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  • Male  (18)
  • American Association for the Advancement of Science (AAAS)  (18)
  • 1
    Publication Date: 2009-04-25
    Description: To understand the biology and evolution of ruminants, the cattle genome was sequenced to about sevenfold coverage. The cattle genome contains a minimum of 22,000 genes, with a core set of 14,345 orthologs shared among seven mammalian species of which 1217 are absent or undetected in noneutherian (marsupial or monotreme) genomes. Cattle-specific evolutionary breakpoint regions in chromosomes have a higher density of segmental duplications, enrichment of repetitive elements, and species-specific variations in genes associated with lactation and immune responsiveness. Genes involved in metabolism are generally highly conserved, although five metabolic genes are deleted or extensively diverged from their human orthologs. The cattle genome sequence thus provides a resource for understanding mammalian evolution and accelerating livestock genetic improvement for milk and meat production.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943200/" 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/PMC2943200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bovine Genome Sequencing and Analysis Consortium -- Elsik, Christine G -- Tellam, Ross L -- Worley, Kim C -- Gibbs, Richard A -- Muzny, Donna M -- Weinstock, George M -- Adelson, David L -- Eichler, Evan E -- Elnitski, Laura -- Guigo, Roderic -- Hamernik, Debora L -- Kappes, Steve M -- Lewin, Harris A -- Lynn, David J -- Nicholas, Frank W -- Reymond, Alexandre -- Rijnkels, Monique -- Skow, Loren C -- Zdobnov, Evgeny M -- Schook, Lawrence -- Womack, James -- Alioto, Tyler -- Antonarakis, Stylianos E -- Astashyn, Alex -- Chapple, Charles E -- Chen, Hsiu-Chuan -- Chrast, Jacqueline -- Camara, Francisco -- Ermolaeva, Olga -- Henrichsen, Charlotte N -- Hlavina, Wratko -- Kapustin, Yuri -- Kiryutin, Boris -- Kitts, Paul -- Kokocinski, Felix -- Landrum, Melissa -- Maglott, Donna -- Pruitt, Kim -- Sapojnikov, Victor -- Searle, Stephen M -- Solovyev, Victor -- Souvorov, Alexandre -- Ucla, Catherine -- Wyss, Carine -- Anzola, Juan M -- Gerlach, Daniel -- Elhaik, Eran -- Graur, Dan -- Reese, Justin T -- Edgar, Robert C -- McEwan, John C -- Payne, Gemma M -- Raison, Joy M -- Junier, Thomas -- Kriventseva, Evgenia V -- Eyras, Eduardo -- Plass, Mireya -- Donthu, Ravikiran -- Larkin, Denis M -- Reecy, James -- Yang, Mary Q -- Chen, Lin -- Cheng, Ze -- Chitko-McKown, Carol G -- Liu, George E -- Matukumalli, Lakshmi K -- Song, Jiuzhou -- Zhu, Bin -- Bradley, Daniel G -- Brinkman, Fiona S L -- Lau, Lilian P L -- Whiteside, Matthew D -- Walker, Angela -- Wheeler, Thomas T -- Casey, Theresa -- German, J Bruce -- Lemay, Danielle G -- Maqbool, Nauman J -- Molenaar, Adrian J -- Seo, Seongwon -- Stothard, Paul -- Baldwin, Cynthia L -- Baxter, Rebecca -- Brinkmeyer-Langford, Candice L -- Brown, Wendy C -- Childers, Christopher P -- Connelley, Timothy -- Ellis, Shirley A -- Fritz, Krista -- Glass, Elizabeth J -- Herzig, Carolyn T A -- Iivanainen, Antti -- Lahmers, Kevin K -- Bennett, Anna K -- Dickens, C Michael -- Gilbert, James G R -- Hagen, Darren E -- Salih, Hanni -- Aerts, Jan -- Caetano, Alexandre R -- Dalrymple, Brian -- Garcia, Jose Fernando -- Gill, Clare A -- Hiendleder, Stefan G -- Memili, Erdogan -- Spurlock, Diane -- Williams, John L -- Alexander, Lee -- Brownstein, Michael J -- Guan, Leluo -- Holt, Robert A -- Jones, Steven J M -- Marra, Marco A -- Moore, Richard -- Moore, Stephen S -- Roberts, Andy -- Taniguchi, Masaaki -- Waterman, Richard C -- Chacko, Joseph -- Chandrabose, Mimi M -- Cree, Andy -- Dao, Marvin Diep -- Dinh, Huyen H -- Gabisi, Ramatu Ayiesha -- Hines, Sandra -- Hume, Jennifer -- Jhangiani, Shalini N -- Joshi, Vandita -- Kovar, Christie L -- Lewis, Lora R -- Liu, Yih-Shin -- Lopez, John -- Morgan, Margaret B -- Nguyen, Ngoc Bich -- Okwuonu, Geoffrey O -- Ruiz, San Juana -- Santibanez, Jireh -- Wright, Rita A -- Buhay, Christian -- Ding, Yan -- Dugan-Rocha, Shannon -- Herdandez, Judith -- Holder, Michael -- Sabo, Aniko -- Egan, Amy -- Goodell, Jason -- Wilczek-Boney, Katarzyna -- Fowler, Gerald R -- Hitchens, Matthew Edward -- Lozado, Ryan J -- Moen, Charles -- Steffen, David -- Warren, James T -- Zhang, Jingkun -- Chiu, Readman -- Schein, Jacqueline E -- Durbin, K James -- Havlak, Paul -- Jiang, Huaiyang -- Liu, Yue -- Qin, Xiang -- Ren, Yanru -- Shen, Yufeng -- Song, Henry -- Bell, Stephanie Nicole -- Davis, Clay -- Johnson, Angela Jolivet -- Lee, Sandra -- Nazareth, Lynne V -- Patel, Bella Mayurkumar -- Pu, Ling-Ling -- Vattathil, Selina -- Williams, Rex Lee Jr -- Curry, Stacey -- Hamilton, Cerissa -- Sodergren, Erica -- Wheeler, David A -- Barris, Wes -- Bennett, Gary L -- Eggen, Andre -- Green, Ronnie D -- Harhay, Gregory P -- Hobbs, Matthew -- Jann, Oliver -- Keele, John W -- Kent, Matthew P -- Lien, Sigbjorn -- McKay, Stephanie D -- McWilliam, Sean -- Ratnakumar, Abhirami -- Schnabel, Robert D -- Smith, Timothy -- Snelling, Warren M -- Sonstegard, Tad S -- Stone, Roger T -- Sugimoto, Yoshikazu -- Takasuga, Akiko -- Taylor, Jeremy F -- Van Tassell, Curtis P -- Macneil, Michael D -- Abatepaulo, Antonio R R -- Abbey, Colette A -- Ahola, Virpi -- Almeida, Iassudara G -- Amadio, Ariel F -- Anatriello, Elen -- Bahadue, Suria M -- Biase, Fernando H -- Boldt, Clayton R -- Carroll, Jeffery A -- Carvalho, Wanessa A -- Cervelatti, Eliane P -- Chacko, Elsa -- Chapin, Jennifer E -- Cheng, Ye -- Choi, Jungwoo -- Colley, Adam J -- de Campos, Tatiana A -- De Donato, Marcos -- Santos, Isabel K F de Miranda -- de Oliveira, Carlo J F -- Deobald, Heather -- Devinoy, Eve -- Donohue, Kaitlin E -- Dovc, Peter -- Eberlein, Annett -- Fitzsimmons, Carolyn J -- Franzin, Alessandra M -- Garcia, Gustavo R -- Genini, Sem -- Gladney, Cody J -- Grant, Jason R -- Greaser, Marion L -- Green, Jonathan A -- Hadsell, Darryl L -- Hakimov, Hatam A -- Halgren, Rob -- Harrow, Jennifer L -- Hart, Elizabeth A -- Hastings, Nicola -- Hernandez, Marta -- Hu, Zhi-Liang -- Ingham, Aaron -- Iso-Touru, Terhi -- Jamis, Catherine -- Jensen, Kirsty -- Kapetis, Dimos -- Kerr, Tovah -- Khalil, Sari S -- Khatib, Hasan -- Kolbehdari, Davood -- Kumar, Charu G -- Kumar, Dinesh -- Leach, Richard -- Lee, Justin C-M -- Li, Changxi -- Logan, Krystin M -- Malinverni, Roberto -- Marques, Elisa -- Martin, William F -- Martins, Natalia F -- Maruyama, Sandra R -- Mazza, Raffaele -- McLean, Kim L -- Medrano, Juan F -- Moreno, Barbara T -- More, Daniela D -- Muntean, Carl T -- Nandakumar, Hari P -- Nogueira, Marcelo F G -- Olsaker, Ingrid -- Pant, Sameer D -- Panzitta, Francesca -- Pastor, Rosemeire C P -- Poli, Mario A -- Poslusny, Nathan -- Rachagani, Satyanarayana -- Ranganathan, Shoba -- Razpet, Andrej -- Riggs, Penny K -- Rincon, Gonzalo -- Rodriguez-Osorio, Nelida -- Rodriguez-Zas, Sandra L -- Romero, Natasha E -- Rosenwald, Anne -- Sando, Lillian -- Schmutz, Sheila M -- Shen, Libing -- Sherman, Laura -- Southey, Bruce R -- Lutzow, Ylva Strandberg -- Sweedler, Jonathan V -- Tammen, Imke -- Telugu, Bhanu Prakash V L -- Urbanski, Jennifer M -- Utsunomiya, Yuri T -- Verschoor, Chris P -- Waardenberg, Ashley J -- Wang, Zhiquan -- Ward, Robert -- Weikard, Rosemarie -- Welsh, Thomas H Jr -- White, Stephen N -- Wilming, Laurens G -- Wunderlich, Kris R -- Yang, Jianqi -- Zhao, Feng-Qi -- 062023/Wellcome Trust/United Kingdom -- 077198/Wellcome Trust/United Kingdom -- BBS/B/13438/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/13446/Biotechnology and Biological Sciences Research Council/United Kingdom -- P30 DA018310/DA/NIDA NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- U54 HG003273-04/HG/NHGRI NIH HHS/ -- U54 HG003273-04S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05/HG/NHGRI NIH HHS/ -- U54 HG003273-05S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05S2/HG/NHGRI NIH HHS/ -- U54 HG003273-06/HG/NHGRI NIH HHS/ -- U54 HG003273-06S1/HG/NHGRI NIH HHS/ -- U54 HG003273-06S2/HG/NHGRI NIH HHS/ -- U54 HG003273-07/HG/NHGRI NIH HHS/ -- U54 HG003273-08/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 24;324(5926):522-8. doi: 10.1126/science.1169588.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19390049" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Animals, Domestic ; *Biological Evolution ; Cattle ; Evolution, Molecular ; Female ; Genetic Variation ; *Genome ; Humans ; Male ; MicroRNAs/genetics ; Molecular Sequence Data ; Proteins/genetics ; Sequence Analysis, DNA ; Species Specificity ; Synteny
    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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  • 2
    Publication Date: 1999-07-03
    Description: Epithelia permit selective and regulated flux from apical to basolateral surfaces by transcellular passage through cells or paracellular flux between cells. Tight junctions constitute the barrier to paracellular conductance; however, little is known about the specific molecules that mediate paracellular permeabilities. Renal magnesium ion (Mg2+) resorption occurs predominantly through a paracellular conductance in the thick ascending limb of Henle (TAL). Here, positional cloning has identified a human gene, paracellin-1 (PCLN-1), mutations in which cause renal Mg2+ wasting. PCLN-1 is located in tight junctions of the TAL and is related to the claudin family of tight junction proteins. These findings provide insight into Mg2+ homeostasis, demonstrate the role of a tight junction protein in human disease, and identify an essential component of a selective paracellular conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simon, D B -- Lu, Y -- Choate, K A -- Velazquez, H -- Al-Sabban, E -- Praga, M -- Casari, G -- Bettinelli, A -- Colussi, G -- Rodriguez-Soriano, J -- McCredie, D -- Milford, D -- Sanjad, S -- Lifton, R P -- F.1/Telethon/Italy -- R01DK51696/DK/NIDDK NIH HHS/ -- TGM06S01/Telethon/Italy -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390358" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Calcium/urine ; Chromosomes, Human, Pair 3/genetics ; Claudins ; Cloning, Molecular ; Female ; Genes, Recessive ; Homeostasis ; Humans ; Kidney Diseases/*genetics/metabolism ; Kidney Tubules/chemistry ; Loop of Henle/chemistry/*metabolism ; Magnesium/blood/*metabolism ; Magnesium Deficiency/*genetics/metabolism ; Male ; Membrane Proteins/analysis/chemistry/genetics/*physiology ; Molecular Sequence Data ; Mutation ; Pedigree ; Physical Chromosome Mapping ; Tight Junctions/*metabolism
    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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  • 3
    Publication Date: 2001-04-28
    Description: Embryonic stem (ES) cells are fully pluripotent in that they can differentiate into all cell types, including gametes. We have derived 35 ES cell lines via nuclear transfer (ntES cell lines) from adult mouse somatic cells of inbred, hybrid, and mutant strains. ntES cells contributed to an extensive variety of cell types, including dopaminergic and serotonergic neurons in vitro and germ cells in vivo. Cloning by transfer of ntES cell nuclei could result in normal development of fertile adults. These studies demonstrate the full pluripotency of ntES cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wakayama, T -- Tabar, V -- Rodriguez, I -- Perry, A C -- Studer, L -- Mombaerts, P -- New York, N.Y. -- Science. 2001 Apr 27;292(5517):740-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Rockefeller University, New York, NY 10021, USA. teru@advancedcell.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11326103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*cytology ; *Cell Differentiation ; Cell Line ; Cell Lineage ; Chimera ; Cloning, Organism ; Crosses, Genetic ; Dopamine/metabolism ; Embryo Transfer ; Female ; Germ Cells/*cytology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Inbred ICR ; Mice, Nude ; Neurons/*cytology ; *Nuclear Transfer Techniques ; Serotonin/metabolism ; Stem Cells/*cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2001-02-22
    Description: A 2.91-billion base pair (bp) consensus sequence of the euchromatic portion of the human genome was generated by the whole-genome shotgun sequencing method. The 14.8-billion bp DNA sequence was generated over 9 months from 27,271,853 high-quality sequence reads (5.11-fold coverage of the genome) from both ends of plasmid clones made from the DNA of five individuals. Two assembly strategies-a whole-genome assembly and a regional chromosome assembly-were used, each combining sequence data from Celera and the publicly funded genome effort. The public data were shredded into 550-bp segments to create a 2.9-fold coverage of those genome regions that had been sequenced, without including biases inherent in the cloning and assembly procedure used by the publicly funded group. This brought the effective coverage in the assemblies to eightfold, reducing the number and size of gaps in the final assembly over what would be obtained with 5.11-fold coverage. The two assembly strategies yielded very similar results that largely agree with independent mapping data. The assemblies effectively cover the euchromatic regions of the human chromosomes. More than 90% of the genome is in scaffold assemblies of 100,000 bp or more, and 25% of the genome is in scaffolds of 10 million bp or larger. Analysis of the genome sequence revealed 26,588 protein-encoding transcripts for which there was strong corroborating evidence and an additional approximately 12,000 computationally derived genes with mouse matches or other weak supporting evidence. Although gene-dense clusters are obvious, almost half the genes are dispersed in low G+C sequence separated by large tracts of apparently noncoding sequence. Only 1.1% of the genome is spanned by exons, whereas 24% is in introns, with 75% of the genome being intergenic DNA. Duplications of segmental blocks, ranging in size up to chromosomal lengths, are abundant throughout the genome and reveal a complex evolutionary history. Comparative genomic analysis indicates vertebrate expansions of genes associated with neuronal function, with tissue-specific developmental regulation, and with the hemostasis and immune systems. DNA sequence comparisons between the consensus sequence and publicly funded genome data provided locations of 2.1 million single-nucleotide polymorphisms (SNPs). A random pair of human haploid genomes differed at a rate of 1 bp per 1250 on average, but there was marked heterogeneity in the level of polymorphism across the genome. Less than 1% of all SNPs resulted in variation in proteins, but the task of determining which SNPs have functional consequences remains an open challenge.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venter, J C -- Adams, M D -- Myers, E W -- Li, P W -- Mural, R J -- Sutton, G G -- Smith, H O -- Yandell, M -- Evans, C A -- Holt, R A -- Gocayne, J D -- Amanatides, P -- Ballew, R M -- Huson, D H -- Wortman, J R -- Zhang, Q -- Kodira, C D -- Zheng, X H -- Chen, L -- Skupski, M -- Subramanian, G -- Thomas, P D -- Zhang, J -- Gabor Miklos, G L -- Nelson, C -- Broder, S -- Clark, A G -- Nadeau, J -- McKusick, V A -- Zinder, N -- Levine, A J -- Roberts, R J -- Simon, M -- Slayman, C -- Hunkapiller, M -- Bolanos, R -- Delcher, A -- Dew, I -- Fasulo, D -- Flanigan, M -- Florea, L -- Halpern, A -- Hannenhalli, S -- Kravitz, S -- Levy, S -- Mobarry, C -- Reinert, K -- Remington, K -- Abu-Threideh, J -- Beasley, E -- Biddick, K -- Bonazzi, V -- Brandon, R -- Cargill, M -- Chandramouliswaran, I -- Charlab, R -- Chaturvedi, K -- Deng, Z -- Di Francesco, V -- Dunn, P -- Eilbeck, K -- Evangelista, C -- Gabrielian, A E -- Gan, W -- Ge, W -- Gong, F -- Gu, Z -- Guan, P -- Heiman, T J -- Higgins, M E -- Ji, R R -- Ke, Z -- Ketchum, K A -- Lai, Z -- Lei, Y -- Li, Z -- Li, J -- Liang, Y -- Lin, X -- Lu, F -- Merkulov, G V -- Milshina, N -- Moore, H M -- Naik, A K -- Narayan, V A -- Neelam, B -- Nusskern, D -- Rusch, D B -- Salzberg, S -- Shao, W -- Shue, B -- Sun, J -- Wang, Z -- Wang, A -- Wang, X -- Wang, J -- Wei, M -- Wides, R -- Xiao, C -- Yan, C -- Yao, A -- Ye, J -- Zhan, M -- Zhang, W -- Zhang, H -- Zhao, Q -- Zheng, L -- Zhong, F -- Zhong, W -- Zhu, S -- Zhao, S -- Gilbert, D -- Baumhueter, S -- Spier, G -- Carter, C -- Cravchik, A -- Woodage, T -- Ali, F -- An, H -- Awe, A -- Baldwin, D -- Baden, H -- Barnstead, M -- Barrow, I -- Beeson, K -- Busam, D -- Carver, A -- Center, A -- Cheng, M L -- Curry, L -- Danaher, S -- Davenport, L -- Desilets, R -- Dietz, S -- Dodson, K -- Doup, L -- Ferriera, S -- Garg, N -- Gluecksmann, A -- Hart, B -- Haynes, J -- Haynes, C -- Heiner, C -- Hladun, S -- Hostin, D -- Houck, J -- Howland, T -- Ibegwam, C -- Johnson, J -- Kalush, F -- Kline, L -- Koduru, S -- Love, A -- Mann, F -- May, D -- McCawley, S -- McIntosh, T -- McMullen, I -- Moy, M -- Moy, L -- Murphy, B -- Nelson, K -- Pfannkoch, C -- Pratts, E -- Puri, V -- Qureshi, H -- Reardon, M -- Rodriguez, R -- Rogers, Y H -- Romblad, D -- Ruhfel, B -- Scott, R -- Sitter, C -- Smallwood, M -- Stewart, E -- Strong, R -- Suh, E -- Thomas, R -- Tint, N N -- Tse, S -- Vech, C -- Wang, G -- Wetter, J -- Williams, S -- Williams, M -- Windsor, S -- Winn-Deen, E -- Wolfe, K -- Zaveri, J -- Zaveri, K -- Abril, J F -- Guigo, R -- Campbell, M J -- Sjolander, K V -- Karlak, B -- Kejariwal, A -- Mi, H -- Lazareva, B -- Hatton, T -- Narechania, A -- Diemer, K -- Muruganujan, A -- Guo, N -- Sato, S -- Bafna, V -- Istrail, S -- Lippert, R -- Schwartz, R -- Walenz, B -- Yooseph, S -- Allen, D -- Basu, A -- Baxendale, J -- Blick, L -- Caminha, M -- Carnes-Stine, J -- Caulk, P -- Chiang, Y H -- Coyne, M -- Dahlke, C -- Mays, A -- Dombroski, M -- Donnelly, M -- Ely, D -- Esparham, S -- Fosler, C -- Gire, H -- Glanowski, S -- Glasser, K -- Glodek, A -- Gorokhov, M -- Graham, K -- Gropman, B -- Harris, M -- Heil, J -- Henderson, S -- Hoover, J -- Jennings, D -- Jordan, C -- Jordan, J -- Kasha, J -- Kagan, L -- Kraft, C -- Levitsky, A -- Lewis, M -- Liu, X -- Lopez, J -- Ma, D -- Majoros, W -- McDaniel, J -- Murphy, S -- Newman, M -- Nguyen, T -- Nguyen, N -- Nodell, M -- Pan, S -- Peck, J -- Peterson, M -- Rowe, W -- Sanders, R -- Scott, J -- Simpson, M -- Smith, T -- Sprague, A -- Stockwell, T -- Turner, R -- Venter, E -- Wang, M -- Wen, M -- Wu, D -- Wu, M -- Xia, A -- Zandieh, A -- Zhu, X -- New York, N.Y. -- Science. 2001 Feb 16;291(5507):1304-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Celera Genomics, 45 West Gude Drive, Rockville, MD 20850, USA. humangenome@celera.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11181995" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Chromosome Banding ; Chromosome Mapping ; Chromosomes, Artificial, Bacterial ; Computational Biology ; Consensus Sequence ; CpG Islands ; DNA, Intergenic ; Databases, Factual ; Evolution, Molecular ; Exons ; Female ; Gene Duplication ; Genes ; Genetic Variation ; *Genome, Human ; *Human Genome Project ; Humans ; Introns ; Male ; Phenotype ; Physical Chromosome Mapping ; Polymorphism, Single Nucleotide ; Proteins/genetics/physiology ; Pseudogenes ; Repetitive Sequences, Nucleic Acid ; Retroelements ; *Sequence Analysis, DNA/methods ; Species Specificity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-05-26
    Description: To function effectively, individuals must voluntarily postpone immediate gratification and persist in goal-directed behavior for the sake of later outcomes. The present research program analyzed the nature of this type of future-oriented self-control and the psychological processes that underlie it. Enduring individual differences in self-control were found as early as the preschool years. Those 4-year-old children who delayed gratification longer in certain laboratory situations developed into more cognitively and socially competent adolescents, achieving higher scholastic performance and coping better with frustration and stress. Experiments in the same research program also identified specific cognitive and attentional processes that allow effective self-regulation early in the course of development. The experimental results, in turn, specified the particular types of preschool delay situations diagnostic for predicting aspects of cognitive and social competence later in life.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mischel, W -- Shoda, Y -- Rodriguez, M I -- New York, N.Y. -- Science. 1989 May 26;244(4907):933-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Columbia University, New York 10027〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2658056" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Psychological ; Attention ; Child ; *Child Development ; Child, Preschool ; *Cognition ; Female ; *Frustration ; Humans ; *Individuality ; Male ; Reward ; Social Adjustment
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  • 6
    Publication Date: 2008-08-02
    Description: MyD88 is a key downstream adapter for most Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs). MyD88 deficiency in mice leads to susceptibility to a broad range of pathogens in experimental settings of infection. We describe a distinct situation in a natural setting of human infection. Nine children with autosomal recessive MyD88 deficiency suffered from life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease. However, these patients were otherwise healthy, with normal resistance to other microbes. Their clinical status improved with age, but not due to any cellular leakiness in MyD88 deficiency. The MyD88-dependent TLRs and IL-1Rs are therefore essential for protective immunity to a small number of pyogenic bacteria, but redundant for host defense to most natural infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688396/" 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/PMC2688396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Bernuth, Horst -- Picard, Capucine -- Jin, Zhongbo -- Pankla, Rungnapa -- Xiao, Hui -- Ku, Cheng-Lung -- Chrabieh, Maya -- Mustapha, Imen Ben -- Ghandil, Pegah -- Camcioglu, Yildiz -- Vasconcelos, Julia -- Sirvent, Nicolas -- Guedes, Margarida -- Vitor, Artur Bonito -- Herrero-Mata, Maria Jose -- Arostegui, Juan Ignacio -- Rodrigo, Carlos -- Alsina, Laia -- Ruiz-Ortiz, Estibaliz -- Juan, Manel -- Fortuny, Claudia -- Yague, Jordi -- Anton, Jordi -- Pascal, Mariona -- Chang, Huey-Hsuan -- Janniere, Lucile -- Rose, Yoann -- Garty, Ben-Zion -- Chapel, Helen -- Issekutz, Andrew -- Marodi, Laszlo -- Rodriguez-Gallego, Carlos -- Banchereau, Jacques -- Abel, Laurent -- Li, Xiaoxia -- Chaussabel, Damien -- Puel, Anne -- Casanova, Jean-Laurent -- U19 AI057234/AI/NIAID NIH HHS/ -- U19 AI057234-02/AI/NIAID NIH HHS/ -- U19 AIO57234-02/PHS HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):691-6. doi: 10.1126/science.1158298.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics of Infectious Diseases, INSERM U550, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669862" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Bacterial Infections/*genetics/*immunology ; Cell Line, Transformed ; Child ; Child, Preschool ; Cytokines/metabolism ; Disease Susceptibility ; Female ; Gene Deletion ; Humans ; Immunity, Innate ; Male ; Mice ; Mutation, Missense ; Myeloid Differentiation Factor 88/*deficiency/genetics/metabolism ; Pneumococcal Infections/genetics/immunology ; Pseudomonas Infections/genetics/immunology ; Receptors, Interleukin-1/immunology/metabolism ; Signal Transduction ; Staphylococcal Infections/genetics/immunology ; Toll-Like Receptors/immunology/metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2010-06-05
    Description: The understanding of natural and sexual selection requires both field and laboratory studies to exploit the advantages and avoid the disadvantages of each approach. However, studies have tended to be polarized among the types of organisms studied, with vertebrates studied in the field and invertebrates in the lab. We used video monitoring combined with DNA profiling of all of the members of a wild population of field crickets across two generations to capture the factors predicting the reproductive success of males and females. The factors that predict a male's success in gaining mates differ from those that predict how many offspring he has. We confirm the fundamental prediction that males vary more in their reproductive success than females, and we find that females as well as males leave more offspring when they mate with more partners.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez-Munoz, R -- Bretman, A -- Slate, J -- Walling, C A -- Tregenza, T -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1269-72. doi: 10.1126/science.1188102.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Ecology and Conservation, School of Biosciences, University of Exeter, Cornwall Campus, Penryn TR10 EZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522773" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; Female ; *Genetic Fitness ; Gryllidae/*genetics/*physiology ; Male ; *Mating Preference, Animal ; Microsatellite Repeats ; Oviposition ; Reproduction ; *Selection, Genetic ; *Sex Characteristics ; Sexual Behavior, Animal ; Vocalization, Animal
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2011-11-05
    Description: Plain-tailed wrens (Pheugopedius euophrys) cooperate to produce a duet song in which males and females rapidly alternate singing syllables. We examined how sensory information from each wren is used to coordinate singing between individuals for the production of this cooperative behavior. Previous findings in nonduetting songbird species suggest that premotor circuits should encode each bird's own contribution to the duet. In contrast, we find that both male and female wrens encode the combined cooperative output of the pair of birds. Further, behavior and neurophysiology show that both sexes coordinate the timing of their singing based on feedback from the partner and suggest that females may lead the duet.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fortune, Eric S -- Rodriguez, Carlos -- Li, David -- Ball, Gregory F -- Coleman, Melissa J -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):666-70. doi: 10.1126/science.1209867.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychological and Brain Sciences, Johns Hopkins University, 3400 North Charles Street, Baltimore, MD 21218, USA. eric.fortune@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053048" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Male ; Neurons/*physiology ; Songbirds/*physiology ; Vocalization, Animal/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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  • 9
    Publication Date: 2011-03-19
    Description: Decreased cardiac contractility is a central feature of systolic heart failure. Existing drugs increase cardiac contractility indirectly through signaling cascades but are limited by their mechanism-related adverse effects. To avoid these limitations, we previously developed omecamtiv mecarbil, a small-molecule, direct activator of cardiac myosin. Here, we show that it binds to the myosin catalytic domain and operates by an allosteric mechanism to increase the transition rate of myosin into the strongly actin-bound force-generating state. Paradoxically, it inhibits adenosine 5'-triphosphate turnover in the absence of actin, which suggests that it stabilizes an actin-bound conformation of myosin. In animal models, omecamtiv mecarbil increases cardiac function by increasing the duration of ejection without changing the rates of contraction. Cardiac myosin activation may provide a new therapeutic approach for systolic heart failure.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090309/" 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/PMC4090309/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malik, Fady I -- Hartman, James J -- Elias, Kathleen A -- Morgan, Bradley P -- Rodriguez, Hector -- Brejc, Katjusa -- Anderson, Robert L -- Sueoka, Sandra H -- Lee, Kenneth H -- Finer, Jeffrey T -- Sakowicz, Roman -- Baliga, Ramesh -- Cox, David R -- Garard, Marc -- Godinez, Guillermo -- Kawas, Raja -- Kraynack, Erica -- Lenzi, David -- Lu, Pu Ping -- Muci, Alexander -- Niu, Congrong -- Qian, Xiangping -- Pierce, Daniel W -- Pokrovskii, Maria -- Suehiro, Ion -- Sylvester, Sheila -- Tochimoto, Todd -- Valdez, Corey -- Wang, Wenyue -- Katori, Tatsuo -- Kass, David A -- Shen, You-Tang -- Vatner, Stephen F -- Morgans, David J -- 1-R43-HL-66647-1/HL/NHLBI NIH HHS/ -- R01 HL106511/HL/NHLBI NIH HHS/ -- R43 HL066647/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 18;331(6023):1439-43. doi: 10.1126/science.1200113.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Preclinical Research and Development, Cytokinetics, Inc., South San Francisco, CA 94080, USA. fmalik@cytokinetics.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21415352" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism ; Actins/metabolism ; Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Adrenergic beta-Agonists/pharmacology ; Allosteric Regulation ; Animals ; Binding Sites ; Calcium/metabolism ; Cardiac Myosins/chemistry/*metabolism ; Cardiac Output/drug effects ; Dogs ; Female ; Heart Failure, Systolic/*drug therapy/physiopathology ; Isoproterenol/pharmacology ; Male ; Myocardial Contraction/*drug effects ; Myocytes, Cardiac/*drug effects/physiology ; Phosphates/metabolism ; Protein Binding ; Protein Conformation ; Protein Isoforms/chemistry/metabolism ; Rats ; Rats, Sprague-Dawley ; Urea/*analogs & derivatives/chemistry/metabolism/pharmacology ; Ventricular Function, Left/drug effects
    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
    Publication Date: 1997-06-27
    Description: Corticotropin-releasing factor (CRF) has been implicated in the mediation of the stress-like and negative affective consequences of withdrawal from drugs of abuse, such as alcohol, cocaine, and opiates. This study sought to determine whether brain CRF systems also have a role in cannabinoid dependence. Rats were treated daily for 2 weeks with the potent synthetic cannabinoid HU-210. Withdrawal, induced by the cannabinoid antagonist SR 141716A, was accompanied by a marked elevation in extracellular CRF concentration and a distinct pattern of Fos activation in the central nucleus of the amygdala. Maximal increases in CRF corresponded to the time when behavioral signs resulting from cannabinoid withdrawal were at a maximum. These data suggest that long-term cannabinoid administration alters CRF function in the limbic system of the brain, in a manner similar to that observed with other drugs of abuse, and also induces neuroadaptive processes that may result in future vulnerability to drug dependence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez de Fonseca, F -- Carrera, M R -- Navarro, M -- Koob, G F -- Weiss, F -- DA 08426/DA/NIDA NIH HHS/ -- DK26741/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2050-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto Complutense de Drogodependencias, Departamento de Psicobiologia, Facultad de Psicologia, Universidad Complutense de Madrid, 28223 Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197270" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/drug effects/*metabolism ; Animals ; Anxiety/chemically induced ; Behavior, Animal/drug effects ; Brain/drug effects/*metabolism ; Corticosterone/blood ; Corticotropin-Releasing Hormone/*metabolism ; Dronabinol/adverse effects/*analogs & derivatives/antagonists & ; inhibitors/pharmacology ; Male ; Microdialysis ; Piperidines/pharmacology ; Proto-Oncogene Proteins c-fos/analysis ; Pyrazoles/pharmacology ; Rats ; Rats, Wistar ; Receptors, Cannabinoid ; Receptors, Drug/antagonists & inhibitors ; Substance Withdrawal Syndrome/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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