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Articles by K. H Chang
Total Records ( 4 ) for K. H Chang
  J. H Kim , K. H Chang , D.G Na , S. H Park , E Kim , D.H Han , H. M Kwon , C. H Sohn and Y.J. Yim
 

BACKGROUND AND PURPOSE: Meningeal inflammatory myofibroblastic tumor (IMT) has been rarely reported, and its prognosis is still unclear. Our purpose was to describe the imaging features of patients with meningeal IMT and their results on follow-up studies.

MATERIALS AND METHODS: Twenty-four MR images in 10 consecutive patients with pathologically proved meningeal IMTs were retrospectively evaluated, focusing on the lesion distribution, signal intensity (SI), and contrast-enhancement pattern with a review of the clinical records.

RESULTS: Eight patients with intracranial IMT showed localized (n = 4) or diffuse (n = 4) dural thickening, a single mass (n = 5) or 2 (n = 2) dural-based masses with surrounding edema, dural venous sinus thrombosis (n = 5), and leptomeningeal involvement (n = 5). Extracranial involvement of the mastoid (n = 2) and orbit (n = 2) was also associated. Each of the 2 patients with intraspinal IMT showed a dural-based mass and a segmental dural thickening, respectively. All of the thickened dura showed low SI on T2-weighted images, iso-SI on T1-weighted images, and diffuse contrast enhancement. Variable recurrences with dural-based masses, mastoid involvement, or nasolacrimal duct involvement were observed in all 4 patients with diffuse intracranial IMT, but not in the others.

CONCLUSIONS: Localized or diffuse dural thickening of T2 low SI and diffuse contrast enhancement combined with dural-based masses are a common MR imaging finding of meningeal intracranial IMT. Adjacent leptomeningeal involvement and dural venous sinus thrombosis are frequently associated. The diffuse type has a tendency toward recurrence.

  J. L Kielczewski , Y. P.R Jarajapu , E. L McFarland , J Cai , A Afzal , S Li Calzi , K. H Chang , T Lydic , L. C Shaw , J Busik , J Hughes , A. J Cardounel , K Wilson , T. J Lyons , M. E Boulton , R. N Mames , T Chan Ling and M. B. Grant
 

Rationale: Insulin-like growth factor binding protein (IGFBP)-3 modulates vascular development by regulating endothelial progenitor cell (EPC) behavior, specifically stimulating EPC cell migration. This study was undertaken to investigate the mechanism of IGFBP-3 effects on EPC function and how IGFBP-3 mediates cytoprotection following vascular injury.

Objective: To examine the mechanism of IGFBP-3–mediated repair following vascular injury.

Methods and Results: We used 2 complementary vascular injury models: laser occlusion of retinal vessels in adult green fluorescent protein (GFP) chimeric mice and oxygen-induced retinopathy in mouse pups. Intravitreal injection of IGFBP-3–expressing plasmid into lasered GFP chimeric mice stimulated homing of EPCs, whereas reversing ischemia induced increases in macrophage infiltration. IGFBP-3 also reduced the retinal ceramide/sphingomyelin ratio that was increased following laser injury. In the OIR model, IGFBP-3 prevented cell death of resident vascular endothelial cells and EPCs, while simultaneously increasing astrocytic ensheathment of vessels. For EPCs to orchestrate repair, these cells must migrate into ischemic tissue. This migratory ability is mediated, in part, by endogenous NO generation. Thus, we asked whether the migratory effects of IGFBP-3 were attributable to stimulation of NO generation. IGFBP-3 increased endothelial NO synthase expression in human EPCs leading to NO generation. IGFBP-3 exposure also led to the redistribution of vasodilator-stimulated phosphoprotein, an NO regulated protein critical for cell migration. IGFBP-3–mediated NO generation required high-density lipoprotein receptor activation and stimulation of phosphatidylinositol 3-kinase/Akt pathway.

Conclusion: These studies support consideration of IGFBP-3 as a novel agent to restore the function of injured vasculature and restore NO generation.

  M Lee , J. L Saver , W. H Huang , J Chow , K. H Chang and B. Ovbiagele
  Background—

Chronic kidney disease is a growing public health problem that carries substantial risk for cardiovascular disease (CVD). Single studies have differentially examined the role of cystatin C, a novel renal index, with varying cut-point use. We undertook a meta-analysis of prospective studies to properly assess the link between cystatin C (dichotomized and continuous) versus CVD.

Methods and Results—

Systematic literature search for studies reporting a multivariate-adjusted estimate, represented as relative risk (RR) with 95% confidence interval (CI), of the association between cystatin C and subsequent risk of (1) any CVD event and (2) specific CVD events. Data were collated from 14 studies, with 13 high cardiovascular risk population cohorts and 1 general population cohort, involving 22 509 subjects with 2321 CVD events, 741 coronary heart disease events, and 828 stroke events. Highest cystatin C category versus lowest was associated with greater risk of CVD (RR, 2.62; 95% CI, 2.05 to 3.37, P<0.001), coronary heart disease (RR, 1.72; 95% CI, 1.27 to 2.34; P<0.001), and stroke (RR, 1.83; 95% CI, 1.12 to 3.00; P=0.02) after adjustment for established cardiovascular risk factors. Each standard deviation rise in cystatin C concentration boosted CVD risk (RR, 1.34; 95% CI, 1.18 to 1.51; P<0.001). Highest cystatin C category was also independently linked to greater risk of all-cause mortality and heart failure.

Conclusions—

The meta-analysis, mostly derived from high cardiovascular populations, showed that cystatin C is strongly and independently associated with subsequent CVD risk. Further investigation is warranted to clarify whether measurement of cystatin C can usefully enhance CVD stratification beyond established predictors already in clinical use.

  K. H Chang , W Lee , D. M Choo , C. S Lee and Y. Kim
 

In this research, using direct measurements and Monte Carlo calculations, the potential dose reduction achieved by bismuth shielding in computed tomography was evaluated. The patient dose was measured using an ionisation chamber in a polymethylmethacrylate (PMMA) phantom that had five measurement points at the centre and periphery. Simulations were performed using the MCNPX code. For both the bare and the bismuth-shielded phantom, the differences of dose values between experiment and simulation were within 9 %. The dose reductions due to the bismuth shielding were 1.2–55 % depending on the measurement points, X-ray tube voltage and the type of shielding. The amount of dose reduction was significant for the positions covered by the bismuth shielding (34 – 46 % for head and 41 – 55 % for body phantom on average) and negligible for other peripheral positions. The artefact on the reconstructed images were minimal when the distance between the shielding and the organs was >1 cm, and hence the shielding should be selectively located to protect critical organs such as the eye lens, thyroid and breast. The simulation results using the PMMA phantom was compared with those using a realistically voxelised phantom (KTMAN-2). For eye and breast, the simulation results using the PMMA and KTMAN-2 phantoms were similar with each other, while for thyroid the simulation results were different due to the discrepancy of locations and the sizes of the phantoms. The dose reductions achieved by bismuth and lead shielding were compared with each other and the results showed that the difference of the dose reductions achieved by the two materials was less than 2–3 %.

 
 
 
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