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  • 1
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    Innovative materials processing strategies: a biomimetic approach (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-28
    Description: Many organisms construct structural ceramic (biomineral) composites from seemingly mundane materials; cell-mediated processes control both the nucleation and growth of mineral and the development of composite microarchitecture. Living systems fabricate biocomposites by: (i) confining biomineralization within specific subunit compartments; (ii) producing a specific mineral with defined crystal size and orientation; and (iii) packaging many incremental units together in a moving front process to form fully densified, macroscopic structures. By adapting biological principles, materials scientists are attempting to produce novel materials. To date, neither the elegance of the biomineral assembly mechanisms nor the intricate composite microarchitectures have been duplicated by nonbiological processing. However, substantial progress has been made in the understanding of how biomineralization occurs, and the first steps are now being taken to exploit the basic principles involved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heuer, A H -- Fink, D J -- Laraia, V J -- Arias, J L -- Calvert, P D -- Kendall, K -- Messing, G L -- Blackwell, J -- Rieke, P C -- Thompson, D H -- New York, N.Y. -- Science. 1992 Feb 28;255(5048):1098-105.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, Case Western Reserve University, Cleveland, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546311" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Matrix ; Calcification, Physiologic ; *Ceramics ; Chickens ; Crystallography
    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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    HIP-70: an isoform of phosphoinositol-specific phospholipase C-alpha (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mobbs, C V -- Fink, G -- Pfaff, D W -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):566-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2382136" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain/enzymology ; Information Systems ; Isoenzymes/*genetics/metabolism ; Type C Phospholipases/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    HIP-70: a protein induced by estrogen in the brain and LH-RH in the pituitary (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-23
    Description: Estrogen and luteinizing hormone-releasing hormone (LH-RH) interact to influence both behavior and gonadotropin release. However, little is known about the biochemical mechanisms that mediate the effects of these hormones or their interactions. The most prominent protein induced by estrogen in the ventromedial hypothalamus has the same amino-terminal sequence as the most prominent protein induced by LH-RH in the pituitary in vitro and in vivo; these proteins comigrate on two-dimensional gels. Furthermore, the hormonal induction may be caused by modification of a constitutive protein with the same molecular weight (70,000) but a slightly more acidic isoelectric point, whose level is inversely related to the level of the induced form after estrogen treatment. Thus estrogen and LH-RH may interact by additively or synergistically inducing this protein, which is called HIP-70.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mobbs, C V -- Fink, G -- Pfaff, D W -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1477-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Behavior, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2181662" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Electrophoresis, Gel, Two-Dimensional ; Estrogens/*pharmacology ; Female ; Gonadotropin-Releasing Hormone/*pharmacology ; Hypothalamus/drug effects/*metabolism ; Molecular Sequence Data ; Nerve Tissue Proteins/*biosynthesis ; Ovariectomy ; Pituitary Gland/drug effects/*metabolism ; *Protein Biosynthesis ; Rats
    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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    Hydrogen is an energy source for hydrothermal vent symbioses (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-08-13
    Description: The discovery of deep-sea hydrothermal vents in 1977 revolutionized our understanding of the energy sources that fuel primary productivity on Earth. Hydrothermal vent ecosystems are dominated by animals that live in symbiosis with chemosynthetic bacteria. So far, only two energy sources have been shown to power chemosynthetic symbioses: reduced sulphur compounds and methane. Using metagenome sequencing, single-gene fluorescence in situ hybridization, immunohistochemistry, shipboard incubations and in situ mass spectrometry, we show here that the symbionts of the hydrothermal vent mussel Bathymodiolus from the Mid-Atlantic Ridge use hydrogen to power primary production. In addition, we show that the symbionts of Bathymodiolus mussels from Pacific vents have hupL, the key gene for hydrogen oxidation. Furthermore, the symbionts of other vent animals such as the tubeworm Riftia pachyptila and the shrimp Rimicaris exoculata also have hupL. We propose that the ability to use hydrogen as an energy source is widespread in hydrothermal vent symbioses, particularly at sites where hydrogen is abundant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, Jillian M -- Zielinski, Frank U -- Pape, Thomas -- Seifert, Richard -- Moraru, Cristina -- Amann, Rudolf -- Hourdez, Stephane -- Girguis, Peter R -- Wankel, Scott D -- Barbe, Valerie -- Pelletier, Eric -- Fink, Dennis -- Borowski, Christian -- Bach, Wolfgang -- Dubilier, Nicole -- England -- Nature. 2011 Aug 10;476(7359):176-80. doi: 10.1038/nature10325.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Marine Microbiology, Celsiusstrasse 1, 28359 Bremen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21833083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atlantic Ocean ; Bivalvia/drug effects/metabolism/*microbiology ; Dose-Response Relationship, Drug ; *Ecosystem ; *Energy Metabolism ; Geologic Sediments/chemistry ; Gills/drug effects/metabolism/microbiology ; Hot Springs/*chemistry/microbiology ; Hydrogen/analysis/*metabolism/pharmacology ; Hydrogenase/genetics/metabolism ; Molecular Sequence Data ; Oxidation-Reduction ; Partial Pressure ; Seawater/chemistry/microbiology ; Sulfides/metabolism ; Sulfur/metabolism ; Symbiosis/drug effects/genetics/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-30
    Description: Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530898/" 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/PMC3530898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biankin, Andrew V -- Waddell, Nicola -- Kassahn, Karin S -- Gingras, Marie-Claude -- Muthuswamy, Lakshmi B -- Johns, Amber L -- Miller, David K -- Wilson, Peter J -- Patch, Ann-Marie -- Wu, Jianmin -- Chang, David K -- Cowley, Mark J -- Gardiner, Brooke B -- Song, Sarah -- Harliwong, Ivon -- Idrisoglu, Senel -- Nourse, Craig -- Nourbakhsh, Ehsan -- Manning, Suzanne -- Wani, Shivangi -- Gongora, Milena -- Pajic, Marina -- Scarlett, Christopher J -- Gill, Anthony J -- Pinho, Andreia V -- Rooman, Ilse -- Anderson, Matthew -- Holmes, Oliver -- Leonard, Conrad -- Taylor, Darrin -- Wood, Scott -- Xu, Qinying -- Nones, Katia -- Fink, J Lynn -- Christ, Angelika -- Bruxner, Tim -- Cloonan, Nicole -- Kolle, Gabriel -- Newell, Felicity -- Pinese, Mark -- Mead, R Scott -- Humphris, Jeremy L -- Kaplan, Warren -- Jones, Marc D -- Colvin, Emily K -- Nagrial, Adnan M -- Humphrey, Emily S -- Chou, Angela -- Chin, Venessa T -- Chantrill, Lorraine A -- Mawson, Amanda -- Samra, Jaswinder S -- Kench, James G -- Lovell, Jessica A -- Daly, Roger J -- Merrett, Neil D -- Toon, Christopher -- Epari, Krishna -- Nguyen, Nam Q -- Barbour, Andrew -- Zeps, Nikolajs -- Australian Pancreatic Cancer Genome Initiative -- Kakkar, Nipun -- Zhao, Fengmei -- Wu, Yuan Qing -- Wang, Min -- Muzny, Donna M -- Fisher, William E -- Brunicardi, F Charles -- Hodges, Sally E -- Reid, Jeffrey G -- Drummond, Jennifer -- Chang, Kyle -- Han, Yi -- Lewis, Lora R -- Dinh, Huyen -- Buhay, Christian J -- Beck, Timothy -- Timms, Lee -- Sam, Michelle -- Begley, Kimberly -- Brown, Andrew -- Pai, Deepa -- Panchal, Ami -- Buchner, Nicholas -- De Borja, Richard -- Denroche, Robert E -- Yung, Christina K -- Serra, Stefano -- Onetto, Nicole -- Mukhopadhyay, Debabrata -- Tsao, Ming-Sound -- Shaw, Patricia A -- Petersen, Gloria M -- Gallinger, Steven -- Hruban, Ralph H -- Maitra, Anirban -- Iacobuzio-Donahue, Christine A -- Schulick, Richard D -- Wolfgang, Christopher L -- Morgan, Richard A -- Lawlor, Rita T -- Capelli, Paola -- Corbo, Vincenzo -- Scardoni, Maria -- Tortora, Giampaolo -- Tempero, Margaret A -- Mann, Karen M -- Jenkins, Nancy A -- Perez-Mancera, Pedro A -- Adams, David J -- Largaespada, David A -- Wessels, Lodewyk F A -- Rust, Alistair G -- Stein, Lincoln D -- Tuveson, David A -- Copeland, Neal G -- Musgrove, Elizabeth A -- Scarpa, Aldo -- Eshleman, James R -- Hudson, Thomas J -- Sutherland, Robert L -- Wheeler, David A -- Pearson, John V -- McPherson, John D -- Gibbs, Richard A -- Grimmond, Sean M -- 13031/Cancer Research UK/United Kingdom -- 2P50CA101955/CA/NCI NIH HHS/ -- P01CA134292/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- P50 CA102701/CA/NCI NIH HHS/ -- P50CA062924/CA/NCI NIH HHS/ -- R01 CA097075/CA/NCI NIH HHS/ -- R01 CA97075/CA/NCI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Nov 15;491(7424):399-405. doi: 10.1038/nature11547. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kinghorn Cancer Centre, 370 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Carcinoma, Pancreatic Ductal/*genetics/*pathology ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genome/*genetics ; Humans ; Kaplan-Meier Estimate ; Mice ; Mutation ; Pancreatic Neoplasms/*genetics/*pathology ; Proteins/genetics ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Presynaptic inhibition of spinal sensory feedback ensures smooth movement (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-05-03
    Description: The precision of skilled movement depends on sensory feedback and its refinement by local inhibitory microcircuits. One specialized set of spinal GABAergic interneurons forms axo-axonic contacts with the central terminals of sensory afferents, exerting presynaptic inhibitory control over sensory-motor transmission. The inability to achieve selective access to the GABAergic neurons responsible for this unorthodox inhibitory mechanism has left unresolved the contribution of presynaptic inhibition to motor behaviour. We used Gad2 as a genetic entry point to manipulate the interneurons that contact sensory terminals, and show that activation of these interneurons in mice elicits the defining physiological characteristics of presynaptic inhibition. Selective genetic ablation of Gad2-expressing interneurons severely perturbs goal-directed reaching movements, uncovering a pronounced and stereotypic forelimb motor oscillation, the core features of which are captured by modelling the consequences of sensory feedback at high gain. Our findings define the neural substrate of a genetically hardwired gain control system crucial for the smooth execution of movement.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4292914/" 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/PMC4292914/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fink, Andrew J P -- Croce, Katherine R -- Huang, Z Josh -- Abbott, L F -- Jessell, Thomas M -- Azim, Eiman -- MH078844/MH/NIMH NIH HHS/ -- MH093338/MH/NIMH NIH HHS/ -- NS033245/NS/NINDS NIH HHS/ -- R01 MH093338/MH/NIMH NIH HHS/ -- R01 NS033245/NS/NINDS NIH HHS/ -- R01 NS080932/NS/NINDS NIH HHS/ -- T32 HD007430/HD/NICHD NIH HHS/ -- U01 MH078844/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 May 1;509(7498):43-8. doi: 10.1038/nature13276.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Kavli Institute for Brain Science, Mortimer B. Zuckerman Mind Brain Behavior Institute, Departments of Neuroscience and Biochemistry and Molecular Biophysics, Columbia University, New York, New York 10032, USA. ; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. ; Center for Theoretical Neuroscience, Departments of Physiology and Neuroscience, Columbia University, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24784215" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Efferent Pathways/physiology ; Feedback, Sensory/*physiology ; Female ; Forelimb/physiology ; GABAergic Neurons/cytology/metabolism ; Glutamate Decarboxylase/genetics/metabolism ; Interneurons/cytology/metabolism ; Male ; Mice ; Models, Neurological ; Motor Skills/*physiology ; Movement/*physiology ; Neural Inhibition/*physiology ; Neurotransmitter Agents/secretion ; Presynaptic Terminals/*physiology ; Spinal Cord/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    CaMKII determines mitochondrial stress responses in heart (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-12
    Description: Myocardial cell death is initiated by excessive mitochondrial Ca(2+) entry causing Ca(2+) overload, mitochondrial permeability transition pore (mPTP) opening and dissipation of the mitochondrial inner membrane potential (DeltaPsim). However, the signalling pathways that control mitochondrial Ca(2+) entry through the inner membrane mitochondrial Ca(2+) uniporter (MCU) are not known. The multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is activated in ischaemia reperfusion, myocardial infarction and neurohumoral injury, common causes of myocardial death and heart failure; these findings suggest that CaMKII could couple disease stress to mitochondrial injury. Here we show that CaMKII promotes mPTP opening and myocardial death by increasing MCU current (I(MCU)). Mitochondrial-targeted CaMKII inhibitory protein or cyclosporin A, an mPTP antagonist with clinical efficacy in ischaemia reperfusion injury, equivalently prevent mPTP opening, DeltaPsim deterioration and diminish mitochondrial disruption and programmed cell death in response to ischaemia reperfusion injury. Mice with myocardial and mitochondrial-targeted CaMKII inhibition have reduced I(MCU) and are resistant to ischaemia reperfusion injury, myocardial infarction and neurohumoral injury, suggesting that pathological actions of CaMKII are substantially mediated by increasing I(MCU). Our findings identify CaMKII activity as a central mechanism for mitochondrial Ca(2+) entry in myocardial cell death, and indicate that mitochondrial-targeted CaMKII inhibition could prevent or reduce myocardial death and heart failure in response to common experimental forms of pathophysiological stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471377/" 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/PMC3471377/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joiner, Mei-Ling A -- Koval, Olha M -- Li, Jingdong -- He, B Julie -- Allamargot, Chantal -- Gao, Zhan -- Luczak, Elizabeth D -- Hall, Duane D -- Fink, Brian D -- Chen, Biyi -- Yang, Jinying -- Moore, Steven A -- Scholz, Thomas D -- Strack, Stefan -- Mohler, Peter J -- Sivitz, William I -- Song, Long-Sheng -- Anderson, Mark E -- R01 HL062494/HL/NHLBI NIH HHS/ -- R01 HL070250/HL/NHLBI NIH HHS/ -- R01 HL079031/HL/NHLBI NIH HHS/ -- R01 HL083422/HL/NHLBI NIH HHS/ -- R01 HL084583/HL/NHLBI NIH HHS/ -- R01 HL090905/HL/NHLBI NIH HHS/ -- R01 HL113001/HL/NHLBI NIH HHS/ -- R01 HL62494/HL/NHLBI NIH HHS/ -- R01 HL70250/HL/NHLBI NIH HHS/ -- R56 NS056244/NS/NINDS NIH HHS/ -- England -- Nature. 2012 Nov 8;491(7423):269-73. doi: 10.1038/nature11444. Epub 2012 Oct 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine and Cardiovascular Center, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA. mei-ling-joiner@uiowa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23051746" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Calcium/*metabolism/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/antagonists & ; inhibitors/chemistry/*metabolism ; Cyclosporine/pharmacology ; Female ; Heart/drug effects/physiopathology ; Heart Failure/drug therapy/prevention & control ; Membrane Potential, Mitochondrial/drug effects/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondria, Heart/enzymology/*metabolism/*pathology ; Mitochondrial Membrane Transport Proteins/metabolism ; Myocardial Infarction/drug therapy/prevention & control ; Myocardium/*enzymology/metabolism/*pathology ; Reperfusion Injury/enzymology/metabolism/pathology/prevention & control ; Serine/metabolism ; *Stress, Physiological/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Joiner et al. reply (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-09-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joiner, Mei-Ling A -- Koval, Olha M -- Li, Jingdong -- He, B Julie -- Allamargot, Chantal -- Gao, Zhan -- Luczak, Elizabeth D -- Hall, Duane D -- Fink, Brian D -- Chen, Biyi -- Yang, Jinying -- Moore, Steven A -- Scholz, Thomas D -- Strack, Stefan -- Mohler, Peter J -- Sivitz, William I -- Song, Long-Sheng -- Anderson, Mark E -- England -- Nature. 2014 Sep 25;513(7519):E3. doi: 10.1038/nature13627.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Internal Medicine and Cardiovascular Center, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA [2] Department of Molecular Physiology &Biophysics, Carver College of Medicine, University of Iowa, 51 Newton Road, Iowa City, Iowa 52242, USA (M.A.J.); The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA (J.L., P.J.M.); Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA (B.J.H.); Johns Hopkins University School of Medicine, 1830 East Monument Street, 9th Floor, Suite 9026, Baltimore, Maryland 21287, USA (E.D.L., M.E.A.). ; Department of Internal Medicine and Cardiovascular Center, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA. ; University of Iowa Central Microscopy Research Facility, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA. ; Iowa City Veterans Affairs Medical, Iowa City, Iowa 52246, USA. ; 1] Department of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA [2] Department of Pathology, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA. ; Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA. ; Department of Pharmacology, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA. ; 1] Department of Internal Medicine and Cardiovascular Center, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA [2] Iowa City Veterans Affairs Medical, Iowa City, Iowa 52246, USA. ; 1] Department of Internal Medicine and Cardiovascular Center, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA [2] Department of Molecular Physiology and Biophysics, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA [3] Department of Molecular Physiology &Biophysics, Carver College of Medicine, University of Iowa, 51 Newton Road, Iowa City, Iowa 52242, USA (M.A.J.); The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA (J.L., P.J.M.); Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA (B.J.H.); Johns Hopkins University School of Medicine, 1830 East Monument Street, 9th Floor, Suite 9026, Baltimore, Maryland 21287, USA (E.D.L., M.E.A.).〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25254481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism ; Female ; Mitochondria, Heart/*metabolism/*pathology ; Myocardium/*enzymology/*pathology ; *Stress, Physiological
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Deployable wireless Fresnel lens (2013)
    In:  CASI
    Details
    Publication Date: 2019-08-27
    Description: Apparatus and methods for enhancing the gain of a wireless signal are provided. In at least one specific embodiment, the apparatus can include a screen comprised of one or more electrically conductive regions for reflecting electromagnetic radiation and one or more non-conductive regions for permitting electromagnetic radiation therethrough. The one or more electrically conductive regions can be disposed adjacent to at least one of the one or more non-conductive regions. The apparatus can also include a support member disposed about at least a portion of the screen. The screen can be capable of collapsing by twisting the support member in opposite screw senses to form interleaved concentric sections.
    Keywords: Electronics and Electrical Engineering
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