http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
개별검색 DB통합검색이 안되는 DB는 DB아이콘을 클릭하여 이용하실 수 있습니다.
통계정보 및 조사
예술 / 패션
<해외전자자료 이용권한 안내>
- 이용 대상 : RISS의 모든 해외전자자료는 교수, 강사, 대학(원)생, 연구원, 대학직원에 한하여(로그인 필수) 이용 가능
- 구독대학 소속 이용자: RISS 해외전자자료 통합검색 및 등록된 대학IP 대역 내에서 24시간 무료 이용
- 미구독대학 소속 이용자: RISS 해외전자자료 통합검색을 통한 오후 4시~익일 오전 9시 무료 이용
※ 단, EBSCO ASC/BSC(오후 5시~익일 오전 9시 무료 이용)
Chang, Sung-A,Kim, Yong-Jin,Lee, Hye-Won,Kim, Dae-Hee,Kim, Hyung-Kwan,Chang, Hyuk-Jae,Sohn, Dae-Won,Oh, Byung-Hee,Park, Young-Bae Ovid Technologies Wolters Kluwer -American Heart A 2009 Hypertension Vol.54 No.3
<P>Hypertensive patients with left ventricular hypertrophy (LVH) are the most common high-risk group to develop heart failure with preserved ejection fraction. Recent reports have noted the favorable effect of statins on LVH. We evaluated the effect of rosuvastatin on cardiac remodeling, function, and progression to heart failure in a hypertensive rat model with established LVH. Dahl salt-sensitive rats were fed a high-salt diet until 13 weeks of age. After LVH was confirmed by echocardiography, rats were randomly assigned to control and statin treatment (n=18 each group). The statin-treated group was treated with rosuvastatin until 21 weeks of ages. Serial echocardiography, blood pressure monitoring, and miniaturized conductance catheter hemodynamic monitoring were performed at 21 weeks. Echocardiographic parameters were not significantly different between the groups. On hemodynamic monitoring, systolic performance parameters were similar between the groups, whereas end diastolic pressure-volume relationships were lower in the statin-treated group (0.014+/-0.008 versus 0.008+/-0.004 mm Hg/muL, P<0.05), suggesting improvement in myocardial stiffness. Pathological analysis showed attenuation of perivascular and interstitial fibrosis in the statin-treated group (P<0.02). Rosuvastatin therapy did not alleviate LVH in hypertensive rats with established LVH, but it attenuated myocardial fibrosis and LV stiffness. It seems that rosuvastatin has limited therapeutic value when used to prevent progression from LVH to heart failure in hypertensive hearts.</P>
Chiang, Chien-Sung,Huang, Ching-Hui,Chieng, Hockling,Chang, Ya-Ting,Chang, Dory,Chen, Ji-Jr,Chen, Yong-Cyuan,Chen, Yen-Hui,Shin, Hee-Sup,Campbell, Kevin P.,Chen, Chien-Chang Ovid Technologies Wolters Kluwer -American Heart A 2009 Circulation research Vol.104 No.4
<P>Voltage-gated T-type Ca(2+) channels (T-channels) are normally expressed during embryonic development in ventricular myocytes but are undetectable in adult ventricular myocytes. Interestingly, T-channels are reexpressed in hypertrophied or failing hearts. It is unclear whether T-channels play a role in the pathogenesis of cardiomyopathy and what the mechanism might be. Here we show that the alpha(1H) voltage-gated T-type Ca(2+) channel (Ca(v)3.2) is involved in the pathogenesis of cardiac hypertrophy via the activation of calcineurin/nuclear factor of activated T cells (NFAT) pathway. Specifically, pressure overload-induced hypertrophy was severely suppressed in mice deficient for Ca(v)3.2 (Ca(v)3.2(-/-)) but not in mice deficient for Ca(v)3.1 (Ca(v)3.1(-/-)). Angiotensin II-induced cardiac hypertrophy was also suppressed in Ca(v)3.2(-/-) mice. Consistent with these findings, cultured neonatal myocytes isolated from Ca(v)3.2(-/-) mice fail to respond hypertrophic stimulation by treatment with angiotensin II. Together, these results demonstrate the importance of Ca(v)3.2 in the development of cardiac hypertrophy both in vitro and in vivo. To test whether Ca(v)3.2 mediates the hypertrophic response through the calcineurin/NFAT pathway, we generated Ca(v)3.2(-/-), NFAT-luciferase reporter mice and showed that NFAT-luciferase reporter activity failed to increase after pressure overload in the Ca(v)3.2(-/-)/NFAT-Luc mice. Our results provide strong genetic evidence that Ca(v)3.2 indeed plays a pivotal role in the induction of calcineurin/NFAT hypertrophic signaling and is crucial for the activation of pathological cardiac hypertrophy.</P>
<P>The endoplasmic reticulum (ER) is a multifunctional intracellular organelle supporting many processes required by virtually every mammalian cell, including cardiomyocytes. It performs diverse functions, including protein synthesis, translocation across the membrane, integration into the membrane, folding, posttranslational modification including N-linked glycosylation, and synthesis of phospholipids and steroids on the cytoplasmic side of the ER membrane, and regulation of Ca(2+) homeostasis. Perturbation of ER-associated functions results in ER stress via the activation of complex cytoplasmic and nuclear signaling pathways, collectively termed the unfolded protein response (UPR) (also known as misfolded protein response), leading to upregulation of expression of ER resident chaperones, inhibition of protein synthesis and activation of protein degradation. The UPR has been associated with numerous human pathologies, and it may play an important role in the pathophysiology of the heart. ER stress responses, ER Ca(2+) buffering, and protein and lipid turnover impact many cardiac functions, including energy metabolism, cardiogenesis, ischemic/reperfusion, cardiomyopathies, and heart failure. ER proteins and ER stress-associated pathways may play a role in the development of novel UPR-targeted therapies for cardiovascular diseases.</P>
Chung, Jong-Won,Kim, Beom Joon,Han, Moon-Ku,Ko, Youngchai,Lee, SooJoo,Kang, Kyusik,Park, Jong-Moo,Park, Sang-Soon,Park, Tai Hwan,Cho, Yong-Jin,Hong, Keun-Sik,Lee, Kyung Bok,Lee, Jun,Ryu, Wi-Sun,Kim, D Ovid Technologies Wolters Kluwer -American Heart A 2016 Stroke Vol.47 No.6
<P>Background and Purpose-Since its introduction, controversy has existed about the administration of intravenous heparin for the treatment of acute ischemic stroke. We studied trends in the intravenous heparin use during a 6-year time period and the potential influence of clinical guidelines in national language on intravenous heparin administration in Korea. Methods-On the basis of a prospective nationwide multicenter stroke registry, we collected data on patients with acute ischemic stroke who arrived within 7 days of symptom onset during the time period 2008 to 2013. We studied patient demographics, prestroke medical history, stroke characteristics, and stroke treatment. Data from a total of 23 425 patients from 12 university hospitals or regional stroke centers were analyzed. Results-The administration of intravenous heparin steadily decreased throughout the study period: 9.7% in 2008, 10.9% in 2009, 9.4% in 2010, 6.0% in 2011, 4.7% in 2012, and 4.3% in 2013 (P for trend < 0.001). The reduced intravenous heparin use was associated with moderate stroke severity, atrial fibrillation, and stroke of cardioembolic, other-, and undetermined etiology. In a multivariable logistic model, increase of 1 calendar year (odds ratio, 0.89; 95% confidence interval, 0.84-0.95; P < 0.001) and release of clinical practice guidelines in Korean (odd ratio, 0.74; 95% confidence interval, 0.59-0.91; P < 0.01) were independent factors associated with reduction in the frequency of intravenous heparin use. Conclusions-Use of intravenous heparin for acute ischemic stroke treatment has decreased in Korea, and this change may be attributable to the spread and successful implementation of regional clinical practice guidelines.</P>
Lee, Chan Joo,Ryu, Jiin,Kim, Hyeon-Chang,Ryu, Dong-Ryeol,Ihm, Sang-Hyun,Kim, Yong-Jin,Shin, Jin-Ho,Pyun, Wook Bum,Kang, Hyoung-Soo,Park, Jong-Heon,Hwang, Jinseub,Park, Sungha Ovid Technologies Wolters Kluwer -American Heart A 2018 Hypertension Vol.72 No.6
Yoo, Joonsang,Baek, Jang-Hyun,Park, Hyungjong,Song, Dongbeom,Kim, Kyoungsub,Hwang, In Gun,Kim, Young Dae,Kim, Seo Hyun,Lee, Hye Sun,Ahn, Seong Hwan,Cho, Han-Jin,Kim, Gyu Sik,Kim, Jinkwon,Lee, Kyung-Yu Ovid Technologies Wolters Kluwer -American Heart A 2018 Stroke Vol.49 No.9
Kim, Hyo Jung,Kim, Min Young,Jin, Hana,Kim, Hyun Joon,Kang, Sang Soo,Kim, Hye Jung,Lee, Jae Heun,Chang, Ki Churl,Hwang, Jin-Yong,Yabe-Nishimura, Chihiro,Kim, Jin-Hoi,Seo, Han Geuk Ovid Technologies Wolters Kluwer -American Heart A 2009 Circulation research Vol.105 No.1
<P>Homeostasis of the extracellular matrix and apoptosis of vascular smooth muscle cells (VSMCs) are key components in the regulation of the stability of atherosclerotic plaques. Here, we demonstrate that peroxisome proliferator-activated receptor (PPAR)delta regulates extracellular matrix synthesis and degradation through transforming growth factor-beta1 and its effector, Smad3. Activation of PPARdelta strongly amplified the expression of types I and III collagen, fibronectin, elastin, and TIMP-3 (tissue inhibitor of metalloproteinases 3), but not of TIMP-1, matrix metalloproteinase-2 or -9. The effect of PPARdelta on the expression of type III collagen was dually regulated by the direct binding of PPARdelta and Smad3 to a direct repeat-1 site and a Smad-binding element, respectively, in the type III collagen gene promoter. The activation of PPARdelta attenuated apoptotic cell death in VSMCs induced by oxidized low-density lipoprotein, and similar antiapoptotic effects were observed on treatment of cells with exogenous type I and/or III collagen. Administration of a PPARdelta ligand GW501516 to mice also suppressed elastase-induced cell death of aortic VSMCs. These results suggest that PPARdelta-induced upregulation of extracellular matrix proteins exerts an antiapoptotic effect, thereby maintaining the stability of atherosclerotic plaques. Specific ligands of PPARdelta may aid in the therapeutic intervention of atherosclerosis by improving plaque stability and patient prognosis.</P>
<P>Conclusions-This study showed that calcified atherosclerosis in the MCA was less frequently symptomatic.</P>
Jeong, Han-Gil,Cha, Bong Geun,Kang, Dong-Wan,Kim, Do Yeon,Ki, Seul Ki,Kim, Song I.,Han, Ju hee,Yang, Wookjin,Kim, Chi Kyung,Kim, Jaeyun,Lee, Seung-Hoon Ovid Technologies Wolters Kluwer -American Heart A 2018 Stroke Vol.49 No.12