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        The Effectiveness of Green Tea or Green Tea Extract on Insulin Resistance and Glycemic Control in Type 2 Diabetes Mellitus: A Meta-Analysis

        Jinyue Yu,Peige Song,Rachel Perry,Chris Penfold,Ashley R. Cooper 대한당뇨병학회 2017 Diabetes and Metabolism Journal Vol.41 No.4

        Green tea or green tea extract (GT/GTE) has been demonstrated to reduce insulin resistance and improve glycemic control. However, evidence for this health beneficial effect is inconsistent. This systematic review evaluated the effect of GT/GTE on insulin resistance and glycemic control in people with pre-diabetes/type 2 diabetes mellitus (T2DM). Ovid MEDLINE, Embase, AMED, Web of Science, and the Cochrane Library were searched up to April 2017 for randomised controlled trials of participants with pre-diabetes or T2DM, where the intervention was GT/GTE. Meta-analysis was performed to assess the standardised mean difference (SMD) in biomarkers of insulin resistance and glycemic control between GT/GTE and placebo groups. Six studies (n=382) were pooled into random-effects meta-analysis. Overall, no differences were found between GT/GTE and the placebo for glycosylated hemoglobin (HbA1c: SMD, –0.32; 95% confidence interval [CI], –0.86 to 0.23), homeostatic model assessment for insulin resistance (HOMA-IR: SMD, 0.10; 95% CI, –0.17 to 0.38), fasting insulin (SMD, –0.25; 95% CI, –0.64 to 0.15), and fasting glucose (SMD, –0.10; 95% CI, –0.50 to 0.30). No evidence support the consumption of GT/GTE could reduce the levels of HbA1c, HOMA-IR, fasting insulin, or fasting glucose in people with pre-diabetes/T2DM. However, the studies included were small and of varying quality.

      • Comparative transcriptome analysis in Arabidopsis <i>ein2</i> / <i>ore3</i> and <i>ahk3</i> / <i>ore12</i> mutants during dark-induced leaf senescence

        Kim, Jeongsik,Park, Su Jin,Lee, Il Hwan,Chu, Hyosub,Penfold, Christopher A,Kim, Jin Hee,Buchanan-Wollaston, Vicky,Nam, Hong Gil,Woo, Hye Ryun,Lim, Pyung Ok Oxford University Press 2018 Journal of experimental botany Vol.69 No.12

        <▼1><P>Ethylene and cytokinin play antagonistic roles in the regulation of leaf senescence via EIN2/ORE3-dependent transcriptional regulation of stress responses and AHK3/ORE12-dependent transcriptional maintenance of the translational machinery, respectively.</P></▼1><▼2><P><B>Abstract</B></P><P>Leaf senescence involves degenerative but active biological processes that require balanced regulation of pro- and anti-senescing activities. Ethylene and cytokinin are major antagonistic regulatory hormones that control the timing and progression rate of leaf senescence. To identify the roles of these hormones in the regulation of leaf senescence in Arabidopsis, global gene expression profiles in detached leaves of the wild type, an ethylene-insensitive mutant (<I>ein2</I>/<I>ore3</I>), and a constitutive cytokinin response mutant (<I>ahk3/ore12</I>) were investigated during dark-induced leaf senescence. Comparative transcriptome analyses revealed that genes involved in oxidative or salt stress response were preferentially altered in the <I>ein2</I>/<I>ore3</I> mutant, whereas genes involved in ribosome biogenesis were affected in the <I>ahk3/ore12</I> mutant during dark-induced leaf senescence. Similar results were also obtained for developmental senescence. Through extensive molecular and physiological analyses in <I>ein2</I>/<I>ore3</I> and <I>ahk3/ore12</I> during dark-induced leaf senescence, together with responses when treated with cytokinin and ethylene inhibitor, we conclude that ethylene acts as a senescence-promoting factor via the transcriptional regulation of stress-related responses, whereas cytokinin acts as an anti-senescing agent by maintaining cellular activities and preserving the translational machinery. These findings provide new insights into how plants utilize two antagonistic hormones, ethylene and cytokinin, to regulate the molecular programming of leaf senescence.</P></▼2>

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        Identifying the major intermediate species by combining time-resolved X-ray solution scattering and X-ray absorption spectroscopy

        Kim, Kyung Hwan,Kim, Jeongho,Oang, Key Young,Lee, Jae Hyuk,Grolimund, Daniel,Milne, Christopher J.,Penfold, Thomas J.,Johnson, Steven L.,Galler, Andreas,Kim, Tae Wu,Kim, Jong Goo,Suh, Deokbeom,Moon, J The Royal Society of Chemistry 2015 Physical chemistry chemical physics Vol.17 No.36

        <P>Identifying the intermediate species along a reaction pathway is a first step towards a complete understanding of the reaction mechanism, but often this task is not trivial. There has been a strong on-going debate: which of the three intermediates, the CHI<SUB>2</SUB> radical, the CHI<SUB>2</SUB>–I isomer, and the CHI<SUB>2</SUB><SUP>+</SUP> ion, is the dominant intermediate species formed in the photolysis of iodoform (CHI<SUB>3</SUB>)? Herein, by combining time-resolved X-ray liquidography (TRXL) and time-resolved X-ray absorption spectroscopy (TR-XAS), we present strong evidence that the CHI<SUB>2</SUB> radical is dominantly formed from the photolysis of CHI<SUB>3</SUB> in methanol at 267 nm within the available time resolution of the techniques (∼20 ps for TRXL and ∼100 ps for TR-XAS). The TRXL measurement, conducted using the time-slicing scheme, detected no CHI<SUB>2</SUB>–I isomer within our signal-to-noise ratio, indicating that, if formed, the CHI<SUB>2</SUB>–I isomer must be a minor intermediate. The TR-XAS transient spectra measured at the iodine L<SUB>1</SUB> and L<SUB>3</SUB> edges support the same conclusion. The present work demonstrates that the application of these two complementary time-resolved X-ray methods to the same system can provide a detailed understanding of the reaction mechanism.</P> <P>Graphic Abstract</P><P>We identify a major transient species formed in the photolysis of CHI<SUB>3</SUB> by combining time-resolved X-ray liquidography (TRXL) and time-resolved X-ray absorption spectroscopy (TR-XAS). <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c5cp03686k'> </P>

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