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Articles by D. H Shin
Total Records ( 2 ) for D. H Shin
  H. E Park , S. A Chang , H. K Kim , D. H Shin , J. H Kim , M. K Seo , Y. J Kim , G. Y Cho , D. W Sohn , B. H Oh and Y. B. Park
 

Background— The effects of left ventricular (LV) loading conditions on LV dyssynchrony have not been elucidated. We modified LV loading conditions to reveal their effects on echocardiography-derived LV dyssynchrony index (LVdys) in patients with documented nonischemic dilated cardiomyopathy.

Methods and Results— Thirty-seven patients were consecutively enrolled. After baseline measurements, pneumatic compression of the lower extremities (Pcom) was used to increase LV afterload. Subsequently, sublingual nitroglycerin (SL-NG) was administered to modify preload. Conventional echocardiographic parameters, LVdys (by speckle-tracking radial strain analysis) and LV end-systolic wall stress (LV-ESWS), were calculated under each condition. LVdys-6 (defined as the maximal difference in time-to-peak radial strain between 6 myocardial segments) and LV-ESWS increased under Pcom (for LVdys-6, 159±117 at baseline versus 239±140 ms under Pcom, P<0.05; for LV-ESWS, 191±63 versus 228±80 g/m2, P<0.05) After SL-NG application, both parameters decreased significantly (for LVdys-6, 239±140 under Pcom versus 147±103 ms after SL-NG, P<0.05; for LV-ESWS, 228±80 under Pcom versus 189±67 g/m2 after SL-NG, P<0.05). When the presence of LV dyssynchrony was defined as the absolute difference in time-to-peak radial strain between the anteroseptal and posterior segments (LVdys-2), the results were unchanged. Using 130 ms as a cutoff value, the proportion of patients with LV dyssynchrony changed significantly (29.7% at baseline, 45.9% under Pcom, and 35.1% after SL-NG). When the presence of LV dyssynchrony was defined as standard deviation of the time to peak radial strain for 6 segments (LVdys-SD), the results were same. LVdys and LV-ESWS showed a modest but significant association with each other (r=0.47, P<0.001 for LVdys-6; r=0.41, P<0.001 for LVdys-2; r=0.46, P<0.001 for LVdys-SD).

Conclusions— To the best of our knowledge, the present study provides the first evidence of a significant association between LVdys and LV loading status, reflective of a dynamic nature of LVdys. Accordingly, LV loading conditions should be taken into account when echocardiographic LVdys is used for clinical decision-making of selecting candidates for cardiac resynchronization therapy or when it is used as a surrogate marker of prognosis.

  H Zheng , J. H Nam , B Pang , D. H Shin , J. S Kim , Y. S Chun , J. W Park , H Bang , W. K Kim , Y. E Earm and S. J. Kim
 

Mouse B cells and their cell line (WEHI-231) express large-conductance background K+ channels (LKbg) that are activated by arachidonic acids, characteristics similar to TREK-2. However, there is no evidence to identify the molecular nature of LKbg; some properties of LKbg were partly different from the reported results of TREK type channels. In this study, we compared the properties of cloned TREK-2 and LKbg in terms of their sensitivities to ATP, phosphatidylinositol 4,5-bisphosphate (PIP2), intracellular pH (pHi), and membrane stretch. Similar to the previous findings of LKbg, TREK-2 showed spontaneous activation after membrane excision (i-o patch) and were inhibited by MgATP or by PIP2. The inhibition by MgATP was prevented by wortmannin, suggesting membrane-delimited regulation of TREKs by phosphoinositide (PI) kinase. The same was observed with the property of LKbg; the activation of TREK-2 by membrane stretch was suppressed by U73122 (PLC inhibitor). As with the known properties of TREK-2, LKbg were activated by acidic pHi and inhibited by PKC activator. Finally, we confirmed the expression of TREK-2 in WEHI-231 by using RT-PCR and immunoblot analyses. The amplitude of background K+ current and the TREK-2 expression in WEHI-231 were commonly decreased by genetic knockdown of TREK-2 using small interfering RNA. The downregulation of TREK-2 attenuated Ca2+-influx induced by arachidonic acid in WEHI-231. As a whole, these results strongly indicate that TREK-2 encodes LKbg in mouse B cells. We also newly suggest that the low activity of TREK-2 in intact cells is due to the inhibition by intrinsic PIP2.

 
 
 
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