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Articles by J. M Kim
Total Records ( 4 ) for J. M Kim
  S. Y Kim , J. E Cho , J. Y Hong , B. N Koo , J. M Kim and H. K. Kil

The administration of low-dose bupivacaine can limit the distribution of spinal block to reduce adverse haemodynamic effects. Intrathecal opioids can enhance analgesia in combination with subtherapeutic doses of local anaesthetics. We aimed at comparing the efficacy of intrathecal fentanyl and sufentanil with low-dose diluted bupivacaine for transurethral prostatectomy (TURP) in elderly patients.


Seventy patients undergoing TURP were randomly allocated into two groups. Group F (n=35) received fentanyl 25 µg+bupivacaine 0.5% (0.8 ml)+normal saline 0.3 ml and Group S (n=35) received sufentanil 5 µg+bupivacaine 0.5% (0.8 ml)+normal saline 0.7 ml—in total, bupivacaine 0.25% (1.6 ml) intrathecally. Onset and duration of the sensory block, the degree of the motor block, side-effects, and the perioperative analgesic requirements were assessed.


The median peak level of the sensory block was significantly higher in Group S than in Group F (P=0.049). Group S required fewer perioperative analgesics than Group F (P=0.008). The time to the first analgesic request was longer in Group S (P=0.025). There were no differences between the groups for the onset and recovery time of the sensory block, degree of the motor block, quality of anaesthesia, or adverse effects.


Low-dose diluted bupivacaine with fentanyl 25 µg or sufentanil 5 µg can provide adequate anaesthesia without haemodynamic instability for TURP in elderly patients. However, sufentanil was superior to fentanyl in the quality of the spinal block produced.

  I. S Song , S. U Kim , N. S Oh , J Kim , D. Y Yu , S. M Huang , J. M Kim , D. S Lee and N. S. Kim

Reactive oxygen species (ROS) have been implicated in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance of many cancers. We evaluated the role of peroxiredoxin (Prx) I in TRAIL resistance governed by coupling of nicotinamide adenosine dinucleotide phosphate oxidase (Nox)-derived ROS signaling with the p38 mitogen-activated protein kinase (MAPK)/caspase-signaling cascade in liver cancer cells. Upregulated Prx I expression was found in neoplastic regions of human patient liver, and Prx I knockdown resulted in accelerated TRAIL-induced cell death in SK-Hep-1 human hepatoma cells. The TRAIL cytotoxicity by Prx I knockdown was dependent on activation of caspase-8/3 cascades, which was ablated by addition of inhibitors for p38 MAPK, ROS or Nox, suggesting the association with Nox-driven redox signaling. Furthermore, we found that Nox4 was constitutively expressed in both SK-Hep-1 cells and tumor regions of patient livers, knockdown of Nox4 expression could alleviate ROS generation and TRAIL-mediated cytotoxicity. In accordance with previous findings, increased activation of both p38 MAPK and caspase cascades by Prx I knockdown was inhibited by either Nox4 knockdown or SB203580 addition. Collectively, these data suggest that Prx I functions to block propagation of Nox-derived ROS signaling to the p38 MAPK/caspase/cell death cascade during TRAIL treatment and also provides a molecular mechanism by which Prx I contributes to TRAIL resistance in liver cancers.

  A. W.Y Chung , H.H. C Yang , J. M Kim , M. K Sigrist , E Chum , W. A Gourlay and A. Levin

Background— Cardiovascular disease is the leading cause of mortality in chronic kidney disease patients on maintenance dialysis. Given the importance of matrix metalloproteinase-2 (MMP-2) in matrix integrity, vascular cell function, and structural stability, we hypothesized that MMP-2 was elevated in the macrovasculature in dialyzed chronic kidney disease patients compared with chronic kidney disease patients not on dialysis and kidney donors.

Methods and Results— Arteries from live kidney donors (Adonor; n=30) and recipients (nondialysis [Anondialyzed], n=17; dialysis [Adialyzed], n=23 [peritoneal dialysis, n=10; hemodialysis, n=13]) were harvested during the transplantation procedure. Compared with Adonor, MMP-2 upregulation was evident in both recipient groups. Protein expression of latent plus active MMP-2 in Adialyzed was 2-fold that in Anondialyzed. MMP-2 activity increased with length of dialysis (r=0.573, P=0.004). In Adialyzed, medial elastic fiber fragmentation was pronounced, and the ratio of external elastic lamina to media was negatively correlated with MMP-2 activity (r=–0.638, P=0.001). Adialyzed was 25% stiffer than Anondialyzed; this increased stiffness correlated with MMP-2 activity (r=0.728, P<0.0001) and the severity of medial calcium deposition (r=0.748, P=0.001). The contractile function and endothelium-dependent relaxation were reduced by 35% to 55% in Adialyzed and were negatively associated with MMP-2 activity (r=–0.608, P=0.002; r=–0.520, P=0.019, respectively). Preincubation with MMP-2 inhibitor significantly improved contractility and relaxation in Adialyzed.

Conclusions— We describe a strong correlation between MMP-2 activation and elastic fiber disorganization, stiffness, calcification, and vasomotor dysfunction in the arterial vasculature in dialyzed chronic kidney disease patients. These findings may contribute to an improved understanding of mechanisms important in vascular health in chronic kidney disease patients.

  S Kim , J. Y Yang , K Lee , K. H Oh , M Gi , J. M Kim , D. J Paik , S Hong and J. Youn

Peripheral naive CD4+ T cells selectively differentiate to type 1 Th, type 2 Th and IL-17-producing Th (Th17) cells, depending on the priming conditions. Since these subsets develop antagonistically to each other to elicit subset-specific adaptive immune responses, balance between these subsets can regulate the susceptibility to diverse immune diseases. The present study was undertaken to determine whether poly--glutamic acid (-PGA), an edible and safe exopolymer that is generated by microorganisms such as Bacillus subtilis, could modulate the development pathways of Th subsets. The presence of -PGA during priming promoted the development of Th1 and Th17 cells but inhibited development of Th2 cells. -PGA up-regulated the expression of T-bet and ROR-t, the master genes of Th1 and Th17 cells, respectively, whereas down-regulating the level of GATA-3, the master gene of Th2 cells. -PGA induced the expression of IL-12p40, CD80 and CD86 in dendritic cells (DC) and macrophages in a Toll-like receptor-4-dependent manner, and the effect of -PGA on Th1/Th2 development was dependent on the presence of antigen-presenting cells (APC). Furthermore, -PGA-stimulated DC favored the polarization of naive CD4+ T cells toward Th1 cells rather than Th2 cells. In contrast, -PGA affected Th17 cell development, regardless of the presence or absence of APC. Thus, these data demonstrate that -PGA has the potential to regulate the development pathways of naive CD4+ T cells through APC-dependent and -independent mechanisms and to be applicable to treating Th2-dominated diseases.

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