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Articles by W. K Kim
Total Records ( 3 ) for W. K Kim
  D.Y Yoon , S.K Chang , C.S Choi , W. K Kim and J. H. Lee

BACKGROUND AND PURPOSE: The aim of our study was to assess the accuracy of multidetector row CT angiography (MDCTA) in the detection of the underlying vascular abnormalities causing spontaneous lobar intracerebral hemorrhage (ICH) compared with conventional digital subtraction angiography (DSA).

MATERIALS AND METHODS: Seventy-eight patients who underwent MDCTA with use of a 16-detector row scanner and DSA were prospectively included in this study. Each study was assessed by 2 independent blinded neuroradiologists; decisions were made in consensus. Findings on CT angiograms, including the original axial data, multiplanar reformations, and volume-rendered images with and without automated bone segmentation, were used to identify the underlying causes of ICH.

RESULTS: Twenty-two of the 78 patients (28.2%) exhibited angiographic abnormalities, including aneurysms of the proximal arteries (n = 9), arteriovenous malformations (n = 7), Moyamoya disease (n = 4), and aneurysms of the distal arteries (n = 2). MDCTA detected the underlying vascular abnormalities in 21 patients except 1 case of small arteriovenous malformation. Overall sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of MDCTA for detection of underlying vascular abnormalities were 95.5%, 100%, 100%, 98.2%, and 98.7%, respectively.

CONCLUSIONS: MDCTA is a highly accurate imaging technique in the diagnosis of underlying vascular abnormalities in patients with spontaneous lobar ICH.

  W. K Kim , V Meliton , K. W Park , C Hong , P Tontonoz , P Niewiadomski , J. A Waschek , S Tetradis and F. Parhami

Hedgehog (Hh) signaling is indispensable in embryonic development, and its dysregulated activity results in severe developmental disorders as shown by genetic models of naturally occurring mutations in animal and human pathologies. Hh signaling also functions in postembryonic development and adult tissue homeostasis, and its aberrant activity causes various human cancers. Better understanding of molecular regulators of Hh signaling is of fundamental importance in finding new strategies for pathway modulation. Here, we identify liver X receptors (LXRs), members of the nuclear hormone receptor family, as previously unrecognized negative regulators of Hh signaling. Activation of LXR by specific pharmacological ligands, TO901317 and GW3965, inhibited the responses of pluripotent bone marrow stromal cells and calvaria organ cultures to sonic Hh, resulting in the inhibition of expression of Hh-target genes, Gli1 and Patched1, and Gli-dependent transcriptional activity. Moreover, LXR ligands inhibited sonic Hh-induced differentiation of bone marrow stromal cells into osteoblasts. Elimination of LXRs by small interfering RNA inhibited ligand-induced inhibition of Hh target gene expression. Furthermore, LXR ligand did not inhibit Hh responsiveness in mouse embryonic fibroblasts that do not express LXRs, whereas introduction of LXR into these cells reestablished the inhibitory effects. Daily oral administration of TO901317 to mice after 3 d significantly inhibited baseline Hh target-gene expression in liver, lung, and spleen. Given the importance of modulating Hh signaling in various physiological and pathological settings, our findings suggest that pharmacological targeting of LXRs may be a novel strategy for Hh pathway modulation.

  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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