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  • Biomass  (48)
  • Mice
  • Chemistry
  • 2015-2019  (56)
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  • 1
    Publication Date: 2021-05-19
    Description: El presente estudio corresponde al levantamiento y análisis de la información biológica-pesquera de la temporada 2010 y la actualización de los indicadores históricos de la pesquería demersal austral (PDA) basada en las especies objetivo merluza del sur (Merluccius australis), congrio dorado (Genypterus blacodes), merluza de tres aletas (Micromesistius australis) y raya volantín (Zearaja chilensis) como también las especies secundarias como cojinoba moteada (Seriolella punctata) y cojinaba ploma (Seriolella punctata) y cojinoba ploma (Seriolelella caerulea). El área de operación de la flota comprende entre las latitudes 37° y 57°S, estableciendo para fines de administración pesquera una zona norte (41°28,6’-47°00’S) y una zona sur (47°01’-57°S) en aguas exteriores (Al oeste de la línea de base recta)
    Description: The present study is to survey and analysis of biological data and fishery of the 2010 season and updating the historical indicators of austral demersal fisheries (PDA) based on the target species in southern hake (Merluccius australis), golden eel (Genypterus blacodes) Southern blue whiting (Micromesistius australis) and kite line (Zearaja chilensis) as well as secondary species such as spotted warehou (Seriolella punctata) and Heermann cushions (Seriolella punctata) and Heermann warehou (Seriolelella caerulea). The area of ​​operation of the fleet between latitudes 37° and 57° S, for administration by establishing a northern fishing (41° 28.6 ’-47° 00’S) and south (47° 01’-57° S) in offshore waters (west of the straight baseline)
    Description: Unpublished
    Keywords: Merluccius australis ; Micromesistius australis ; Zearaja chilensis ; Seriolella caerulea ; Genypterus blacodes ; marine environment ; Benthic environment ; Pelagic fisheries ; Stock assessment ; Trap fishing ; Bathymetric data ; Biomass ; Age determination ; Size-at-age ; Length-weight relationships ; Spawning ; Salinity ; Recruitment
    Repository Name: AquaDocs
    Type: Report , Non-Refereed , Article
    Format: 193pp. & Anexos
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  • 2
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-05-27
    Description: Biomass-degrading microorganisms use lytic polysaccharide monooxygenase (LPMO) enzymes to help digest cellulose, chitin, and starch. By cleaving otherwise inaccessible crystalline cellulose chains, these enzymes provide access to hydrolytic enzymes. LPMOs are of interest to biotechnology because efficient depolymerization of cellulose is a major bottleneck for the production of biologically based chemicals and fuels. On page 1098 of this issue, Kracher et al. (1) compare LPMO-reducing substrates in fungi from different taxonomic groups and lifestyles, based on both biochemical and genomic evidence. The results provide insights into reductive activation of LPMO that are important for developing more efficient industrial enzymes for lignocellulose biorefineries. Author: Angel T. Martínez
    Keywords: Chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2018-07-06
    Description: Conical intersections play a critical role in excited-state dynamics of polyatomic molecules because they govern the reaction pathways of many nonadiabatic processes. However, ultrafast probes have lacked sufficient spatial resolution to image wave-packet trajectories through these intersections directly. Here, we present the simultaneous experimental characterization of one-photon and two-photon excitation channels in isolated CF 3 I molecules using ultrafast gas-phase electron diffraction. In the two-photon channel, we have mapped out the real-space trajectories of a coherent nuclear wave packet, which bifurcates onto two potential energy surfaces when passing through a conical intersection. In the one-photon channel, we have resolved excitation of both the umbrella and the breathing vibrational modes in the CF 3 fragment in multiple nuclear dimensions. These findings benchmark and validate ab initio nonadiabatic dynamics calculations.
    Keywords: Chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2015-07-15
    Description: Human inborn errors of immunity mediated by the cytokines interleukin-17A and interleukin-17F (IL-17A/F) underlie mucocutaneous candidiasis, whereas inborn errors of interferon-gamma (IFN-gamma) immunity underlie mycobacterial disease. We report the discovery of bi-allelic RORC loss-of-function mutations in seven individuals from three kindreds of different ethnic origins with both candidiasis and mycobacteriosis. The lack of functional RORgamma and RORgammaT isoforms resulted in the absence of IL-17A/F-producing T cells in these individuals, probably accounting for their chronic candidiasis. Unexpectedly, leukocytes from RORgamma- and RORgammaT-deficient individuals also displayed an impaired IFN-gamma response to Mycobacterium. This principally reflected profoundly defective IFN-gamma production by circulating gammadelta T cells and CD4(+)CCR6(+)CXCR3(+) alphabeta T cells. In humans, both mucocutaneous immunity to Candida and systemic immunity to Mycobacterium require RORgamma, RORgammaT, or both.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668938/" 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/PMC4668938/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Satoshi -- Markle, Janet G -- Deenick, Elissa K -- Mele, Federico -- Averbuch, Dina -- Lagos, Macarena -- Alzahrani, Mohammed -- Al-Muhsen, Saleh -- Halwani, Rabih -- Ma, Cindy S -- Wong, Natalie -- Soudais, Claire -- Henderson, Lauren A -- Marzouqa, Hiyam -- Shamma, Jamal -- Gonzalez, Marcela -- Martinez-Barricarte, Ruben -- Okada, Chizuru -- Avery, Danielle T -- Latorre, Daniela -- Deswarte, Caroline -- Jabot-Hanin, Fabienne -- Torrado, Egidio -- Fountain, Jeffrey -- Belkadi, Aziz -- Itan, Yuval -- Boisson, Bertrand -- Migaud, Melanie -- Arlehamn, Cecilia S Lindestam -- Sette, Alessandro -- Breton, Sylvain -- McCluskey, James -- Rossjohn, Jamie -- de Villartay, Jean-Pierre -- Moshous, Despina -- Hambleton, Sophie -- Latour, Sylvain -- Arkwright, Peter D -- Picard, Capucine -- Lantz, Olivier -- Engelhard, Dan -- Kobayashi, Masao -- Abel, Laurent -- Cooper, Andrea M -- Notarangelo, Luigi D -- Boisson-Dupuis, Stephanie -- Puel, Anne -- Sallusto, Federica -- Bustamante, Jacinta -- Tangye, Stuart G -- Casanova, Jean-Laurent -- 8UL1TR000043/TR/NCATS NIH HHS/ -- HHSN272200900044C/AI/NIAID NIH HHS/ -- HHSN272200900044C/PHS HHS/ -- R37 AI095983/AI/NIAID NIH HHS/ -- R37AI095983/AI/NIAID NIH HHS/ -- T32 AI007512/AI/NIAID NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Aug 7;349(6248):606-13. doi: 10.1126/science.aaa4282. Epub 2015 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Department of Pediatrics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. jmarkle@rockefeller.edu jean-laurent.casanova@rockefeller.edu. ; Immunology Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia. St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia. ; Institute for Research in Biomedicine, University of Italian Switzerland, Bellinzona, Switzerland. ; Department of Pediatrics, Hadassah University Hospital, Jerusalem, Israel. ; Department of Immunology, School of Medicine, Universidad de Valparaiso, Santiago, Chile. Department of Pediatrics, Padre Hurtado Hospital and Clinica Alemana, Santiago, Chile. ; Department of Pediatrics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. ; Department of Pediatrics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. Department of Pediatrics, Prince Naif Center for Immunology Research, College of Medicine, King Saud University, Riyadh, Saudi Arabia. ; Department of Pediatrics, Prince Naif Center for Immunology Research, College of Medicine, King Saud University, Riyadh, Saudi Arabia. ; Immunology Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia. ; Institut Curie, INSERM U932, Paris, France. ; Division of Immunology, Boston Children's Hospital, Boston, MA 02115, USA. ; Caritas Baby Hospital, Post Office Box 11535, Jerusalem, Israel. ; Department of Immunology, School of Medicine, Universidad de Valparaiso, Santiago, Chile. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. ; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. ; Trudeau Institute, Saranac Lake, NY 12983, USA. ; La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA. ; Department of Radiology, Assistance Publique-Hopitaux de Paris (AP-HP), Necker Hospital for Sick Children, Paris, France. ; Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria, Australia. ; Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University, Clayton, Victoria, Australia. Australian Research Council Centre of Excellence for Advanced Molecular Imaging, Monash University, Clayton, Victoria, Australia. Institute of Infection and Immunity, Cardiff University, School of Medicine, Heath Park, Cardiff CF14 4XN, UK. ; Laboratoire Dynamique du Genome et Systeme Immunitaire, INSERM UMR 1163, Universite Paris Descartes-Sorbonne Paris Cite, Imagine Institute, Paris, France. ; Laboratoire Dynamique du Genome et Systeme Immunitaire, INSERM UMR 1163, Universite Paris Descartes-Sorbonne Paris Cite, Imagine Institute, Paris, France. Pediatric Hematology-Immunology Unit, AP-HP, Necker Hospital for Sick Children, Paris, France. ; Institute of Cellular Medicine, Newcastle University and Great North Children's Hospital, Newcastle upon Tyne NE4 6BE, UK. ; Laboratory of Lymphocyte Activation and Susceptibility to EBV Infection, INSERM UMR 1163, Universite Paris Descartes-Sorbonne Paris Cite, Imagine Institute, Paris, France. ; Department of Paediatric Allergy Immunology, University of Manchester, Royal Manchester Children's Hospital, Manchester, UK. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. Pediatric Hematology-Immunology Unit, AP-HP, Necker Hospital for Sick Children, Paris, France. Center for the Study of Primary Immunodeficiencies, AP-HP, Necker Hospital for Sick Children, Paris, France. ; Department of Pediatrics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. ; Division of Immunology, Boston Children's Hospital, Boston, MA 02115, USA. Manton Center for Orphan Disease Research, Children's Hospital, Boston, MA 02115, USA. ; Institute for Research in Biomedicine, University of Italian Switzerland, Bellinzona, Switzerland. Center of Medical Immunology, Institute for Research in Biomedicine, University of Italian Switzerland, Bellinzona, Switzerland. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. Center for the Study of Primary Immunodeficiencies, AP-HP, Necker Hospital for Sick Children, Paris, France. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. Pediatric Hematology-Immunology Unit, AP-HP, Necker Hospital for Sick Children, Paris, France. Howard Hughes Medical Institute, New York, NY 10065, USA. jmarkle@rockefeller.edu jean-laurent.casanova@rockefeller.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26160376" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Candida albicans/*immunology ; Candidiasis, Chronic Mucocutaneous/complications/*genetics/immunology ; Cattle ; Child ; Child, Preschool ; DNA Mutational Analysis ; Exome/genetics ; Female ; Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor ; Humans ; Immunity/*genetics ; Interferon-gamma/immunology ; Interleukin-17/immunology ; Mice ; Mutation ; Mycobacterium bovis/immunology/isolation & purification ; Mycobacterium tuberculosis/immunology/isolation & purification ; Nuclear Receptor Subfamily 1, Group F, Member 3/*genetics ; Pedigree ; Receptors, Antigen, T-Cell, alpha-beta/genetics/immunology ; Receptors, Antigen, T-Cell, gamma-delta/genetics/immunology ; Severe Combined Immunodeficiency/*genetics ; T-Lymphocytes/immunology ; Thymus Gland/abnormalities/immunology ; Tuberculosis, Bovine/*genetics/immunology ; Tuberculosis, Pulmonary/*genetics/immunology
    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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  • 5
    Publication Date: 2017-08-04
    Description: Biological systems sense and respond to mechanical stimuli in a complex manner. In an effort to develop synthetic materials that transduce mechanical force into multifold changes in their intrinsic properties, we report on a mechanochemically responsive nonconjugated polymer that converts to a conjugated polymer via an extensive rearrangement of the macromolecular structure in response to force. Our design is based on the facile mechanochemical unzipping of polyladderene, a polymer inspired by a lipid natural product structure and prepared via direct metathesis polymerization. The resultant polyacetylene block copolymers exhibit long conjugation length and uniform trans-configuration and self-assemble into semiconducting nanowires. Calculations support a tandem unzipping mechanism of the ladderene units.
    Keywords: Chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2016-03-17
    Description: The integrated stress response (ISR) is a homeostatic mechanism by which eukaryotic cells sense and respond to stress-inducing signals, such as amino acid starvation. General controlled non-repressed (GCN2) kinase is a key orchestrator of the ISR, and modulates protein synthesis in response to amino acid starvation. Here we demonstrate in mice that GCN2 controls intestinal inflammation by suppressing inflammasome activation. Enhanced activation of ISR was observed in intestinal antigen presenting cells (APCs) and epithelial cells during amino acid starvation, or intestinal inflammation. Genetic deletion of Gcn2 (also known as Eif2ka4) in CD11c(+) APCs or intestinal epithelial cells resulted in enhanced intestinal inflammation and T helper 17 cell (TH17) responses, owing to enhanced inflammasome activation and interleukin (IL)-1beta production. This was caused by reduced autophagy in Gcn2(-/-) intestinal APCs and epithelial cells, leading to increased reactive oxygen species (ROS), a potent activator of inflammasomes. Thus, conditional ablation of Atg5 or Atg7 in intestinal APCs resulted in enhanced ROS and TH17 responses. Furthermore, in vivo blockade of ROS and IL-1beta resulted in inhibition of TH17 responses and reduced inflammation in Gcn2(-/-) mice. Importantly, acute amino acid starvation suppressed intestinal inflammation via a mechanism dependent on GCN2. These results reveal a mechanism that couples amino acid sensing with control of intestinal inflammation via GCN2.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854628/" 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/PMC4854628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ravindran, Rajesh -- Loebbermann, Jens -- Nakaya, Helder I -- Khan, Nooruddin -- Ma, Hualing -- Gama, Leonardo -- Machiah, Deepa K -- Lawson, Benton -- Hakimpour, Paul -- Wang, Yi-chong -- Li, Shuzhao -- Sharma, Prachi -- Kaufman, Randal J -- Martinez, Jennifer -- Pulendran, Bali -- R01 DK088227/DK/NIDDK NIH HHS/ -- R01 DK103185/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK042394/DK/NIDDK NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19 AI090023/AI/NIAID NIH HHS/ -- ZIA ES103286-01/Intramural NIH HHS/ -- England -- Nature. 2016 Mar 24;531(7595):523-7. doi: 10.1038/nature17186. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo 05508, Brazil. ; Department of Biotechnology and Bioinformatics, School of Life Sciences, University of Hyderabad, Hyderabad 500 046, India. ; Division of Pathology, Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; Virology Core, Emory Vaccine Center and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; Degenerative Disease Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037 USA. ; National Institute of Environmental Health Sciences, Mail Drop D2-01 Research Triangle Park, North Carolina 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982722" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/administration & dosage/deficiency/*metabolism/pharmacology ; Animals ; Antigen-Presenting Cells/immunology/metabolism ; Autophagy ; Colitis/etiology/*metabolism/pathology/prevention & control ; Disease Models, Animal ; Epithelial Cells/metabolism ; Female ; Humans ; Inflammasomes/*antagonists & inhibitors/metabolism ; Inflammation/etiology/*metabolism/pathology/prevention & control ; Interleukin-1beta/immunology ; Intestines/*metabolism/*pathology ; Male ; Mice ; Microtubule-Associated Proteins/deficiency/metabolism ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Reactive Oxygen Species/metabolism ; Stress, Physiological ; Th17 Cells/immunology ; Ubiquitin-Activating Enzymes/deficiency/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
    Publication Date: 2016-01-08
    Description: During ageing, muscle stem-cell regenerative function declines. At advanced geriatric age, this decline is maximal owing to transition from a normal quiescence into an irreversible senescence state. How satellite cells maintain quiescence and avoid senescence until advanced age remains unknown. Here we report that basal autophagy is essential to maintain the stem-cell quiescent state in mice. Failure of autophagy in physiologically aged satellite cells or genetic impairment of autophagy in young cells causes entry into senescence by loss of proteostasis, increased mitochondrial dysfunction and oxidative stress, resulting in a decline in the function and number of satellite cells. Re-establishment of autophagy reverses senescence and restores regenerative functions in geriatric satellite cells. As autophagy also declines in human geriatric satellite cells, our findings reveal autophagy to be a decisive stem-cell-fate regulator, with implications for fostering muscle regeneration in sarcopenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia-Prat, Laura -- Martinez-Vicente, Marta -- Perdiguero, Eusebio -- Ortet, Laura -- Rodriguez-Ubreva, Javier -- Rebollo, Elena -- Ruiz-Bonilla, Vanessa -- Gutarra, Susana -- Ballestar, Esteban -- Serrano, Antonio L -- Sandri, Marco -- Munoz-Canoves, Pura -- England -- Nature. 2016 Jan 7;529(7584):37-42. doi: 10.1038/nature16187.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University (UPF), CIBER on Neurodegenerative diseases (CIBERNED), E-08003 Barcelona, Spain. ; Neurodegenerative Diseases Research Group, Vall d'Hebron Research Institute-CIBERNED, E-08035 Barcelona, Spain. ; Chromatin and Disease Group, Cancer Epigenetics and Biology Programme (PEBC), Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, E-08907 Barcelona, Spain. ; Advanced Fluorescence Microscopy Unit, Molecular Biology Institute of Barcelona (IBMB-CSIC), E-08028 Barcelona, Spain. ; Department of Biomedical Science, University of Padova, 35100 Padova, Italy. ; Telethon Institute of Genetics and Medicine (TIGEM), 80131 Napoli, Italy. ; ICREA, E-08908 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26738589" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/pathology ; Animals ; Autophagy/*physiology ; *Cell Aging ; Cell Count ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Epigenesis, Genetic ; Homeostasis ; Humans ; Male ; Mice ; Mitochondria/metabolism/pathology ; Mitochondrial Degradation ; Muscle, Skeletal/cytology/pathology ; Organelles/metabolism ; Oxidative Stress ; Proteins/metabolism ; Reactive Oxygen Species/metabolism ; Regeneration ; Sarcopenia/pathology/prevention & control ; Satellite Cells, Skeletal Muscle/*cytology/pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2016-04-21
    Description: Defects in clearance of dying cells have been proposed to underlie the pathogenesis of systemic lupus erythematosus (SLE). Mice lacking molecules associated with dying cell clearance develop SLE-like disease, and phagocytes from patients with SLE often display defective clearance and increased inflammatory cytokine production when exposed to dying cells in vitro. Previously, we and others described a form of noncanonical autophagy known as LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles, including dying cells, recruit elements of the autophagy pathway to facilitate maturation of phagosomes and digestion of their contents. Genome-wide association studies have identified polymorphisms in the Atg5 (ref. 8) and possibly Atg7 (ref. 9) genes, involved in both canonical autophagy and LAP, as markers of a predisposition for SLE. Here we describe the consequences of defective LAP in vivo. Mice lacking any of several components of the LAP pathway show increased serum levels of inflammatory cytokines and autoantibodies, glomerular immune complex deposition, and evidence of kidney damage. When dying cells are injected into LAP-deficient mice, they are engulfed but not efficiently degraded and trigger acute elevation of pro-inflammatory cytokines but not anti-inflammatory interleukin (IL)-10. Repeated injection of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated the development of SLE-like disease, including increased serum levels of autoantibodies. By contrast, mice deficient in genes required for canonical autophagy but not LAP do not display defective dying cell clearance, inflammatory cytokine production, or SLE-like disease, and, like wild-type mice, produce IL-10 in response to dying cells. Therefore, defects in LAP, rather than canonical autophagy, can cause SLE-like phenomena, and may contribute to the pathogenesis of SLE.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860026/" 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/PMC4860026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, Jennifer -- Cunha, Larissa D -- Park, Sunmin -- Yang, Mao -- Lu, Qun -- Orchard, Robert -- Li, Quan-Zhen -- Yan, Mei -- Janke, Laura -- Guy, Cliff -- Linkermann, Andreas -- Virgin, Herbert W -- Green, Douglas R -- 1ZIAES10328601/PHS HHS/ -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI40646/AI/NIAID NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- ZIA ES103286-01/Intramural NIH HHS/ -- England -- Nature. 2016 May 5;533(7601):115-9. doi: 10.1038/nature17950. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, North Carolina 27709, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Division of Nephrology and Hypertension, Christian-Albrechts-University, Kiel 24105, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096368" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/metabolism ; Autoantibodies/blood ; *Autophagy/genetics ; Cytokines/biosynthesis/blood ; Inflammation/blood/genetics/*pathology ; Interleukin-10/biosynthesis ; Kidney/metabolism/pathology ; Lupus Erythematosus, Systemic/blood/genetics/*immunology/*pathology ; Male ; Mice ; Microtubule-Associated Proteins/metabolism ; Phagocytes/cytology/physiology ; Phagosomes/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2015-03-20
    Description: Atmospheric carbon dioxide records indicate that the land surface has acted as a strong global carbon sink over recent decades, with a substantial fraction of this sink probably located in the tropics, particularly in the Amazon. Nevertheless, it is unclear how the terrestrial carbon sink will evolve as climate and atmospheric composition continue to change. Here we analyse the historical evolution of the biomass dynamics of the Amazon rainforest over three decades using a distributed network of 321 plots. While this analysis confirms that Amazon forests have acted as a long-term net biomass sink, we find a long-term decreasing trend of carbon accumulation. Rates of net increase in above-ground biomass declined by one-third during the past decade compared to the 1990s. This is a consequence of growth rate increases levelling off recently, while biomass mortality persistently increased throughout, leading to a shortening of carbon residence times. Potential drivers for the mortality increase include greater climate variability, and feedbacks of faster growth on mortality, resulting in shortened tree longevity. The observed decline of the Amazon sink diverges markedly from the recent increase in terrestrial carbon uptake at the global scale, and is contrary to expectations based on models.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brienen, R J W -- Phillips, O L -- Feldpausch, T R -- Gloor, E -- Baker, T R -- Lloyd, J -- Lopez-Gonzalez, G -- Monteagudo-Mendoza, A -- Malhi, Y -- Lewis, S L -- Vasquez Martinez, R -- Alexiades, M -- Alvarez Davila, E -- Alvarez-Loayza, P -- Andrade, A -- Aragao, L E O C -- Araujo-Murakami, A -- Arets, E J M M -- Arroyo, L -- Aymard C, G A -- Banki, O S -- Baraloto, C -- Barroso, J -- Bonal, D -- Boot, R G A -- Camargo, J L C -- Castilho, C V -- Chama, V -- Chao, K J -- Chave, J -- Comiskey, J A -- Cornejo Valverde, F -- da Costa, L -- de Oliveira, E A -- Di Fiore, A -- Erwin, T L -- Fauset, S -- Forsthofer, M -- Galbraith, D R -- Grahame, E S -- Groot, N -- Herault, B -- Higuchi, N -- Honorio Coronado, E N -- Keeling, H -- Killeen, T J -- Laurance, W F -- Laurance, S -- Licona, J -- Magnussen, W E -- Marimon, B S -- Marimon-Junior, B H -- Mendoza, C -- Neill, D A -- Nogueira, E M -- Nunez, P -- Pallqui Camacho, N C -- Parada, A -- Pardo-Molina, G -- Peacock, J -- Pena-Claros, M -- Pickavance, G C -- Pitman, N C A -- Poorter, L -- Prieto, A -- Quesada, C A -- Ramirez, F -- Ramirez-Angulo, H -- Restrepo, Z -- Roopsind, A -- Rudas, A -- Salomao, R P -- Schwarz, M -- Silva, N -- Silva-Espejo, J E -- Silveira, M -- Stropp, J -- Talbot, J -- ter Steege, H -- Teran-Aguilar, J -- Terborgh, J -- Thomas-Caesar, R -- Toledo, M -- Torello-Raventos, M -- Umetsu, R K -- van der Heijden, G M F -- van der Hout, P -- Guimaraes Vieira, I C -- Vieira, S A -- Vilanova, E -- Vos, V A -- Zagt, R J -- England -- Nature. 2015 Mar 19;519(7543):344-8. doi: 10.1038/nature14283.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Geography, University of Leeds, Leeds LS2 9JT, UK. ; 1] School of Geography, University of Leeds, Leeds LS2 9JT, UK. [2] Geography, College of Life and Environmental Sciences, University of Exeter, Rennes Drive, Exeter EX4 4RJ, UK. ; 1] Department of Life Sciences, Imperial College London, Silwood Park Campus, Buckhurst Road, Ascot, Berkshire SL5 7PY, UK. [2] School of Marine and Tropical Biology, James Cook University, Cairns, 4870 Queenland, Australia. ; Jardin Botanico de Missouri, Prolongacion Bolognesi Mz.e, Lote 6, Oxapampa, Pasco, Peru. ; Environmental Change Institute, School of Geography and the Environment, University of Oxford, Oxford OX1 3QK, UK. ; 1] School of Geography, University of Leeds, Leeds LS2 9JT, UK. [2] Department of Geography, University College London, Pearson Building, Gower Street, London WC1E 6BT, UK. ; School of Anthropology and Conservation, Marlowe Building, University of Kent, Canterbury CT1 3EH, UK. ; Servicios Ecosistemicos y Cambio Climatico, Jardin Botanico de Medellin, Calle 73 no. 51 D-14, C.P. 050010, Medellin, Colombia. ; Center for Tropical Conservation, Duke University, Box 90381, Durham, North Carolina 27708, USA. ; Biological Dynamics of Forest Fragment Project (INPA &STRI), C.P. 478, Manaus AM 69011-970, Brazil. ; 1] Geography, College of Life and Environmental Sciences, University of Exeter, Rennes Drive, Exeter EX4 4RJ, UK. [2] National Institute for Space Research (INPE), Av. Dos Astronautas, 1758, Sao Jose dos Campos, Sao Paulo 12227-010, Brazil. ; Museo de Historia Natural Noel Kempff Mercado, Universidad Autonoma Gabriel Rene Moreno, Casilla 2489, Av. Irala 565, Santa Cruz, Bolivia. ; Alterra, Wageningen University and Research Centre, PO Box 47, 6700 AA Wageningen, The Netherlands. ; UNELLEZ-Guanare, Programa de Ciencias del Agro y el Mar, Herbario Universitario (PORT), Mesa de Cavacas, Estado Portuguesa, 3350 Venezuela. ; Biodiversiteit en Ecosysteem Dynamica, University of Amsterdam, Postbus 94248, 1090 GE Amsterdam, The Netherlands. ; 1] Institut National de la Recherche Agronomique, UMR EcoFoG, Campus Agronomique, 97310 Kourou, French Guiana. [2] International Center for Tropical Botany, Department of Biological Sciences, Florida International University, Miami, Florida 33199, USA. ; Universidade Federal do Acre, Campus de Cruzeiro do Sul, Rio Branco, Brazil. ; INRA, UMR 1137 ''Ecologie et Ecophysiologie Forestiere'' 54280 Champenoux, France. ; Embrapa Roraima, Caixa Postal 133, Boa Vista, RR, CEP 69301-970, Brazil. ; Universidad Nacional San Antonio Abad del Cusco, Av. de la Cultura N degrees 733, Cusco, Peru. ; 1] School of Geography, University of Leeds, Leeds LS2 9JT, UK. [2] International Master Program of Agriculture, College of Agriculture and Natural Resources, National Chung Hsing University, Taichung 40227, Taiwan. ; Universite Paul Sabatier CNRS, UMR 5174 Evolution et Diversite Biologique, Batiment 4R1, 31062 Toulouse, France. ; Northeast Region Inventory and Monitoring Program, National Park Service, 120 Chatham Lane, Fredericksburg, Virginia 22405, USA. ; Andes to Amazon Biodiversity Program, Puerto Maldonado, Madre de Dios, Peru. ; Universidade Federal do Para, Centro de Geociencias, Belem, CEP 66017-970 Para, Brazil. ; Universidade do Estado de Mato Grosso, Campus de Nova Xavantina, Caixa Postal 08, CEP 78.690-000, Nova Xavantina MT, Brazil. ; Department of Anthropology, University of Texas at Austin, SAC Room 5.150, 2201 Speedway Stop C3200, Austin, Texas 78712, USA. ; Department of Entomology, Smithsonian Institution, PO Box 37012, MRC 187, Washington DC 20013-7012, USA. ; Cirad, UMR Ecologie des Forets de Guyane, Campus Agronomique, 97310 Kourou, French Guiana. ; 1] School of Geography, University of Leeds, Leeds LS2 9JT, UK. [2] Instituto de Investigaciones de la Amazonia Peruana, Av. A. Jose Quinones km 2.5, Iquitos, Peru. ; World Wildlife Fund, 1250 24th Street NW, Washington DC 20037, USA. ; Centre for Tropical Environmental and Sustainability Science (TESS) and School of Marine and Environmental Sciences, James Cook University, Cairns, Queensland 4878, Australia. ; Instituto Boliviano de Investigacion Forestal, C.P. 6201, Santa Cruz de la Sierra, Bolivia. ; National Institute for Research in Amazonia (INPA), C.P. 478, Manaus, Amazonas, CEP 69011-970, Brazil. ; 1] FOMABO, Manejo Forestal en las Tierras Tropicales de Bolivia, Sacta, Bolivia. [2] Escuela de Ciencias Forestales (ESFOR), Universidad Mayor de San Simon (UMSS), Sacta, Bolivia. ; Universidad Estatal Amazonica, Facultad de Ingenieria Ambiental, Paso lateral km 2 1/2 via Napo, Puyo, Pastaza, Ecuador. ; National Institute for Research in Amazonia (INPA), C.P. 2223, 69080-971, Manaus, Amazonas, Brazil. ; Universidad Autonoma del Beni, Campus Universitario, Av. Ejercito Nacional, Riberalta, Beni, Bolivia. ; 1] Instituto Boliviano de Investigacion Forestal, C.P. 6201, Santa Cruz de la Sierra, Bolivia. [2] Forest Ecology and Forest Management Group, Wageningen University, PO Box 47, 6700 AA Wageningen, The Netherlands. ; 1] Center for Tropical Conservation, Duke University, Box 90381, Durham, North Carolina 27708, USA. [2] The Field Museum, 1400 South Lake Shore Drive, Chicago, Illinois 60605-2496, USA. ; Forest Ecology and Forest Management Group, Wageningen University, PO Box 47, 6700 AA Wageningen, The Netherlands. ; Universidad Nacional de la Amazonia Peruana, Iquitos, Loreto, Peru. ; Instituto de Investigaciones para el Desarrollo Forestal (INDEFOR), Universidad de Los Andes, Facultad de Ciencias Forestales y Ambientales, Conjunto Forestal, C.P. 5101, Merida, Venezuela. ; Iwokrama International Centre for Rainforest Conservation and Development, 77 High Street Kingston, Georgetown, Guyana. ; Museu Paraense Emilio Goeldi, Av. Magalhaes Barata, 376 - Sao Braz, CEP 66040-170, Belem PA, Brazil. ; UFRA, Av. Presidente Tancredo Neves 2501, CEP 66.077-901, Belem, Para, Brazil. ; Museu Universitario, Universidade Federal do Acre, Rio Branco AC 69910-900, Brazil. ; European Commission - DG Joint Research Centre, Institute for Environment and Sustainability, Via Enrico Fermi 274, 21010 Ispra, Italy. ; 1] Naturalis Biodiversity Center, PO Box, 2300 RA, Leiden, The Netherlands. [2] Ecology and Biodiversity Group, Utrecht University, PO Box 80084, 3508 TB Utrecht, The Netherlands. ; Museo de Historia Natural Alcide D'Orbigny, Av. Potosi no 1458, Cochabamba, Bolivia. ; 1] School of Earth and Environmental Science, James Cook University, Cairns, Queensland 4870, Australia. [2] Centre for Tropical Environmental and Sustainability Science (TESS) and School of Marine and Tropical Biology, James Cook University, Cairns, Queensland 4878, Australia. ; 1] Northumbria University, School of Geography, Ellison Place, Newcastle upon Tyne, Newcastle NE1 8ST, UK. [2] University of Wisconsin, Milwaukee, Wisconsin 53202, USA. [3] Smithsonian Tropical Research Institute, Apartado Postal 0843-03092, Panama, Republic of Panama. ; Van der Hout Forestry Consulting, Jan Trooststraat 6, 3078 HP Rotterdam, The Netherlands. ; Universidade Estadual de Campinas, NEPAM, Rua dos Flamboyants, 155- Cidade Universitaria Zeferino Vaz, Campinas, CEP 13083-867, Sao Paulo, Brazil. ; 1] Universidad Autonoma del Beni, Campus Universitario, Av. Ejercito Nacional, Riberalta, Beni, Bolivia. [2] Centro de Investigacion y Promocion del Campesinado, regional Norte Amazonico, C/ Nicanor Gonzalo Salvatierra N degrees 362, Casilla 16, Riberalta, Bolivia. ; Tropenbos International, PO Box 232, 6700 AE Wageningen, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25788097" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/chemistry ; Biomass ; Brazil ; Carbon/analysis/metabolism ; Carbon Dioxide/*analysis/metabolism ; *Carbon Sequestration ; Plant Stems/metabolism ; *Rainforest ; Trees/growth & development/metabolism ; Tropical Climate ; Wood/analysis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Publication Date: 2017-11-03
    Description: The irradiation of gold nanorod colloids with a femtosecond laser can be tuned to induce controlled nanorod reshaping, yielding colloids with exceptionally narrow localized surface plasmon resonance bands. The process relies on a regime characterized by a gentle multishot reduction of the aspect ratio, whereas the rod shape and volume are barely affected. Successful reshaping can only occur within a narrow window of the heat dissipation rate: Low cooling rates lead to drastic morphological changes, and fast cooling has nearly no effect. Hence, a delicate balance must be achieved between irradiation fluence and surface density of the surfactant on the nanorods. This perfection process is appealing because it provides a simple, fast, reproducible, and scalable route toward gold nanorods with an optical response of exceptional quality, near the theoretical limit.
    Keywords: Chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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