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  • 1
    Publication Date: 2010-02-27
    Description: The beta1- and beta2-adrenergic receptors (betaARs) on the surface of cardiomyocytes mediate distinct effects on cardiac function and the development of heart failure by regulating production of the second messenger cyclic adenosine monophosphate (cAMP). The spatial localization in cardiomyocytes of these betaARs, which are coupled to heterotrimeric guanine nucleotide-binding proteins (G proteins), and the functional implications of their localization have been unclear. We combined nanoscale live-cell scanning ion conductance and fluorescence resonance energy transfer microscopy techniques and found that, in cardiomyocytes from healthy adult rats and mice, spatially confined beta2AR-induced cAMP signals are localized exclusively to the deep transverse tubules, whereas functional beta1ARs are distributed across the entire cell surface. In cardiomyocytes derived from a rat model of chronic heart failure, beta2ARs were redistributed from the transverse tubules to the cell crest, which led to diffuse receptor-mediated cAMP signaling. Thus, the redistribution of beta(2)ARs in heart failure changes compartmentation of cAMP and might contribute to the failing myocardial phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nikolaev, Viacheslav O -- Moshkov, Alexey -- Lyon, Alexander R -- Miragoli, Michele -- Novak, Pavel -- Paur, Helen -- Lohse, Martin J -- Korchev, Yuri E -- Harding, Sian E -- Gorelik, Julia -- 084064/Wellcome Trust/United Kingdom -- BB/D020875/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0500373/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1653-7. doi: 10.1126/science.1185988. Epub 2010 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiac Medicine, National Heart and Lung Institute, Imperial College London, Dovehouse Street, London SW3 6LY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Membrane/*metabolism/ultrastructure ; Chronic Disease ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cytosol/metabolism ; Fluorescence Resonance Energy Transfer ; Heart Failure/*metabolism/*pathology ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Microscopy/methods ; Myocytes, Cardiac/*metabolism/ultrastructure ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta-1/genetics/metabolism ; Receptors, Adrenergic, beta-2/genetics/*metabolism ; Sarcolemma/*metabolism/ultrastructure ; Signal Transduction
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  • 2
    Publication Date: 2010-08-07
    Description: Visual, acoustic, and olfactory stimuli associated with a highly charged emotional situation take on the affective qualities of that situation. Where the emotional meaning of a given sensory experience is stored is a matter of debate. We found that excitotoxic lesions of auditory, visual, or olfactory secondary sensory cortices impaired remote, but not recent, fear memories in rats. Amnesia was modality-specific and not due to an interference with sensory or emotional processes. In these sites, memory persistence was dependent on ongoing protein kinase Mzeta activity and was associated with an increased activity of layers II-IV, thus suggesting a synaptic strengthening of corticocortical connections. Lesions of the same areas left intact the memory of sensory stimuli not associated with any emotional charge. We propose that secondary sensory cortices support memory storage and retrieval of sensory stimuli that have acquired a behavioral salience with the experience.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sacco, Tiziana -- Sacchetti, Benedetto -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):649-56. doi: 10.1126/science.1183165.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Turin, Corso Raffaello 30, I-10125 Turin, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20689011" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Amnesia/physiopathology ; Amygdala/physiology ; Animals ; Auditory Cortex/*physiology ; Conditioning (Psychology) ; Early Growth Response Protein 1/genetics/metabolism ; *Emotions ; *Fear ; Habituation, Psychophysiologic ; Male ; Memory/*physiology ; Odors ; Olfactory Pathways/*physiology ; Photic Stimulation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Rats ; Rats, Wistar ; Synapses/physiology ; Visual Cortex/*physiology
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2010-05-15
    Description: Active invasion of the dendritic tree by action potentials (APs) generated in the axon is essential for associative synaptic plasticity and neuronal ensemble formation. In cortical pyramidal cells (PCs), this AP back-propagation is supported by dendritic voltage-gated Na+ (Nav) channels, whose molecular identity is unknown. Using a highly sensitive electron microscopic immunogold technique, we revealed the presence of the Nav1.6 subunit in hippocampal CA1 PC proximal and distal dendrites. Here, the subunit density is lower by a factor of 35 to 80 than that found in axon initial segments. A gradual decrease in Nav1.6 density along the proximodistal axis of the dendritic tree was also detected without any labeling in dendritic spines. Our results reveal the characteristic subcellular distribution of the Nav1.6 subunit, identifying this molecule as a key substrate enabling dendritic excitability.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546315/" 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/PMC3546315/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorincz, Andrea -- Nusser, Zoltan -- 083484/Wellcome Trust/United Kingdom -- 090197/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 May 14;328(5980):906-9. doi: 10.1126/science.1187958.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary. lorincz@koki.hu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466935" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/chemistry/physiology ; CA1 Region, Hippocampal/*chemistry/physiology/ultrastructure ; Cell Membrane/chemistry ; Dendrites/*chemistry/physiology/ultrastructure ; Dendritic Spines/chemistry ; Fluorescent Antibody Technique ; Freeze Fracturing ; Immunohistochemistry ; Ion Channel Gating ; Male ; Microscopy, Immunoelectron ; NAV1.1 Voltage-Gated Sodium Channel ; NAV1.6 Voltage-Gated Sodium Channel ; Nerve Tissue Proteins/analysis ; Ranvier's Nodes/chemistry ; Rats ; Rats, Wistar ; Sodium Channels/*analysis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2010-06-26
    Description: Chronic exposure to drugs of abuse induces countless modifications in brain physiology. However, the neurobiological adaptations specifically associated with the transition to addiction are unknown. Cocaine self-administration rapidly suppresses long-term depression (LTD), an important form of synaptic plasticity in the nucleus accumbens. Using a rat model of addiction, we found that animals that progressively develop the behavioral hallmarks of addiction have permanently impaired LTD, whereas LTD is progressively recovered in nonaddicted rats maintaining a controlled drug intake. By making drug seeking consistently resistant to modulation by environmental contingencies and consequently more and more inflexible, a persistently impaired LTD could mediate the transition to addiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasanetz, Fernando -- Deroche-Gamonet, Veronique -- Berson, Nadege -- Balado, Eric -- Lafourcade, Mathieu -- Manzoni, Olivier -- Piazza, Pier Vincenzo -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1709-12. doi: 10.1126/science.1187801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U862, NeuroCentre Magendie, 147 Rue Leo Saignat, 33077, Bordeaux Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576893" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Cocaine/administration & dosage ; Cocaine-Related Disorders/*physiopathology ; Disease Models, Animal ; Glutamic Acid/metabolism ; *Long-Term Synaptic Depression ; Nucleus Accumbens/*physiopathology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Self Administration ; Synaptic Transmission
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2010-09-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sauvageau, Guy -- Humphries, R Keith -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1291-2. doi: 10.1126/science.1195173.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics of Stem Cells Laboratory, Institute of Research in Immunology and Cancer, University of Montreal, Montreal, QC H3C 3J7, Canada. guy.sauvageau@umontreal.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829472" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Fetal Blood/cytology ; *Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology/*drug effects/physiology ; Humans ; Mice ; Purines/chemistry/metabolism/*pharmacology ; Receptors, Aryl Hydrocarbon/*antagonists & inhibitors/metabolism ; Small Molecule Libraries ; Species Specificity
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2010-08-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhatia, Mickie -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1024-5. doi: 10.1126/science.1194919.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell and Cancer Research Institute, McMaster University, Hamilton, Ontario L8N 3Z5, Canada. mbhatia@mcmaster.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798306" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques/*methods ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Elasticity ; Humans ; Hydrogels ; Mice ; Muscle Fibers, Skeletal/*cytology/physiology ; Myoblasts, Skeletal/cytology/physiology ; Regeneration ; Stem Cell Niche/*physiology ; Stem Cell Transplantation ; Stem Cells/*physiology
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  • 7
    Publication Date: 2010-07-22
    Description: Astrocytes provide structural and metabolic support for neuronal networks, but direct evidence demonstrating their active role in complex behaviors is limited. Central respiratory chemosensitivity is an essential mechanism that, via regulation of breathing, maintains constant levels of blood and brain pH and partial pressure of CO2. We found that astrocytes of the brainstem chemoreceptor areas are highly chemosensitive. They responded to physiological decreases in pH with vigorous elevations in intracellular Ca2+ and release of adenosine triphosphate (ATP). ATP propagated astrocytic Ca2+ excitation, activated chemoreceptor neurons, and induced adaptive increases in breathing. Mimicking pH-evoked Ca2+ responses by means of optogenetic stimulation of astrocytes expressing channelrhodopsin-2 activated chemoreceptor neurons via an ATP-dependent mechanism and triggered robust respiratory responses in vivo. This demonstrates a potentially crucial role for brain glial cells in mediating a fundamental physiological reflex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160742/" 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/PMC3160742/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gourine, Alexander V -- Kasymov, Vitaliy -- Marina, Nephtali -- Tang, Feige -- Figueiredo, Melina F -- Lane, Samantha -- Teschemacher, Anja G -- Spyer, K Michael -- Deisseroth, Karl -- Kasparov, Sergey -- 079040/Wellcome Trust/United Kingdom -- PG/09/064/27886/British Heart Foundation/United Kingdom -- British Heart Foundation/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):571-5. doi: 10.1126/science.1190721. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience, Physiology, and Pharmacology, University College London, London WC1E 6BT, UK. a.gourine@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647426" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Astrocytes/*physiology ; Brain Stem/cytology/*physiology ; Calcium/metabolism ; Carbon Dioxide/analysis/blood ; Cells, Cultured ; Chemoreceptor Cells/*physiology ; Exocytosis ; Gap Junctions/metabolism ; Hydrogen-Ion Concentration ; In Vitro Techniques ; Light ; Medulla Oblongata/cytology/*physiology ; Membrane Potentials ; Rats ; Rats, Sprague-Dawley ; Receptors, Purinergic P2/metabolism ; *Respiration ; Rhodopsin/genetics/metabolism
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  • 8
    Publication Date: 2010-08-07
    Description: Using optical trapping and fluorescence imaging techniques, we measured the step size and stiffness of single skeletal myosins interacting with actin filaments and arranged on myosin-rod cofilaments that approximate myosin mechanics during muscle contraction. Stiffness is dramatically lower for negatively compared to positively strained myosins, consistent with buckling of myosin's subfragment 2 rod domain. Low stiffness minimizes drag of negatively strained myosins during contraction at loaded conditions. Myosin's elastic portion is stretched during active force generation, reducing apparent step size with increasing load, even though the working stroke is approximately constant at about 8 nanometers. Taking account of the nonlinear nature of myosin elasticity is essential to relate myosin's internal structural changes to physiological force generation and filament sliding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaya, Motoshi -- Higuchi, Hideo -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):686-9. doi: 10.1126/science.1191484.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, Graduate School of Science, University of Tokyo, 7-3-1 Hongo, Bunkyou-ku, Tokyo, 113-0033 Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20689017" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*physiology ; Actomyosin/chemistry/physiology ; Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Compliance ; Elasticity ; Models, Biological ; *Muscle Contraction ; Muscle Fibers, Skeletal/chemistry/physiology ; Muscle, Skeletal ; Myosin Subfragments/physiology ; Myosins/chemistry/*physiology ; Quantum Dots ; Rabbits
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  • 9
    Publication Date: 2010-01-30
    Description: In addition to their pivotal role in thrombosis and wound repair, platelets participate in inflammatory responses. We investigated the role of platelets in the autoimmune disease rheumatoid arthritis. We identified platelet microparticles--submicrometer vesicles elaborated by activated platelets--in joint fluid from patients with rheumatoid arthritis and other forms of inflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via interleukin-1. Consistent with these findings, depletion of platelets attenuated murine inflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis pathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets and their activation-induced microparticles in inflammatory joint diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927861/" 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/PMC2927861/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boilard, Eric -- Nigrovic, Peter A -- Larabee, Katherine -- Watts, Gerald F M -- Coblyn, Jonathan S -- Weinblatt, Michael E -- Massarotti, Elena M -- Remold-O'Donnell, Eileen -- Farndale, Richard W -- Ware, Jerry -- Lee, David M -- G0500707/Medical Research Council/United Kingdom -- HL091269/HL/NHLBI NIH HHS/ -- HL50545/HL/NHLBI NIH HHS/ -- K08AR051321/AR/NIAMS NIH HHS/ -- P01 AI065858/AI/NIAID NIH HHS/ -- R01 HL050545/HL/NHLBI NIH HHS/ -- R01 HL050545-16/HL/NHLBI NIH HHS/ -- R01 HL050545-18/HL/NHLBI NIH HHS/ -- R21 HL091269/HL/NHLBI NIH HHS/ -- R21 HL091269-01A2/HL/NHLBI NIH HHS/ -- RG/09/003/27122/British Heart Foundation/United Kingdom -- British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):580-3. doi: 10.1126/science.1181928.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Immunology and Allergy, 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/20110505" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/blood/immunology ; Arthritis, Rheumatoid/*blood/*immunology/physiopathology ; Blood Platelets/cytology/*physiology/ultrastructure ; Cell-Derived Microparticles/metabolism/*physiology ; Cells, Cultured ; Collagen/*metabolism ; Cytokines/*metabolism ; Extracellular Matrix/metabolism ; Fibroblasts/immunology/metabolism ; Humans ; Interleukin-1/metabolism ; Mice ; Mice, Transgenic ; Platelet Activation ; Platelet Membrane Glycoproteins/metabolism ; Receptors, Collagen/metabolism ; Synovial Fluid/cytology/*immunology ; Synovial Membrane/cytology/immunology
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  • 10
    Publication Date: 2010-07-22
    Description: Stem cells that naturally reside in adult tissues, such as muscle stem cells (MuSCs), exhibit robust regenerative capacity in vivo that is rapidly lost in culture. Using a bioengineered substrate to recapitulate key biophysical and biochemical niche features in conjunction with a highly automated single-cell tracking algorithm, we show that substrate elasticity is a potent regulator of MuSC fate in culture. Unlike MuSCs on rigid plastic dishes (approximately 10(6) kilopascals), MuSCs cultured on soft hydrogel substrates that mimic the elasticity of muscle (12 kilopascals) self-renew in vitro and contribute extensively to muscle regeneration when subsequently transplanted into mice and assayed histologically and quantitatively by noninvasive bioluminescence imaging. Our studies provide novel evidence that by recapitulating physiological tissue rigidity, propagation of adult muscle stem cells is possible, enabling future cell-based therapies for muscle-wasting diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929271/" 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/PMC2929271/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilbert, P M -- Havenstrite, K L -- Magnusson, K E G -- Sacco, A -- Leonardi, N A -- Kraft, P -- Nguyen, N K -- Thrun, S -- Lutolf, M P -- Blau, H M -- 2 T32 HD007249/HD/NICHD NIH HHS/ -- 52005886/Howard Hughes Medical Institute/ -- AG009521/AG/NIA NIH HHS/ -- AG020961/AG/NIA NIH HHS/ -- CA09151/CA/NCI NIH HHS/ -- HL096113/HL/NHLBI NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG020961/AG/NIA NIH HHS/ -- R01 AG020961-06A2/AG/NIA NIH HHS/ -- R01 AG020961-07/AG/NIA NIH HHS/ -- R01 HL096113/HL/NHLBI NIH HHS/ -- R01 HL096113-03/HL/NHLBI NIH HHS/ -- T32 CA009151/CA/NCI NIH HHS/ -- T32 CA009151-35/CA/NCI NIH HHS/ -- T32 HD007249/HD/NICHD NIH HHS/ -- T32 HD007249-25/HD/NICHD NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- U01 HL100397-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1078-81. doi: 10.1126/science.1191035. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647425" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cell Count ; Cell Culture Techniques/*methods ; Cell Death ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Separation ; Cell Survival ; Cells, Cultured ; Elastic Modulus ; Hydrogels ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Muscle Fibers, Skeletal/*cytology/physiology ; Muscle, Skeletal/*cytology ; Polyethylene Glycols ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology ; Stem Cell Niche/*physiology ; Stem Cell Transplantation ; Stem Cells/cytology/*physiology
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