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Articles by Y Kim
Total Records ( 4 ) for Y Kim
  H. K Roy , A. J Gomes , S Ruderman , L. K Bianchi , M. J Goldberg , V Stoyneva , J. D Rogers , V Turzhitsky , Y Kim , E Yen , M Jameel , A Bogojevic and V. Backman
 

Flexible sigmoidoscopy is a robust, clinically validated, and widely available colorectal cancer screening technique that is currently sanctioned by major guideline organizations. Given that endoscopic visualization is generally limited to the distal third of the colon and women tend to have a proclivity for proximal lesions, the flexible sigmoidoscopy performance is markedly inferior in women than in men. Our group has shown that by using a novel light-scattering approach, we were able to detect an early increase in blood supply (EIBS) in the distal colonic mucosa, which served as a marker of field carcinogenesis and, hence, proximal neoplasia. Therefore, we sought to ascertain whether rectal EIBS would improve flexible sigmoidoscopy, especially in women. A polarization-gated spectroscopy fiber-optic probe was used to assess EIBS in the endoscopically normal rectum (n = 366). When compared with gender-matched neoplasia-free controls, females with advanced proximal neoplasia (n = 10) had a robust (60%; P = 0.002) increase in rectal mucosal oxyhemoglobin content whereas the effect size in males was less marked (33%; P = 0.052). In women, addition of rectal oxyhemoglobin tripled the sensitivity for advanced neoplasia over flexible sigmoidoscopy alone. Indeed, the performance characteristics seemed to be excellent (sensitivity, 100%; specificity, 76.8%; positive predictive value, 32.6%; and negative predictive value, 100%). A variety of nonneoplastic factors were assessed and did not confound the relationship between rectal EIBS and advanced neoplasia. Therefore, using rectal EIBS in combination with flexible sigmoidoscopy mitigated the gender gap and may allow flexible sigmoidoscopy to be considered as a viable colorectal cancer screening test in women. Cancer Prev Res; 3(7); 844–51. ©2010 AACR.

  R Shantouf , C. P Kovesdy , Y Kim , N Ahmadi , A Luna , C Luna , M Rambod , A. R Nissenson , M. J Budoff and K. Kalantar Zadeh
 

Background and objectives: Recent in vitro studies have shown a link between alkaline phosphatase and vascular calcification in patients with chronic kidney disease (CKD). High serum levels of alkaline phosphatase are associated with increased death risk in epidemiologic studies of maintenance hemodialysis (MHD) patients. We hypothesized that coronary artery calcification is independently associated with increased serum alkaline phosphatase levels in MHD patients.

Design, setting, participants, & measurements: We examined the association of coronary artery calcification score (CACS) and alkaline phosphatase in 137 randomly selected MHD patients for whom markers of malnutrition, inflammation, and bone and mineral disorders were also measured.

Results: Serum alkaline phosphatase was the only measure with significant and robust association with CACS (P < 0.003), whereas either other biochemical markers had no association with CACS or their association was eliminated after controlling for case-mix variables. Serum alkaline phosphatase >120 IU/L was a robust predictor of higher CACS and was particularly associated with the likelihood of CACS >400 (multivariate odds ratio 5.0 95% confidence interval 1.6 to 16.3; P = 0.007). Serum alkaline phosphatase of approximately 85 IU/L seemed to be associated with the lowest likelihood of severe coronary artery calcification, but in the lowest tertile of alkaline phosphatase, the CACS predictability was not statistically significant.

Conclusions: An association between serum alkaline phosphatase level and CACS exists in MHD patients. Given the high burden of vascular calcification in patients with CKD, examining potential therapeutic interventions to modulate the alkaline phosphatase pathway may be warranted.

  J Park , Y Kim and J. Chung
  Jeehye Park, Yongsung Kim, and Jongkyeong Chung

Parkinson’s disease (PD), one of the most common neurodegenerative disorders worldwide, currently lacks a cure. Although most PD cases occur sporadically, studies from rare genetic mutations give significant insights into addressing the pathological mechanism of not only familial PD, but also sporadic PD. Recent PD research focuses on generating genetic mutant animal models that recapitulate the features of human PD patients. Significant advances in PD research have resulted from studying Drosophila mutants of several identified PD-associated genes because they show strikingly visible phenotypes. In particular, previous studies with the Drosophila mutants parkin and PINK1, which are two common causative genes among PD familial forms, have suggested strongly that mitochondrial dysfunction is the prominent cause for the PD pathogenesis and that these two PD genes are in a common pathway, with Parkin downstream of PINK1. Recent genetic studies have revealed that the PINK1-Parkin pathway is involved in regulating the mitochondrial remodeling...

  B Kim , Y Lee , Y Kim , K. H Lee , S Chun , K Rhee , J. T Seo , S. W Kim and J. S. Paick
  BACKGROUND

DAZ is a male infertility gene located at the AZFc region of the Y chromosome. There are four copies of the DAZ gene that share a strong homology but are not identical to one another. In the present study, we carried out cDNA cloning and immunoblot analyses to determine whether all of the DAZ genes are actively expressed in the human testis.

METHODS

AZFc deletion was detected by sequence-tagged site polymerase chain reaction (PCR) of genomic DNA isolated from blood samples. DAZ cDNAs were cloned with RT–PCR followed by sequence analysis. The expression of DAZ proteins in human testis was determined by immunoblot and compared with DAZ cDNA expression.

RESULTS

Immunoblot analysis revealed four DAZ protein bands in testis samples that showed no deletions in the AZFc region. No specific bands were observed in samples from AZFc deletion patients. Testis samples from individuals with the partial AZFc deletion, gr/gr, showed two DAZ-specific bands. Interestingly, the sizes of DAZ-specific bands varied among individuals. Analysis of DAZ transcripts in testis samples revealed that the DAZ proteins were translated from the largest of the multiple transcripts originating from each single DAZ gene.

CONCLUSIONS

All four DAZ genes are expressed in the human testis, and their products are highly polymorphic among men.

 
 
 
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