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  • Female  (2,049)
  • Chemistry
  • 2010-2014  (2,065)
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  • 1
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    Influence of protozoan grazing on the marine geochemistry of particle reactive trace metals (2012)
    Massachusetts Institute of Technology and Woods Hole Oceanographic Institution
    Details
    Publication Date: 2022-05-25
    Description: Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy at the Massachusetts Institute of Technology and the Woods Hole Oceanographic Institution May 1998
    Description: Planktonic protozoan grazers have the potential to significantly affect the chemistry of particle-associated trace metals. This is due both to the importance of protists as consumers of bacterial-sized particles, and to the unique low-pH, enzyme-rich microenvironment of the grazer food vacuole. This thesis examines the role of protozoan grazers in the marine geochemistry of strongly hydrolyzed, particle-reactive trace metals, in particular Th and Fe. A series of tracer experiments was carried out in model systems in order to determine the effect of grazer-mediated transformations on the chemical speciation and partitioning of radioisotopes C9Fe, 234Th, 51Cr) associated with prey cells. Results indicate that protozoan grazers are equally able to mobilize intracellular and extracellular trace metals. In some cases, protozoan regeneration of trace metals appears to lead to the formation of metal-organic complexes. Protozoan grazing may generate colloidal material that can scavenge trace metals and, via aggregation, lead to an increase in the metal/organic carbon ratio of aggregated particles. Model system experiments were also conducted in order to determine the effect of grazers on mineral phases, specifically colloidal iron oxide (ferrihydrite). Several independent techniques were employed, including size fractionation ors9Fe-labeled colloids, competitive ligand exchange, and iron-limited diatoms as "probes" for bioavailable Fe. Experimental evidence strongly suggests that protozoan grazing can affect the surface chemistry and increase the dissolution rate of iron oxide phases through phagotrophic ingestion. In further work on protozoan-mediated dissolution of colloidal Fe oxides, a novel tracer technique was developed based on the synthesis of colloidal ferrihydrite impregnated with 133Ba as an inert tracer. This technique was shown to be a sensitive, quantitative indicator for the extent of ferrihydrite dissolution/alteration by a variety of mechanisms, including photochemical reduction and ligand-mediated dissolution. In field experiments using this technique, grazing by naturally occuring protistan assemblages was shown to significantly enhance the dissolution rate of colloidal ferrihydrite over that in non-grazing controls. Laboratory and field results indicate that, when integrated temporally over the entire euphotic zone, protozoan grazing may equal or exceed photoreduction as a pathway for the dissolution of iron oxides.
    Description: This work was financially supported by a Department of Defense ONR-NDSEG Graduate Fellowship, Office ofNaval Research AASERT Award (N00014-94-1-0711), and the National Science Foundation EGB Program (OCE-9523910).
    Keywords: Protozoa ; Water chemistry ; Trace elements in water ; Marine zooplankton ; Chemistry
    Repository Name: Woods Hole Open Access Server
    Type: Thesis
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  • 2
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    Repair of UVB-Damaged Skin by the antioxidant sulphated flavone glycoside Thalassiolin B Isolated from the marine plant Thalassia testudinum Banks ex König (2011)
    Details
    Publication Date: 2021-05-19
    Description: Daily topical application of the aqueous ethanolic extract of the marine sea grass, Thalassia testudinum, on mice skin exposed to UVB radiation resulted in a dose dependent recovery of the skin macroscopic alterations over a 6-day period. Maximal effect (90%) occurred at a dose of 240 μg/cm2, with no additional effects at higher doses. Bioassay-guided fractionation of the plant extract resulted in the isolation of thalassiolin B (1). Topical application of 1 (240 μg/cm2) markedly reduces skin UVB-induced damage. In addition, thalassiolin B scavenged 2,2-diphenyl-2-picrylhydrazyl radical with an EC50=100 μg/ml. These results suggest that thalassiolin B is responsible for the skin regenerating effects of the crude extract of T. testudinum
    Description: Published
    Description: Flavonoids, Thalassiolin B, DPPH scavenged, antioxidant activity, Skin regenerating activity, Thalassia testudinum
    Keywords: Chemistry ; Pharmacology ; Chemistry ; Pharmacology
    Repository Name: AquaDocs
    Type: Journal Contribution
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  • 3
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    Bromopyrrole alkaloids from the Caribbean sponge Agelas cerebrum (2011)
    Sociedade Brasileira de Química
    Details
    Publication Date: 2021-05-19
    Description: Bioguided fractionation of Agelas cerebrum crude extract resulted in isolation of four bromopyrrole and four bromopyrrole aminoimidazole alkaloids, identified as 5-bromopyrrole-2-carboxylic acid (1), 4-bromopyrrole-2-carboxylic acid (2), 3,4-bromopyrrole-2-carboxylic acid (3), 4,5-bromopyrrole-2-carboxylic acid (4), oroidin (5), bromoageliferin (6), dibromoageliferin (7) and dibromosceptrin (8) on the basis of spectroscopic data analyses (UV, IR, HRMS, 1D and 2D NMR) and comparison with literature data. This is the first report of compounds 2 and 3 in a marine sponge belonging to the Agelas genus and the first evidence of the presence of 1 from a natural source.
    Description: Published
    Description: Agelas cerebrum, bromopyrrole alkaloids, antitumoral, antiprotozoal activity
    Keywords: Chemistry ; Alkaloids ; Sponges ; Alkaloids ; Sponges ; Chemistry
    Repository Name: AquaDocs
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  • 4
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    Der Abbau von p-Hydroxybenzoesäure, Protocatechusäure und Gallussäure im Boden (2010)
    Details
    Publication Date: 2021-05-19
    Description: La velocidad de descomposición de tres fenólicos, el p-hidroxibenzoico, el protocatecúico y el gálico, los cuales se diferencian en el número de grupos OH, fue investigada en el suelo. Con el aumento de grupos OH aumenta también la velocidad de descomposición microbial. El ácido gálico se descompone más rápido que el protocatecúico y este a su vez más rápido que el phidroxibenzoico.
    Description: The rate of decomposition of the three phenolics, p-hydroxybenzoic acid, protocatechuic acid and gallic acid, whose difference is the amount of OH-groups, was investigated in the soil. With the increase in OH-groups increases the rate of microbial decomposition. Gallic acid decomposes faster than protocatecuic acid and this again faster than p-hydroxybenzoic acid.
    Description: Published
    Keywords: Chemical decomposition ; OH Groups ; Microbes ; Phenols ; Chemistry ; Phenols ; Chemistry
    Repository Name: AquaDocs
    Type: Journal Contribution
    Format: pp.141-143
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  • 5
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    Meikin is a conserved regulator of meiosis-I-specific kinetochore function (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-12-24
    Description: The kinetochore is the crucial apparatus regulating chromosome segregation in mitosis and meiosis. Particularly in meiosis I, unlike in mitosis, sister kinetochores are captured by microtubules emanating from the same spindle pole (mono-orientation) and centromeric cohesion mediated by cohesin is protected in the following anaphase. Although meiotic kinetochore factors have been identified only in budding and fission yeasts, these molecules and their functions are thought to have diverged earlier. Therefore, a conserved mechanism for meiotic kinetochore regulation remains elusive. Here we have identified in mouse a meiosis-specific kinetochore factor that we termed MEIKIN, which functions in meiosis I but not in meiosis II or mitosis. MEIKIN plays a crucial role in both mono-orientation and centromeric cohesion protection, partly by stabilizing the localization of the cohesin protector shugoshin. These functions are mediated mainly by the activity of Polo-like kinase PLK1, which is enriched to kinetochores in a MEIKIN-dependent manner. Our integrative analysis indicates that the long-awaited key regulator of meiotic kinetochore function is Meikin, which is conserved from yeasts to humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jihye -- Ishiguro, Kei-ichiro -- Nambu, Aya -- Akiyoshi, Bungo -- Yokobayashi, Shihori -- Kagami, Ayano -- Ishiguro, Tadashi -- Pendas, Alberto M -- Takeda, Naoki -- Sakakibara, Yogo -- Kitajima, Tomoya S -- Tanno, Yuji -- Sakuno, Takeshi -- Watanabe, Yoshinori -- England -- Nature. 2015 Jan 22;517(7535):466-71. doi: 10.1038/nature14097. Epub 2014 Dec 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1Yayoi, Tokyo 113-0032, Japan. ; Instituto de Biologia Molecular y Celular del Cancer (CSIC-USAL), 37007 Salamanca, Spain. ; Center for Animal Resources and Development, Kumamoto University, 2-2-1 Honjo, Kumamoto 860-0811 Japan. ; Laboratory for Chromosome Segregation, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-Minamimachi, Chuo-ku, Kobe 650-0047, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25533956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle Proteins/metabolism ; Centromere/metabolism ; Chromosomal Proteins, Non-Histone/deficiency/genetics/*metabolism ; *Conserved Sequence ; Female ; Humans ; Infertility/genetics/metabolism ; Kinetochores/*metabolism ; Male ; *Meiosis ; Mice ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; Schizosaccharomyces pombe Proteins/metabolism
    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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    Lineage-negative progenitors mobilize to regenerate lung epithelium after major injury (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-12-24
    Description: Broadly, tissue regeneration is achieved in two ways: by proliferation of common differentiated cells and/or by deployment of specialized stem/progenitor cells. Which of these pathways applies is both organ- and injury-specific. Current models in the lung posit that epithelial repair can be attributed to cells expressing mature lineage markers. By contrast, here we define the regenerative role of previously uncharacterized, rare lineage-negative epithelial stem/progenitor (LNEP) cells present within normal distal lung. Quiescent LNEPs activate a DeltaNp63 (a p63 splice variant) and cytokeratin 5 remodelling program after influenza or bleomycin injury in mice. Activated cells proliferate and migrate widely to occupy heavily injured areas depleted of mature lineages, at which point they differentiate towards mature epithelium. Lineage tracing revealed scant contribution of pre-existing mature epithelial cells in such repair, whereas orthotopic transplantation of LNEPs, isolated by a definitive surface profile identified through single-cell sequencing, directly demonstrated the proliferative capacity and multipotency of this population. LNEPs require Notch signalling to activate the DeltaNp63 and cytokeratin 5 program, and subsequent Notch blockade promotes an alveolar cell fate. Persistent Notch signalling after injury led to parenchymal 'micro-honeycombing' (alveolar cysts), indicative of failed regeneration. Lungs from patients with fibrosis show analogous honeycomb cysts with evidence of hyperactive Notch signalling. Our findings indicate that distinct stem/progenitor cell pools repopulate injured tissue depending on the extent of the injury, and the outcomes of regeneration or fibrosis may depend in part on the dynamics of LNEP Notch signalling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4312207/" 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/PMC4312207/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vaughan, Andrew E -- Brumwell, Alexis N -- Xi, Ying -- Gotts, Jeffrey E -- Brownfield, Doug G -- Treutlein, Barbara -- Tan, Kevin -- Tan, Victor -- Liu, Feng Chun -- Looney, Mark R -- Matthay, Michael A -- Rock, Jason R -- Chapman, Harold A -- F32 HL117600-01/HL/NHLBI NIH HHS/ -- R01 HL44712/HL/NHLBI NIH HHS/ -- U01 HL099995/HL/NHLBI NIH HHS/ -- U01 HL099999/HL/NHLBI NIH HHS/ -- U01 HL111054/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Jan 29;517(7536):621-5. doi: 10.1038/nature14112. Epub 2014 Dec 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA. ; Department of Biochemistry, Stanford University School of Medicine and Howard Hughes Medical Institute, Stanford, California 94305, USA. ; Max Planck Institute for Evolutionary Anthropology, Department of Evolutionary Genetics, Deutscher Platz 6, 04103 Leipzig, Germany. ; Department of Anatomy, School of Medicine, University of California, San Francisco (UCSF), San Francisco, California 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25533958" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bleomycin ; Cell Lineage ; Cell Proliferation ; Cell Separation ; Cysts/metabolism/pathology ; Epithelial Cells/*cytology/metabolism/*pathology ; Female ; Humans ; Keratin-5/metabolism ; Lung/*cytology/*pathology/physiology ; Lung Injury/chemically induced/*pathology/virology ; Male ; Mice ; Orthomyxoviridae Infections/pathology/virology ; Phosphoproteins/genetics/metabolism ; *Re-Epithelialization ; Receptors, Notch/metabolism ; Signal Transduction ; Stem Cell Transplantation ; Stem Cells/*cytology/metabolism ; Trans-Activators/genetics/metabolism
    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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    Large-scale discovery of novel genetic causes of developmental disorders (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-12-24
    Description: Despite three decades of successful, predominantly phenotype-driven discovery of the genetic causes of monogenic disorders, up to half of children with severe developmental disorders of probable genetic origin remain without a genetic diagnosis. Particularly challenging are those disorders rare enough to have eluded recognition as a discrete clinical entity, those with highly variable clinical manifestations, and those that are difficult to distinguish from other, very similar, disorders. Here we demonstrate the power of using an unbiased genotype-driven approach to identify subsets of patients with similar disorders. By studying 1,133 children with severe, undiagnosed developmental disorders, and their parents, using a combination of exome sequencing and array-based detection of chromosomal rearrangements, we discovered 12 novel genes associated with developmental disorders. These newly implicated genes increase by 10% (from 28% to 31%) the proportion of children that could be diagnosed. Clustering of missense mutations in six of these newly implicated genes suggests that normal development is being perturbed by an activating or dominant-negative mechanism. Our findings demonstrate the value of adopting a comprehensive strategy, both genome-wide and nationwide, to elucidate the underlying causes of rare genetic disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deciphering Developmental Disorders Study -- 098395/Wellcome Trust/United Kingdom -- 100140/Wellcome Trust/United Kingdom -- CZD/16/6/Chief Scientist Office/United Kingdom -- WT098051/Wellcome Trust/United Kingdom -- Department of Health/United Kingdom -- England -- Nature. 2015 Mar 12;519(7542):223-8. doi: 10.1038/nature14135. Epub 2014 Dec 24.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25533962" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Carrier Proteins/genetics ; Child ; Child, Preschool ; Chromosomal Proteins, Non-Histone/genetics ; Chromosome Aberrations ; DEAD-box RNA Helicases/genetics ; DNA-Binding Proteins/genetics ; Developmental Disabilities/*diagnosis/*genetics ; Dynamin I/genetics ; Exome/genetics ; Female ; Gene Expression Regulation, Developmental ; Genes, Dominant/genetics ; Genome, Human/genetics ; Great Britain ; Guanine Nucleotide Exchange Factors/genetics ; Homeodomain Proteins/genetics ; Humans ; Infant ; Infant, Newborn ; Male ; Mutation, Missense/genetics ; Nerve Tissue Proteins/genetics ; Nuclear Proteins/genetics ; Parents ; Phosphoproteins/genetics ; Polycomb Repressive Complex 1/genetics ; Protein Phosphatase 2/genetics ; Protein-Serine-Threonine Kinases/genetics ; Rare Diseases/genetics ; Transcription Factors/genetics ; Transposases/genetics ; Zebrafish/genetics
    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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    Cell division: Hold on and let go (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tachibana-Konwalski, Kikue -- England -- Nature. 2015 Jan 22;517(7535):441-2. doi: 10.1038/nature14087. Epub 2014 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), 1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25533954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomal Proteins, Non-Histone/*metabolism ; *Conserved Sequence ; Female ; Humans ; Kinetochores/*metabolism ; Male ; *Meiosis
    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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    Mechanosensory interactions drive collective behaviour in Drosophila (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-12-24
    Description: Collective behaviour enhances environmental sensing and decision-making in groups of animals. Experimental and theoretical investigations of schooling fish, flocking birds and human crowds have demonstrated that simple interactions between individuals can explain emergent group dynamics. These findings indicate the existence of neural circuits that support distributed behaviours, but the molecular and cellular identities of relevant sensory pathways are unknown. Here we show that Drosophila melanogaster exhibits collective responses to an aversive odour: individual flies weakly avoid the stimulus, but groups show enhanced escape reactions. Using high-resolution behavioural tracking, computational simulations, genetic perturbations, neural silencing and optogenetic activation we demonstrate that this collective odour avoidance arises from cascades of appendage touch interactions between pairs of flies. Inter-fly touch sensing and collective behaviour require the activity of distal leg mechanosensory sensilla neurons and the mechanosensory channel NOMPC. Remarkably, through these inter-fly encounters, wild-type flies can elicit avoidance behaviour in mutant animals that cannot sense the odour--a basic form of communication. Our data highlight the unexpected importance of social context in the sensory responses of a solitary species and open the door to a neural-circuit-level understanding of collective behaviour in animal groups.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4359906/" 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/PMC4359906/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramdya, Pavan -- Lichocki, Pawel -- Cruchet, Steeve -- Frisch, Lukas -- Tse, Winnie -- Floreano, Dario -- Benton, Richard -- 205202/European Research Council/International -- 615094/European Research Council/International -- England -- Nature. 2015 Mar 12;519(7542):233-6. doi: 10.1038/nature14024. Epub 2014 Dec 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, Lausanne CH-1015, Switzerland [2] Laboratory of Intelligent Systems, Institute of Microengineering, Ecole Polytechnique Federale de Lausanne, Lausanne CH-1015, Switzerland. ; 1] Laboratory of Intelligent Systems, Institute of Microengineering, Ecole Polytechnique Federale de Lausanne, Lausanne CH-1015, Switzerland [2] Department of Ecology and Evolution, University of Lausanne, Lausanne CH-1015, Switzerland. ; Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, Lausanne CH-1015, Switzerland. ; Master's Program in Microengineering, Institute of Microengineering, Ecole Polytechnique Federale de Lausanne, Lausanne CH-1015, Switzerland. ; Laboratory of Intelligent Systems, Institute of Microengineering, Ecole Polytechnique Federale de Lausanne, Lausanne CH-1015, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25533959" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Communication ; Animals ; Avoidance Learning/physiology ; Computer Simulation ; Drosophila Proteins/metabolism ; Drosophila melanogaster/cytology/genetics/*physiology ; Escape Reaction/*physiology ; Extremities/physiology ; Female ; Male ; *Mass Behavior ; Mechanoreceptors/cytology/*physiology ; Mechanotransduction, Cellular ; Odors/*analysis ; Optogenetics ; Sensilla/cytology/*physiology ; Touch/physiology ; Transient Receptor Potential Channels/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Group 2 innate lymphoid cells promote beiging of white adipose tissue and limit obesity (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-12-24
    Description: Obesity is an increasingly prevalent disease regulated by genetic and environmental factors. Emerging studies indicate that immune cells, including monocytes, granulocytes and lymphocytes, regulate metabolic homeostasis and are dysregulated in obesity. Group 2 innate lymphoid cells (ILC2s) can regulate adaptive immunity and eosinophil and alternatively activated macrophage responses, and were recently identified in murine white adipose tissue (WAT) where they may act to limit the development of obesity. However, ILC2s have not been identified in human adipose tissue, and the mechanisms by which ILC2s regulate metabolic homeostasis remain unknown. Here we identify ILC2s in human WAT and demonstrate that decreased ILC2 responses in WAT are a conserved characteristic of obesity in humans and mice. Interleukin (IL)-33 was found to be critical for the maintenance of ILC2s in WAT and in limiting adiposity in mice by increasing caloric expenditure. This was associated with recruitment of uncoupling protein 1 (UCP1)(+) beige adipocytes in WAT, a process known as beiging or browning that regulates caloric expenditure. IL-33-induced beiging was dependent on ILC2s, and IL-33 treatment or transfer of IL-33-elicited ILC2s was sufficient to drive beiging independently of the adaptive immune system, eosinophils or IL-4 receptor signalling. We found that ILC2s produce methionine-enkephalin peptides that can act directly on adipocytes to upregulate Ucp1 expression in vitro and that promote beiging in vivo. Collectively, these studies indicate that, in addition to responding to infection or tissue damage, ILC2s can regulate adipose function and metabolic homeostasis in part via production of enkephalin peptides that elicit beiging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447235/" 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/PMC4447235/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brestoff, Jonathan R -- Kim, Brian S -- Saenz, Steven A -- Stine, Rachel R -- Monticelli, Laurel A -- Sonnenberg, Gregory F -- Thome, Joseph J -- Farber, Donna L -- Lutfy, Kabirullah -- Seale, Patrick -- Artis, David -- 2-P30 CA016520/CA/NCI NIH HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI097333/AI/NIAID NIH HHS/ -- AI102942/AI/NIAID NIH HHS/ -- DP2 OD007288/OD/NIH HHS/ -- DP2OD007288/OD/NIH HHS/ -- DP5 OD012116/OD/NIH HHS/ -- DP5OD012116/OD/NIH HHS/ -- F30 AI112023/AI/NIAID NIH HHS/ -- F30-AI112023/AI/NIAID NIH HHS/ -- F31 AG047003/AG/NIA NIH HHS/ -- F31AG047003/AG/NIA NIH HHS/ -- K08 AR065577/AR/NIAMS NIH HHS/ -- KL2-RR024132/RR/NCRR NIH HHS/ -- P01 AI106697/AI/NIAID NIH HHS/ -- P01AI06697/AI/NIAID NIH HHS/ -- P30 AR057217/AR/NIAMS NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- P30-DK050306/DK/NIDDK NIH HHS/ -- P30DK19525/DK/NIDDK 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/ -- T32 AI060516/AI/NIAID NIH HHS/ -- T32-AI007532/AI/NIAID NIH HHS/ -- T32-AI060516/AI/NIAID NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- England -- Nature. 2015 Mar 12;519(7542):242-6. doi: 10.1038/nature14115. Epub 2014 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Jill Roberts Institute for Research in IBD, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, New York 10021, USA [2] Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Institute for Diabetes, Obesity and Metabolism, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Jill Roberts Institute for Research in IBD, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, New York 10021, USA. ; 1] Columbia Center for Translational Immunology, Columbia University Medical Center, New York, New York 10032, USA [2] Department of Microbiology and Immunology, Columbia University Medical Center, New York, New York 10032, USA. ; 1] Columbia Center for Translational Immunology, Columbia University Medical Center, New York, New York 10032, USA [2] Department of Microbiology and Immunology, Columbia University Medical Center, New York, New York 10032, USA [3] Department of Surgery, Columbia University Medical Center, New York, New York 10032, USA. ; Department of Pharmaceutical Sciences, College of Pharmacy, Western University of Health Sciences, Pomona, California 91766, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25533952" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/drug effects ; Adipose Tissue, White/*cytology/*immunology ; Animals ; Energy Metabolism/immunology ; Enkephalin, Methionine/biosynthesis/metabolism ; Eosinophils/immunology/metabolism ; Female ; Homeostasis/drug effects ; Humans ; Immunity, Innate/*immunology ; Interleukins/immunology/pharmacology ; Ion Channels/metabolism ; Lymphocytes/cytology/immunology/*physiology ; Male ; Mice ; Mitochondrial Proteins/metabolism ; Obesity/*immunology/pathology ; Receptors, Interleukin-4/immunology/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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