What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Wednesday, 2014 June 25
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

View complete results in PubMed (results may change over time).

Edit saved search settings, or unsubscribe from these e-mail updates.

PubMed Results

Items 1 - 7 of 7

1.	N Engl J Med. 2014 Jun 12;370(24):2342-5. doi: 10.1056/NEJMcibr1403629. Translating the genomic revolution - targeted genome editing in primates. Cathomen T, Ehl S.
	PMID: 24918378 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2014 May 8;509(7499):162-3. doi: 10.1038/509162a. Q&A: Canopy composer. Jones D, Hoffman J.
	PMID: 24805330 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nature. 2014 May 8;509(7499):148-9. doi: 10.1038/509148a. Imaging: Cancer caught in the act. Lok C. Author information: Nature in Cambridge, Massachusetts.
	PMID: 24805326 [PubMed - indexed for MEDLINE]
	Related citations

4.	Nature. 2014 May 8;509(7499):171-2. doi: 10.1038/nature13332. Epub 2014 Apr 30. Biodiversity: Supply and demand. Mooers AO. Author information: Biology Department and the Human Evolutionary Studies Program, Simon Fraser University, Burnaby, British Columbia V5A1S6, Canada. Comment on Niche filling slows the diversification of Himalayan songbirds. [Nature. 2014] Niche filling slows the diversification of Himalayan songbirds.Price TD, Hooper DM, Buchanan CD, Johansson US, Tietze DT, Alström P, Olsson U, Ghosh-Harihar M, Ishtiaq F, Gupta SK, et al. Nature. 2014 May 8; 509(7499):222-5. Epub 2014 Apr 30.
	PMID: 24776802 [PubMed - indexed for MEDLINE]
	Related citations

5.	Nature. 2014 May 8;509(7499):222-5. doi: 10.1038/nature13272. Epub 2014 Apr 30. Niche filling slows the diversification of Himalayan songbirds. Price TD1, Hooper DM1, Buchanan CD1, Johansson US2, Tietze DT3, Alström P4, Olsson U5, Ghosh-Harihar M6, Ishtiaq F6, Gupta SK6, Martens J7, Harr B8, Singh P6, Mohan D6. Author information: 1Department of Ecology and Evolution, University of Chicago, Chicago, Illinois 60637, USA. 21] Department of Ecology and Evolution, University of Chicago, Chicago, Illinois 60637, USA [2] Department of Zoology, Swedish Museum of Natural History, 10405 Stockholm, Sweden. 31] Department of Ecology and Evolution, University of Chicago, Chicago, Illinois 60637, USA [2] Institute of Pharmacy and Molecular Biotechnology, University of Heidelberg, Im Neuenheimer Feld 364, 69120 Heidelberg, Germany. 41] Key Laboratory of Zoological Systematics and Evolution, Institute of Zoology, Chinese Academy of Sciences, 1 Beichen West Road, Chaoyang District, Beijing 100101, China [2] Swedish Species Information Centre, Swedish University of Agricultural Sciences, Box 7007, 75007 Uppsala, Sweden. 5Systematics and Biodiversity, Department of Biology and Environmental Sciences, University of Gothenburg, 40530 Gothenburg, Sweden. 6Wildlife Institute of India, PO Box 18, Chandrabani, Dehradun 248001, India. 7Institute of Zoology, Johannes Gutenberg University, Mainz 55099, Germany. 8Max Planck Institute for Evolutionary Biology, August Thienemannstrasse 2, 24306 Plön, Germany. Comment in Biodiversity: Supply and demand. [Nature. 2014] Biodiversity: Supply and demand.Mooers AO. Nature. 2014 May 8; 509(7499):171-2. Epub 2014 Apr 30. Abstract Speciation generally involves a three-step process--range expansion, range fragmentation and the development of reproductive isolation between spatially separated populations. Speciation relies on cycling through these three steps and each may limit the rate at which new species form. We estimate phylogenetic relationships among all Himalayan songbirds to ask whether the development of reproductive isolation and ecological competition, both factors that limit range expansions, set an ultimate limit on speciation. Based on a phylogeny for all 358 species distributed along the eastern elevational gradient, here we show that body size and shape differences evolved early in the radiation, with the elevational band occupied by a species evolving later. These results are consistent with competition for niche space limiting species accumulation. Even the elevation dimension seems to be approaching ecological saturation, because the closest relatives both inside the assemblage and elsewhere in the Himalayas are on average separated by more than five million years, which is longer than it generally takes for reproductive isolation to be completed; also, elevational distributions are well explained by resource availability, notably the abundance of arthropods, and not by differences in diversification rates in different elevational zones. Our results imply that speciation rate is ultimately set by niche filling (that is, ecological competition for resources), rather than by the rate of acquisition of reproductive isolation.
	PMID: 24776798 [PubMed - indexed for MEDLINE]
	Related citations

6.	Nature. 2014 May 8;509(7499):230-4. doi: 10.1038/nature13168. Epub 2014 Apr 13. Listeria monocytogenes exploits efferocytosis to promote cell-to-cell spread. Czuczman MA1, Fattouh R2, van Rijn JM3, Canadien V2, Osborne S2, Muise AM4, Kuchroo VK5, Higgins DE6, Brumell JH7. Author information: 11] Cell Biology Program, Hospital for Sick Children, Toronto, Ontario M5G0A4, Canada [2] Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S1A8, Canada. 2Cell Biology Program, Hospital for Sick Children, Toronto, Ontario M5G0A4, Canada. 3Department of Cell Biology and Institute of Biomembranes, University Medical Center Utrecht, 3584 CX Utrecht, the Netherlands. 41] Cell Biology Program, Hospital for Sick Children, Toronto, Ontario M5G0A4, Canada [2] Division of Gastroenterology, Hepatology, and Nutrition, Department of Paediatrics, Hospital for Sick Children, Toronto, Ontario M5G1X8, Canada [3] Institute of Medical Science, University of Toronto, Toronto, Ontario M5S1A8, Canada [4] Sickkids IBD Centre, Hospital for Sick Children, Toronto, Ontario M5G1X8, Canada. 5Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. 6Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA. 71] Cell Biology Program, Hospital for Sick Children, Toronto, Ontario M5G0A4, Canada [2] Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S1A8, Canada [3] Institute of Medical Science, University of Toronto, Toronto, Ontario M5S1A8, Canada [4] Sickkids IBD Centre, Hospital for Sick Children, Toronto, Ontario M5G1X8, Canada. Comment in Bacterial pathogenesis: Pirate bacteria hijack efferocytosis. [Nat Rev Microbiol. 2014] Bacterial pathogenesis: Pirate bacteria hijack efferocytosis.Kåhrström CT. Nat Rev Microbiol. 2014 Jun; 12(6):396-7. Epub 2014 Apr 28. Abstract Efferocytosis, the process by which dying or dead cells are removed by phagocytosis, has an important role in development, tissue homeostasis and innate immunity. Efferocytosis is mediated, in part, by receptors that bind to exofacial phosphatidylserine (PS) on cells or cellular debris after loss of plasma membrane asymmetry. Here we show that a bacterial pathogen, Listeria monocytogenes, can exploit efferocytosis to promote cell-to-cell spread during infection. These bacteria can escape the phagosome in host cells by using the pore-forming toxin listeriolysin O (LLO) and two phospholipase C enzymes. Expression of the cell surface protein ActA allows L. monocytogenes to activate host actin regulatory factors and undergo actin-based motility in the cytosol, eventually leading to formation of actin-rich protrusions at the cell surface. Here we show that protrusion formation is associated with plasma membrane damage due to LLO's pore-forming activity. LLO also promotes the release of bacteria-containing protrusions from the host cell, generating membrane-derived vesicles with exofacial PS. The PS-binding receptor TIM-4 (encoded by the Timd4 gene) contributes to efficient cell-to-cell spread by L. monocytogenes in macrophages in vitro and growth of these bacteria is impaired in Timd4(-/-) mice. Thus, L. monocytogenes promotes its dissemination in a host by exploiting efferocytosis. Our results indicate that PS-targeted therapeutics may be useful in the fight against infections by L. monocytogenes and other bacteria that use similar strategies of cell-to-cell spread during infection.
	PMID: 24739967 [PubMed - indexed for MEDLINE]
	Related citations

7.	Nature. 2014 May 8;509(7499):235-9. doi: 10.1038/nature13152. Epub 2014 Apr 13. NRROS negatively regulates reactive oxygen species during host defence and autoimmunity. Noubade R1, Wong K2, Ota N2, Rutz S2, Eidenschenk C2, Valdez PA1, Ding J2, Peng I2, Sebrell A3, Caplazi P4, DeVoss J2, Soriano RH5, Sai T3, Lu R2, Modrusan Z5, Hackney J6, Ouyang W2. Author information: 11] Department of Immunology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA [2] Flexus Biosciences, 75 Shoreway Road, Suite D, San Carlos, California 94070, USA (R.N.); American Society for Biochemistry and Molecular Biology, 11200 Rockville Pike, Suite 302, Rockville, Maryland 20852, USA (P.A.V.). 2Department of Immunology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. 3Department of Antibody Engineering, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. 4Department of Pathology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. 5Department of Molecular Biology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. 6Department of Bioinformatics, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. Abstract Reactive oxygen species (ROS) produced by phagocytes are essential for host defence against bacterial and fungal infections. Individuals with defective ROS production machinery develop chronic granulomatous disease. Conversely, excessive ROS can cause collateral tissue damage during inflammatory processes and therefore needs to be tightly regulated. Here we describe a protein, we termed negative regulator of ROS (NRROS), which limits ROS generation by phagocytes during inflammatory responses. NRROS expression in phagocytes can be repressed by inflammatory signals. NRROS-deficient phagocytes produce increased ROS upon inflammatory challenges, and mice lacking NRROS in their phagocytes show enhanced bactericidal activity against Escherichia coli and Listeria monocytogenes. Conversely, these mice develop severe experimental autoimmune encephalomyelitis owing to oxidative tissue damage in the central nervous system. Mechanistically, NRROS is localized to the endoplasmic reticulum, where it directly interacts with nascent NOX2 (also known as gp91(phox) and encoded by Cybb) monomer, one of the membrane-bound subunits of the NADPH oxidase complex, and facilitates the degradation of NOX2 through the endoplasmic-reticulum-associated degradation pathway. Thus, NRROS provides a hitherto undefined mechanism for regulating ROS production--one that enables phagocytes to produce higher amounts of ROS, if required to control invading pathogens, while minimizing unwanted collateral tissue damage.
	PMID: 24739962 [PubMed - indexed for MEDLINE]
	Related citations