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Articles by H. W Kim
Total Records ( 4 ) for H. W Kim
  E Jeon , H. W Kim and J. H. Jang

Fibroblast growth factor-1 (FGF1) is one of the most potent angiogenic growth factors, and also plays an important role in regulating cellular functions including cell proliferation, motility, differentiation, survival, and tissue regeneration processes. Here we described a novel fusion protein that was designed by combining the cell adhesion sequence from fibronectin with FGF1. The F1–Fn fusion protein functions as a minimized protein that directs integrin-dependent cell adhesion and stimulates cellular responses including cell proliferation and differentiation. Moreover, our results indicate that Fn-mediated signaling synergizes with signals from FGF1 in promoting cellular adhesion, proliferation, and differentiation in MG63 cells.

  P. C Walker , S. J Bernstein , J. N. T Jones , J Piersma , H. W Kim , R. E Regal , L Kuhn and S. A. Flanders

Background  Medication discrepancies are common at hospital discharge and can result in adverse events, hospital readmissions, and emergency department visits. Our objectives were to characterize medication discrepancies at hospital discharge and test the effects of a pharmacist intervention on health care utilization following discharge.

Methods  We used a prospective, alternating month quasi-experimental design to compare outcomes of patients receiving the intervention (n = 358) with controls (n = 366). All patients were discharged to home and were at high risk for medication-related problems following discharge because of the number or types of medications they were prescribed, multiple medication changes during hospitalization, or problems managing medications. The intervention consisted of medication therapy assessment, medication reconciliation, screening for adherence concerns, patient counseling and education, and postdischarge telephone follow-up. The primary outcomes were 14-day and 30-day readmission rates and emergency department visits within 72 hours of discharge. Medication discrepancies occurring at discharge were also characterized.

Results  Medication discrepancies at discharge were identified in 33.5% of intervention patients and 59.6% of control patients (P < .001). Although all discrepancies were resolved in the intervention group prior to discharge, readmission rates did not differ significantly between groups at 14 days (12.6% vs 11.5%; P = .65) and 30 days (22.1% vs 18%; P = .17), nor did emergency department visits (2.8% vs 2.2%, respectively; P = .60).

Conclusion  While our intervention improved the quality of patient discharge by identifying and reconciling medication discrepancies at discharge, there was no effect on postdischarge health care resource utilization.

  M. R Patel , P. J Cawley , J. F Heitner , I Klem , M. A Parker , W. A Jaroudi , T. J Meine , J. B White , M. D Elliott , H. W Kim , R. M Judd and R. J. Kim

Background— In patients with sarcoidosis, sudden death is a leading cause of mortality, which may represent unrecognized cardiac involvement. Delayed-enhancement cardiovascular magnetic resonance (DE-CMR) can detect minute amounts of myocardial damage. We sought to compare DE-CMR with standard clinical evaluation for the identification of cardiac involvement.

Methods and Results— Eighty-one consecutive patients with biopsy-proven extracardiac sarcoidosis were prospectively recruited for a parallel and masked comparison of cardiac involvement between (1) DE-CMR and (2) standard clinical evaluation with the use of consensus criteria (modified Japanese Ministry of Health [JMH] guidelines). Standard evaluation included 12-lead ECG and at least 1 dedicated non-CMR cardiac study (echocardiography, radionuclide scintigraphy, or cardiac catheterization). Patients were followed for 21±8 months for major adverse events (death, defibrillator shock, or pacemaker requirement). Patients were predominantly middle-aged (46±11 years), female (62%), and black (73%) and had chronic sarcoidosis (median, 7 years) and preserved left ventricular ejection fraction (median, 56%). DE-CMR identified cardiac involvement in 21 patients (26%) and JMH criteria in 10 (12%, 8 overlapping), a >2-fold higher rate for DE-CMR (P=0.005). All patients with myocardial damage on DE-CMR had coronary disease excluded by x-ray angiography. Pathology evaluation in 15 patients (19%) identified 4 with cardiac sarcoidosis; all 4 were positive by DE-CMR, whereas 2 were JMH positive. On follow-up, 8 had adverse events, including 5 cardiac deaths. Patients with myocardial damage on DE-CMR had a 9-fold higher rate of adverse events and an 11.5-fold higher rate of cardiac death than patients without damage.

Conclusions— In patients with sarcoidosis, DE-CMR is more than twice as sensitive for cardiac involvement as current consensus criteria. Myocardial damage detected by DE-CMR appears to be associated with future adverse events including cardiac death, but events were few, and this needs confirmation in a larger cohort.

  G. H Kim , K Park , S. Y Yeom , K. J Lee , G Kim , J Ko , D. K Rhee , Y. H Kim , H. K Lee , H. W Kim , G. T Oh , K. U Lee , J. W Lee and S. W. Kim

Activating signal cointegrator-2 (ASC-2) functions as a transcriptional coactivator of many nuclear receptors and also plays important roles in the physiology of the liver and pancreas by interacting with liver X receptors (LXRs), which antagonize the development of atherosclerosis. This study was undertaken to establish the specific function of ASC-2 in macrophages and atherogenesis. Intriguingly, ASC-2 was more highly expressed in macrophages than in the liver and pancreas. To inhibit LXR-specific activity of ASC-2, we used DN2, which contains the C-terminal LXXLL motif of ASC-2 and thereby acts as an LXR-specific, dominant-negative mutant of ASC-2. In DN2-overexpressing transgenic macrophages, cellular cholesterol content was higher and cholesterol efflux lower than in control macrophages. DN2 reduced LXR ligand-dependent increases in the levels of ABCA1, ABCG1, and apolipoprotein E (apoE) transcripts as well as the activity of luciferase reporters driven by the LXR response elements (LXREs) of ABCA1, ABCG1, and apoE genes. These inhibitory effects of DN2 were reversed by overexpression of ASC-2. Chromatin immunoprecipitation analysis demonstrated that ASC-2 was recruited to the LXREs of the ABCA1, ABCG1, and apoE genes in a ligand-dependent manner and that DN2 interfered with the recruitment of ASC-2 to these LXREs. Furthermore, low-density lipoprotein receptor (LDLR)-null mice receiving bone marrow transplantation from DN2-transgenic mice showed accelerated atherogenesis when administered a high-fat diet. Taken together, these results indicate that suppression of the LXR-specific activity of ASC-2 results in both defective cholesterol metabolism in macrophages and accelerated atherogenesis, suggesting that ASC-2 is an antiatherogenic coactivator of LXRs in macrophages.

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