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Articles by J. Y Lee
Total Records ( 8 ) for J. Y Lee
  J. Y Choi , M. J Kim , J. Y Lee , J. S Lim , J. J Chung , K. W Kim and H. S. Yoo
 

OBJECTIVE. The purpose of this article is to present the typical and atypical manifestations of serous cystadenoma, which can be visualized with cross-sectional imaging.

CONCLUSION. Serous cystadenomas of the pancreas have various distinguishing imaging features. Typically, a serous cystadenoma is morphologically classified as having either a polycystic, honeycomb, or oligocystic pattern. Atypical manifestations of serous cystadenoma can include giant tumors with ductal dilatation, intratumoral hemorrhages, solid variants, unilocular cystic tumors, interval growth, and a disseminated form.

  J. Y Lee , A. K Park , K. M Lee , S. K Park , S Han , W Han , D. Y Noh , K. Y Yoo , H Kim , S. J Chanock , N Rothman and D. Kang
 

Objectives: This study was conducted to investigate the role of common variation in innate immunity-related genes as susceptibility factors to breast cancer risk in Korean women. Methods: Total 1536 single-nucleotide polymorphisms (SNPs) in 203 genes were analyzed by Illumina GoldenGate assay in 209 cases and the same numbers of controls. Both SNP and gene-based tests were used to evaluate the association with breast cancer risk. The robustness of results was further evaluated with permutation method, false discovery rate and haplotype analyses. Results: Both SNP and gene-based analyses showed promising associations with breast cancer risk for 17 genes: OR10J3, FCER1A, NCF4, CNTNAP1, CTNNB1, KLKB1, ITGB2, ALOX12B, KLK2, IRAK3, KLK4, STAT6, NCF2, CCL1, C1QR1, MBP and NOS1. The most significant association with breast cancer risk was observed for the OR10J3 SNP (rs2494251, P-value = 1.2 x 10–4) and FCER1A SNP (rs7548864, P-value = 7.7 x 10–4). Gene-based permutation and false discovery rate P-values for OR10J3 SNP (rs2494251) with breast cancer risk were also significant (P = 4 x 10–5 and 0.008, respectively). Haplotype analyses supported these findings that OR10J3 and FCER1A were most significantly associated with risk for breast cancer (P = 2 x 10–4 and 0.004, respectively). Conclusion: This study suggests that common genetic variants in the OR10J3 and FCER1A be strongly associated with breast cancer risk among Korean women.

  D. W Park , S. C Yun , J. Y Lee , W. J Kim , S. J Kang , S. W Lee , Y. H Kim , C. W Lee , J. J Kim , S. W Park and S. J. Park
 

Background— Although C-reactive protein (CRP) has been proposed as a useful biomarker for predicting atherothrombosis, the association between CRP and stent thrombosis after drug-eluting stent implantation has not been defined.

Methods and Results— We prospectively evaluated 2691 patients treated with drug-eluting stents who had a baseline CRP measurement. The primary outcome was stent thrombosis; secondary outcomes were death, myocardial infarction (MI), death or MI, and target vessel revascularization. During follow-up (median, 3.9 years), 32 patients had definite or probable stent thrombosis, 137 patients died, 227 had an MI, and 195 underwent target vessel revascularization. In multivariable Cox proportional-hazards models, elevated levels of CRP were significantly associated with increased risk of stent thrombosis (hazard ratio, 3.86; 95% confidence interval, 1.82 to 8.18; P<0.001). Elevated CRP levels also significantly predicted the risks of death (hazard ratio, 1.61; 95% confidence interval, 1.13 to 2.28; P=0.008), MI (hazard ratio, 1.63; 95% confidence interval, 1.25 to 2.12; P=0.001), and death or MI (hazard ratio, 1.61; 95% confidence interval, 1.29 to 2.00; P<0.001) but not target vessel revascularization (hazard ratio, 1.20; 95% confidence interval, 0.90 to 1.61; P=0.21). The incorporation of CRP into a model with patient, lesion, and procedural factors resulted in a significant increase in the C statistic for the prediction of stent thrombosis, MI, and the composite of death or MI.

Conclusions— Elevated CRP levels were significantly associated with increased risks of stent thrombosis, death, and MI in patients receiving drug-eluting stents, suggesting the usefulness of inflammatory risk assessment with CRP. Given the relatively infrequent occurrence of stent thrombosis, death, and MI, larger studies with longer-term follow-up are required to confirm the novel relationship.

  S. Y Min , D. W Park , S. C Yun , Y. H Kim , J. Y Lee , S. J Kang , S. W Lee , C. W Lee , J. J Kim , S. W Park and S. J. Park
 

Background— The clinical characteristics that identify high-risk subsets of patients with unprotected left main coronary artery disease undergoing percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) have not been well established.

Methods and Results— Between January 2000 and June 2006, 2240 patients with unprotected left main coronary artery disease underwent PCI (n=1102) or CABG (n=1138). Twenty-six preprocedural parameters were evaluated by univariate and multivariate Cox regression analysis to identify independent predictors of all-cause mortality and target-vessel revascularization. Interaction tests were performed to compare heterogeneities of effects of preprocedural parameters depending on the revascularization methods. During follow-up (median of 3.1 years), 187 patients died (78 PCI and 109 CABG) and 149 patients had target-vessel revascularization (121 PCI and 28 CABG). EuroSCORE ≥6 was an independent predictor of death in both groups. Additional independent predictors were chronic renal failure and previous congestive heart failure in the PCI group and age ≥75 years, atrial fibrillation, right coronary artery disease, and left main distal bifurcation disease in the CABG group. Interaction analysis showed no heterogeneities of the effects of variables depending on the revascularization methods. Independent predictors of target-vessel revascularization were acute coronary syndrome and left main distal bifurcation disease in the PCI group and history of coronary intervention in the CABG group. The interaction between previous PCI and treatment remained after adjustment for all independent predictors of target-vessel revascularization (interaction P=0.0345).

Conclusions— Several clinical characteristics were identified as important preprocedural predictors of long-term adverse outcomes after percutaneous or surgical revascularization in patients with unprotected left main coronary artery disease.

  A. M Caputo , J. Y Lee , C. E Spritzer , M. E Easley , J. K DeOrio , J. A Nunley and L. E. DeFrate
  Background

Previous studies have suggested that injury to the anterior talofibular ligament (ATFL) may be linked to altered kinematics and the development of osteoarthritis of the ankle joint. However, the effects of ATFL injury on the in vivo kinematics of the ankle joint are unclear.

Hypothesis

Based on the orientation of the ATFL fibers, ATFL deficiency leads to increased anterior translation and increased internal rotation of the talus relative to the tibia.

Study Design

Descriptive laboratory study.

Methods

The ankles of 9 patients with unilateral ATFL injuries were compared as they stepped onto a level surface. Kinematic measurements were made as a function of increasing load. With use of magnetic resonance imaging and orthogonal fluoroscopy, the in vivo kinematics of the tibiotalar joint were measured in the ATFL-deficient and intact ankles of the same individuals.

Results

A statistically significant increase in internal rotation, anterior translation, and superior translation of the talus was measured in ATFL-deficient ankles, as compared with the intact contralateral controls. For example, at 100% body weight, ATFL-deficient ankles demonstrated an increase of 0.9 ± 0.5 mm in anterior translation (P = .008), an increase of 5.7° ± 3.6° in internal rotation (P = .008), and a slight increase of 0.2 ± 0.2 mm in the superior translation (P = .02) relative to the intact contralateral ankles.

Conclusion

Deficiency of the ATFL increases anterior translation, internal rotation, and superior translation of the talus.

Clinical Relevance

Altered kinematics may contribute to the degenerative changes observed with chronic lateral ankle instability. These findings might help to explain the degenerative changes frequently observed on the medial talus in patients with chronic ATFL insufficiency and so provide a baseline for improving ankle ligament reconstructions aimed at restoring normal joint motion.

  S. B Jang , C Ma , J. Y Lee , J. H Kim , S. J Park , A. R Kwon and B. J. Lee
 

The HP0827 protein is an 82-residue protein identified as a putative ss-DNA-binding protein 12RNP2 Precursor from Helicobacter pylori. Here, we have determined 3D structure of HP0827 using Nuclear Magnetic Resonance. It has a ferredoxin-like fold, β1–1–β2–β3–2–β4 (; -helix and β; β-sheet) and ribonucleoprotein (RNP) motifs which are thought to be important in RNA binding. By using structural homologues search and analyzing electrostatic potential of surface, we could compared HP0827 with other RNA-binding proteins (sex-lethal, T-cell restricted intracellular antigen-1, U1A) to predict RNA-binding sites of HP0827. We could predict that β sheets of HP0827, especially β1 and β3, are primary region for RNA binding. Consequently, similar to other RNA-binding proteins, RNP motifs (Y5, F45, F47), positively charged and hydrophobic regions (K32, R37, K40, K41, K43, R70, R73) are proposed as a putative RNA-binding sites. In addition, differences in amino acids composition of RNP motifs, N, C-terminal residues, loop-region fold and the orientation of 1-helix with other RNA recognition motif proteins could give specific biological functions to HP0827. Finally, the study on natural RNA target is also important to completely understand the biological function of HP0827.

  J. Y Lee , Y Nagano , J. P Taylor , K. L Lim and T. P. Yao
 

Parkin catalyzes mitochondrial ubiquitination, recruiting autophagic components that clear damaged mitochondria. Defects in this pathway are implicated in Parkinson's disease.

  L Li , J. Y Lee , J Gross , S. H Song , A Dean and P. E. Love
 

During erythrocyte development, the nuclear cofactor Lim domain binding protein 1 (Ldb1) functions as a core subunit of multiprotein DNA binding complexes that include the transcription factors Scl and Gata-1 and the Lim-only adapter Lmo2. Scl, Gata-1, and Lmo2 are each required for erythropoiesis, suggesting that Ldb1-nucleated transcription complexes regulate key steps during erythropoiesis. We documented a requirement for Ldb1 in erythropoiesis in mice. Analysis of ldb1–/– embryos revealed a critical requirement for Ldb1 during primitive erythropoiesis, and conditional inactivation of ldb1 at later stages of gestation and in adult mice demonstrated that Ldb1 is continuously required for both definitive erythropoiesis and megakaryopoiesis. Down-regulation of Ldb1 in erythroblasts inhibited the expression of multiple erythroid-specific and prosurvival genes. These results represent the first unequivocal demonstration of a role for Ldb1 in erythropoiesis in vivo and establish a critical function for Ldb1-nucleated complexes in regulating the erythroid/megakaryocyte transcriptional program.

 
 
 
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