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Articles by J. Y Kim
Total Records ( 9 ) for J. Y Kim
  H. K Sung , Y. W Kim , S. J Choi , J. Y Kim , K. H Jeune , K. C Won , J. K Kim , G. Y Koh and S. Y. Park
 

To test whether chronic enhanced blood flow alters insulin-stimulated glucose uptake, we measured skeletal muscle glucose uptake in chow-fed and high-fat-fed mice injected with adenovirus containing modified angiopoietin-1, COMP-Ang1, via euglycemic-hyperinsulinemic clamp. Blood flow rates and platelet endothelial cell adhesion molecule-1 positive endothelial cells in the hindlimb skeletal muscle were elevated in COMP-Ang1 compared with control LacZ. Whole body glucose uptake and whole body glycogen/lipid synthesis were elevated in COMP-Ang1 compared with LacZ in chow diet. High-fat diet significantly reduced whole body glucose uptake and whole body glycolysis in LacZ mice, whereas high-fat-fed COMP-Ang1 showed a level of whole body glucose uptake that was comparable with chow-fed LacZ and showed increased glucose uptake compared with high-fat-fed LacZ. Glucose uptake and glycolysis in gastrocnemius muscle of chow-fed COMP-Ang1 were increased compared with chow-fed LacZ. High-fat diet-induced whole body insulin resistance in the LacZ was mostly due to ~40% decrease in insulin-stimulated glucose uptake in skeletal muscle. In contrast, COMP-Ang1 prevented diet-induced skeletal muscle insulin resistance compared with high-fat-fed LacZ. Akt phosphorylation in skeletal muscle was increased in COMP-Ang1 compared with LacZ in both chow-fed and high-fat-fed groups. These results suggest that increased blood flow by COMP-Ang1 increases insulin-stimulated glucose uptake and prevents high-fat diet-induced insulin resistance in skeletal muscle.

  K Liu , S Zhou , J. Y Kim , K Tillison , D Majors , D Rearick , J. H Lee , R. F Fernandez Boyanapalli , K Barricklow , M. S Houston and C. M. Smas
 

The adipocyte-specific protein FSP27, also known as CIDEC, is one of three cell death-inducing DFF45-like effector (CIDE) proteins. The first known function for CIDEs was promotion of apoptosis upon ectopic expression in mammalian cells. Recent studies in endogenous settings demonstrated key roles for CIDEs in energy metabolism. FSP27 is a lipid droplet-associated protein whose heterologous expression enhances formation of enlarged lipid droplets and is required for unilocular lipid droplets typical of white adipocytes in vivo. Here, we delineate relationships between apoptotic function and lipid droplet localization of FSP27. We demonstrate that ectopic expression of FSP27 induces enlarged lipid droplets in multiple human cell lines, which is indicative that its mechanism involves ubiquitously present, rather than adipocyte-specific, cellular machinery. Furthermore, promotion of lipid droplet formation in HeLa cells via culture in exogenous oleic acid offsets FSP27-mediated apoptosis. Using transient cotransfections and analysis of lipid droplets in HeLa cells stably expressing FSP27, we show that FSP27 does not protect lipid droplets from action of ATGL lipase. Domain mapping with eGFP-FSP27 deletion constructs indicates that lipid droplet localization of FSP27 requires amino acids 174–192 of its CIDE C domain. The apoptotic mechanism of FSP27, which we show involves caspase-9 and mitochondrial cytochrome c, also requires this 19-amino acid region. Interaction assays determine the FSP27 CIDE C domain complexes with CIDEA, and Western blot reveals that FSP27 protein levels are reduced by coexpression of CIDEA. Overall, our findings demonstrate the function of the FSP27 CIDE C domain and/or regions thereof for apoptosis, lipid droplet localization, and CIDEA interaction.

  H. J Kwak , J. Y Kim , S. K Min , J. S Kim and J. Y. Kim
  Background

The goals of this study were to determine the effective bolus dose of alfentanil required for successful tracheal intubation during inhalation induction using sevoflurane 5% without neuromuscular block in children, and whether nitrous oxide reduces these doses.

Methods

Fifty paediatric patients, aged 3–10 yr, were randomly assigned to one of the two groups. Subjects received either sevoflurane 5% in oxygen 100% (O2 group, n=25) or sevoflurane 5% in oxygen 40% and nitrous oxide 60% (N2O group, n=25) through a face mask. One minute after inhalation induction, a predetermined dose of alfentanil was injected over 15 s. The alfentanil dose was determined using Dixon's up-and-down method, starting from alfentanil 14 µg kg–1. The trachea was intubated 3 min after inducing anaesthesia.

Results

The ED50 [95% confidence interval (CI)] of alfentanil for successful tracheal intubation was 11.5 (9.9–13.1) and 8.6 (7.4–9.8) µg kg–1 in the O2 and N2O groups, respectively. The ED50 of the N2O group was significantly lower than that of the O2 group (P=0.0146). From isotonic regression, 50% effective dose (ED50) (95% CI) of alfentanil in the O2 and N2O groups was 11.4 (9.9–13.0) and 6.5 (5.0–8.1) µg kg–1, respectively.

Conclusions

The effective bolus dose of alfentanil for successful tracheal intubation was 11.5 µg kg–1 in 50% of children during inhalation induction using sevoflurane 5% without neuromuscular blocking agent. Addition of nitrous oxide 60% in oxygen reduced the effective alfentanil dose by 25%.

  J. Y Hong , J. Y Kim , Y. D Choi , K. H Rha , S. J Yoon and H. K. Kil
  Background

Robotic-assisted laparoscopic radical prostatectomy (RALRP) is gaining popularity as a less traumatic and minimally invasive alternative to open radical retropubic prostatectomy (RRP). The aim of this study was to evaluate the incidence and grade of venous gas embolism (VGE) during RALRP compared with those during RRP using transoesophageal echocardiography (TOE).

Methods

Fifty-two patients undergoing RRP (n=26) or RALRP (n=26) were consecutively enrolled. TOE was continuously applied during surgery and VGE was graded by an independent researcher.

Results

The total incidence of VGE (proportion, 95% CI) in the RRP group was higher than that in the RALRP group [20/25 (0.80, 0.60–0.92) and 10/26 (0.38, 0.22–0.58), respectively]. Most VGE in the RALRP group occurred during the transection of the deep dorsal venous complex. There was no difference in the incidence of severe VGE between the two groups. No patients with cardiorespiratory instabilities even with severe VGE were observed in this study.

Conclusions

In contrast to general belief, VGE occurred less frequently during RALRP. Although the VGE in this study did not cause any cardiorespiratory instability, close monitoring for possibly fatal VGE must be considered during both types of radical prostatectomy because those who undergo radical prostatectomy frequently have cardiopulmonary co-morbidities.

  J. Y Kim , E. H Kim , S. U Kim , T. K Kwon and K. S. Choi
 

Capsaicin, a pungent ingredient of red chili peppers, has been reported to possess antitumor activities. Here, we show that subtoxic doses of capsaicin effectively sensitize multiple malignant glioma cell lines to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Although TRAIL alone mediated partial proteolytic processing of procaspase-3 in glioma cells, cotreatment with capsaicin and TRAIL efficiently restored complete activation of caspases. We found that treatment of various gliomas with capsaicin significantly upregulated DR5, a death receptor of TRAIL, and downregulated the caspase inhibitor survivin. The induction of DR5 was mediated by CHOP/GADD153. The reduction in survivin protein level was associated with downregulation of cyclin B and Cdc2 expression, suggesting that inhibition of Cdc2 activity might contribute to capsaicin-induced survivin downregulation. Taken together, these results indicate that the activity of capsaicin toward DR5 and survivin contributes to the amplification of caspase cascades, thereby restoring TRAIL sensitivity in malignant glioma cells. Interestingly, normal astrocytes were resistant to combined treatment with capsaicin and TRAIL. Neither capsaicin-induced DR5 upregulation/survivin downregulation nor the partial processing of procaspase-3 by TRAIL was induced in astrocytes. Thus, a combined regimen using capsaicin and TRAIL may provide a safe and effective strategy for treating malignant gliomas.

  J. Y Kim , H. J Cho , J. J Sir , B. K Kim , J Hur , S. W Youn , H. M Yang , S. I Jun , K. W Park , S. J Hwang , Y. W Kwon , H. Y Lee , H. J Kang , B. H Oh , Y. B Park and H. S. Kim
  Aims

Inflammation, and the subsequent proliferative activity of vascular smooth muscle cells (VSMCs), is one of the major pathophysiological mechanisms associated with neointimal hyperplasia following vascular injury. Although sulfasalazine (SSZ) has been used as an anti-inflammatory and immune-modulatory agent in various inflammatory diseases, its primary targets and therapeutic effects on vascular disease have not yet been determined. We investigated whether SSZ could suppress VSMC growth and prevent neointimal hyperplasia.

Methods and results

SSZ was found to have pro-apoptotic and anti-proliferative activity in cultured VSMCs. Unexpectedly, these effects were not mediated by nuclear factor kappa B (NF-B) inhibition, which has been suggested to be the anti-inflammatory mechanism associated with the effects of SSZ. Instead, cell-cycle arrest of the VSMCs was observed, which was mediated by induction of haem oxygenase-1 (HO-1) followed by an increased expression of p21waf1/Cip1. The underlying mechanism for SSZ-induced HO-1 expression was by reactive oxygen species (ROS)-dependent nuclear translocation and activation of nuclear factor erythroid-2-related factor 2 (Nrf2). In a rat carotid artery balloon injury model, administration of SSZ significantly suppressed neointimal growth. In a series of reverse experiments, inhibition of HO-1 by shRNA, ROS by N-acetylcysteine (NAC) or Nrf2 by dominant-negative Nrf2 abrogated the beneficial effects of SSZ.

Conclusion

Our data demonstrate that SSZ inhibits VSMC proliferation in vitro and in vivo through a novel signalling pathway and may be a promising therapeutic option for the treatment of proliferative vascular disease.

  T. H Lee , S. H Song , K. L Kim , J. Y Yi , G. H Shin , J. Y Kim , J Kim , Y. M Han , S. H Lee , S. H Shim and W. Suh
 

Rationale: Generation of induced pluripotent stem (iPS) cells has been intensively studied by a variety of reprogramming methods, but the molecular and functional properties of the cells differentiated from iPS cells have not been well characterized.

Objective: To address this issue, we generated iPS cells from human aortic vascular smooth muscle cells (HASMCs) using lentiviral transduction of defined transcription factors and differentiated these iPS cells back into smooth muscle cells (SMCs).

Methods and Results: Established iPS cells were shown to possess properties equivalent to human embryonic stem cells, in terms of the cell surface markers, global mRNA and microRNA expression patterns, epigenetic status of OCT4, REX1, and NANOG promoters, and in vitro/in vivo pluripotency. The cells were differentiated into SMCs to enable a direct, comparative analysis with HASMCs, from which the iPS cells originated. We observed that iPS cell–derived SMCs were very similar to parental HASMCs in gene expression patterns, epigenetic modifications of pluripotency-related genes, and in vitro functional properties. However, the iPS cells still expressed a significant amount of lentiviral transgenes (OCT4 and LIN28) because of partial gene silencing.

Conclusions: Our study reports, for the first time, the generation of iPS cells from HASMCs and their differentiation into SMCs. Moreover, a parallel comparative analysis of human iPS cell–derived SMCs and parental HASMCs revealed that iPS-derived cells possessed representative molecular and in vitro functional characteristics of parental HASMCs, suggesting that iPS cells hold great promise as an autologous cell source for patient-specific cell therapy.

  J. H Oh , H. K Lee , J. Y Kim , S. H Kim and H. S. Gong
  Background

Although arthroscopic glenoid labrum repair using the BioKnotless anchor is common, the benefits and efficacy have not been fully evaluated.

Hypothesis

BioKnotless suture anchor is a clinically and radiologically suitable material for arthroscopic labral repair.

Study Design

Case series; Level of evidence, 4.

Methods

Ninety-seven patients underwent arthroscopic glenoid labrum repair with BioKnotless anchor between July 2004 and December 2005. Thirty-seven patients had traumatic anterior instability and 60 patients had an isolated superior labrum, anterior-posterior (SLAP) lesion. The mean age at surgery was 36.0 years (range, 15–66); the average follow-up was 34.1 months (range, 24–54). Clinical outcomes were evaluated using range of motion and various functional evaluation scores including sports activity. Pain and patient satisfaction were measured using a visual analog scale (VAS). Computed tomography arthrography was conducted in 73 patients at least 1 year after surgery for radiologic evaluation.

Results

In patients with instability, the Western Ontario Shoulder Instability index and Rowe score improved from 53.2 to 85.9 and from 68.7 to 92.7, respectively. Return to normal recreation and sports were possible in 30 patients (81.1%); the mean satisfaction VAS was 9.2. There was 1 postoperative dislocation, and the apprehension test was positive in 1 case. Postoperative range of motion including external rotation was not different. In patients with a SLAP lesion, the American Shoulder and Elbow Surgeons score and Constant score improved from 67.3 to 96.0 and 79.1 to 96.8, respectively. Pain VAS decreased from 6.0 to 0.4, and the mean satisfaction VAS was 9.4. Return to normal recreation and sports were possible in 50 patients (83.3%). All labra were found to have firmly healed to bony glenoid rim without anchor-related osteolysis in postoperative CT arthrography.

Conclusion

Clinically and radiologically, the BioKnotless anchor appears to be an acceptable alternative for arthroscopic labrum repair, and a suitable material allowing the avoidance of certain troublesome drawbacks of the conventional knot-tying suture anchor.

  J. R Kim , H. J Kee , J. Y Kim , H Joung , K. I Nam , G. H Eom , N Choe , H. S Kim , J. C Kim , H Kook , S. B Seo and H. Kook
 

Skeletal muscle differentiation is well regulated by a series of transcription factors. We reported previously that enhancer of polycomb1 (Epc1), a chromatin protein, can modulate skeletal muscle differentiation, although the mechanisms of this action have yet to be defined. Here we report that Epc1 recruits both serum response factor (SRF) and p300 to induce skeletal muscle differentiation. Epc1 interacted physically with SRF. Transfection of Epc1 to myoblast cells potentiated the SRF-induced expression of skeletal muscle-specific genes as well as multinucleation. Proximal CArG box in the skeletal -actin promoter was responsible for the synergistic activation of the promoter-luciferase. Epc1 knockdown caused a decrease in the acetylation of histones associated with serum response element (SRE) of the skeletal -actin promoter. The Epc1·SRF complex bound to the SRE, and the knockdown of Epc1 resulted in a decrease in SRF binding to the skeletal -actin promoter. Epc1 recruited histone acetyltransferase activity, which was potentiated by cotransfection with p300 but abolished by si-p300. Epc1 directly bound to p300 in myoblast cells. Epc1+/– mice showed distortion of skeletal -actin, and the isolated myoblasts from the mice had impaired muscle differentiation. These results suggest that Epc1 is required for skeletal muscle differentiation by recruiting both SRF and p300 to the SRE of muscle-specific gene promoters.

 
 
 
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