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  • Animals  (3)
  • United States  (2)
  • American Association for the Advancement of Science (AAAS)  (5)
  • 2010-2014  (1)
  • 1980-1984  (4)
  • 1950-1954
  • 1
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    Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-05
    Description: Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by expansion of a translated CAG repeat in Ataxin-1 (ATXN1). To determine the long-term effects of exercise, we implemented a mild exercise regimen in a mouse model of SCA1 and found a considerable improvement in survival accompanied by up-regulation of epidermal growth factor and consequential down-regulation of Capicua, which is an ATXN1 interactor. Offspring of Capicua mutant mice bred to SCA1 mice showed significant improvement of all disease phenotypes. Although polyglutamine-expanded Atxn1 caused some loss of Capicua function, further reduction of Capicua levels--either genetically or by exercise--mitigated the disease phenotypes by dampening the toxic gain of function. Thus, exercise might have long-term beneficial effects in other ataxias and neurodegenerative diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232424/" 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/PMC3232424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fryer, John D -- Yu, Peng -- Kang, Hyojin -- Mandel-Brehm, Caleigh -- Carter, Angela N -- Crespo-Barreto, Juan -- Gao, Yan -- Flora, Adriano -- Shaw, Chad -- Orr, Harry T -- Zoghbi, Huda Y -- 1F32NS055545/NS/NINDS NIH HHS/ -- HD24064/HD/NICHD NIH HHS/ -- NS022920/NS/NINDS NIH HHS/ -- NS045667/NS/NINDS NIH HHS/ -- NS27699/NS/NINDS NIH HHS/ -- NS27699-20S1/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- P30 HD024064-23/HD/NICHD NIH HHS/ -- R01 NS027699/NS/NINDS NIH HHS/ -- R01 NS027699-20S1/NS/NINDS NIH HHS/ -- R01 NS027699-21/NS/NINDS NIH HHS/ -- R01 NS027699-22/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):690-3. doi: 10.1126/science.1212673.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxin-1 ; Ataxins ; Cerebellum/metabolism ; Disease Models, Animal ; *Exercise Therapy ; Gene Knock-In Techniques ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Nerve Tissue Proteins/genetics ; Nuclear Proteins/genetics ; Repressor Proteins/genetics/*physiology ; Spinocerebellar Ataxias/genetics/*therapy
    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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  • 2
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    Funding more NIH research grants (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-07-22
    Description: Because of the prospect of a serious decline in the nation's biomedical research capacity owing to diminished federal appropriations, temporary measures should be initiated promptly by the National Institutes of Health to preserve the stability of resources and diversity of research required for future productivity. It is recommended that the available funds be distributed in such a way as to permit some support for 50 percent of competing grant applications approved by the National Institutes of Health study sections. Measures proposed for consideration are a sliding scale for funding, a greater across-the-board reduction, a limit on support for an individual laboratory, and a review of indirect costs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mandel, H G -- New York, N.Y. -- Science. 1983 Jul 22;221(4608):338-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6867712" target="_blank"〉PubMed〈/a〉
    Keywords: *National Institutes of Health (U.S.)/organization & administration ; *Research Support as Topic/economics ; United States
    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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  • 3
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    Amiloride directly inhibits the Na,K-ATPase activity of rabbit kidney proximal tubules (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-05-27
    Description: Amiloride inhibited the ouabain-sensitive rate of oxygen consumption (QO2) of a suspension of rabbit intact proximal tubules in the presence of different concentrations of extracellular sodium. Measurements of the ouabain-sensitive QO2 in the presence of nystatin, the tissue sodium and potassium contents of the tubules in suspension, and the sodium- and potassium-dependent adenosinetriphosphatase (Na,K-ATPase) activity of lysed tubule membranes indicated that the effect of amiloride was due to a direct inhibition of the Na,K-ATPase activity of the proximal tubule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soltoff, S P -- Mandel, L J -- AM26816/AM/NIADDK NIH HHS/ -- GM29256/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1983 May 27;220(4600):957-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6302840" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/*pharmacology ; Animals ; Dose-Response Relationship, Drug ; Female ; Ion Channels/drug effects ; Kidney Tubules, Proximal/drug effects/*enzymology ; Nystatin/pharmacology ; Ouabain/pharmacology ; Oxygen Consumption/drug effects ; Pyrazines/*pharmacology ; Rabbits ; Rats ; Sodium/metabolism ; Sodium-Potassium-Exchanging ATPase/*antagonists & inhibitors/metabolism
    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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  • 4
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    Crisis in NIH funding (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vesell, E S -- Mandel, H G -- New York, N.Y. -- Science. 1982 Feb 26;215(4536):1026-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7063837" target="_blank"〉PubMed〈/a〉
    Keywords: *National Institutes of Health (U.S.) ; Research Support as Topic/*economics ; United States
    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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  • 5
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    Oxygen consumption and cellular ion transport: evidence for adenosine triphosphate to O2 ratio near 6 in intact cell (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-06-06
    Description: Oxygen (O2) consumption and net K+ uptake were measured simultaneously upon reintroduction of K+ into a K+-depleted suspension of renal tubules. The K+/O2 stoichiometries of 11.8 +/- 0.2 and 8.4 +/- 0.6 were obtained for reduced nicotinamide adenine dinucleotide- and flavoprotein-linked substrates, respectively. These values complement classical K+ to adenosine triphosphate (ATP) and ATP/O2 stoichiometries, thereby demonstrating a remarkably efficient coupling between the processes of Na+- and K+-dependent adenosinetriphosphatase-mediated ion transport and oxidative phosphorylation within the intact cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harris, S I -- Balaban, R S -- Mandel, L J -- New York, N.Y. -- Science. 1980 Jun 6;208(4448):1148-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6246581" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Biological Transport, Active ; Kidney Tubules/metabolism ; Mitochondria/metabolism ; NAD/metabolism ; Ouabain/pharmacology ; *Oxidative Phosphorylation ; *Oxygen Consumption/drug effects ; Potassium/*metabolism ; Rabbits ; Sodium-Potassium-Exchanging ATPase/*metabolism
    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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