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  • Mice, Inbred C57BL  (16)
  • Cosmochemistry Special Feature
  • Organic Synthesis Toward Small-Molecule Probes and Drugs Special Feature
  • 2010-2014  (21)
  • 1
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    Combining meteorites and missions to explore Mars [Geology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-11-30
    Description: Laboratory studies of meteorites and robotic exploration of Mars reveal scant atmosphere, no evidence of plate tectonics, past evidence for abundant water, and a protracted igneous evolution. Despite indirect hints, direct evidence of a martian origin came with the discovery of trapped atmospheric gases in one meteorite. Since then, the study of martian meteorites and findings from missions have been linked. Although the meteorite source locations are unknown, impact ejection modeling and spectral mapping of Mars suggest derivation from small craters in terrains of Amazonian to Hesperian age. Whereas most martian meteorites are young (  4.5 Ga and formation of enriched and depleted reservoirs. However, the history inferred from martian meteorites conflicts with results from recent Mars missions, calling into doubt whether the igneous histor y inferred from the meteorites is applicable to Mars as a whole. Allan Hills 84001 dates to 4.09 Ga and contains fluid-deposited carbonates. Accompanying debate about the mechanism and temperature of origin of the carbonates came several features suggestive of past microbial life in the carbonates. Although highly disputed, the suggestion spurred interest in habitable extreme environments on Earth and throughout the Solar System. A flotilla of subsequent spacecraft has redefined Mars from a volcanic planet to a hydrologically active planet that may have harbored life. Understanding the history and habitability of Mars depends on understanding the coupling of the atmosphere, surface, and subsurface. Sample return that brings back direct evidence from these diverse reservoirs is essential.
    Keywords: Cosmochemistry Special Feature
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    Global epigenomic reconfiguration during mammalian brain development (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-06
    Description: DNA methylation is implicated in mammalian brain development and plasticity underlying learning and memory. We report the genome-wide composition, patterning, cell specificity, and dynamics of DNA methylation at single-base resolution in human and mouse frontal cortex throughout their lifespan. Widespread methylome reconfiguration occurs during fetal to young adult development, coincident with synaptogenesis. During this period, highly conserved non-CG methylation (mCH) accumulates in neurons, but not glia, to become the dominant form of methylation in the human neuronal genome. Moreover, we found an mCH signature that identifies genes escaping X-chromosome inactivation. Last, whole-genome single-base resolution 5-hydroxymethylcytosine (hmC) maps revealed that hmC marks fetal brain cell genomes at putative regulatory regions that are CG-demethylated and activated in the adult brain and that CG demethylation at these hmC-poised loci depends on Tet2 activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3785061/" 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/PMC3785061/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lister, Ryan -- Mukamel, Eran A -- Nery, Joseph R -- Urich, Mark -- Puddifoot, Clare A -- Johnson, Nicholas D -- Lucero, Jacinta -- Huang, Yun -- Dwork, Andrew J -- Schultz, Matthew D -- Yu, Miao -- Tonti-Filippini, Julian -- Heyn, Holger -- Hu, Shijun -- Wu, Joseph C -- Rao, Anjana -- Esteller, Manel -- He, Chuan -- Haghighi, Fatemeh G -- Sejnowski, Terrence J -- Behrens, M Margarita -- Ecker, Joseph R -- AI44432/AI/NIAID NIH HHS/ -- CA151535/CA/NCI NIH HHS/ -- HD065812/HD/NICHD NIH HHS/ -- HG006827/HG/NHGRI NIH HHS/ -- K99NS080911/NS/NINDS NIH HHS/ -- MH094670/MH/NIMH NIH HHS/ -- R01 AI044432/AI/NIAID NIH HHS/ -- R01 CA151535/CA/NCI NIH HHS/ -- R01 HD065812/HD/NICHD NIH HHS/ -- R01 HG006827/HG/NHGRI NIH HHS/ -- R01 MH094670/MH/NIMH NIH HHS/ -- R01 MH094774/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):1237905. doi: 10.1126/science.1237905. Epub 2013 Jul 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomic Analysis Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA. ryan.lister@uwa.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23828890" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Adult ; Animals ; Base Sequence ; Conserved Sequence ; Cytosine/*analogs & derivatives/metabolism ; *DNA Methylation ; *Epigenesis, Genetic ; Epigenomics ; Frontal Lobe/*growth & development ; *Gene Expression Regulation, Developmental ; Genome-Wide Association Study ; Humans ; Longevity ; Mice ; Mice, Inbred C57BL ; X Chromosome Inactivation/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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    Creating a false memory in the hippocampus (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-28
    Description: Memories can be unreliable. We created a false memory in mice by optogenetically manipulating memory engram-bearing cells in the hippocampus. Dentate gyrus (DG) or CA1 neurons activated by exposure to a particular context were labeled with channelrhodopsin-2. These neurons were later optically reactivated during fear conditioning in a different context. The DG experimental group showed increased freezing in the original context, in which a foot shock was never delivered. The recall of this false memory was context-specific, activated similar downstream regions engaged during natural fear memory recall, and was also capable of driving an active fear response. Our data demonstrate that it is possible to generate an internally represented and behaviorally expressed fear memory via artificial means.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramirez, Steve -- Liu, Xu -- Lin, Pei-Ann -- Suh, Junghyup -- Pignatelli, Michele -- Redondo, Roger L -- Ryan, Tomas J -- Tonegawa, Susumu -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jul 26;341(6144):387-91. doi: 10.1126/science.1239073.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN-Massachusetts Institute of Technology Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory, Department of Biology, MIT, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23888038" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/physiology ; Animals ; Association ; CA1 Region, Hippocampal/cytology/*physiology ; *Conditioning (Psychology) ; Dentate Gyrus/cytology/*physiology ; Dependovirus/genetics ; Doxycycline/administration & dosage ; Fear ; Genes, fos ; Light ; Memory/*physiology ; Mental Recall/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neurons/*physiology ; Optogenetics ; Rhodopsin/genetics/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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  • 4
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    Retinal waves coordinate patterned activity throughout the developing visual system (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-13
    Description: The morphological and functional development of the vertebrate nervous system is initially governed by genetic factors and subsequently refined by neuronal activity. However, fundamental features of the nervous system emerge before sensory experience is possible. Thus, activity-dependent development occurring before the onset of experience must be driven by spontaneous activity, but the origin and nature of activity in vivo remains largely untested. Here we use optical methods to show in live neonatal mice that waves of spontaneous retinal activity are present and propagate throughout the entire visual system before eye opening. This patterned activity encompassed the visual field, relied on cholinergic neurotransmission, preferentially initiated in the binocular retina and exhibited spatiotemporal correlations between the two hemispheres. Retinal waves were the primary source of activity in the midbrain and primary visual cortex, but only modulated ongoing activity in secondary visual areas. Thus, spontaneous retinal activity is transmitted through the entire visual system and carries patterned information capable of guiding the activity-dependent development of complex intra- and inter-hemispheric circuits before the onset of vision.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962269/" 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/PMC3962269/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ackman, James B -- Burbridge, Timothy J -- Crair, Michael C -- P30 EY000785/EY/NEI NIH HHS/ -- R01 EY015788/EY/NEI NIH HHS/ -- R01 EY023105/EY/NEI NIH HHS/ -- T15LM070506/LM/NLM NIH HHS/ -- T32 EY017353/EY/NEI NIH HHS/ -- T32 EY022312/EY/NEI NIH HHS/ -- T32 NS007224/NS/NINDS NIH HHS/ -- T32NS007224/NS/NINDS NIH HHS/ -- England -- Nature. 2012 Oct 11;490(7419):219-25. doi: 10.1038/nature11529.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23060192" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Bicyclo Compounds, Heterocyclic/pharmacology ; Calcium/metabolism ; Gene Expression Regulation, Developmental/drug effects ; Mice ; Mice, Inbred C57BL ; Nicotinic Agonists/pharmacology ; Pyridines/pharmacology ; Retina/drug effects/growth & development ; Retinal Neurons/cytology/drug effects ; Visual Cortex/cytology/drug effects/*growth & development
    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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    Reconstructing lineage hierarchies of the distal lung epithelium using single-cell RNA-seq (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-04-18
    Description: The mammalian lung is a highly branched network in which the distal regions of the bronchial tree transform during development into a densely packed honeycomb of alveolar air sacs that mediate gas exchange. Although this transformation has been studied by marker expression analysis and fate-mapping, the mechanisms that control the progression of lung progenitors along distinct lineages into mature alveolar cell types are still incompletely known, in part because of the limited number of lineage markers and the effects of ensemble averaging in conventional transcriptome analysis experiments on cell populations. Here we show that single-cell transcriptome analysis circumvents these problems and enables direct measurement of the various cell types and hierarchies in the developing lung. We used microfluidic single-cell RNA sequencing (RNA-seq) on 198 individual cells at four different stages encompassing alveolar differentiation to measure the transcriptional states which define the developmental and cellular hierarchy of the distal mouse lung epithelium. We empirically classified cells into distinct groups by using an unbiased genome-wide approach that did not require a priori knowledge of the underlying cell types or the previous purification of cell populations. The results confirmed the basic outlines of the classical model of epithelial cell-type diversity in the distal lung and led to the discovery of many previously unknown cell-type markers, including transcriptional regulators that discriminate between the different populations. We reconstructed the molecular steps during maturation of bipotential progenitors along both alveolar lineages and elucidated the full life cycle of the alveolar type 2 cell lineage. This single-cell genomics approach is applicable to any developing or mature tissue to robustly delineate molecularly distinct cell types, define progenitors and lineage hierarchies, and identify lineage-specific regulatory factors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4145853/" 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/PMC4145853/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Treutlein, Barbara -- Brownfield, Doug G -- Wu, Angela R -- Neff, Norma F -- Mantalas, Gary L -- Espinoza, F Hernan -- Desai, Tushar J -- Krasnow, Mark A -- Quake, Stephen R -- 5K08HL084095/HL/NHLBI NIH HHS/ -- K08 HL084095/HL/NHLBI NIH HHS/ -- T32 HD007249/HD/NICHD NIH HHS/ -- T32HD007249/HD/NICHD NIH HHS/ -- U01 HL099995/HL/NHLBI NIH HHS/ -- U01 HL099999/HL/NHLBI NIH HHS/ -- U01HL099995/HL/NHLBI NIH HHS/ -- U01HL099999/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 May 15;509(7500):371-5. doi: 10.1038/nature13173. Epub 2014 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Departments of Bioengineering and Applied Physics, Stanford University School of Medicine and Howard Hughes Medical Institute, Stanford, California 94305, USA [2]. ; 1] Department of Biochemistry, Stanford University School of Medicine and Howard Hughes Medical Institute, Stanford, California 94305, USA [2]. ; Departments of Bioengineering and Applied Physics, Stanford University School of Medicine and Howard Hughes Medical Institute, Stanford, California 94305, USA. ; Department of Biochemistry, Stanford University School of Medicine and Howard Hughes Medical Institute, Stanford, California 94305, USA. ; Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24739965" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bronchi/cytology ; Cell Differentiation/genetics ; Cell Lineage/*genetics ; Epithelial Cells/classification/*cytology/*metabolism ; Female ; Genetic Markers ; Genome/genetics ; Genomics ; Lung/*cytology/embryology ; Mice ; Mice, Inbred C57BL ; Pulmonary Alveoli/cytology ; Pulmonary Gas Exchange ; Sequence Analysis, RNA/*methods ; Single-Cell Analysis/*methods ; Stem Cells/cytology ; Transcriptome/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    mTORC1-mediated translational elongation limits intestinal tumour initiation and growth (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-11-11
    Description: Inactivation of APC is a strongly predisposing event in the development of colorectal cancer, prompting the search for vulnerabilities specific to cells that have lost APC function. Signalling through the mTOR pathway is known to be required for epithelial cell proliferation and tumour growth, and the current paradigm suggests that a critical function of mTOR activity is to upregulate translational initiation through phosphorylation of 4EBP1 (refs 6, 7). This model predicts that the mTOR inhibitor rapamycin, which does not efficiently inhibit 4EBP1 (ref. 8), would be ineffective in limiting cancer progression in APC-deficient lesions. Here we show in mice that mTOR complex 1 (mTORC1) activity is absolutely required for the proliferation of Apc-deficient (but not wild-type) enterocytes, revealing an unexpected opportunity for therapeutic intervention. Although APC-deficient cells show the expected increases in protein synthesis, our study reveals that it is translation elongation, and not initiation, which is the rate-limiting component. Mechanistically, mTORC1-mediated inhibition of eEF2 kinase is required for the proliferation of APC-deficient cells. Importantly, treatment of established APC-deficient adenomas with rapamycin (which can target eEF2 through the mTORC1-S6K-eEF2K axis) causes tumour cells to undergo growth arrest and differentiation. Taken together, our data suggest that inhibition of translation elongation using existing, clinically approved drugs, such as the rapalogs, would provide clear therapeutic benefit for patients at high risk of developing colorectal cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304784/" 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/PMC4304784/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faller, William J -- Jackson, Thomas J -- Knight, John R P -- Ridgway, Rachel A -- Jamieson, Thomas -- Karim, Saadia A -- Jones, Carolyn -- Radulescu, Sorina -- Huels, David J -- Myant, Kevin B -- Dudek, Kate M -- Casey, Helen A -- Scopelliti, Alessandro -- Cordero, Julia B -- Vidal, Marcos -- Pende, Mario -- Ryazanov, Alexey G -- Sonenberg, Nahum -- Meyuhas, Oded -- Hall, Michael N -- Bushell, Martin -- Willis, Anne E -- Sansom, Owen J -- 311301/European Research Council/International -- A7130/Cancer Research UK/United Kingdom -- G1000078/1/National Centre for the Replacement, Refinement and Reduction of Animals in Research/United Kingdom -- MC_UP_A600_1023/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2015 Jan 22;517(7535):497-500. doi: 10.1038/nature13896. Epub 2014 Nov 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK Beatson Institute, Glasgow G61 1BD, UK. ; Medical Research Council Toxicology Unit, Leicester LE1 9HN, UK. ; Institut Necker-Enfants Malades, CS 61431, Paris, France Institut National de la Sante et de la Recherche Medicale, U1151, F-75014 Paris, France Universite Paris Descartes, Sorbonne Paris Cite, 75006 Paris, France. ; Department of Pharmacology, Rutgers The State University of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA. ; Department of Biochemistry and Goodman Cancer Research Center, McGill University, Montreal, Quebec H3A 1A3, Canada. ; Department of Biochemistry and Molecular Biology, IMRIC, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel. ; Biozentrum, University of Basel, CH-4056 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25383520" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein/deficiency/genetics ; Animals ; Cell Proliferation ; Cell Transformation, Neoplastic/metabolism/*pathology ; Elongation Factor 2 Kinase/deficiency/genetics/metabolism ; Enzyme Activation ; Genes, APC ; Intestinal Neoplasms/genetics/*metabolism/*pathology ; Male ; Mice ; Mice, Inbred C57BL ; Multiprotein Complexes/*metabolism ; Oncogene Protein p55(v-myc)/metabolism ; *Peptide Chain Elongation, Translational ; Peptide Elongation Factor 2/metabolism ; Ribosomal Protein S6 Kinases/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/*metabolism ; Wnt Proteins/metabolism
    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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  • 7
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    Elementary Ca2+ signals through endothelial TRPV4 channels regulate vascular function (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-05
    Description: Major features of the transcellular signaling mechanism responsible for endothelium-dependent regulation of vascular smooth muscle tone are unresolved. We identified local calcium (Ca(2+)) signals ("sparklets") in the vascular endothelium of resistance arteries that represent Ca(2+) influx through single TRPV4 cation channels. Gating of individual TRPV4 channels within a four-channel cluster was cooperative, with activation of as few as three channels per cell causing maximal dilation through activation of endothelial cell intermediate (IK)- and small (SK)-conductance, Ca(2+)-sensitive potassium (K(+)) channels. Endothelial-dependent muscarinic receptor signaling also acted largely through TRPV4 sparklet-mediated stimulation of IK and SK channels to promote vasodilation. These results support the concept that Ca(2+) influx through single TRPV4 channels is leveraged by the amplifier effect of cooperative channel gating and the high Ca(2+) sensitivity of IK and SK channels to cause vasodilation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3715993/" 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/PMC3715993/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sonkusare, Swapnil K -- Bonev, Adrian D -- Ledoux, Jonathan -- Liedtke, Wolfgang -- Kotlikoff, Michael I -- Heppner, Thomas J -- Hill-Eubanks, David C -- Nelson, Mark T -- 1P01HL095488/HL/NHLBI NIH HHS/ -- 2-P20-RR-016435-06/RR/NCRR NIH HHS/ -- GM086736/GM/NIGMS NIH HHS/ -- HL044455/HL/NHLBI NIH HHS/ -- P01 HL095488/HL/NHLBI NIH HHS/ -- R01 HL098243/HL/NHLBI NIH HHS/ -- R01HL098243/HL/NHLBI NIH HHS/ -- R37 DK053832/DK/NIDDK NIH HHS/ -- R37DK053832/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 May 4;336(6081):597-601. doi: 10.1126/science.1216283.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, College of Medicine, University of Vermont, Burlington, VT 05405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22556255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; *Calcium Signaling ; Endothelial Cells/drug effects/*metabolism/physiology ; Endothelium, Vascular/drug effects/metabolism/physiology ; Intermediate-Conductance Calcium-Activated Potassium Channels/metabolism ; Ion Channel Gating ; Leucine/analogs & derivatives/pharmacology ; Mesenteric Arteries/drug effects/*metabolism/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Patch-Clamp Techniques ; Receptors, Muscarinic/metabolism ; Signal Transduction ; Small-Conductance Calcium-Activated Potassium Channels/metabolism ; Sulfonamides/pharmacology ; TRPV Cation Channels/agonists/antagonists & inhibitors/*metabolism ; *Vasodilation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Coinfection. Virus-helminth coinfection reveals a microbiota-independent mechanism of immunomodulation (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-08-02
    Description: The mammalian intestine is colonized by beneficial commensal bacteria and is a site of infection by pathogens, including helminth parasites. Helminths induce potent immunomodulatory effects, but whether these effects are mediated by direct regulation of host immunity or indirectly through eliciting changes in the microbiota is unknown. We tested this in the context of virus-helminth coinfection. Helminth coinfection resulted in impaired antiviral immunity and was associated with changes in the microbiota and STAT6-dependent helminth-induced alternative activation of macrophages. Notably, helminth-induced impairment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-like molecule that is associated with alternatively activated macrophages, could partially restore antiviral immunity. These data indicate that helminth-induced immunomodulation occurs independently of changes in the microbiota but is dependent on Ym1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548887/" 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/PMC4548887/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osborne, Lisa C -- Monticelli, Laurel A -- Nice, Timothy J -- Sutherland, Tara E -- Siracusa, Mark C -- Hepworth, Matthew R -- Tomov, Vesselin T -- Kobuley, Dmytro -- Tran, Sara V -- Bittinger, Kyle -- Bailey, Aubrey G -- Laughlin, Alice L -- Boucher, Jean-Luc -- Wherry, E John -- Bushman, Frederic D -- Allen, Judith E -- Virgin, Herbert W -- Artis, David -- 095831/Wellcome Trust/United Kingdom -- 2-P30 CA016520/CA/NCI NIH HHS/ -- 5T32A100716334/PHS HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI082630/AI/NIAID NIH HHS/ -- AI083022/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI097333/AI/NIAID NIH HHS/ -- AI102942/AI/NIAID NIH HHS/ -- AI106697/AI/NIAID NIH HHS/ -- F32 AI085828/AI/NIAID NIH HHS/ -- F32-AI085828/AI/NIAID NIH HHS/ -- HHSN272201300006C/PHS HHS/ -- K08 DK097301/DK/NIDDK NIH HHS/ -- K08-DK097301/DK/NIDDK NIH HHS/ -- MR/J001929/1/Medical Research Council/United Kingdom -- P01 AI106697/AI/NIAID NIH HHS/ -- P30-AI045008/AI/NIAID NIH HHS/ -- P30-DK050306/DK/NIDDK NIH HHS/ -- R01 AI 084887/AI/NIAID NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI097333/AI/NIAID NIH HHS/ -- R01 AI102942/AI/NIAID NIH HHS/ -- R21 AI087990/AI/NIAID NIH HHS/ -- T32-AI007532/AI/NIAID NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 1;345(6196):578-82. doi: 10.1126/science.1256942. Epub 2014 Jul 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques, Universite Paris Descartes, Paris, France. ; Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. dartis@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25082704" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/immunology ; Caliciviridae Infections/*immunology ; Coinfection/*immunology/microbiology/parasitology ; Gastroenteritis/*immunology/virology ; Germ-Free Life ; *Immunomodulation ; Intestines/immunology/microbiology/virology ; Lectins/*immunology ; Macrophage Activation ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Microbiota/*immunology ; Norovirus/*immunology ; Trichinella/*immunology ; Trichinellosis/*immunology ; beta-N-Acetylhexosaminidases/*immunology
    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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  • 9
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    Interferon-lambda cures persistent murine norovirus infection in the absence of adaptive immunity (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-29
    Description: Norovirus gastroenteritis is a major public health burden worldwide. Although fecal shedding is important for transmission of enteric viruses, little is known about the immune factors that restrict persistent enteric infection. We report here that although the cytokines interferon-alpha (IFN-alpha) and IFN-beta prevented the systemic spread of murine norovirus (MNoV), only IFN-lambda controlled persistent enteric infection. Infection-dependent induction of IFN-lambda was governed by the MNoV capsid protein and correlated with diminished enteric persistence. Treatment of established infection with IFN-lambda cured mice in a manner requiring nonhematopoietic cell expression of the IFN-lambda receptor, Ifnlr1, and independent of adaptive immunity. These results suggest the therapeutic potential of IFN-lambda for curing virus infections in the gastrointestinal tract.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398891/" 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/PMC4398891/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nice, Timothy J -- Baldridge, Megan T -- McCune, Broc T -- Norman, Jason M -- Lazear, Helen M -- Artyomov, Maxim -- Diamond, Michael S -- Virgin, Herbert W -- 5T32A100716334/PHS HHS/ -- 5T32AI007163/AI/NIAID NIH HHS/ -- 5T32CA009547/CA/NCI NIH HHS/ -- F31 CA177194/CA/NCI NIH HHS/ -- F31CA177194-01/CA/NCI NIH HHS/ -- R01 AI084887/AI/NIAID NIH HHS/ -- T32 AI007163/AI/NIAID NIH HHS/ -- T32 CA009547/CA/NCI NIH HHS/ -- U19 AI083019/AI/NIAID NIH HHS/ -- U19 AI106772/AI/NIAID NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 16;347(6219):269-73. doi: 10.1126/science.1258100. Epub 2014 Nov 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. virgin@wustl.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25431489" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Caliciviridae Infections/*drug therapy/*immunology/virology ; Capsid Proteins/immunology/metabolism ; Cells, Cultured ; Cytokines/biosynthesis/*immunology/*therapeutic use ; Feces/virology ; Gastroenteritis/drug therapy/*immunology/virology ; Immunity, Innate ; Interferon-alpha/biosynthesis/immunology ; Interferon-beta/biosynthesis/immunology ; Mice ; Mice, Inbred C57BL ; Norovirus/*immunology/*physiology ; Virus Replication ; Virus Shedding
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    Commensal microbes and interferon-lambda determine persistence of enteric murine norovirus infection (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-29
    Description: The capacity of human norovirus (NoV), which causes 〉90% of global epidemic nonbacterial gastroenteritis, to infect a subset of people persistently may contribute to its spread. How such enteric viruses establish persistent infections is not well understood. We found that antibiotics prevented persistent murine norovirus (MNoV) infection, an effect that was reversed by replenishment of the bacterial microbiota. Antibiotics did not prevent tissue infection or affect systemic viral replication but acted specifically in the intestine. The receptor for the antiviral cytokine interferon-lambda, Ifnlr1, as well as the transcription factors Stat1 and Irf3, were required for antibiotics to prevent viral persistence. Thus, the bacterial microbiome fosters enteric viral persistence in a manner counteracted by specific components of the innate immune system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4409937/" 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/PMC4409937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldridge, Megan T -- Nice, Timothy J -- McCune, Broc T -- Yokoyama, Christine C -- Kambal, Amal -- Wheadon, Michael -- Diamond, Michael S -- Ivanova, Yulia -- Artyomov, Maxim -- Virgin, Herbert W -- 1F31CA177194/CA/NCI NIH HHS/ -- 5T32AI007163/AI/NIAID NIH HHS/ -- 5T32CA009547/CA/NCI NIH HHS/ -- F31 CA177194/CA/NCI NIH HHS/ -- R01 AI084887/AI/NIAID NIH HHS/ -- T32 AI007163/AI/NIAID NIH HHS/ -- T32 CA009547/CA/NCI NIH HHS/ -- U19 AI083019/AI/NIAID NIH HHS/ -- U19 AI106772/AI/NIAID NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 16;347(6219):266-9. doi: 10.1126/science.1258025. Epub 2014 Nov 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Departments of Medicine and Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. virgin@wustl.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25431490" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Caliciviridae Infections/drug therapy/immunology/microbiology/*virology ; Cytokines/*physiology ; Female ; Gastroenteritis/drug therapy/immunology/microbiology/*virology ; Intestines/*microbiology/virology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; *Microbiota/drug effects ; Norovirus/immunology/*physiology ; Receptors, Cytokine/genetics/metabolism ; Signal Transduction ; *Symbiosis ; Viral Load ; Virus Replication ; Virus Shedding
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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