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( Sook Jin Seong ),( Young Ran Yoon ),( Mi Sun Lim ) 영남대학교 약품개발연구소 2016 영남대학교 약품개발연구소 연구업적집 Vol.26 No.-
Te1misartan is an angiotensin II receptor antagonist and chlorthalidone is a thiazide-like diuret-ics. In this study, we report serious adverse events (SAEs) during clinical trial for pharmacokinetic interaction between telmisartan and chlorthalidone in healthy Korean subjects. Two separate, ran-domized, multiple-dose, two-period, one-sequence studies were conducted at Kyungpook National University Hospital. In part A, 43 volunteers received telmisartan for 7 days, and then chlorthali-done for 14 days (days 8-21). Telrnisartan was co-administered during day 15-21 to evaluate the effects of chlorthalidone on the pharmacokinetics of telmisartan at steady state. A healthy 36-year-old male in part A was referred to the emergency room due to severe nausea and vomiting developed about 3 h after administration of chlorthalidone on day 9. Hypokalemia and QT prolongation were observed during his initial laboratory examination and electrocardiogram (ECG) monitoring in the emergency wilt. Nausea and vomiting improved after conservative management with hos-pitalization for 9 days. We consider that the episodes of excessive nausea and vomiting resulted in hypokalemic state which was potentiated by chlorthalidone. And the hypokalemic state caused the lengthening of the QT interval on ECG.
Lim, Sang Woo,Kim, Hye Ran,Kim, Hwan Young,Huh, Jung Wook,Kim, Young Jin,Shin, Jong Hee,Suh, Soon Pal,Ryang, Dong Wook,Kim, Hyeong Rok,Shin, Myung Geun Wiley Subscription Services, Inc., A Wiley Company 2012 International journal of cancer: Journal internati Vol.131 No.6
<P><B>Abstract</B></P><P>Most studies of mitochondrial DNA (mtDNA) mutations in colorectal cancer have used case‐control and case‐database comparisons without searching their clinical relevance. This study was to investigate colorectal cancer tissue‐specific mtDNA mutations from 54 matched colorectal cancer and adjacent normal tissues and then to evaluate their clinical values. This study focused on analyzing control region including mtDNA minisatellites and coding regions. Cancer tissue‐specific mtDNA mutations were found in over half of the patients (59%). The patterns of mtDNA mutations were substitution only (13%), mtDNA minisatellite instability (mtMSI) (20%) and both mutations combined (26%). mtMSI in colorectal cancer was mainly occurred in the 303 polyC (35%) and 16184 poly C (19%) minisatellite. mtDNA copy number and hydrogen peroxide level were significantly increased in colorectal cancer tissue. The amount of mtDNA large deletions was significantly decreased in colorectal cancer tissue compared with those from matched normal mucosa (<I>p</I> = 0.03). The activity of the mitochondrial respiratory chain enzyme complexes I, II and III in colorectal cancer tissues was impaired. mtDNA haplogroup B4 might be closely associated with colorectal cancer risk. The patient group harboring cancer tissue‐specific mtDNA mutations showed larger tumor sizes (<I>p</I> = 0.005) and more advanced TNM stages (<I>p</I> = 0.002). Thus, mtDNA mutations in colorectal cancer might be implicated in risk factors that induce poor outcomes and tumorigenesis.</P>
Lim, Ae Ran,Jeong, Se-Young IOP Pub 2006 Journal of Physics, Condensed Matter Vol.18 No.29
<P><I>T</I><SUB>1</SUB>, <I>T</I><SUB>1ρ</SUB> and <I>T</I><SUB>2</SUB> for the <SUP>1</SUP>H and <SUP>2</SUP>H nuclei in (NH<SUB>4</SUB>)<SUB>3</SUB>H(SO<SUB>4</SUB>)<SUB>2</SUB> and (ND<SUB>4</SUB>)<SUB>3</SUB>D(SO<SUB>4</SUB>)<SUB>2</SUB> single crystals grown using the slow evaporation method were measured for phases I, II, III, IV and V. The <SUP>1</SUP>H <I>T</I><SUB>1</SUB>, <I>T</I><SUB>1ρ</SUB>, and <I>T</I><SUB>2</SUB> values were found to exhibit different trends in phases II and III: <I>T</I><SUB>1</SUB>, <I>T</I><SUB>1ρ</SUB> and <I>T</I><SUB>2</SUB> for <SUP>1</SUP>H do not change significantly near the phase transition at 265 K, whereas near 413 K they change discontinuously. We conclude that the NH<SUB>4</SUB><SUP>+</SUP> and H(SO<SUB>4</SUB>)<SUB>2</SUB><SUP>−</SUP> ions do not play an important role in the III–II phase transition, but do play important roles in the II–I phase transition. The liquid-like nature of the <SUP>1</SUP>H <I>T</I><SUB>1ρ</SUB> and <I>T</I><SUB>2</SUB> above 413 K is indicative of the destruction and reconstruction of hydrogen bonds. Moreover, the phase transitions of the (NH<SUB>4</SUB>)<SUB>3</SUB>H(SO<SUB>4</SUB>)<SUB>2</SUB> crystal are accompanied by changes in the molecular motion of the (NH<SUB>4</SUB>)<SUP>+</SUP> ions. The variations with temperature of the <SUP>2</SUP>H <I>T</I><SUB>1</SUB> and <I>T</I><SUB>2</SUB> of (ND<SUB>4</SUB>)<SUB>3</SUB>D(SO<SUB>4</SUB>)<SUB>2</SUB> crystals are not similar to those observed for the <SUP>1</SUP>H <I>T</I><SUB>1</SUB> and <I>T</I><SUB>2</SUB>. Our comparison of the results for (NH<SUB>4</SUB>)<SUB>3</SUB>H(SO<SUB>4</SUB>)<SUB>2</SUB> and (ND<SUB>4</SUB>)<SUB>3</SUB>D(SO<SUB>4</SUB>)<SUB>2</SUB> crystals indicates the following: the <SUP>1</SUP>H <I>T</I><SUB>1ρ</SUB> and <I>T</I><SUB>2</SUB> of the (NH<SUB>4</SUB>)<SUP>+</SUP> and H(SO<SUB>4</SUB>)<SUB>2</SUB><SUP>−</SUP> ions above <I>T</I><SUB>C1</SUB> are characteristic of fast, liquid-like motion, which is not the case for (ND<SUB>4</SUB>)<SUB>3</SUB>D(SO<SUB>4</SUB>)<SUB>2</SUB>; and the <SUP>2</SUP>H <I>T</I><SUB>1</SUB> of D(SO<SUB>4</SUB>)<SUB>2</SUB><SUP>−</SUP> in (ND<SUB>4</SUB>)<SUB>3</SUB>D(SO<SUB>4</SUB>)<SUB>2</SUB> is longer than the <SUP>2</SUP>H <I>T</I><SUB>1</SUB> of (ND<SUB>4</SUB>)<SUP>+</SUP> in contrast to the results for (NH<SUB>4</SUB>)<SUB>3</SUB>H(SO<SUB>4</SUB>)<SUB>2</SUB> crystals.</P>