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Articles by K Lee
Total Records ( 5 ) for K Lee
  C Marsland , P Larsen , R Segal , S Hunter , J Morris , P Mezzavia , A Walpole , B di Luca , K Lee and W. Lim
  Background

Proficient manipulation of the fibreoptic bronchoscope is an important component of competent bronchoscopic airway management. We studied the duration of specialized bench training necessary to achieve this proficiency and the subsequent transfer of this psychomotor skill to human subjects.

Methods

Twenty-nine novice endoscopists undertook the training associated with a commercial non-anatomic endoscopic dexterity training system, DexterTM. Bronchoscopic driving performance was assessed after each hour of self-directed training, using a global rating scale from 1 (unskilled) to 5 (expert) with a score of 3 linked to proficiency. The scale was applied to anonymized recordings of the endoscopic view as the bronchoscope was manipulated from the mouth to the carina of an anatomic manikin. Once bench proficiency was achieved, the ability of participants to perform the skill on volunteer co-participants was assessed.

Results

Ninety-six per cent of participants achieved proficiency on the manikin within 4 h of practice. Ninety-three per cent then drove the bronchoscope proficiently from the mouth to the carina of clinical volunteers on the first attempt.

Conclusions

The endoscopic dexterity required to proficiently drive a bronchoscope in human subjects to an anatomic endpoint relevant to fibreoptic intubation is achievable after 2–4 h of specialized bench training. Training in the local environment may be more conducive to success than in time-limited workshops. Achieving a defined proficiency standard on bench models contributes to the development of basic bronchoscopic competence. This has the potential to protect patients from novice learning curves, optimize clinical education and efficiency, and assist compliance with difficult airway algorithms.

  B. K Seo , K Lee and X. Wang
 

This article investigates longitudinal changes in the relative performance of business groups utilizing data on listed companies in China over a 10-year period (1994–2003). Using a measure of firm value in the stock market and panel regression methods, this article finds the initially superior and eventually worsening performance of group-affiliated firms compared with stand-alone firms. To explain the downward performance, this article considers several alternative hypotheses, namely, institutional development, increasing competition, diversification discount, agency costs from state-ownership, and agents asset diversion behavior. This article has found certain differences in the explanatory power of each hypothesis. While the institutional development hypothesis is somewhat weak, the increasing discount for unrelated diversification as well as serious agency costs revealed in asset diversion in the business groups can better explain the longitudinal decrease in the performance of business groups. We find that while diversification still creates values, its marginal contribution has decreased over time, and that while the state-ownership variable negatively affects the values of firms in general, it is not the cause of the worsening valuation of business groups.

  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.

  M Park , E Shin , M Won , J. H Kim , H Go , H. L Kim , J. J Ko , K Lee and J. Bae
 

Mutations in FOXL2 are responsible for blepharophimosis-ptosis-epicanthus inversus syndrome (BPES) type I, in which affected women exhibit premature ovarian failure. FOXL2-null mice showed defects in granulosa cell development during folliculogenesis. We screened a rat ovarian yeast two-hybrid cDNA library to identify FOXL2-interacting proteins and found steroidogenic factor-1 (SF-1). Here, we show that human FOXL2 and SF-1 proteins interact in human granulosa cells and that FOXL2 negatively regulates the transcriptional activation of a steroidogenic enzyme, CYP17, by SF-1. Furthermore, FOXL2 mutants found in blepharophimosis-ptosis-epicanthus inversus syndrome type I patients lost the ability to repress CYP17 induction mediated by SF-1. Chromatin immunoprecipitation and EMSA results further revealed that FOXL2 inhibited the binding of SF-1 to the CYP17 promoter, whereas the FOXL2 mutants failed to block this interaction. Therefore, this study identifies a novel regulatory role for FOXL2 on a key steroidogenic enzyme and provides a possible mechanism by which mutations in FOXL2 disrupt normal ovarian follicle development.

  K. Y Renkema , K Lee , C. N Topala , M Goossens , P Houillier , R. J Bindels and J. G. Hoenderop
 

Background. Kidney stone formation is a major socioeconomic problem in humans, involving pain, recurrent treatment and renal insufficiency. As most renal precipitates contain calcium as a major component, hypercalciuria is the main risk factor for renal stone formation. Different forms of hypercalciuria can be classified, which primarily arise from defects in the main organs involved in calcium homeostasis. A distinction can be made between renal, absorptive and resorptive hypercalciuria, originating from disturbed calcium handling in kidney, intestine and bone, respectively. A positive family history predisposes individuals to an increased risk of stone formation, which strongly indicates the involvement of genetic susceptibility factors. TRPV5 is the renal epithelial calcium channel that is the gatekeeper protein in active calcium reabsorption in the kidney. TRPV5 gene ablation in mice leads to severe hypercalciuria, implying that TRPV5 is an interesting candidate gene for renal hypercalciuria in humans. This study aims to identify and functionally characterize TRPV5 gene aberrations in patients with renal hypercalciuria.

Methods. The TRPV5 coding region and intron–exon boundaries were screened for gene mutations in 20 subjects displaying renal hypercalciuria after which identified non-synonymous polymorphisms were functionally characterized by patch-clamp analysis. Wild-type and TRPV5 channels including polymorphisms were transiently expressed in human embryonic kidney (HEK) 293 cells and functionally characterized by path-clamp analysis.

Results. Genotyping TRPV5 in renal hypercalciuria patients revealed three non-synonymous and five synonymous polymorphisms. Electrophysiological characterization of the TRPV5 mutants did not reveal significant functional changes compared to wild-type TRPV5 channel recordings.

Conclusions. In this specific patient cohort, our data do not support a primary role for TRPV5 in the pathogenesis of renal hypercalciuria. However, TRPV5 cannot be excluded as a candidate gene in hypercalciuria.

 
 
 
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