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

Sent on Tuesday, 2014 April 29
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]))

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1.	Science. 2014 Apr 18;344(6181):255. doi: 10.1126/science.344.6181.255-a. Uganda homosexuality report in context. Wayengera M. Author information: Unit of Genetics and Genomics, Department of Pathology, School of Biomedical Sciences, Makerere University College of Health Sciences, Kampala, Uganda. Comment on Science and politics. Science misused to justify Ugandan antigay law. [Science. 2014] Science and politics. Science misused to justify Ugandan antigay law.Balter M. Science. 2014 Feb 28; 343(6174):956.
	PMID: 24744358 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Apr 11;344(6180):208-11. doi: 10.1126/science.1250217. Mapping the cellular response to small molecules using chemogenomic fitness signatures. Lee AY1, St Onge RP, Proctor MJ, Wallace IM, Nile AH, Spagnuolo PA, Jitkova Y, Gronda M, Wu Y, Kim MK, Cheung-Ong K, Torres NP, Spear ED, Han MK, Schlecht U, Suresh S, Duby G, Heisler LE, Surendra A, Fung E, Urbanus ML, Gebbia M, Lissina E, Miranda M, Chiang JH, Aparicio AM, Zeghouf M, Davis RW, Cherfils J, Boutry M, Kaiser CA, Cummins CL, Trimble WS, Brown GW, Schimmer AD, Bankaitis VA, Nislow C, Bader GD, Giaever G. Author information: 1The Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada. Abstract Genome-wide characterization of the in vivo cellular response to perturbation is fundamental to understanding how cells survive stress. Identifying the proteins and pathways perturbed by small molecules affects biology and medicine by revealing the mechanisms of drug action. We used a yeast chemogenomics platform that quantifies the requirement for each gene for resistance to a compound in vivo to profile 3250 small molecules in a systematic and unbiased manner. We identified 317 compounds that specifically perturb the function of 121 genes and characterized the mechanism of specific compounds. Global analysis revealed that the cellular response to small molecules is limited and described by a network of 45 major chemogenomic signatures. Our results provide a resource for the discovery of functional interactions among genes, chemicals, and biological processes.
	PMID: 24723613 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2014 Mar;20(3):239-41. doi: 10.1038/nm.3501. Regulating innate immunity with dopamine and electroacupuncture. Chavan SS, Tracey KJ. Author information: Feinstein Institute for Medical Research, Laboratory of Biomedical Science, Manhasset, New York, USA. Comment on Dopamine mediates vagal modulation of the immune system by electroacupuncture. [Nat Med. 2014] Dopamine mediates vagal modulation of the immune system by electroacupuncture.Torres-Rosas R, Yehia G, Peña G, Mishra P, del Rocio Thompson-Bonilla M, Moreno-Eutimio MA, Arriaga-Pizano LA, Isibasi A, Ulloa L. Nat Med. 2014 Mar; 20(3):291-5. Epub 2014 Feb 23.
	PMID: 24603793 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2014 Mar;20(3):291-5. doi: 10.1038/nm.3479. Epub 2014 Feb 23. Dopamine mediates vagal modulation of the immune system by electroacupuncture. Torres-Rosas R1, Yehia G2, Peña G2, Mishra P2, del Rocio Thompson-Bonilla M3, Moreno-Eutimio MA4, Arriaga-Pizano LA5, Isibasi A5, Ulloa L6. Author information: 11] Laboratory of Anti-inflammatory Signaling, Department of Surgery, Rutgers University New Jersey Medical School, Newark, New Jersey, USA. [2] Medical Research Unit on Immunochemistry, National Medical Center Siglo XXI, Mexico City, Mexico. 2Laboratory of Anti-inflammatory Signaling, Department of Surgery, Rutgers University New Jersey Medical School, Newark, New Jersey, USA. 31] Laboratory of Anti-inflammatory Signaling, Department of Surgery, Rutgers University New Jersey Medical School, Newark, New Jersey, USA. [2] The Institute for Social Security and Services for the State's Employees Research Institute, Mexico City, Mexico. 4Laboratory of Immunobiology, Hospital Juárez de México, Mexico City, Mexico. 5Medical Research Unit on Immunochemistry, National Medical Center Siglo XXI, Mexico City, Mexico. 61] Laboratory of Anti-inflammatory Signaling, Department of Surgery, Rutgers University New Jersey Medical School, Newark, New Jersey, USA. [2] Center of Immunology and Inflammation, Rutgers University New Jersey Medical School, Newark, New Jersey, USA. Comment in Regulating innate immunity with dopamine and electroacupuncture. [Nat Med. 2014] Regulating innate immunity with dopamine and electroacupuncture.Chavan SS, Tracey KJ. Nat Med. 2014 Mar; 20(3):239-41. Abstract Previous anti-inflammatory strategies against sepsis, a leading cause of death in hospitals, had limited efficacy in clinical trials, in part because they targeted single cytokines and the experimental models failed to mimic clinical settings. Neuronal networks represent physiological mechanisms, selected by evolution to control inflammation, that can be exploited for the treatment of inflammatory and infectious disorders. Here, we report that sciatic nerve activation with electroacupuncture controls systemic inflammation and rescues mice from polymicrobial peritonitis. Electroacupuncture at the sciatic nerve controls systemic inflammation by inducing vagal activation of aromatic L-amino acid decarboxylase, leading to the production of dopamine in the adrenal medulla. Experimental models with adrenolectomized mice mimic clinical adrenal insufficiency, increase the susceptibility to sepsis and prevent the anti-inflammatory effects of electroacupuncture. Dopamine inhibits cytokine production via dopamine type 1 (D1) receptors. D1 receptor agonists suppress systemic inflammation and rescue mice with adrenal insufficiency from polymicrobial peritonitis. Our results suggest a new anti-inflammatory mechanism mediated by the sciatic and vagus nerves that modulates the production of catecholamines in the adrenal glands. From a pharmacological perspective, the effects of selective dopamine agonists mimic the anti-inflammatory effects of electroacupuncture and can provide therapeutic advantages to control inflammation in infectious and inflammatory disorders. PMCID: PMC3949155 [Available on 2014/9/1]
	PMID: 24562381 [PubMed - indexed for MEDLINE]
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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]))

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1.	Nat Genet. 2014 Mar;46(3):220-4. doi: 10.1038/ng.2896. Epub 2014 Feb 9. The deleterious mutation load is insensitive to recent population history. Simons YB1, Turchin MC2, Pritchard JK3, Sella G4. Author information: 11] Department of Ecology, Evolution and Behavior, Hebrew University of Jerusalem, Jerusalem, Israel. [2]. 21] Department of Human Genetics, University of Chicago, Chicago, Illinois, USA. [2]. 31] Department of Human Genetics, University of Chicago, Chicago, Illinois, USA. [2] Howard Hughes Medical Institute, Stanford University, Stanford, California, USA. [3] Department of Biology, Stanford University, Stanford, California, USA. [4] Department of Genetics, Stanford University, Stanford, California, USA. 41] Department of Ecology and Evolution, University of Chicago, Chicago, Illinois, USA. [2]. Abstract Human populations have undergone major changes in population size in the past 100,000 years, including recent rapid growth. How these demographic events have affected the burden of deleterious mutations in individuals and the frequencies of disease mutations in populations remains unclear. We use population genetic models to show that recent human demography has probably had little impact on the average burden of deleterious mutations. This prediction is supported by two exome sequence data sets showing that individuals of west African and European ancestry carry very similar burdens of damaging mutations. We further show that for many diseases, rare alleles are unlikely to contribute a large fraction of the heritable variation, and therefore the impact of recent growth is likely to be modest. However, for those diseases that have a direct impact on fitness, strongly deleterious rare mutations probably do have an important role, and recent growth will have increased their impact. PMCID: PMC3953611 [Available on 2014/9/1]
	PMID: 24509481 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2014 Mar;46(3):225-33. doi: 10.1038/ng.2891. Epub 2014 Feb 2. Genomic architecture and evolution of clear cell renal cell carcinomas defined by multiregion sequencing. Gerlinger M1, Horswell S2, Larkin J3, Rowan AJ1, Salm MP2, Varela I4, Fisher R5, McGranahan N6, Matthews N7, Santos CR6, Martinez P6, Phillimore B7, Begum S7, Rabinowitz A7, Spencer-Dene B8, Gulati S9, Bates PA9, Stamp G8, Pickering L5, Gore M5, Nicol DL10, Hazell S11, Futreal PA12, Stewart A13, Swanton C14. Author information: 11] Translational Cancer Therapeutics Laboratory, Cancer Research UK London Research Institute, London, UK. [2]. 21] Bioinformatics and Biostatistics, Cancer Research UK London Research Institute, London, UK. [2]. 31] Department of Medicine, Royal Marsden Hospital, London, UK. [2]. 4Instituto de Biomedicina y Biotecnología de Cantabria (CSIC-UC-Sodercan), Departamento de Biología Molecular, Universidad de Cantabria, Santander, Spain. 5Department of Medicine, Royal Marsden Hospital, London, UK. 6Translational Cancer Therapeutics Laboratory, Cancer Research UK London Research Institute, London, UK. 7Advanced Sequencing Facility, Cancer Research UK London Research Institute, London, UK. 8Experimental Histopathology, Cancer Research UK London Research Institute, London, UK. 9Biomolecular Modelling, Cancer Research UK London Research Institute, London, UK. 10Department of Urology, Royal Marsden Hospital, London, UK. 11Department of Pathology, Royal Marsden Hospital, London, UK. 12Department of Genomic Medicine, MD Anderson Cancer Center, Houston, Texas, USA. 13Bioinformatics and Biostatistics, Cancer Research UK London Research Institute, London, UK. 141] Translational Cancer Therapeutics Laboratory, Cancer Research UK London Research Institute, London, UK. [2] University College London Cancer Institute, University College London, London, UK. Comment in Kidney cancer: Intratumoral differences analysed. [Nat Rev Urol. 2014] Kidney cancer: Intratumoral differences analysed.Payton S. Nat Rev Urol. 2014 Mar; 11(3):127. Epub 2014 Feb 25. Abstract Clear cell renal carcinomas (ccRCCs) can display intratumor heterogeneity (ITH). We applied multiregion exome sequencing (M-seq) to resolve the genetic architecture and evolutionary histories of ten ccRCCs. Ultra-deep sequencing identified ITH in all cases. We found that 73-75% of identified ccRCC driver aberrations were subclonal, confounding estimates of driver mutation prevalence. ITH increased with the number of biopsies analyzed, without evidence of saturation in most tumors. Chromosome 3p loss and VHL aberrations were the only ubiquitous events. The proportion of C>T transitions at CpG sites increased during tumor progression. M-seq permits the temporal resolution of ccRCC evolution and refines mutational signatures occurring during tumor development.
	PMID: 24487277 [PubMed - indexed for MEDLINE]
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3.	PLoS One. 2013 Jun 28;8(6):e68306. doi: 10.1371/journal.pone.0068306. Print 2013. Regulated expression of PTPRJ/CD148 and an antisense long noncoding RNA in macrophages by proinflammatory stimuli. Dave RK1, Dinger ME, Andrew M, Askarian-Amiri M, Hume DA, Kellie S. Author information: 1The University of Queensland, Institute for Molecular Bioscience, Brisbane, Australia. Abstract PTPRJ/CD148 is a tyrosine phosphatase that has tumour suppressor-like activity. Quantitative PCR of various cells and tissues revealed that it is preferentially expressed in macrophage-enriched tissues. Within lymphoid tissues immunohistochemistry revealed that PTPRJ/CD148 co-localised with F4/80, indicating that macrophages most strongly express the protein. Macrophages express the highest basal level of ptprj, and this is elevated further by treatment with LPS and other Toll-like receptor ligands. In contrast, CSF-1 treatment reduced basal and stimulated Ptprj expression in human and mouse cells, and interferon also repressed Ptprj expression. We identified a 1006 nucleotide long noncoding RNA species, Ptprj-as1 that is transcribed antisense to Ptprj. Ptprj-as1 was highly expressed in macrophage-enriched tissue and was transiently induced by Toll-like receptor ligands with a similar time course to Ptprj. Finally, putative transcription factor binding sites in the promoter region of Ptprj were identified. PMCID: PMC3695918 Free PMC Article
	PMID: 23840844 [PubMed - indexed for MEDLINE]
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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]))

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1.	Nature. 2014 Apr 3;508(7494):S6-7. doi: 10.1038/508S6a. Genetics: Unravelling complexity. Wright J.
	PMID: 24695335 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Apr 3;508(7494):22. doi: 10.1038/508022a. Epigenomics starts to make its mark. Callaway E.
	PMID: 24695296 [PubMed - indexed for MEDLINE]
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Sent on Tuesday, 2014 April 22
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]))

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1.	Science. 2014 Apr 4;344(6179):30. doi: 10.1126/science.344.6179.30. The well-heeled: Donald Bowden. Servick K.
	PMID: 24700840 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Mar 27;507(7493):414-6. doi: 10.1038/507414a. Human evolution: The Neanderthal in the family. Callaway E.
	PMID: 24670743 [PubMed - indexed for MEDLINE]
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3.	Lancet. 2014 Feb 26;383 Suppl 1:S1-2. doi: 10.1016/S0140-6736(14)60049-0. Shaping academic medicine. Tooke J1, Wass J2, Horton R3. Author information: 1Academy of Medical Sciences, London, UK; University College London, London, UK. Electronic address: john.tooke@acmedsci.ac.uk. 2Royal College of Physicians, London, UK; Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK. 3The Lancet, London, UK.
	PMID: 24581623 [PubMed - indexed for MEDLINE]
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1.	N Engl J Med. 2014 Apr 10;370(15):1412-21. doi: 10.1056/NEJMoa1305727. Epub 2014 Mar 18. Albumin replacement in patients with severe sepsis or septic shock. Caironi P1, Tognoni G, Masson S, Fumagalli R, Pesenti A, Romero M, Fanizza C, Caspani L, Faenza S, Grasselli G, Iapichino G, Antonelli M, Parrini V, Fiore G, Latini R, Gattinoni L; ALBIOS Study Investigators. Collaborators: Gattinoni L, Caironi P, Pesenti A, Fumagalli R, Tognoni G, Romero M, Latini R, Masson S, Vincent JL, Suter PM, Valsecchi MG, Santosuosso A, Cavana M, Ortu A, Gabini R, Perno S, Anelli A, Amoruso R, Ferraris S, Borelli M, Massei R, Riva I, Poli G, Papagni G, Bortone F, Mamprin F, Keim R, Brivio M, Colageo U, Mimii EP, Sangiorgi G, Siniscalchi A, Pierucci E, Giovannitti A, Gentile C, Pascucci F, Antonini B, Zummo U, Valsecchi R, Cerisara M, Trezzi T, Dossena A, Ribola A, Tamayo L, Zoppellari R, Volta CA, Mangani V, Fanfani E, Chelazzi C, Bartoli T, Parrini V, Oggioni R, Fedele A, Molin A, Berri C, Guarino A, Isetta M, Bonfiglio M, Tissino F, Silvestri L, Milanesi M, Sbrana G, Motta E, Iannaco I, Casadio MC, Pasetti GS, Palandini A, Cascione C, Puscio D, Cellai F, Boccalatte D, Silvestri S, Fausto CI, Lupo V, Zompanti V, Iacobone E, Gattari D, Ronzoni G, Beck E, Francesconi S, Colombo R, Raimondi F, Castelli A, De Gasperi A, Radrizzani D, Ferla LE, Giudici R, Bellato V, Bordone G, Gavazzeni V, Lesmo A, Ripamonti D, Vesconi S, Papoff A, Rossi A, Noto A, Pezzi A, Zanforlin G, Kandil H, Ballotta A, Bettini F, Vaghi GM, Rossi S, Pessina C, Casagrande D, Trivellato A, Costagli V, Moise G, Furla M, Marelli S, Caspani L, Panigada M, Bruzzone P, Isgrò S, Abbruzzese C, Tagliabue P, Solca M, Bonazzi M, Cattaneo A, Rossi N, Andreoni P, Pasetto A, Girardis M, Barbieri E, Piazza O, Giarratano A, Raineri SM, Cortegiani A, Zagara G, Bono M, Galzerano A, Garzilli T, Dentini N, Bindi M, Biancofiore G, Mercante WP, Disconzi MM, Todesco N, Lunardi S, Sani E, Carli M, Bracciotti G, Gori V, Braccini P, Maggio G, Braschi A, Bottazzi A, Iotti G, Nicora B, Salati G, Salsi P, Antonelli M, Pennisi MA, Bello G, Caccese R, D'Ambrosio M, Rocco M, Sanseverino M, Gatta A, Nastasi M, Corsi A, Facondini F, Franchi F, Mongelli P, Ferrario M, Carulli F, Del Curto S, Schiappacasse G, Dalpiaz C, Armani S, Verderosa I, Marzullo A, Tonetti F, De Piero ME, Livigni S, Fiore G, Cerutti A, Erbetta S, Napolitano R, Pastorelli M, Bona F, Debernardi F, Gallo M, Segala V, Parigi L, Perzolla D, Marson F, Chiarandini P, Cammarano C, Sermann G, De Lucia S, Frigerio A, Distaso F, Franco R, Bossi E, Laudi C, De Nardin M, Violo T, Lazzari F, Vestali A, Della Mora E, Polati E, Martini A, Cristallini S, Totaro C, Milan B, Dan M, Ruberti S, Danzi V. Author information: 1From Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Ca' Granda-Ospedale Maggiore Policlinico, Università degli Studi di Milano (P.C., G.I., L.G.), Dipartimento di Anestesia, Rianimazione e Terapia del Dolore, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico (P.C., L.C., L.G.), IRCCS-Istituto di Ricerche Farmacologiche Mario Negri (S.M., R.L.), Dipartimento di Scienze della Salute, Università degli Studi di Milano Bicocca (R.F., A.P.), and Dipartimento di Emergenza-Urgenza, Azienda Ospedaliera S. Paolo-Polo Universitario (G.I.), Milan, Consorzio Mario Negri Sud, Santa Maria Imbaro (G.T., M.R., C.F.), Anestesiologia e Rianimazione, Dipartimento Emergenza-Urgenza, Chirurgia Generale e dei Trapianti, Policlinico Universitario S. Orsola Malpighi, Bologna (S.F.), Dipartimento di Emergenza-Urgenza, Azienda Ospedaliera S. Gerardo, Monza (G.G.), Policlinico Universitario A. Gemelli, Università Cattolica, Rome (M.A.), Ospedale del Mugello-Azienda Sanitaria di Firenze, Florence (V.P.), and Ospedale S. Croce, Moncalieri (G.F.) - all in Italy. Abstract BACKGROUND: Although previous studies have suggested the potential advantages of albumin administration in patients with severe sepsis, its efficacy has not been fully established. METHODS: In this multicenter, open-label trial, we randomly assigned 1818 patients with severe sepsis, in 100 intensive care units (ICUs), to receive either 20% albumin and crystalloid solution or crystalloid solution alone. In the albumin group, the target serum albumin concentration was 30 g per liter or more until discharge from the ICU or 28 days after randomization. The primary outcome was death from any cause at 28 days. Secondary outcomes were death from any cause at 90 days, the number of patients with organ dysfunction and the degree of dysfunction, and length of stay in the ICU and the hospital. RESULTS: During the first 7 days, patients in the albumin group, as compared with those in the crystalloid group, had a higher mean arterial pressure (P=0.03) and lower net fluid balance (P<0.001). The total daily amount of administered fluid did not differ significantly between the two groups (P=0.10). At 28 days, 285 of 895 patients (31.8%) in the albumin group and 288 of 900 (32.0%) in the crystalloid group had died (relative risk in the albumin group, 1.00; 95% confidence interval [CI], 0.87 to 1.14; P=0.94). At 90 days, 365 of 888 patients (41.1%) in the albumin group and 389 of 893 (43.6%) in the crystalloid group had died (relative risk, 0.94; 95% CI, 0.85 to 1.05; P=0.29). No significant differences in other secondary outcomes were observed between the two groups. CONCLUSIONS: In patients with severe sepsis, albumin replacement in addition to crystalloids, as compared with crystalloids alone, did not improve the rate of survival at 28 and 90 days. (Funded by the Italian Medicines Agency; ALBIOS ClinicalTrials.gov number, NCT00707122.).
	PMID: 24635772 [PubMed - indexed for MEDLINE]

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1.	N Engl J Med. 2014 Mar 27;370(13):1238-48. doi: 10.1056/NEJMcpc1304162. Case records of the Massachusetts General Hospital. Case 10-2014. A 45-year-old man with a rash. Chiappa V, Chang CY, Sellas MI, Pierce VM, Kradin RL.
	PMID: 24670171 [PubMed - indexed for MEDLINE]

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1.	Science. 2014 Mar 28;343(6178):1439-40. doi: 10.1126/science.1252785. Immunology. The axis of tolerance. Aychek T1, Jung S. Author information: 1Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel. Comment on Microbiota-dependent crosstalk between macrophages and ILC3 promotes intestinal homeostasis. [Science. 2014] Microbiota-dependent crosstalk between macrophages and ILC3 promotes intestinal homeostasis.Mortha A, Chudnovskiy A, Hashimoto D, Bogunovic M, Spencer SP, Belkaid Y, Merad M. Science. 2014 Mar 28; 343(6178):1249288. Epub 2014 Mar 13.
	PMID: 24675941 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Mar 28;343(6178):1249288. doi: 10.1126/science.1249288. Epub 2014 Mar 13. Microbiota-dependent crosstalk between macrophages and ILC3 promotes intestinal homeostasis. Mortha A1, Chudnovskiy A, Hashimoto D, Bogunovic M, Spencer SP, Belkaid Y, Merad M. Author information: 1Department of Oncological Sciences, 1470 Madison Avenue, New York, NY 10029, USA. Comment in Immunology. The axis of tolerance. [Science. 2014] Immunology. The axis of tolerance.Aychek T, Jung S. Science. 2014 Mar 28; 343(6178):1439-40. Abstract The intestinal microbiota and tissue-resident myeloid cells promote immune responses that maintain intestinal homeostasis in the host. However, the cellular cues that translate microbial signals into intestinal homeostasis remain unclear. Here, we show that deficient granulocyte-macrophage colony-stimulating factor (GM-CSF) production altered mononuclear phagocyte effector functions and led to reduced regulatory T cell (T(reg)) numbers and impaired oral tolerance. We observed that RORγt(+) innate lymphoid cells (ILCs) are the primary source of GM-CSF in the gut and that ILC-driven GM-CSF production was dependent on the ability of macrophages to sense microbial signals and produce interleukin-1β. Our findings reveal that commensal microbes promote a crosstalk between innate myeloid and lymphoid cells that leads to immune homeostasis in the intestine.
	PMID: 24625929 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

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PubMed Results

Items 1 - 5 of 5

1.	Nature. 2014 Mar 20;507(7492):273-4. How to get ahead. [No authors listed]
	PMID: 24654276 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Mar 20;507(7492):294-5. doi: 10.1038/507294a. Technology: The $1,000 genome. Hayden EC.
	PMID: 24646979 [PubMed - indexed for MEDLINE]
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3.	Science. 2014 Feb 28;343(6174):956. doi: 10.1126/science.343.6174.956. Science and politics. Science misused to justify Ugandan antigay law. Balter M.
	PMID: 24578555 [PubMed - indexed for MEDLINE]
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4.	Nature. 2014 Mar 20;507(7492):366-70. doi: 10.1038/nature12979. Epub 2014 Feb 23. IL-35-producing B cells are critical regulators of immunity during autoimmune and infectious diseases. Shen P1, Roch T2, Lampropoulou V3, O'Connor RA4, Stervbo U3, Hilgenberg E3, Ries S3, Dang VD3, Jaimes Y3, Daridon C5, Li R6, Jouneau L7, Boudinot P7, Wilantri S3, Sakwa I3, Miyazaki Y6, Leech MD4, McPherson RC4, Wirtz S8, Neurath M8, Hoehlig K3, Meinl E9, Grützkau A3, Grün JR3, Horn K3, Kühl AA10, Dörner T5, Bar-Or A6, Kaufmann SH11, Anderton SM4, Fillatreau S3. Author information: 11] Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany [2]. 21] Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany [2] Institute of Biomaterial Science, Helmholtz-Zentrum Geesthacht, Centre for Materials and Coastal Research, Kantstraße 55, 14513 Teltow, Germany. [3]. 3Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany. 4University of Edinburgh, Centre for Inflammation Research and Centre for Multiple Sclerosis Research, Queen's Medical Research Institute, Edinburgh EH16 4TJ, UK. 51] Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany [2] Charité Universitätsmedizin Berlin, CC12, Department of Medicine/Rheumatology and Clinical Immunology, 10117 Berlin, Germany. 6Neuroimmunology Unit, Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec H3A2B4, Canada. 7Virologie et Immunologie Moléculaires, INRA, 78352 Jouy-en-Josas, France. 8Medical Clinic 1, Kussmaul Campus for Medical Research, University of Erlangen-Nürnberg, 91054 Erlangen, Germany. 9Institut für Klinische Neuroimmunologie Klinikum der Ludwig-Maximilians-Universität München, 81377 München, Germany. 10Immunpathologie, Research Center ImmunoSciences, 12203 Berlin, Germany. 11Max Planck Institute of Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany. Abstract B lymphocytes have critical roles as positive and negative regulators of immunity. Their inhibitory function has been associated primarily with interleukin 10 (IL-10) because B-cell-derived IL-10 can protect against autoimmune disease and increase susceptibility to pathogens. Here we identify IL-35-producing B cells as key players in the negative regulation of immunity. Mice in which only B cells did not express IL-35 lost their ability to recover from the T-cell-mediated demyelinating autoimmune disease experimental autoimmune encephalomyelitis (EAE). In contrast, these mice displayed a markedly improved resistance to infection with the intracellular bacterial pathogen Salmonella enterica serovar Typhimurium as shown by their superior containment of the bacterial growth and their prolonged survival after primary infection, and upon secondary challenge, compared to control mice. The increased immunity found in mice lacking IL-35 production by B cells was associated with a higher activation of macrophages and inflammatory T cells, as well as an increased function of B cells as antigen-presenting cells (APCs). During Salmonella infection, IL-35- and IL-10-producing B cells corresponded to two largely distinct sets of surface-IgM(+)CD138(hi)TACI(+)CXCR4(+)CD1d(int)Tim1(int) plasma cells expressing the transcription factor Blimp1 (also known as Prdm1). During EAE, CD138(+) plasma cells were also the main source of B-cell-derived IL-35 and IL-10. Collectively, our data show the importance of IL-35-producing B cells in regulation of immunity and highlight IL-35 production by B cells as a potential therapeutic target for autoimmune and infectious diseases. This study reveals the central role of activated B cells, particularly plasma cells, and their production of cytokines in the regulation of immune responses in health and disease.
	PMID: 24572363 [PubMed - indexed for MEDLINE]
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5.	Nature. 2014 Mar 20;507(7492):354-7. doi: 10.1038/nature12961. Epub 2014 Jan 29. The genomic landscape of Neanderthal ancestry in present-day humans. Sankararaman S1, Mallick S1, Dannemann M2, Prüfer K2, Kelso J2, Pääbo S2, Patterson N1, Reich D3. Author information: 11] Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA. 2Max Planck Institute for Evolutionary Anthropology, Leipzig 04103, Germany. 31] Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA [3] Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. Abstract Genomic studies have shown that Neanderthals interbred with modern humans, and that non-Africans today are the products of this mixture. The antiquity of Neanderthal gene flow into modern humans means that genomic regions that derive from Neanderthals in any one human today are usually less than a hundred kilobases in size. However, Neanderthal haplotypes are also distinctive enough that several studies have been able to detect Neanderthal ancestry at specific loci. We systematically infer Neanderthal haplotypes in the genomes of 1,004 present-day humans. Regions that harbour a high frequency of Neanderthal alleles are enriched for genes affecting keratin filaments, suggesting that Neanderthal alleles may have helped modern humans to adapt to non-African environments. We identify multiple Neanderthal-derived alleles that confer risk for disease, suggesting that Neanderthal alleles continue to shape human biology. An unexpected finding is that regions with reduced Neanderthal ancestry are enriched in genes, implying selection to remove genetic material derived from Neanderthals. Genes that are more highly expressed in testes than in any other tissue are especially reduced in Neanderthal ancestry, and there is an approximately fivefold reduction of Neanderthal ancestry on the X chromosome, which is known from studies of diverse species to be especially dense in male hybrid sterility genes. These results suggest that part of the explanation for genomic regions of reduced Neanderthal ancestry is Neanderthal alleles that caused decreased fertility in males when moved to a modern human genetic background.
	PMID: 24476815 [PubMed - indexed for MEDLINE]
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