -- Science. 2012 Sep 21;337(6101):1468-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22997318" target="_blank"〉PubMed〈/a〉
    Keywords: *Advisory Committees ; Breast Neoplasms/diagnosis/*prevention & control ; *Early Detection of Cancer/statistics & numerical data ; Evidence-Based Medicine ; Female ; Health Policy ; Humans ; Male ; *Mammography/statistics & numerical data ; Prostate-Specific Antigen/blood ; Prostatic Neoplasms/diagnosis/*prevention & control ; Public Opinion ; United States ; United States Dept. of Health and Human Services/*organization & administration
    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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    China's push in tissue engineering (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hvistendahl, Mara -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):900-2. doi: 10.1126/science.338.6109.900.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23161989" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; China ; Government Programs ; Humans ; Mice ; Nerve Regeneration ; Peripheral Nerves/physiology/transplantation ; Tissue Engineering/*economics/*trends
    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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    Public health. Korea tackles a mushrooming problem (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Normile, Dennis -- New York, N.Y. -- Science. 2012 Nov 23;338(6110):1026-7. doi: 10.1126/science.338.6110.1026.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23180842" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Age Factors ; Aged ; Aged, 80 and over ; Child ; Female ; Humans ; Mental Disorders/epidemiology ; Middle Aged ; Republic of Korea/epidemiology ; Sex Factors ; Suicide/*statistics & numerical data/*trends ; Young Adult
    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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    Neuroethics. When a brain scan bears bad news (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2012 Oct 26;338(6106):455. doi: 10.1126/science.338.6106.455.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23112304" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/abnormalities/blood supply ; Female ; Humans ; *Incidental Findings ; Magnetic Resonance Imaging/*ethics ; Neuroimaging/*ethics ; *Practice Guidelines as Topic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genetics. A genetic intervention stands a skip away from clinical tests (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chamberlain, Jeffrey S -- R37 AR040864/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Dec 14;338(6113):1431-2. doi: 10.1126/science.1233074.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, School of Medicine, University of Washington, 1959 N.E. Pacific Street, Seattle, WA 98195-7720, USA. Jsc5@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23239725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Channel Blockers/administration & dosage/therapeutic use ; Clinical Trials as Topic ; Dantrolene/administration & dosage/*therapeutic use ; Disease Models, Animal ; Dystrophin/*biosynthesis/genetics ; Exons/genetics ; Mice ; Muscle Relaxants, Central/administration & dosage/*therapeutic use ; Muscular Dystrophy, Duchenne/genetics/*therapy ; Oligonucleotides, Antisense/administration & dosage/*therapeutic use ; RNA Precursors/genetics ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sequence Deletion
    Print ISSN: 0036-8075
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    Adaptive sleep loss in polygynous pectoral sandpipers (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-11
    Description: The functions of sleep remain elusive. Extensive evidence suggests that sleep performs restorative processes that sustain waking brain performance. An alternative view proposes that sleep simply enforces adaptive inactivity to conserve energy when activity is unproductive. Under this hypothesis, animals may evolve the ability to dispense with sleep when ecological demands favor wakefulness. Here, we show that male pectoral sandpipers (Calidris melanotos), a polygynous Arctic breeding shorebird, are able to maintain high neurobehavioral performance despite greatly reducing their time spent sleeping during a 3-week period of intense male-male competition for access to fertile females. Males that slept the least sired the most offspring. Our results challenge the view that decreased performance is an inescapable outcome of sleep loss.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lesku, John A -- Rattenborg, Niels C -- Valcu, Mihai -- Vyssotski, Alexei L -- Kuhn, Sylvia -- Kuemmeth, Franz -- Heidrich, Wolfgang -- Kempenaers, Bart -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1654-8. Epub 2012 Aug 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Avian Sleep Group, Max Planck Institute for Ornithology, Seewiesen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22878501" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Charadriiformes/*physiology ; Energy Metabolism ; Female ; Male ; *Reproduction ; *Sexual Behavior, Animal ; Sleep/*physiology
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    My microbiome and me (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hvistendahl, Mara -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1248-50. doi: 10.1126/science.336.6086.1248. Epub 2012 Jun 6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22674327" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*growth & development/metabolism ; Berberine/therapeutic use ; China ; Diet ; Drugs, Chinese Herbal/*therapeutic use ; Gastrointestinal Tract/*microbiology ; History, 20th Century ; History, 21st Century ; Humans ; Mice ; Obesity/diet therapy/drug therapy/*microbiology/*therapy ; Prebiotics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    IRE1alpha cleaves select microRNAs during ER stress to derepress translation of proapoptotic Caspase-2 (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-09
    Description: The endoplasmic reticulum (ER) is the primary organelle for folding and maturation of secretory and transmembrane proteins. Inability to meet protein-folding demand leads to "ER stress," and activates IRE1alpha, an ER transmembrane kinase-endoribonuclease (RNase). IRE1alpha promotes adaptation through splicing Xbp1 mRNA or apoptosis through incompletely understood mechanisms. Here, we found that sustained IRE1alpha RNase activation caused rapid decay of select microRNAs (miRs -17, -34a, -96, and -125b) that normally repress translation of Caspase-2 mRNA, and thus sharply elevates protein levels of this initiator protease of the mitochondrial apoptotic pathway. In cell-free systems, recombinant IRE1alpha endonucleolytically cleaved microRNA precursors at sites distinct from DICER. Thus, IRE1alpha regulates translation of a proapoptotic protein through terminating microRNA biogenesis, and noncoding RNAs are part of the ER stress response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742121/" 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/PMC3742121/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Upton, John-Paul -- Wang, Likun -- Han, Dan -- Wang, Eric S -- Huskey, Noelle E -- Lim, Lionel -- Truitt, Morgan -- McManus, Michael T -- Ruggero, Davide -- Goga, Andrei -- Papa, Feroz R -- Oakes, Scott A -- DK063720/DK/NIDDK NIH HHS/ -- DP2 OD001925/OD/NIH HHS/ -- DP2OD001925/OD/NIH HHS/ -- GM080783/GM/NIGMS NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- R01 CA136577/CA/NCI NIH HHS/ -- R01 CA136717/CA/NCI NIH HHS/ -- R01 CA140456/CA/NCI NIH HHS/ -- R01 CA154916/CA/NCI NIH HHS/ -- R01 DK080955/DK/NIDDK NIH HHS/ -- R01 GM080783/GM/NIGMS NIH HHS/ -- R01CA136577/CA/NCI NIH HHS/ -- R01CA136717/CA/NCI NIH HHS/ -- R01CA140456/CA/NCI NIH HHS/ -- R01CA154916/CA/NCI NIH HHS/ -- R01DK080955/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):818-22. doi: 10.1126/science.1226191. Epub 2012 Oct 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23042294" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Apoptosis ; Brefeldin A/pharmacology ; Caspase 2/*genetics/*metabolism ; Cell-Free System ; Cells, Cultured ; Cysteine Endopeptidases/*genetics/*metabolism ; Down-Regulation ; Endoplasmic Reticulum/metabolism ; *Endoplasmic Reticulum Stress ; Endoribonucleases/chemistry/genetics/*metabolism ; Enzyme Activation ; HEK293 Cells ; Humans ; Mice ; Mice, Knockout ; MicroRNAs/*metabolism ; Mutant Proteins ; Protein Biosynthesis ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; RNA Stability ; RNA, Messenger/genetics/metabolism ; Up-Regulation
    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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    Gender and violence (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hvistendahl, Mara -- New York, N.Y. -- Science. 2012 May 18;336(6083):839-40. doi: 10.1126/science.336.6083.839.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22605756" target="_blank"〉PubMed〈/a〉
    Keywords: Conflict (Psychology) ; Female ; Humans ; Male ; Sex Factors ; *Social Values ; *Violence ; *Warfare ; *Women's Rights/statistics & numerical data
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    Avian influenza. Public at last, H5N1 study offers insight into virus's possible path to pandemic (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1494-7. doi: 10.1126/science.336.6088.1494.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723387" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Evolution, Molecular ; Female ; *Ferrets ; Hemagglutinin Glycoproteins, Influenza Virus/*genetics ; Humans ; Influenza A Virus, H5N1 Subtype/*genetics/*pathogenicity ; Influenza, Human/*virology ; Orthomyxoviridae Infections/*virology ; RNA Replicase/*genetics ; Respiratory System/*virology ; Viral Proteins/*genetics
    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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    A stem cell-based approach to cartilage repair (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-12
    Description: Osteoarthritis (OA) is a degenerative joint disease that involves the destruction of articular cartilage and eventually leads to disability. Molecules that promote the selective differentiation of multipotent mesenchymal stem cells (MSCs) into chondrocytes may stimulate the repair of damaged cartilage. Using an image-based high-throughput screen, we identified the small molecule kartogenin, which promotes chondrocyte differentiation (median effective concentration = 100 nM), shows chondroprotective effects in vitro, and is efficacious in two OA animal models. Kartogenin binds filamin A, disrupts its interaction with the transcription factor core-binding factor beta subunit (CBFbeta), and induces chondrogenesis by regulating the CBFbeta-RUNX1 transcriptional program. This work provides new insights into the control of chondrogenesis that may ultimately lead to a stem cell-based therapy for osteoarthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Kristen -- Zhu, Shoutian -- Tremblay, Matthew S -- Payette, Joshua N -- Wang, Jianing -- Bouchez, Laure C -- Meeusen, Shelly -- Althage, Alana -- Cho, Charles Y -- Wu, Xu -- Schultz, Peter G -- New York, N.Y. -- Science. 2012 May 11;336(6082):717-21. doi: 10.1126/science.1215157. Epub 2012 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomics Institute of the Novartis Research Foundation, 10675 John Jay Hopkins Drive, San Diego, CA 92121, USA. kjohnson@gnf.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22491093" target="_blank"〉PubMed〈/a〉
    Keywords: Anilides/administration & dosage/chemistry/*pharmacology/therapeutic use ; Animals ; Cartilage, Articular/*cytology ; Cattle ; Cell Nucleus/metabolism ; Chondrocytes/cytology/*drug effects/metabolism/physiology ; *Chondrogenesis ; Contractile Proteins/metabolism ; Core Binding Factor Alpha 2 Subunit/metabolism ; Core Binding Factor beta Subunit/metabolism ; Disease Models, Animal ; Filamins ; High-Throughput Screening Assays ; Humans ; Mesenchymal Stromal Cells/cytology/*drug effects/physiology ; Mice ; Microfilament Proteins/metabolism ; Osteoarthritis/*drug therapy/pathology/physiopathology ; Phthalic Acids/administration & dosage/chemistry/*pharmacology/therapeutic use ; Regeneration ; Small Molecule Libraries ; Structure-Activity Relationship
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    Akt-mediated regulation of autophagy and tumorigenesis through Beclin 1 phosphorylation (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-01
    Description: Aberrant signaling through the class I phosphatidylinositol 3-kinase (PI3K)-Akt axis is frequent in human cancer. Here, we show that Beclin 1, an essential autophagy and tumor suppressor protein, is a target of the protein kinase Akt. Expression of a Beclin 1 mutant resistant to Akt-mediated phosphorylation increased autophagy, reduced anchorage-independent growth, and inhibited Akt-driven tumorigenesis. Akt-mediated phosphorylation of Beclin 1 enhanced its interactions with 14-3-3 and vimentin intermediate filament proteins, and vimentin depletion increased autophagy and inhibited Akt-driven transformation. Thus, Akt-mediated phosphorylation of Beclin 1 functions in autophagy inhibition, oncogenesis, and the formation of an autophagy-inhibitory Beclin 1/14-3-3/vimentin intermediate filament complex. These findings have broad implications for understanding the role of Akt signaling and intermediate filament proteins in autophagy and cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507442/" 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/PMC3507442/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Richard C -- Wei, Yongjie -- An, Zhenyi -- Zou, Zhongju -- Xiao, Guanghua -- Bhagat, Govind -- White, Michael -- Reichelt, Julia -- Levine, Beth -- K08 CA164047/CA/NCI NIH HHS/ -- P30 CA142543/CA/NCI NIH HHS/ -- R01 CA071443/CA/NCI NIH HHS/ -- R01 CA084254/CA/NCI NIH HHS/ -- R01 CA109618/CA/NCI NIH HHS/ -- R01 CA129451/CA/NCI NIH HHS/ -- R01 CA84254-S1/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):956-9. doi: 10.1126/science.1225967. Epub 2012 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23112296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins/genetics/*metabolism ; *Autophagy ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/*metabolism ; Fibroblasts/metabolism/pathology ; HeLa Cells ; Humans ; Membrane Proteins/genetics/*metabolism ; Mice ; Phosphorylation ; Proto-Oncogene Proteins c-akt/genetics/*metabolism ; RNA, Small Interfering/genetics ; Rats ; Transduction, Genetic ; Vimentin/genetics ; Xenograft Model Antitumor Assays
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    Evolution of shape by multiple regulatory changes to a growth gene (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-01
    Description: The genetic changes responsible for morphological differences between species are largely unidentified. Such changes can involve modifications of growth that are relevant to understanding evolution, development, and disease. We identified a gene that induces male-specific wing size and shape differences between Nasonia wasp species. Fine-scale mapping and in situ hybridization reveal that changes in at least three regions (two strictly in noncoding sequence) around the gene unpaired-like (upd-like) cause changes in spatial and temporal expression of upd-like in the developing wing and corresponding changes in wing width. Upd-like shows homology to the Drosophila unpaired gene, a well-studied signaling protein that regulates cell proliferation and differentiation. Our results indicate how multiple changes in the regulation of upd-like are involved in microevolution of morphological and sex-specific differences between species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3520604/" 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/PMC3520604/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loehlin, David W -- Werren, John H -- 5R01 GM070026-04/GM/NIGMS NIH HHS/ -- 5R24 GM084917-04/GM/NIGMS NIH HHS/ -- R01 GM070026/GM/NIGMS NIH HHS/ -- R24 GM084917/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Feb 24;335(6071):943-7. doi: 10.1126/science.1215193.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Rochester, Rochester, NY 14627, USA. loehlin@wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22363002" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Biological Evolution ; Cloning, Molecular ; Drosophila/genetics ; Drosophila Proteins/genetics ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genes, Insect ; Insect Proteins/*genetics/metabolism ; Male ; Molecular Sequence Data ; Morphogenesis/genetics ; Organ Size ; Quantitative Trait Loci ; Sex Characteristics ; Species Specificity ; Transcription Factors/genetics ; Wasps/anatomy & histology/*genetics/*growth & development ; Wings, Animal/*anatomy & histology/*growth & development/metabolism
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    Fetal and early childhood undernutrition, mortality, and lifelong health (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-22
    Description: Child undernutrition is a major public health challenge, estimated to be responsible for 2.2 million annual deaths. Implementation of available interventions could prevent one-third of these deaths. Emerging evidence suggests that breast-feeding can lead to improvements in intelligence quotient in children and lower risks of noncommunicable diseases in mothers and children decades later. Nonetheless, breast-feeding and complementary feeding practices differ greatly from global recommendations. Although the World Health Organization recommends that infants receive solely breast milk for the first 6 months of life, only about one-third of infants in low-income countries meet this goal, just one-third of children 6 to 24 months old in low-income countries meet the minimum criteria for dietary diversity, and only one in five who are breast-fed receive a minimum acceptable diet. Although the potential effects of improved breast-feeding and complementary feeding appear large, funding for research and greater use of existing effective interventions seems low compared with other life-saving child health interventions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lutter, Chessa K -- Lutter, Randall -- New York, N.Y. -- Science. 2012 Sep 21;337(6101):1495-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pan American Health Organization/World Health Organization, 525 23rd Street NW, Washington, DC 20037-2895, USA. lutterch@paho.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22997328" target="_blank"〉PubMed〈/a〉
    Keywords: *Breast Feeding ; *Child Nutrition Disorders/epidemiology/mortality/prevention & control ; Child, Preschool ; Developed Countries ; Developing Countries ; Female ; *Fetal Nutrition Disorders/epidemiology/mortality/prevention & control ; *Health ; Health Promotion ; Humans ; Infant ; Infant Food ; *Infant Nutrition Disorders/epidemiology/mortality/prevention & control ; *Infant Nutritional Physiological Phenomena ; Infant, Newborn
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    Circadian rhythm of redox state regulates excitability in suprachiasmatic nucleus neurons (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-04
    Description: Daily rhythms of mammalian physiology, metabolism, and behavior parallel the day-night cycle. They are orchestrated by a central circadian clock in the brain, the suprachiasmatic nucleus (SCN). Transcription of clock genes is sensitive to metabolic changes in reduction and oxidation (redox); however, circadian cycles in protein oxidation have been reported in anucleate cells, where no transcription occurs. We investigated whether the SCN also expresses redox cycles and how such metabolic oscillations might affect neuronal physiology. We detected self-sustained circadian rhythms of SCN redox state that required the molecular clockwork. The redox oscillation could determine the excitability of SCN neurons through nontranscriptional modulation of multiple potassium (K(+)) channels. Thus, dynamic regulation of SCN excitability appears to be closely tied to metabolism that engages the clockwork machinery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3490628/" 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/PMC3490628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Tongfei A -- Yu, Yanxun V -- Govindaiah, Gubbi -- Ye, Xiaoying -- Artinian, Liana -- Coleman, Todd P -- Sweedler, Jonathan V -- Cox, Charles L -- Gillette, Martha U -- EY014024/EY/NEI NIH HHS/ -- P30 DA018310/DA/NIDA NIH HHS/ -- P30DA018310/DA/NIDA NIH HHS/ -- R01 EY014024/EY/NEI NIH HHS/ -- R01 HL086870/HL/NHLBI NIH HHS/ -- R01 HL092571/HL/NHLBI NIH HHS/ -- R01HL086870/HL/NHLBI NIH HHS/ -- R01HL092571/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 17;337(6096):839-42. doi: 10.1126/science.1222826. Epub 2012 Aug 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859819" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics ; Animals ; *Circadian Rhythm ; Fluorometry ; Glutathione/metabolism ; Membrane Potentials ; Mice ; Mice, Mutant Strains ; NADP/metabolism ; Neurons/metabolism/*physiology ; Oxidation-Reduction ; Potassium Channels/metabolism ; Rats ; Suprachiasmatic Nucleus/cytology/metabolism/*physiology
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    Washington, District of Columbia. HIV/AIDS response renovated in capital (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):182. doi: 10.1126/science.337.6091.182-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798605" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/statistics & numerical data ; Community Health Services ; District of Columbia/epidemiology ; Epidemics ; Female ; HIV Infections/diagnosis/*epidemiology/prevention & control/transmission ; Homosexuality, Male/statistics & numerical data ; Humans ; Male ; Patient Compliance ; Substance Abuse, Intravenous/complications ; Viral Load
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    Baltimore, Maryland. Dancing the night away; keeping HIV at bay (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):181-2. doi: 10.1126/science.337.6091.181.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798604" target="_blank"〉PubMed〈/a〉
    Keywords: *African Americans ; Baltimore/epidemiology ; *Dancing ; *Epidemics ; Female ; HIV Infections/*epidemiology ; *Homosexuality, Male ; Humans ; Incidence ; Male ; Prevalence ; Public Health ; *Risk-Taking ; Sex Workers ; Unsafe Sex
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    Single-sex education: results one-sided (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kalkus, Olen Anthony -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):165; author reply 166-8. doi: 10.1126/science.335.6065.165-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246751" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiology ; Education/*methods/*standards ; Female ; Humans ; *Learning ; Male ; *Sex Characteristics
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    The transcription factor c-Maf controls touch receptor development and function (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-22
    Description: The sense of touch relies on detection of mechanical stimuli by specialized mechanosensory neurons. The scarcity of molecular data has made it difficult to analyze development of mechanoreceptors and to define the basis of their diversity and function. We show that the transcription factor c-Maf/c-MAF is crucial for mechanosensory function in mice and humans. The development and function of several rapidly adapting mechanoreceptor types are disrupted in c-Maf mutant mice. In particular, Pacinian corpuscles, a type of mechanoreceptor specialized to detect high-frequency vibrations, are severely atrophied. In line with this, sensitivity to high-frequency vibration is reduced in humans carrying a dominant mutation in the c-MAF gene. Thus, our work identifies a key transcription factor specifying development and function of mechanoreceptors and their end organs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wende, Hagen -- Lechner, Stefan G -- Cheret, Cyril -- Bourane, Steeve -- Kolanczyk, Maria E -- Pattyn, Alexandre -- Reuter, Katja -- Munier, Francis L -- Carroll, Patrick -- Lewin, Gary R -- Birchmeier, Carmen -- New York, N.Y. -- Science. 2012 Mar 16;335(6074):1373-6. doi: 10.1126/science.1214314. Epub 2012 Feb 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology, Max Delbruck Center (MDC) for Molecular Medicine, Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22345400" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ganglia, Spinal/cytology/embryology ; Gene Expression Regulation, Developmental ; Humans ; Maf Transcription Factors, Large/genetics/metabolism ; Mechanoreceptors/*cytology/*physiology ; Mice ; Mutation ; Pacinian Corpuscles/cytology/physiology ; Proto-Oncogene Proteins c-maf/genetics/*metabolism ; Proto-Oncogene Proteins c-ret/genetics/metabolism ; Skin/innervation ; *Touch ; Vibration
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    Regulated virulence controls the ability of a pathogen to compete with the gut microbiota (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-15
    Description: The virulence mechanisms that allow pathogens to colonize the intestine remain unclear. Here, we show that germ-free animals are unable to eradicate Citrobacter rodentium, a model for human infections with attaching and effacing bacteria. Early in infection, virulence genes were expressed and required for pathogen growth in conventionally raised mice but not germ-free mice. Virulence gene expression was down-regulated during the late phase of infection, which led to relocation of the pathogen to the intestinal lumen where it was outcompeted by commensals. The ability of commensals to outcompete C. rodentium was determined, at least in part, by the capacity of the pathogen and commensals to grow on structurally similar carbohydrates. Thus, pathogen colonization is controlled by bacterial virulence and through competition with metabolically related commensals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439148/" 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/PMC3439148/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamada, Nobuhiko -- Kim, Yun-Gi -- Sham, Ho Pan -- Vallance, Bruce A -- Puente, Jose L -- Martens, Eric C -- Nunez, Gabriel -- DK091191/DK/NIDDK NIH HHS/ -- DK61707/DK/NIDDK NIH HHS/ -- R01 DK061707/DK/NIDDK NIH HHS/ -- R01 DK091191/DK/NIDDK NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1325-9. doi: 10.1126/science.1222195. Epub 2012 May 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582016" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Load ; Bacterial Proteins/genetics/metabolism ; Bacteroides/*growth & development ; Citrobacter rodentium/genetics/growth & development/immunology/*pathogenicity ; Enterobacteriaceae Infections/immunology/*microbiology ; Escherichia coli/*growth & development ; Feces/microbiology ; Gene Expression Regulation, Bacterial ; Germ-Free Life ; Intestinal Mucosa/*microbiology ; Intestines/*microbiology ; *Metagenome ; Mice ; Mice, Inbred C57BL ; *Microbial Interactions ; Specific Pathogen-Free Organisms ; Virulence Factors/genetics/metabolism
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    Single-sex education: parameters too narrow (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palaima, Thomas G -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):166; author reply 166-8. doi: 10.1126/science.335.6065.166-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246754" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiology ; Education/*methods/*standards ; Female ; Humans ; *Learning ; Male ; *Sex Characteristics
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    San Diego, California, and Tijuana, Mexico. My virus is your virus (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):177-8. doi: 10.1126/science.337.6091.177.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798600" target="_blank"〉PubMed〈/a〉
    Keywords: California/epidemiology ; Emigration and Immigration ; Female ; HIV Infections/*complications/*epidemiology/transmission ; Humans ; International Cooperation ; Male ; Mexico/epidemiology ; Needle Sharing ; Sex Workers ; Substance Abuse, Intravenous/*complications/epidemiology
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    Progenitor and terminal subsets of CD8+ T cells cooperate to contain chronic viral infection (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-01
    Description: Chronic infections strain the regenerative capacity of antiviral T lymphocyte populations, leading to failure in long-term immunity. The cellular and molecular events controlling this regenerative capacity, however, are unknown. We found that two distinct states of virus-specific CD8(+) T cells exist in chronically infected mice and humans. Differential expression of the T-box transcription factors T-bet and Eomesodermin (Eomes) facilitated the cooperative maintenance of the pool of antiviral CD8(+) T cells during chronic viral infection. T-bet(hi) cells displayed low intrinsic turnover but proliferated in response to persisting antigen, giving rise to Eomes(hi) terminal progeny. Genetic elimination of either subset resulted in failure to control chronic infection, which suggests that an imbalance in differentiation and renewal could underlie the collapse of immunity in humans with chronic infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653769/" 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/PMC3653769/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paley, Michael A -- Kroy, Daniela C -- Odorizzi, Pamela M -- Johnnidis, Jonathan B -- Dolfi, Douglas V -- Barnett, Burton E -- Bikoff, Elizabeth K -- Robertson, Elizabeth J -- Lauer, Georg M -- Reiner, Steven L -- Wherry, E John -- 059312/Wellcome Trust/United Kingdom -- AI061699/AI/NIAID NIH HHS/ -- AI0663445/AI/NIAID NIH HHS/ -- AI076458/AI/NIAID NIH HHS/ -- AI078897/AI/NIAID NIH HHS/ -- AI082630/AI/NIAID NIH HHS/ -- AI083022/AI/NIAID NIH HHS/ -- HHSN266200500030C/AI/NIAID NIH HHS/ -- HHSN266200500030C/PHS HHS/ -- P01 AI078897/AI/NIAID NIH HHS/ -- P30 CA016520/CA/NCI NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 AI042370/AI/NIAID NIH HHS/ -- R01 AI061699/AI/NIAID NIH HHS/ -- R01 AI076458/AI/NIAID NIH HHS/ -- T32 AI007632/AI/NIAID NIH HHS/ -- T32-AI-07324/AI/NIAID NIH HHS/ -- U19 AI082630/AI/NIAID NIH HHS/ -- U19 AI083022/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 30;338(6111):1220-5. doi: 10.1126/science.1229620.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23197535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology ; Hepatitis B, Chronic/*immunology ; Humans ; Liver/virology ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Stem Cells/immunology ; T-Box Domain Proteins/genetics/*metabolism ; T-Lymphocyte Subsets/*immunology
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    San Francisco, California. A concerted effort to lighten the load (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):175-6. doi: 10.1126/science.337.6091.175.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798598" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/therapeutic use ; Female ; HIV Infections/drug therapy/*epidemiology/virology ; Homosexuality, Male ; Humans ; Male ; *Outpatient Clinics, Hospital ; Patient Compliance ; *Public Health Practice ; San Francisco/epidemiology ; *Viral Load
    Print ISSN: 0036-8075
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  • 89
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    Glucocorticoids can induce PTSD-like memory impairments in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-01
    Description: Posttraumatic stress disorder (PTSD) is characterized by a hypermnesia of the trauma and by a memory impairment that decreases the ability to restrict fear to the appropriate context. Infusion of glucocorticoids in the hippocampus after fear conditioning induces PTSD-like memory impairments and an altered pattern of neural activation in the hippocampal-amygdalar circuit. Mice become unable to identify the context as the correct predictor of the threat and show fear responses to a discrete cue not predicting the threat in normal conditions. These data demonstrate PTSD-like memory impairments in rodents and identify a potential pathophysiological mechanism of this condition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaouane, Nadia -- Porte, Yves -- Vallee, Monique -- Brayda-Bruno, Laurent -- Mons, Nicole -- Calandreau, Ludovic -- Marighetto, Aline -- Piazza, Pier Vincenzo -- Desmedt, Aline -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1510-3. doi: 10.1126/science.1207615. Epub 2012 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS UMR 5228, Centre de Neurosciences Integratives et Cognitives, Talence, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22362879" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*physiopathology ; Animals ; Conditioning (Psychology) ; Corticosterone/*administration & dosage/blood/metabolism/pharmacology ; Cues ; Electroshock ; *Fear ; Hippocampus/*physiopathology ; Male ; Memory Disorders/chemically induced/*physiopathology ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-fos/metabolism ; Restraint, Physical ; Stress Disorders, Post-Traumatic/*physiopathology ; Stress, Psychological
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    Removal of shelterin reveals the telomere end-protection problem (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-05
    Description: The telomere end-protection problem is defined by the aggregate of DNA damage signaling and repair pathways that require repression at telomeres. To define the end-protection problem, we removed the whole shelterin complex from mouse telomeres through conditional deletion of TRF1 and TRF2 in nonhomologous end-joining (NHEJ) deficient cells. The data reveal two DNA damage response pathways not previously observed upon deletion of individual shelterin proteins. The shelterin-free telomeres are processed by microhomology-mediated alternative-NHEJ when Ku70/80 is absent and are attacked by nucleolytic degradation in the absence of 53BP1. The data establish that the end-protection problem is specified by six pathways [ATM (ataxia telangiectasia mutated) and ATR (ataxia telangiectasia and Rad3 related) signaling, classical-NHEJ, alt-NHEJ, homologous recombination, and resection] and show how shelterin acts with general DNA damage response factors to solve this problem.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3477646/" 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/PMC3477646/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sfeir, Agnel -- de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- GM49046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 CA076027/CA/NCI NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 May 4;336(6081):593-7. doi: 10.1126/science.1218498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22556254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Nuclear/genetics/metabolism ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/metabolism ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA Ligases/metabolism ; DNA Repair ; DNA-Binding Proteins/genetics/metabolism ; Homologous Recombination ; Mice ; Mice, Knockout ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Telomere/*metabolism/ultrastructure ; *Telomere Homeostasis ; Telomere-Binding Proteins/genetics/*metabolism ; Telomeric Repeat Binding Protein 1/genetics/metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism ; Tumor Suppressor Proteins/metabolism
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    The many states of HIV in America (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):168-71. doi: 10.1126/science.337.6091.168.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798593" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/statistics & numerical data ; Anti-HIV Agents/therapeutic use ; *Epidemics ; Female ; HIV Infections/diagnosis/drug therapy/*epidemiology/transmission ; Heterosexuality/statistics & numerical data ; Hispanic Americans/statistics & numerical data ; Homosexuality, Male/statistics & numerical data ; Humans ; Male ; Medication Adherence ; Prevalence ; Socioeconomic Factors ; Southeastern United States/epidemiology ; United States/epidemiology ; Urban Health/statistics & numerical data
    Print ISSN: 0036-8075
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  • 92
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    Some consequences of having too little (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-03
    Description: Poor individuals often engage in behaviors, such as excessive borrowing, that reinforce the conditions of poverty. Some explanations for these behaviors focus on personality traits of the poor. Others emphasize environmental factors such as housing or financial access. We instead consider how certain behaviors stem simply from having less. We suggest that scarcity changes how people allocate attention: It leads them to engage more deeply in some problems while neglecting others. Across several experiments, we show that scarcity leads to attentional shifts that can help to explain behaviors such as overborrowing. We discuss how this mechanism might also explain other puzzles of poverty.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shah, Anuj K -- Mullainathan, Sendhil -- Shafir, Eldar -- New York, N.Y. -- Science. 2012 Nov 2;338(6107):682-5. doi: 10.1126/science.1222426.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Booth School of Business, University of Chicago, Chicago, IL 60637, USA. anuj.shah@chicagobooth.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23118192" target="_blank"〉PubMed〈/a〉
    Keywords: *Attention ; *Decision Making ; Female ; Financing, Personal ; Games, Experimental ; Humans ; Male ; Poverty/*psychology ; *Socioeconomic Factors
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    Infectious disease. HIV prevention and cure insights come from failure and success (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2012 Mar 16;335(6074):1291. doi: 10.1126/science.335.6074.1291.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22422953" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/administration & dosage/blood/*therapeutic use ; Controlled Clinical Trials as Topic ; Female ; HIV/drug effects/immunology/*physiology ; HIV Infections/*drug therapy/immunology/*prevention & control/virology ; Humans ; Male ; Medication Adherence ; Virus Activation ; Virus Latency
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    Single-sex education: positive effects (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Hyunjoon -- Behrman, Jere R -- Choi, Jaesung -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):165-6; author reply 166-8. doi: 10.1126/science.335.6065.165-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246752" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiology ; Education/*methods/*standards ; Female ; Humans ; *Learning ; Male ; *Sex Characteristics
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    Microbial exposure during early life has persistent effects on natural killer T cell function (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-24
    Description: Exposure to microbes during early childhood is associated with protection from immune-mediated diseases such as inflammatory bowel disease (IBD) and asthma. Here, we show that in germ-free (GF) mice, invariant natural killer T (iNKT) cells accumulate in the colonic lamina propria and lung, resulting in increased morbidity in models of IBD and allergic asthma as compared with that of specific pathogen-free mice. This was associated with increased intestinal and pulmonary expression of the chemokine ligand CXCL16, which was associated with increased mucosal iNKT cells. Colonization of neonatal-but not adult-GF mice with a conventional microbiota protected the animals from mucosal iNKT accumulation and related pathology. These results indicate that age-sensitive contact with commensal microbes is critical for establishing mucosal iNKT cell tolerance to later environmental exposures.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437652/" 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/PMC3437652/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olszak, Torsten -- An, Dingding -- Zeissig, Sebastian -- Vera, Miguel Pinilla -- Richter, Julia -- Franke, Andre -- Glickman, Jonathan N -- Siebert, Reiner -- Baron, Rebecca M -- Kasper, Dennis L -- Blumberg, Richard S -- AI090102/AI/NIAID NIH HHS/ -- DK034854/DK/NIDDK NIH HHS/ -- DK44319/DK/NIDDK NIH HHS/ -- DK51362/DK/NIDDK NIH HHS/ -- DK53056/DK/NIDDK NIH HHS/ -- DK88199/DK/NIDDK NIH HHS/ -- P30 DK034854/DK/NIDDK NIH HHS/ -- R01 DK044319/DK/NIDDK NIH HHS/ -- R01 DK088199/DK/NIDDK NIH HHS/ -- R37 DK044319/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):489-93. doi: 10.1126/science.1219328. Epub 2012 Mar 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442383" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Antigens, CD1d/immunology ; Asthma/*immunology ; Bacteria/*growth & development ; Chemokine CXCL6/genetics/metabolism ; Colitis, Ulcerative/chemically induced/*immunology ; Colon/immunology/microbiology ; DNA Methylation ; Disease Models, Animal ; Disease Susceptibility ; Germ-Free Life ; Intestinal Mucosa/*immunology ; Intestines/immunology/*microbiology ; Lung/*immunology ; Mice ; Mice, Inbred C57BL ; Natural Killer T-Cells/*immunology ; Oxazolone ; Receptors, CXCR/genetics/metabolism ; Specific Pathogen-Free Organisms
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    Multiplex targeted sequencing identifies recurrently mutated genes in autism spectrum disorders (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-20
    Description: Exome sequencing studies of autism spectrum disorders (ASDs) have identified many de novo mutations but few recurrently disrupted genes. We therefore developed a modified molecular inversion probe method enabling ultra-low-cost candidate gene resequencing in very large cohorts. To demonstrate the power of this approach, we captured and sequenced 44 candidate genes in 2446 ASD probands. We discovered 27 de novo events in 16 genes, 59% of which are predicted to truncate proteins or disrupt splicing. We estimate that recurrent disruptive mutations in six genes-CHD8, DYRK1A, GRIN2B, TBR1, PTEN, and TBL1XR1-may contribute to 1% of sporadic ASDs. Our data support associations between specific genes and reciprocal subphenotypes (CHD8-macrocephaly and DYRK1A-microcephaly) and replicate the importance of a beta-catenin-chromatin-remodeling network to ASD etiology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528801/" 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/PMC3528801/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Roak, Brian J -- Vives, Laura -- Fu, Wenqing -- Egertson, Jarrett D -- Stanaway, Ian B -- Phelps, Ian G -- Carvill, Gemma -- Kumar, Akash -- Lee, Choli -- Ankenman, Katy -- Munson, Jeff -- Hiatt, Joseph B -- Turner, Emily H -- Levy, Roie -- O'Day, Diana R -- Krumm, Niklas -- Coe, Bradley P -- Martin, Beth K -- Borenstein, Elhanan -- Nickerson, Deborah A -- Mefford, Heather C -- Doherty, Dan -- Akey, Joshua M -- Bernier, Raphael -- Eichler, Evan E -- Shendure, Jay -- HD065285/HD/NICHD NIH HHS/ -- HL-102923/HL/NHLBI NIH HHS/ -- HL-102924/HL/NHLBI NIH HHS/ -- HL-102925/HL/NHLBI NIH HHS/ -- HL-102926/HL/NHLBI NIH HHS/ -- HL-103010/HL/NHLBI NIH HHS/ -- NS069605/NS/NINDS NIH HHS/ -- R01 HD065285/HD/NICHD NIH HHS/ -- R01 NS064077/NS/NINDS NIH HHS/ -- R01 NS069605/NS/NINDS NIH HHS/ -- RC2 HL102926/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Dec 21;338(6114):1619-22. doi: 10.1126/science.1227764. Epub 2012 Nov 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23160955" target="_blank"〉PubMed〈/a〉
    Keywords: Cephalometry ; Child ; Child Development Disorders, Pervasive/*genetics ; Child, Preschool ; Chromatin Assembly and Disassembly ; Cohort Studies ; DNA Probes ; DNA-Binding Proteins/genetics ; Exome ; Female ; *Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Male ; Megalencephaly/genetics ; Microcephaly/genetics ; *Mutation ; Nuclear Proteins/genetics ; PTEN Phosphohydrolase/genetics ; Protein-Serine-Threonine Kinases/genetics ; Protein-Tyrosine Kinases/genetics ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, N-Methyl-D-Aspartate/genetics ; Repressor Proteins/genetics ; Sequence Analysis, DNA/*methods ; T-Box Domain Proteins/genetics ; Transcription Factors/genetics ; beta Catenin/genetics/metabolism
    Print ISSN: 0036-8075
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    Dedifferentiation of neurons and astrocytes by oncogenes can induce gliomas in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-23
    Description: Glioblastoma multiforme (GBM) is the most common and aggressive malignant primary brain tumor in humans. Here we show that gliomas can originate from differentiated cells in the central nervous system (CNS), including cortical neurons. Transduction by oncogenic lentiviral vectors of neural stem cells (NSCs), astrocytes, or even mature neurons in the brains of mice can give rise to malignant gliomas. All the tumors, irrespective of the site of lentiviral vector injection (the initiating population), shared common features of high expression of stem or progenitor markers and low expression of differentiation markers. Microarray analysis revealed that tumors of astrocytic and neuronal origin match the mesenchymal GBM subtype. We propose that most differentiated cells in the CNS upon defined genetic alterations undergo dedifferentiation to generate a NSC or progenitor state to initiate and maintain the tumor progression, as well as to give rise to the heterogeneous populations observed in malignant gliomas.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3595315/" 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/PMC3595315/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friedmann-Morvinski, Dinorah -- Bushong, Eric A -- Ke, Eugene -- Soda, Yasushi -- Marumoto, Tomotoshi -- Singer, Oded -- Ellisman, Mark H -- Verma, Inder M -- 5P41RR004050/RR/NCRR NIH HHS/ -- HL053670/HL/NHLBI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- P30 CA014195-38/CA/NCI NIH HHS/ -- R01 HL053670/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 23;338(6110):1080-4. doi: 10.1126/science.1226929. Epub 2012 Oct 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23087000" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/metabolism/*pathology ; Brain Neoplasms/*genetics/*pathology ; Genes, Neurofibromatosis 1 ; Genes, p53 ; Glioblastoma/genetics/pathology ; Glioma/*genetics/*pathology ; Lentivirus ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/genetics ; Neural Stem Cells/metabolism/pathology ; Neurons/metabolism/*pathology ; *Oncogenes ; Transduction, Genetic
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    Neuroscience. Preventable forms of autism? (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-23
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4102925/" 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/PMC4102925/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beaudet, Arthur L -- M01 RR000188/RR/NCRR NIH HHS/ -- U01 HG006485/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):342-3. doi: 10.1126/science.1229178.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human and Molecular Genetics, Baylor College of Medicine, Houston, TX 77030, USA. abeaudet@bcm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23087240" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)/*administration & ; dosage/*genetics ; Animals ; Autistic Disorder/*diet therapy/*genetics ; Epilepsy/*diet therapy/*genetics ; Female ; Humans ; Male
    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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    dSarm/Sarm1 is required for activation of an injury-induced axon death pathway (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-09
    Description: Axonal and synaptic degeneration is a hallmark of peripheral neuropathy, brain injury, and neurodegenerative disease. Axonal degeneration has been proposed to be mediated by an active autodestruction program, akin to apoptotic cell death; however, loss-of-function mutations capable of potently blocking axon self-destruction have not been described. Here, we show that loss of the Drosophila Toll receptor adaptor dSarm (sterile alpha/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy. Severed mouse Sarm1 null axons exhibit remarkable long-term survival both in vivo and in vitro, indicating that Sarm1 prodegenerative signaling is conserved in mammals. Our results provide direct evidence that axons actively promote their own destruction after injury and identify dSarm/Sarm1 as a member of an ancient axon death signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osterloh, Jeannette M -- Yang, Jing -- Rooney, Timothy M -- Fox, A Nicole -- Adalbert, Robert -- Powell, Eric H -- Sheehan, Amy E -- Avery, Michelle A -- Hackett, Rachel -- Logan, Mary A -- MacDonald, Jennifer M -- Ziegenfuss, Jennifer S -- Milde, Stefan -- Hou, Ying-Ju -- Nathan, Carl -- Ding, Aihao -- Brown, Robert H Jr -- Conforti, Laura -- Coleman, Michael -- Tessier-Lavigne, Marc -- Zuchner, Stephan -- Freeman, Marc R -- 5R01-NS050557-05/NS/NINDS NIH HHS/ -- AI030165/AI/NIAID NIH HHS/ -- R01NS059991/NS/NINDS NIH HHS/ -- R01NS072248/NS/NINDS NIH HHS/ -- RC2-NS070-342/NS/NINDS NIH HHS/ -- U54NS065712/NS/NINDS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):481-4. doi: 10.1126/science.1223899. Epub 2012 Jun 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22678360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Apoptosis ; Armadillo Domain Proteins/analysis/*genetics/*physiology ; Axons/*physiology/ultrastructure ; Axotomy ; Cell Survival ; Cells, Cultured ; Cytoskeletal Proteins/analysis/*genetics/*physiology ; Denervation ; Drosophila/embryology/genetics/physiology ; Drosophila Proteins/analysis/*genetics/*physiology ; Mice ; Mutation ; Neurons/*physiology ; Sciatic Nerve/injuries/physiology ; Signal Transduction ; Superior Cervical Ganglion/cytology ; Tissue Culture Techniques ; *Wallerian Degeneration
    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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  • 100
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    Ecology. When paths to cooperation converge (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sherratt, Thomas N -- Roberts, Gilbert -- New York, N.Y. -- Science. 2012 Sep 14;337(6100):1304-5. doi: 10.1126/science.1226328.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Carleton University, Ottawa, ON K1S 5B6, Canada. tom_sherratt@carleton.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22984060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; *Biological Evolution ; *Cooperative Behavior ; Female ; Male ; Sexual Behavior, Animal
    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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