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Articles by K Park
Total Records ( 3 ) for K Park
  M Wang , J. J Wang , J Li , K Park , X Qian , J. x Ma and S. X. Zhang
 

We previously reported that circulating levels of pigment epithelium-derived factor (PEDF), a newly identified adipokine, are increased in patients with type 2 diabetes, correlating with body mass index. However, the role of PEDF in adipogenesis remains elusive. In the present study, we have investigated the effects and mechanisms of PEDF on adipocyte differentiation in 3T3-L1 preadipocytes. Differentiation of 3T3-L1 preadipocytes was induced in the presence or absence of human recombinant PEDF protein. The effects of PEDF on adipogenic gene expression, mitotic clonal expansion (MCE), and MAPK activation were investigated. Physiological concentrations of human PEDF protein inhibited adipocyte differentiation, evidenced by decreased lipid accumulation, downregulation of adipocyte markers, and inhibition of master adipogenic transcription factors such as C/EBP- and PPAR. The antiadipogenic effects of PEDF were observed only when PEDF was added to the cells on day 0, but not on day 3 during differentiation, suggesting that PEDF targets some early adipogenic events. Similarly, overexpression of PEDF by adenovirus attenuated adipocyte differentiation. Further studies revealed that PEDF, or U-0126, a specific MAPK/ERK inhibitor, sequentially inhibited the early activation of ERK and MCE. Moreover, PEDF attenuated expression and the phosphorylation of C/EBP-β at Thr188, an essential step for transcriptional activation of C/EBP-β. In addition, PEDF expression was decreased significantly in the first 24 h during adipocyte differentiation, suggesting that downregulation of PEDF may be essential for the initiation of MCE and adipogenesis. We conclude that PEDF inhibits adipogenesis in 3T3-L1 preadipocytes partially because of inhibition of the MAPK/ERK signaling pathway and MCE.

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

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.

Methods

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).

Results

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.

Conclusions

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.

  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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