Friday, 12 October 2012

What's new for 'JKB_daily1' in PubMed

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

Sent on Friday, 2012 October 12
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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PubMed Results
Items 1 - 8 of 8

1. N Engl J Med. 2012 Sep 27;367(13):1266-7; author reply 1267.

Protocols, physiology, and trials of hydroxyethyl starch.

Wise R, Fourie C, Richards GA.

Comment on

PMID: 23013091 [PubMed - indexed for MEDLINE]
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2. N Engl J Med. 2012 Sep 27;367(13):1266; author reply 1267.

Protocols, physiology, and trials of hydroxyethyl starch.

Chappell D, Jacob M.

Comment on

PMID: 23013090 [PubMed - indexed for MEDLINE]
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3. N Engl J Med. 2012 Sep 27;367(13):1265-6; author reply 1267.

Protocols, physiology, and trials of hydroxyethyl starch.

von Heymann C, Sander M, Spies CD.

Comment on

PMID: 23013089 [PubMed - indexed for MEDLINE]
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4. N Engl J Med. 2012 Sep 27;367(13):1265; author reply 1267.

Protocols, physiology, and trials of hydroxyethyl starch.

Magder S.

Comment on

PMID: 23013088 [PubMed - indexed for MEDLINE]
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5. Nature. 2012 Aug 30;488(7413):609-14. doi: 10.1038/nature11360.

A Cenozoic record of the equatorial Pacific carbonate compensation depth.

Pälike H, Lyle MW, Nishi H, Raffi I, Ridgwell A, Gamage K, Klaus A, Acton G, Anderson L, Backman J, Baldauf J, Beltran C, Bohaty SM, Bown P, Busch W, Channell JE, Chun CO, Delaney M, Dewangan P, Dunkley Jones T, Edgar KM, Evans H, Fitch P, Foster GL, Gussone N, Hasegawa H, Hathorne EC, Hayashi H, Herrle JO, Holbourn A, Hovan S, Hyeong K, Iijima K, Ito T, Kamikuri S, Kimoto K, Kuroda J, Leon-Rodriguez L, Malinverno A, Moore TC Jr, Murphy BH, Murphy DP, Nakamura H, Ogane K, Ohneiser C, Richter C, Robinson R, Rohling EJ, Romero O, Sawada K, Scher H, Schneider L, Sluijs A, Takata H, Tian J, Tsujimoto A, Wade BS, Westerhold T, Wilkens R, Williams T, Wilson PA, Yamamoto Y, Yamamoto S, Yamazaki T, Zeebe RE.

Source

Ocean and Earth Science, National Oceanography Centre Southampton, University of Southampton, Waterfront Campus, European Way, Southampton SO14 3ZH, UK. hpaelike@marum.de

Comment in

Abstract

Atmospheric carbon dioxide concentrations and climate are regulated on geological timescales by the balance between carbon input from volcanic and metamorphic outgassing and its removal by weathering feedbacks; these feedbacks involve the erosion of silicate rocks and organic-carbon-bearing rocks. The integrated effect of these processes is reflected in the calcium carbonate compensation depth, which is the oceanic depth at which calcium carbonate is dissolved. Here we present a carbonate accumulation record that covers the past 53 million years from a depth transect in the equatorial Pacific Ocean. The carbonate compensation depth tracks long-term ocean cooling, deepening from 3.0-3.5 kilometres during the early Cenozoic (approximately 55 million years ago) to 4.6 kilometres at present, consistent with an overall Cenozoic increase in weathering. We find large superimposed fluctuations in carbonate compensation depth during the middle and late Eocene. Using Earth system models, we identify changes in weathering and the mode of organic-carbon delivery as two key processes to explain these large-scale Eocene fluctuations of the carbonate compensation depth.

PMID: 22932385 [PubMed - indexed for MEDLINE]
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6. Nature. 2012 Aug 30;488(7413):596-7. doi: 10.1038/488596a.

Ocean science: Ancient burial at sea.

Stoll H.

Comment on

PMID: 22932380 [PubMed - indexed for MEDLINE]
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7. Nature. 2012 Aug 30;488(7413):591. doi: 10.1038/488591a.

Publishing: Curb temptation to skip quality control.

Tse H.

Comment on

PMID: 22932375 [PubMed - indexed for MEDLINE]
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8. Nature. 2012 Aug 30;488(7413):670-4. doi: 10.1038/nature11290.

Novel role of PKR in inflammasome activation and HMGB1 release.

Lu B, Nakamura T, Inouye K, Li J, Tang Y, Lundbäck P, Valdes-Ferrer SI, Olofsson PS, Kalb T, Roth J, Zou Y, Erlandsson-Harris H, Yang H, Ting JP, Wang H, Andersson U, Antoine DJ, Chavan SS, Hotamisligil GS, Tracey KJ.

Source

Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York 11030, USA. blu@nshs.edu

Abstract

The inflammasome regulates the release of caspase activation-dependent cytokines, including interleukin (IL)-1β, IL-18 and high-mobility group box 1 (HMGB1). By studying HMGB1 release mechanisms, here we identify a role for double-stranded RNA-dependent protein kinase (PKR, also known as EIF2AK2) in inflammasome activation. Exposure of macrophages to inflammasome agonists induced PKR autophosphorylation. PKR inactivation by genetic deletion or pharmacological inhibition severely impaired inflammasome activation in response to double-stranded RNA, ATP, monosodium urate, adjuvant aluminium, rotenone, live Escherichia coli, anthrax lethal toxin, DNA transfection and Salmonella typhimurium infection. PKR deficiency significantly inhibited the secretion of IL-1β, IL-18 and HMGB1 in E. coli-induced peritonitis. PKR physically interacts with several inflammasome components, including NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3), NLRP1, NLR family CARD domain-containing protein 4 (NLRC4), absent in melanoma 2 (AIM2), and broadly regulates inflammasome activation. PKR autophosphorylation in a cell-free system with recombinant NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC, also known as PYCARD) and pro-caspase-1 reconstitutes inflammasome activity. These results show a crucial role for PKR in inflammasome activation, and indicate that it should be possible to pharmacologically target this molecule to treat inflammation.

PMID: 22801494 [PubMed - indexed for MEDLINE]
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