- 関
- co-translational、cotranslate、cotranslation、cotranslational
WordNet
- subject to movement in which every part of the body moves parallel to and the same distance as every other point on the body
- change from one form or medium into another; "Braque translated collage into oil" (同)transform
- restate (words) from one language into another language; "I have to translate when my in-laws from Austria visit the U.S."; "Can you interpret the speech of the visiting dignitaries?"; "She rendered the French poem into English"; "He translates for the U. (同)interpret, render
- be equivalent in effect; "the growth in income translates into greater purchasing power"
- be translatable, or be translatable in a certain way; "poetry often does not translate"; "Tolstoys novels translate well into English"
- bring to a certain spiritual state
- change the position of (figures or bodies) in space without rotation
- determine the amino-acid sequence of a protein during its synthesis by using information on the messenger RNA
- express, as in simple and less technical language; "Can you translate the instructions in this manual for a layman?"; "Is there a need to translate the psychiatrists remarks?"
- major food fish of Arctic and cold-temperate waters (同)codfish
- lean white flesh of important North Atlantic food fish; usually baked or poached (同)codfish
- lettuce with long dark-green leaves in a loosely packed elongated head (同)cos_lettuce, romaine, romaine lettuce
PrepTutorEJDIC
- (ある言吾から他の言吾へ)〈話・文章〉‘を'『翻訳する』《+名+from+名+into+名》 / …‘を'他の言葉で説明する;(…に)…‘を'言い換える《+名+into+名》 / 《文》(…に)…‘の'性質(状態など)を変える,‘を'変化させる《+名+into+名》 / 『翻訳する』,翻訳者を務める / 〈文章などが〉(…に)翻訳できる《+into+名》
- =codfish 1
- 〈人〉'を'ばかにする
- cosine
- =because
- Colorado
- cobaltの化学記号
UpToDate Contents
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English Journal
- Translating molecular physiology of intestinal transport into pharmacologic treatment of diarrhea: stimulation of na(+) absorption.
- Singh V1, Yang J1, Chen TE1, Zachos NC1, Kovbasnjuk O1, Verkman AS2, Donowitz M3.Author information 1Departments of Physiology and Medicine, Gastroenterology Division, Johns Hopkins University School of Medicine, Baltimore, Maryland.2Departments of Medicine and Physiology, University of California, San Francisco, San Francisco, California.3Departments of Physiology and Medicine, Gastroenterology Division, Johns Hopkins University School of Medicine, Baltimore, Maryland. Electronic address: mdonowit@jhmi.edu.AbstractDiarrheal diseases remain a leading cause of morbidity and mortality for children in developing countries, while representing an important cause of morbidity worldwide. The World Health Organization recommended that low osmolarity oral rehydration solutions plus zinc save lives in patients with acute diarrhea, but there are no approved, safe drugs that have been shown to be effective against most causes of acute diarrhea. Identification of abnormalities in electrolyte handling by the intestine in diarrhea, including increased intestinal anion secretion and reduced Na(+) absorption, suggest a number of potential drug targets. This is based on the view that successful drug therapy for diarrhea will result from correcting the abnormalities in electrolyte transport that are pathophysiologic for diarrhea. We review the molecular mechanisms of physiologic regulation of intestinal ion transport and changes that occur in diarrhea and the status of drugs being developed to correct the transport abnormalities in Na(+) absorption that occur in diarrhea. Mechanisms of Cl(-) secretion and approaches to anti-Cl(-) secretory therapies of diarrhea are discussed in a companion review.
- Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association.Clin Gastroenterol Hepatol.2014 Jan;12(1):27-31. doi: 10.1016/j.cgh.2013.10.020. Epub 2013 Oct 31.
- Diarrheal diseases remain a leading cause of morbidity and mortality for children in developing countries, while representing an important cause of morbidity worldwide. The World Health Organization recommended that low osmolarity oral rehydration solutions plus zinc save lives in patients with acut
- PMID 24184676
- Mitochondrial bioenergetics and therapeutic intervention in cardiovascular disease.
- Mercer JR.Author information University of Glasgow, Institute of Cardiovascular & Medical Sciences, BHF Glasgow Cardiovascular Research Centre, 126 University Place, Glasgow G12 8TA, United Kingdom. Electronic address: john.mercer@glasgow.ac.uk.AbstractCardiovascular disease remains the commonest form of mortality and morbidity in the Western World. It accounts for more deaths than the combined incidence of all cancers. There remains an urgency to identify and translate therapies to reduce the effects of this disease and its associated co-morbidities. Atherosclerotic disease accounts for over two thirds of all cardiovascular related deaths. Arterial vessel wall plaques rupture and cause death due to loss of integrity of the overlaying vascular smooth muscle cell (VSMC) cap. Although plaques contain a heterogeneous pool of different cell types, it is the VSMCs that by their nature are responsible for rupture. VSMC are the primary source of extracellular matrix and collagen and it has been suggested that loss of viability and vitality of these cells contributes to plaque vulnerability and rupture. While DNA damage has long been associated with atherosclerotic plaques only relatively recently has the contribution of mitochondrial DNA damage been suggested to play a role. The mitochondrial respiratory chain is a source of ATP that the cell requires for all its energetic functions but is also a source of free radicals that produce reactive species (RS). While these RS exacerbate DNA damage and attack lipids and proteins, it is the loss of ATP that may ultimately be more detrimental. Therapeutic intervention for mitochondria dysfunction is one route on alleviating this burden. Finding alternative sources of ATP synthesis by energetic reconfiguration may also provide a vital link in delaying the kinetics of plaque rupture.
- Pharmacology & therapeutics.Pharmacol Ther.2014 Jan;141(1):13-20. doi: 10.1016/j.pharmthera.2013.07.011. Epub 2013 Jul 31.
- Cardiovascular disease remains the commonest form of mortality and morbidity in the Western World. It accounts for more deaths than the combined incidence of all cancers. There remains an urgency to identify and translate therapies to reduce the effects of this disease and its associated co-morbidit
- PMID 23911986
- Carbon monoxide-based therapy ameliorates acute pancreatitis via TLR4 inhibition.
- Xue J, Habtezion A.AbstractThe protective role of hemeoxygenase-1 (HO-1) in various inflammatory conditions is mediated in part by its products, carbon monoxide (CO) and biliverdin. Here we investigated a therapeutic role for CO and CO-primed cells in acute pancreatitis (AP). In a mouse model of AP, treatment with CO-releasing molecule-2 (CORM-2) decreased mortality, pancreatic damage, and lung injury. CORM-2 decreased systemic inflammatory cytokines, suppressed systemic and pancreatic macrophage TNF-α secretion, and inhibited macrophage TLR4 receptor complex expression. In both human and mouse cells, CORM-2 inhibited endogenous and exogenous ligand-dependent TLR4 activation, which indicates that CORM-2 could be therapeutic for both early and late stages of AP, which involve sterile- and endotoxin-mediated inflammation, respectively. Mice engrafted with TLR4-deficient hematopoietic cells were protected against caerulein-induced AP. In the absence of leukocyte TLR4 expression, CORM-2 did not confer additional protection, which indicates that CORM-2-dependent effects are mediated via suppression of macrophage TLR4 activation. We determined that CO was directly responsible for the protective effects of CORM-2 in AP, as inactive forms of CORM-2 were ineffective. Importantly, adoptive transfer of CORM-2-primed cells reduced AP. Such a therapeutic approach would translate the beneficial effects of CO-based therapies, avoiding CO- or CORM-mediated toxicities in AP and a wide range of diseases.
- The Journal of clinical investigation.J Clin Invest.2013 Dec 16. pii: 71362. doi: 10.1172/JCI71362. [Epub ahead of print]
- The protective role of hemeoxygenase-1 (HO-1) in various inflammatory conditions is mediated in part by its products, carbon monoxide (CO) and biliverdin. Here we investigated a therapeutic role for CO and CO-primed cells in acute pancreatitis (AP). In a mouse model of AP, treatment with CO-releasin
- PMID 24334457
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★リンクテーブル★
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- 関
- co-translate、cotranslate、cotranslation、cotranslational
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- 関
- co-translate、co-translational、cotranslation、cotranslational
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- 英
- cotranslation、cotranslate、co-translate、cotranslational、co-translational
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- 関
- co-translate、co-translational、cotranslate、cotranslation
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- 関
- co-translate、co-translational、cotranslate、cotranslational
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- 関
- translation、translational、translationally
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タラ
- 関
- Gadiformes
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コバルト cobalt
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