WordNet

set the speed, duration, or execution of; "we time the process to manufacture our cars very precisely"
a period of time considered as a resource under your control and sufficient to accomplish something; "take time to smell the roses"; "I didnt have time to finish"; "it took more than half my time"
a suitable moment; "it is time to go"
adjust so that a force is applied and an action occurs at the desired time; "The good player times his swing so as to hit the ball squarely"
an indefinite period (usually marked by specific attributes or activities); "he waited a long time"; "the time of year for planting"; "he was a great actor in his time"
regulate or set the time of; "time the clock"
the continuum of experience in which events pass from the future through the present to the past
an instance or single occasion for some event; "this time he succeeded"; "he called four times"; "he could do ten at a clip" (同)clip
a persons experience on a particular occasion; "he had a time holding back the tears"; "they had a good time together"
assign a time for an activity or event; "The candidate carefully timed his appearance at the disaster scene"
(physics) a rate of decrease in velocity
a decrease in rate of change; "the deceleration of the arms race" (同)slowing, retardation
the act of decelerating; decreasing the speed; "he initiated deceleration by braking"
shrub with terminal tufts of elongated leaves used locally for thatching and clothing; thick sweet roots are used as food; tropical southeastern Asia, Australia and Hawaii (同)Cordyline terminalis
the syllable naming the seventh (subtonic) note of any musical scale in solmization (同)te, si
the regulation of occurrence, pace, or coordination to achieve a desired effect (as in music, theater, athletics, mechanics)
the time when something happens
a more or less definite period of time now or previously present; "it was a sign of the times"

PrepTutorEJDIC

〈U〉《冠詞をつけずに》(空間に対しての)『時間』,時 / 〈U〉(時計で示される)『時刻』 / 〈U〉(ある方式で決められる)『時間』,標準時 / 〈C〉〈U〉(特定の)『時』,おり,ころ / 〈U〉《しばしば A ~》(ある長さの)『時間』,期間 / 〈U〉(要する)『時間』;暇 / 《しばしば複数形で》(歴史上の)『時代』 / 《複数形で》時勢,景気 / 《one's ~》(個人の)一生;若いころ;生涯の特定の時期 / 〈U〉《しばしば A ~》(ある経験をした)『時間』 / 〈C〉『…回』,度 / 〈C〉『…倍』 / …の時間を定める / (…に)…の調子を合わせる《+名+to+名》 / …の時間を計る
減速
シ(全音階の第7音)
時間の調節;時間を測定[記録]すること
…掛ける

UpToDate Contents

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1. ST上昇型心筋梗塞におけるプライマリ経皮的冠動脈インターベンション：転帰の決定因子 primary percutaneous coronary intervention in acute st elevation myocardial infarction determinants of outcome
2. 出血症状を有する小児に対するアプローチ approach to the child with bleeding symptoms
3. 左心室の評価における経食道心エコー transesophageal echocardiography in the evaluation of the left ventricle
4. 左室拡張機能の心エコー評価 echocardiographic evaluation of left ventricular diastolic function
5. 凝固検査の臨床使用 clinical use of coagulation tests

English Journal

Deficiency of cardiac Acyl-CoA synthetase-1 induces diastolic dysfunction, but pathologic hypertrophy is reversed by rapamycin.

Paul DS1, Grevengoed TJ2, Pascual F3, Ellis JM4, Willis MS5, Coleman RA6.Author information 1McAllister Heart Institute, University of NC at Chapel Hill, 27599, USA. Electronic address: david_paul@med.unc.edu.2Department of Nutrition, University of NC at Chapel Hill, 27599, USA. Electronic address: tgrevengoed@gmail.com.3Department of Nutrition, University of NC at Chapel Hill, 27599, USA. Electronic address: fpascual@live.unc.edu.4Department of Nutrition, University of NC at Chapel Hill, 27599, USA. Electronic address: jessie.ellis@gmail.com.5McAllister Heart Institute, University of NC at Chapel Hill, 27599, USA; Department of Pathology and Laboratory Medicine, University of NC at Chapel Hill, 27599, USA. Electronic address: monte_willis@med.unc.edu.6Department of Nutrition, University of NC at Chapel Hill, 27599, USA; McAllister Heart Institute, University of NC at Chapel Hill, 27599, USA. Electronic address: rcoleman@unc.edu.AbstractIn mice with temporally-induced cardiac-specific deficiency of acyl-CoA synthetase-1 (Acsl1(H-/-)), the heart is unable to oxidize long-chain fatty acids and relies primarily on glucose for energy. These metabolic changes result in the development of both a spontaneous cardiac hypertrophy and increased phosphorylated S6 kinase (S6K), a substrate of the mechanistic target of rapamycin, mTOR. Doppler echocardiography revealed evidence of significant diastolic dysfunction, indicated by a reduced E/A ratio and increased mean performance index, although the deceleration time and the expression of sarco/endoplasmic reticulum calcium ATPase and phospholamban showed no difference between genotypes. To determine the role of mTOR in the development of cardiac hypertrophy, we treated Acsl1(H-/-) mice with rapamycin. Six to eight week old Acsl1(H-/-) mice and their littermate controls were given i.p. tamoxifen to eliminate cardiac Acsl1, then concomitantly treated for 10weeks with i.p. rapamycin or vehicle alone. Rapamycin completely blocked the enhanced ventricular S6K phosphorylation and cardiac hypertrophy and attenuated the expression of hypertrophy-associated fetal genes, including α-skeletal actin and B-type natriuretic peptide. mTOR activation of the related Acsl3 gene, usually associated with pathologic hypertrophy, was also attenuated in the Acsl1(H-/-) hearts, indicating that alternative pathways of fatty acid activation did not compensate for the loss of Acsl1. Compared to controls, Acsl1(H-/-) hearts exhibited an 8-fold higher uptake of 2-deoxy[1-(14)C]glucose and a 35% lower uptake of the fatty acid analog 2-bromo[1-(14)C]palmitate. These data indicate that Acsl1-deficiency causes diastolic dysfunction and that mTOR activation is linked to the development of cardiac hypertrophy in Acsl1(H-/-) mice.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Jun;1841(6):880-7. doi: 10.1016/j.bbalip.2014.03.001. Epub 2014 Mar 12.
In mice with temporally-induced cardiac-specific deficiency of acyl-CoA synthetase-1 (Acsl1(H-/-)), the heart is unable to oxidize long-chain fatty acids and relies primarily on glucose for energy. These metabolic changes result in the development of both a spontaneous cardiac hypertrophy and increa
PMID 24631848

Inconvenient truth: Cancer biomarker development by using proteomics.

Kondo T.Author information Division of Pharmacoproteomics, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. Electronic address: takondo@ncc.go.jp.AbstractA biomarker is a crucial tool for measuring the progress of disease and the effects of treatment for better clinical outcomes in cancer patients. Diagnostic, predictive, and prognostic biomarkers are required in various clinical settings. The proteome, a functional translation of the genome, is considered a rich source of biomarkers; therefore, sizable time and funding have been spent in proteomics to develop biomarkers. Although significant progress has been made in technologies toward comprehensive protein expression profiling, and many biomarker candidates published, none of the reported biomarkers have proven to be beneficial for cancer patients. The present deceleration in biomarker research can be attributed to technical limitations. Additional efforts are required to further technical progress; however, there are many examples demonstrating that problems in biomarker research are not so much with the technology but in the study design. In the study of biomarkers for early diagnosis, candidates are screened and validated by comparing cases and controls of similar sample size, and the low prevalence of disease is often ignored. Although it is reasonable to take advantage of multiple rather than single biomarkers when studying diverse disease mechanisms, the annotation of individual components of reported multiple biomarkers does not often explain the variety of molecular events underlying the clinical observations. In tissue biomarker studies, the heterogeneity of disease tissues and pathological observations are often not considered, and tissues are homogenized as a whole for protein extraction. In addition to the challenge of technical limitations, the fundamental aspects of biomarker development in a disease study need to be addressed. This article is part of a Special Issue entitled: Biomarkers: A Proteomic Challenge.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 May;1844(5):861-865. doi: 10.1016/j.bbapap.2013.07.009. Epub 2013 Jul 27.
A biomarker is a crucial tool for measuring the progress of disease and the effects of treatment for better clinical outcomes in cancer patients. Diagnostic, predictive, and prognostic biomarkers are required in various clinical settings. The proteome, a functional translation of the genome, is cons
PMID 23896458

Tumor necrosis factor alpha antagonists in the treatment of axial spondyloarthritis.

Braun J1, Baraliakos X, Heldmann F, Kiltz U.Author information 1Rheumazentrum Ruhrgebiet , Landgrafenstr. 15, 44652 Herne , Germany +49 2325 592 131 ; + 49 2325 592 136 ; braun@elisabethgruppe.de.AbstractIntroduction: The introduction of therapy with tumor necrosis factor antagonists (aTNF) was a cornerstone of treatment modalities in patients with ankylosing spondylitis (AS). After > 10 years of using aTNF, the introduction of aTNF therapy was a major step forward in the medical management of patients with spondyloarthritis (SpA), but there are still a number of scientific questions that have not been resolved. Areas covered: This review includes both subtypes of axial spondyloarthritis (axSpA), non-radiographic axial SpA (nr-axSpA), and AS. It covers all five aTNF adalimumab, certolizumab, etanercept, golimumab, and infliximab, which are approved for patients with active AS. Expert opinion: aTNF are efficacious and effective in reducing signs and symptoms of patients with axSpA. While aTNF reduce spinal inflammation, the effects on new bone formation are less clear. There may be a deceleration of radiographic progression in 4 years. The development of fatty lesions in vertebral edges seems to be relevant for that - especially when inflammation also persists. Reduction of aTNF doses seems to be possible in selected patients over time. In case of failure, switching to another aTNF works in the majority of cases. Long-term data suggest a favorable safety profile of aTNF.
Expert opinion on investigational drugs.Expert Opin Investig Drugs.2014 May;23(5):647-59. doi: 10.1517/13543784.2014.899351. Epub 2014 Mar 22.
Introduction: The introduction of therapy with tumor necrosis factor antagonists (aTNF) was a cornerstone of treatment modalities in patients with ankylosing spondylitis (AS). After > 10 years of using aTNF, the introduction of aTNF therapy was a major step forward in the medical management of pa
PMID 24654630

Japanese Journal

Acceleration signal in GRACE time-variable gravity in relation to interannual hydrological changes

Ogawa Ryoko,Chao Benjamin F.,Heki Kosuke
Geophysical Journal International 184(2), 673-679, 2011-02
… We solve for such signals in the form of not only linear trend but also quadratic term (acceleration/deceleration) of mass variations globally at a spatial resolution of 500 km. … Comparison studies of geographical patterns of the quadratic (representing acceleration/ deceleration) terms show interesting agreement of the hydrological model GLDAS with GRACE data in many major areas, providing independent assessment as to the quality and validity of the hydrological models for interannual applications. …
NAID 120002725566