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Articles by H. J Kim
Total Records ( 13 ) for H. J Kim
  H. J Kim , H Moradi , J Yuan , K Norris and N. D. Vaziri

A significant reduction of renal mass results in proteinuria, glomerulosclerosis, and tubulointerstitial injury, culminating in end-stage chronic renal failure (CRF). The accumulation of lipids in the kidney can cause renal disease. Uptake of oxidized lipoproteins via scavenger receptors, reabsorption of filtered protein-bound lipids via the megalin-cubilin complex, and increased glucose load per nephron can promote lipid accumulation in glomerular, tubular, and interstitial cells in CRF. Cellular lipid homeostasis is regulated by lipid influx, synthesis, catabolism, and efflux. We examined lipid-regulatory factors in the remnant kidney of rats 11 wk after nephrectomy (CRF) or sham operation. CRF resulted in azotemia, proteinuria, lipid accumulation in the kidney, upregulation of megalin, cubilin, mediators of lipid influx (scavenger receptor class A and lectin-like oxidized receptor-1), lipid efflux (liver X receptor /β and ATP-binding cassette transporter), and fatty acid biosynthesis (carbohydrate-response element binding protein, fatty acid synthase, and acetyl-CoA carboxylase). However, factors involved in cholesterol biosynthesis (sterol regulatory element binding protein, 3-hydroxy-3-methylglutaryl coenzyme A reductase, SCAP, Insig-1, and Insig-2) and fatty acid oxidation (peroxisome proliferator-activated receptor, acyl-CoA oxidase, and liver-type fatty acid binding protein) were reduced in the remnant kidney. Thus CRF results in heavy lipid accumulation in the remnant kidney, which is mediated by upregulation of pathways involved in tubular reabsorption of filtered protein-bound lipids, influx of oxidized lipoproteins and synthesis of fatty acids, and downregulation of pathways involved in fatty acid catabolism.

  H Seo , K. H Lee , H. J Kim , K Kim , S. B Kang , S. Y Kim and Y. H. Kim

OBJECTIVE. The purpose of this study was to compare low-dose unenhanced CT with standard-dose IV contrast-enhanced CT in the diagnosis of appendicitis.

MATERIALS AND METHODS. Two hundred seven adults with suspected appendicitis underwent CT with mean effective doses of both 4.2 and 8.0 mSv. Two radiologists retrospectively reviewed thin-section images by sliding a 5-mm-thick ray-sum slab. They rated the likelihood of appendicitis and appendiceal visualization on 5- and 3-point scales, respectively, and proposed alternative diagnoses. Likelihood ≥ 3 was considered a positive diagnosis. Receiver operating characteristics analysis, the McNemar test, and the Wilcoxon's signed-rank test were used.

RESULTS. Seventy-eight patients had appendicitis. The values of the area under the receiver operating characteristics curve were 0.98 for the low-dose unenhanced acquisition and 0.97 for the standard-dose contrast-enhanced acquisition for reader 1 (95% CI for the difference, -0.02 to 0.03) and 0.99 and 0.98 (-0.02 to 0.02) for reader 2. Sensitivity was 98.7% for low-dose unenhanced CT and 100% for standard-dose contrast-enhanced CT for reader 1 (p = 1.00) and 100% for both techniques for reader 2. Specificity was 95.3% and 93.0% (p = 0.25) and 96.9% and 96.9%. The interpretation was indeterminate (score 3) in 0.5% and 1.4% of cases for reader 1 (p = 0.63) and 0.5% and 0% for reader 2 (p = 1.00). A normal appendix was not visualized in 5.4% and 3.9% of cases by reader 1 (p = 0.63) and 3.9% and 2.3% of cases by reader 2 (p = 0.50). None of the patients whose appendix was not visualized had appendicitis. Diagnostic confidence, visualization score for a normal appendix, and correct alternative diagnosis tended to be compromised with use of low-dose unenhanced CT, showing a significant difference for a reader's confidence in the diagnosis of appendicitis (p = 0.004). The two techniques were comparable in the diagnosis of appendiceal perforation.

CONCLUSION. Low-dose unenhanced CT is potentially useful in the diagnosis of appendicitis.

  S. A Lee , Y. M Kim , T. K Kwak , H. J Kim , S Kim , W Ko , S. H Kim , K. H Park , M Cho and J. W. Lee

Four-transmembrane L6 family member 5 (TM4SF5) and its homolog L6, a tumor antigen, form a four-transmembrane L6 family. TM4SF5 expression causes uncontrolled cell proliferation and angiogenesis. Although other genuine transmembrane 4 superfamily (TM4SF) members co-operate with integrins for cell migration, roles of TM4SF5 in the cellular spreading and migration are unknown. Using hepatocarcinoma cell clones that ectopically express TM4SF5, we found that cross talks via an extracellular interaction between TM4SF5 and integrin 2 in collagen type I environment inhibited integrin 2 functions such as spreading on and migration toward collagen I, which were recovered by suppression of TM4SF5 or structural disturbance of its second extracellular loop using a peptide or mutagenesis. Altogether, the observations suggest that TM4SF5 in hepatocytes negatively regulates integrin 2 function via an interaction between the extracellular loop 2 of TM4SF5 and integrin 2 during cell spreading on and migration through collagen I environment.

  S. H Lee , K. H Koo , J. W Park , H. J Kim , S. K Ye , J. B Park , B. K Park and Y. N. Kim

The plasma membrane microdomains, lipid rafts, are involved in regulation of cellular functions such as cell survival and adhesion. Cholesterol is a critical component of lipid rafts in terms of their integrity and functions and rafts disruption by cholesterol depletion can induce detachment-induced cell death. Hypoxia inducible factor-1 (HIF-1) is stabilized in hypoxia and transactivates numerous genes required for cellular adaptation to hypoxia. It is also induced by non-hypoxic stimuli and contributes to cell survival. Because hypoxia inhibits cholesterol synthesis and HIF-1 plays a role in this process, we here explored a possible connection between lipid rafts and HIF-1. We investigated whether HIF-1 is regulated during cholesterol depletion/rafts disruption in A431 cells in normoxic conditions. Methyl-beta cyclodextrin (MβCD), which induces cholesterol depletion, upregulated HIF-1 even under normoxic conditions and this upregulation required epidermal growth factor receptor (EGFR) and extracellular signal-regulated kinase 1 and 2 activation, but not Akt activation. MβCD treatment induced HIF-1 upregulation at both the transcriptional and translational levels but not at the posttranslational levels. In addition, MβCD robustly induced vascular endothelial growth factor production and stimulated an hypoxia response element-driven luciferase reporter activity under normoxic conditions, indicating that MβCD-induced HIF-1 is functionally activated. Both EGFR activity and HIF-1 expression were higher in the attached cells than in the detached cells after MβCD treatment. Furthermore, inhibition of HIF-1 by RNA interference accelerated cell detachment, thus increasing cell death, indicating that HIF-1 expression attenuates MβCD-induced anoikis-like cell death. These data suggest that, depending on cholesterol levels, lipid rafts or membrane fluidity are probably to regulate HIF-1 expression in normoxia by modulating rafts protein activities such as EGFR, and this connection between lipid rafts and HIF-1 regulation may provide cell survival under membrane-disturbing stress.

  S. W Han , H. J Kim , S Kim and K. H. Ryu

Comprehensive aortic root and valve repair (CARVAR) surgery using specially designed aortic rings was introduced as a new surgical technique for aortic valve disease. We present five consecutive cases of iatrogenic coronary ostial stenosis after CARVAR surgery in patients with aortic stenosis. The preoperative coronary angiography confirmed that all the patients had normal coronary arteries. They underwent aortic valvuloplasty by aortic leaflet extension and insertion of specially designed inner and outer rings at the level of the sinotubular junction. Within 6 months after surgery, all the patients complained of resting chest pain and dyspnea with changes of electrocardiography. Repeated coronary angiography demonstrated right coronary artery (RCA) ostial stenosis in one patient and left main (LM) ostial stenosis in the other four patients. Intravascular ultrasonography demonstrated severe ostial stenosis and extensive echogenic tissue in the extravascular area. Four patients with LM ostial disease successfully underwent coronary bypass graft surgery, and percutaneous coronary intervention with stenting was performed in one case of RCA ostial stenosis. Because the mechanism of this complication is not fully confirmed, more clinical study is required to confirm the safety issues of CARVAR surgery.

  H. J Kim , H. J Lee , H Kim , S. W Cho and J. S. Kim

Broad applications of zinc finger nuclease (ZFN) technology—which allows targeted genome editing—in research, medicine, and biotechnology are hampered by the lack of a convenient, rapid, and publicly available method for the synthesis of functional ZFNs. Here we describe an efficient and easy-to-practice modular-assembly method using publicly available zinc fingers to make ZFNs that can modify the DNA sequences of predetermined genomic sites in human cells. We synthesized and tested hundreds of ZFNs to target dozens of different sites in the human CCR5 gene—a co-receptor required for HIV infection—and found that many of these nucleases induced site-specific mutations in the CCR5 sequence. Because human cells that harbor CCR5 null mutations are functional and normal, these ZFNs might be used for (1) knocking out CCR5 to produce T-cells that are resistant to HIV infection in AIDS patients or (2) inserting therapeutic genes at "safe sites" in gene therapy applications.

  K Park , J. H Park , H. J Kim and B. Y. Park

We analyzed information surveyed from a community-based sample of Korean women older than 40 years of age to understand the relationships between health status and screening behavior.


In a cross-sectional population-based study, a two-stage, geographically stratified household-based sampling design was used for assembly of a probability sample of women aged 40–69 years living in Gunpo in Korea, resulting in a total sample size of 503 women. The primary outcome variable for this analysis was the respondent's intention to obtain a mammogram. Predictor variables included health status and other factors known to influence the use of cancer screening, such as age, education, income, marital status and the presence of co-morbid illnesses. Health status was assessed by using the EuroQol (EQ-5D).


The median EQ visual analogue scale score was 75.0, ranging from 20 to 100. In bivariate analyses, the percentage of women reporting to have intention toward mammography use decreased with worsening health status. Women who had problems with mobility or anxiety/depression showed lower intention to undergo future screening mammography. Multivariate logistic regression confirmed that health status was significantly associated with intention toward mammography use. Anxiety or depression was an independent predictor of future screening mammography use.


Health status is significantly associated with intention regarding screening mammography use. Physicians or other health professionals should be aware that health status is an important component for health promotion, and should pay more attention to clients' possible vulnerability in screening mammography use due to their poor health status.

  K Uk Hong , H. J Kim , H. S Kim , Y. S Seong , K. M Hong , C. D Bae and J. Park

During mitosis, establishment of structurally and functionally sound bipolar spindles is necessary for maintaining the fidelity of chromosome segregation. Tumor-associated microtubule-associated protein (TMAP), also known as cytoskeleton-associated protein 2 (CKAP2), is a mitotic spindle-associated protein whose level is frequently up-regulated in various malignancies. Previous reports have suggested that TMAP is a potential regulator of mitotic spindle assembly and dynamics and that it is required for chromosome segregation to occur properly. So far, there have been no reports on how its mitosis-related functions are regulated. Here, we report that TMAP is hyper-phosphorylated at the C terminus specifically during mitosis. At least four different residues (Thr-578, Thr-596, Thr-622, and Ser-627) were responsible for the mitosis-specific phosphorylation of TMAP. Among these, Thr-622 was specifically phosphorylated by Cdk1-cyclin B1 both in vitro and in vivo. Interestingly, compared with the wild type, a phosphorylation-deficient mutant form of TMAP, in which Thr-622 had been replaced with an alanine (T622A), induced a significant increase in the frequency of metaphase cells with abnormal bipolar spindles, which often displayed disorganized, asymmetrical, or narrow and elongated morphologies. Formation of these abnormal bipolar spindles subsequently resulted in misalignment of metaphase chromosomes and ultimately caused a delay in the entry into anaphase. Moreover, such defects resulting from the T622A mutation were associated with a decrease in the rate of protein turnover at spindle microtubules. These findings suggest that Cdk1-cyclin B1-mediated phosphorylation of TMAP is important for and contributes to proper regulation of microtubule dynamics and establishment of functional bipolar spindles during mitosis.

  J Nolting , C Daniel , S Reuter , C Stuelten , P Li , H Sucov , B. G Kim , J. J Letterio , K Kretschmer , H. J Kim and H. von Boehmer

It has been reported that retinoic acid (RA) enhances regulatory T (T reg) cell conversion by inhibiting the secretion of cytokines that interfere with conversion. This report shows that these conclusions provide a partial explanation at best. First, RA not only interfered with cytokine secretion but also with the ability of these cytokines to inhibit T reg cell conversion of naive T cells. Furthermore, RA enhanced conversion even in the absence of inhibitory cytokines. The latter effect depended on the RA receptor (RAR) but did not require Smad3, despite the fact that RA enhanced Smad3 expression. The RAR1 isoform was not essential for RA-dependent enhancement of transforming growth factor β–driven conversion, suggesting that conversion can also be mediated by RAR2. Interleukin (IL)-6 strongly reduced RAR expression levels such that a deficiency of the predominant RAR1 isoform leaves too little RAR2 for RA to inhibit the generation of Th17 cells in the presence of IL-6.

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