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Articles by J. H Park
Total Records ( 7 ) for J. H Park
  J. H Kim , H. Y Song , Y. D Li , J. H Shin , J. H Park , C. S Yu and J. C. Kim
 

OBJECTIVE. The purpose of this study was to compare, focusing on colonic perforation and stent migration, the clinical safety and efficacy of dual-design expandable colorectal stents with flared ends with those of stents with bent ends in the treatment of patients with malignant colorectal obstruction.

SUBJECTS AND METHODS. A total of 122 patients with malignant colorectal obstruction underwent implantation of dual-design stents with flared (n = 69) or bent (n = 53) ends.

RESULTS. Stent placement was technically successful in 116 of 122 patients (95.1%), 65 of 69 patients (94.2%) with flared-end stents and 51 of 53 patients (96.2%) with bent-end stents (p > 0.05). Clinical success was achieved within 2 days in 61 of 65 patients (93.8%) with bent-end stents and in 46 of 51 patients (90.2%) with flared-end stents (p > 0.05). Complications included seven cases of colonic perforation (6%), seven cases of stent migration (6%), three cases of tumor overgrowth (2.6%), four cases of severe rectal pain (3.4%), and four cases of bleeding (3.4%). There were no significant differences between the rates of colonic perforation and stent migration in the two groups (6.2% vs 5.9%), and the overall complication rates were similar (p > 0.05).

CONCLUSION. Dual-design expandable colorectal stents with flared ends and those with bent ends are equally safe and effective, having similar perforation and migration rates.

  Y. S Park , J. H Park , S. H Kim , M. H Lee , Y. S Lee , S. C Yang and J. S. Kang
 

Limaprost, a prostaglandin E1 analogue, with a strong vasodilatory and antiplatelet activity has been used to release from the symptoms of thromboangiitis obliterans (TAO), which is more prevalent in Korea and Japan, and lumbar spinal canal stenosis (LSCS). In spite of many uses of limaprost, the pharmacokinetics (PK) of it has not been studied in the Korean population. Therefore, a preliminary PK study was designed at a clinical oral dosage of 30-µg limaprost in 5 healthy Korean volunteers. Blood samples were obtained at 14 consecutive time points for 12 hours after dosing and analyzed by liquid chromatography—tandem mass spectrometry with electrospray ionization (LC-ESI/MS/ MS) at a very low detection limit of 0.5 pg/mL of limaprost in human plasma with considerably short run time (18 minutes). Pharmacokinetic characteristics resulted in ‘‘time for maximal concentrations (Tmax 0.5 hour),’’ ‘‘elimination half-life (T1/2 1.64 hours),’’ ‘‘maximal concentration (Cmax 13.37 pg/mL),’’ ‘‘area under the curve (AUC12 hours 18.60 pg · h/mL),’’ ‘‘AUC extrapolated to infinity (AUCinfinity 22.98 pg · h/mL),’’ ‘‘extrapolation (AUCinfinity — 12 hours/AUCinfinity 0.15%),’’ ‘‘elimination rate constant (ke 0.68 h—1),’’ ‘‘systemic clearance (CL 1.77 L/h),’’ and ‘‘mean residence time (MRT 1.74 hours).’’ These results showed that orally administered 30-µg limaprost was rapidly and highly absorbed, and it was considerably eliminated fast from the blood stream in the healthy Korean volunteers.

  D Zou , J. H Park , T. H Kim and X. Chen
 

The requirements for access control have been increased significantly in smart home systems. Many factors such as user ID, user location, service usage conditions and so on, regarded as authorization attributes, are important in making authorization decision in smart home systems. We investigate into the dynamic characteristics of the authorization in smart home systems and propose a new access-control model, SH-CRBAC, which aims to combine the advantages of attribute-based authorization mechanism and role-based access-control mechanism, and imposes attribute and status constraints on the RBAC model and enhances the generality and flexibility of authorization significantly in smart home systems. The status consistency of SH-CRBAC is analysed, and we also analyse the characteristics of SH-CRBAC through comparison with other popular existing authorization models in smart home systems.

  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.

  M. N Lee , S. N Lee , S. H Kim , B Kim , B. K Jung , J. H Seo , J. H Park , J. H Choi , S. H Yim , M. R Lee , J. G Park , J. Y Yoo , J. H Kim , S. T Lee , H. M Kim , S Ryeom , K. W Kim and G. T. Oh
  Background

Vascular endothelial growth factor A (VEGFA), a critical mediator of tumor angiogenesis, is a well-characterized target of hypoxia-inducible factor 1 (HIF-1). Murine arrest-defective protein 1A (mARD1A225) acetylates HIF-1, triggering its degradation, and thus may play a role in decreased expression of VEGFA.

Methods

We generated ApcMin/+/mARD1A225 transgenic mice and quantified growth of intestinal polyps. Human gastric MKN74 and murine melanoma B16F10 cells overexpressing mARD1A225 were injected into mice, and tumor growth and metastasis were measured. VEGFA expression and microvessel density in tumors were assessed using immunohistochemistry. To evaluate the role of mARD1A225 acetylation of Lys532 in HIF-1, we injected B16F10-mARD1A225 cell lines stably expressing mutant HIF-1/K532R into mice and measured metastasis. All statistical tests were two-sided, and P values less than .05 were considered statistically significant.

Results

ApcMin/+/mARD1A225 transgenic mice (n = 25) had statistically significantly fewer intestinal polyps than ApcMin/+ mice (n = 21) (number of intestinal polyps per mouse: ApcMin/+ mice vs ApcMin/+/mARD1A225 transgenic mice, mean = 83.4 vs 38.0 polyps, difference = 45.4 polyps, 95% confidence interval [CI] = 41.8 to 48.6; P < .001). The growth and metastases of transplanted tumors were also statistically significantly reduced in mice injected with mARD1A225-overexpressing cells than in mice injected with control cells (P < .01). Moreover, overexpression of mARD1A225 decreased VEGFA expression and microvessel density in tumor xenografts (P < .04) and ApcMin/+ intestinal polyps (P = .001). Mutation of lysine 532 of HIF-1 in B16F10-mARD1A225 cells prevented HIF-1 degradation and inhibited the antimetastatic effect of mARD1A225 (P < .001).

Conclusion

mARD1A225 may be a novel upstream target that blocks VEGFA expression and tumor-related angiogenesis.

  D Cho , M Zheng , C Min , L Ma , H Kurose , J. H Park and K. M. Kim
 

The regulatory mechanisms and functional roles of agonist-induced internalization of G protein-coupled receptors (GPCRs) were analyzed using mutant dopamine D2 receptors (D2Rs) in which all possible GPCR kinase (GRK) phosphorylation sites were mutated or the affinity for β-arrestins was altered. Agonist-induced internalization of D2Rs involved a phosphorylation-dependent component, which was mediated by serine/threonine (S/T) residues in the second loop and T225 in the third loop, and a phosphorylation-independent component. GRK2-mediated enhancement of the internalization and inhibition of D2R signaling did not involve receptor phosphorylation, and only the former required the enzymatic activity of GRK2. The phosphorylation-deficient mutant (D2R-intracellular loop 2/3) recycled more slowly and showed more agonist-induced desensitization than did the wild-type D2R, suggesting that receptor phosphorylation mediates the recycling of the internalized receptors and enhances receptor resensitization. Blockade of the agonist-induced internalization of D2R-intracellular loop 2/3 provoked desensitization as in wild-type D2R, suggesting that certain cellular processes other than receptor dephosphorylation occurring within the endocytic vesicle are responsible for the resensitization of D2R. When dissociation between D2R and β-arrestin was inhibited or when the expression of cellular β-arrestins was decreased, agonist-induced desensitization of D2R did not occur, suggesting that dissociation from β-arrestin is the main cellular process required for resensitization of D2R and is achieved through agonist-induced internalization. These results indicate that, in the regulation of some GPCRs, phosphorylation-independent association with β-arrestin plays a major role in agonist-induced desensitization.

  J. H Park and H. J. Han
 

The involvement of caveolin-1 in the regulation of embryonic stem (ES) cell growth by epidermal growth factor (EGF) is by no means clear cut. Thus we examined the relationship between EGF and caveolin-1 in mouse ES cell migration and proliferation. The results revealed that EGF increased Src, caveolin-1, focal adhesion kinase (FAK), Akt, and extracellular signal-regulated kinase-1/2 (ERK) phosphorylation levels. Especially, phosphorylation of caveolin-1 is attenuated by AG1478, herbimycin A (tyrosine kinase inhibitors), and pyrazolopyrimidine 2 (PP2, Src inhibitor) and EGF-induced ERK activation was blocked by PP2, methyl-β-cyclodextrin (MβCD), caveolin-1 small interfering RNA (siRNA), LY-294002 [phosphoinositol-3 kinase inhibitor (PI3K)], and Akt inhibitor. In addition, EGF promoted the cell migration, which was attenuated by PP2, caveolin-1 siRNA, FAK siRNA, LY-294002, Akt inhibitor, and PD-98059. EGF also increased matrix metalloproteinase (MMP-2) expression levels and EGF-induced MMP2 expression was inhibited by caveolin-1 siRNA, FAK siRNA, LY-294002, Akt inhibitor, and PD-98059. Furthermore, EGF-induced increase of cell cycle proteins expression level and [3H]thymidine incorporation was blocked by MMP inhibitor. EGF also significantly increases [3H]thymidine incorporation and cell number, which were significantly blocked by AG 1478, PP2, MβCD, caveolin-1 siRNA, FAK siRNA, LY-294002, and PD-98059 (ERK inhibitor). EGF-induced increase of protooncogenes (c-fos, c-myc, and c-Jun) and cell cycle regulatory proteins (cyclin D1, CDK4, cyclin E, and CDK2) expression levels were also attenuated by caveolin-1 siRNA and FAK siRNA. In conclusion, these results demonstrated that EGF-induced DNA synthesis and cell migration are mediated by caveolin-1, which is activated by Src, FAK, PI3K/Akt, ERK, and MMP-2 signals in mouse ES cells.

 
 
 
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