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( Jin Ju Kim ),( Young Min Choi ),( Jin Hwa Kang ),( Kyu Ri Hwang ),( Soo Jin Chae ),( Sun Mie Kim ),( Seung Yup Ku ),( Seok Hyun Kim ),( Jung Gu Kim ),( Shin Yong Moon ) 대한산부인과학회 2013 Obstetrics & Gynecology Science Vol.56 No.4
Objective: Metabolic disturbances are well-recognized clinical features of polycystic ovary syndrome (PCOS). Carotid intima-media thickness (CIMT) has been widely used as a surrogate marker of atherosclerosis and cardiovascular disease (CVD). CIMT in women with PCOS has been investigated in many studies, but there has been only one report in the Korean population. The aim of the present study was to compare the presence of subclinical atherosclerosis in young untreated Korean women with PCOS and age-matched controls, specifically by measuring their CIMT. Methods; CIMT was measured by one radiologist in 56 PCOS patients and 56 controls. To compare the CIMT according to PCOS phenotypes, women with PCOS were divided into two subgroups according to the presence of hyperandrogenism. Results; Although PCOS patients were more obese and had higher blood pressure and insulin resistance index than the age-matched controls, the CIMT was not different between the two groups (0.49 ± 0.09 mm in PCOS patients vs. 0.50 ± 0.11 mm in controls, respectively, p = 0.562). When the CIMT in the control group was compared with hyperandrogenic and non-hyperandrogenic PCOS groups, also no significant differences were found. Conclusion; Despite the significant differences in some vascular risk factors between women with PCOS and controls, PCOS patients did not have a significantly higher CIMT (even in the hyperandrogenic subgroups). Although our study did not show the increased risk of subclinical atherosclerosis in PCOS patients, the role of CIMT continues to be investigated considering the importance of screening and monitoring CVD risk factors in women with PCOS.
Lim, Yong,Kim, Tack-Joong,Jin, Yong-Ri,Kim, Dong-Woon,Kwon, Jin-Sook,Son, Ju-Hee,Jung, Jae-Chul,Avery, Mitchell A,Son, Dong Ju,Hong, Jin Tae,Yun, Yeo-Pyo Williams Wilkins 2007 The Journal of Pharmacology and Experimental Thera Vol.321 No.2
<P>The abnormal proliferation of vascular smooth muscle cells (VSMCs) in arterial walls is an important pathogenetic factor of vascular disorders such as atherosclerosis and restenosis after angioplasty. Epothilone B, a novel potential antitumor compound, has a potent effect on preventing postangioplasty restenosis. Therefore, we established an in vivo rat carotid injury model and examined the potential effects of epothilone B on cardiovascular disease. We found that epothilone B potently prevented neointimal formation and in vivo VSMCs proliferation. In addition, we also showed that epothilone B significantly inhibited 5% fetal bovine serum (FBS)- and 50 ng/ml platelet-derived growth factor (PDGF)-BB-induced proliferation and cell cycle progression in rat aortic VSMCs. Furthermore, FBS and PDGF-BB induced the activations of extracellular signal-regulated kinases 1 and 2, Akt, phospholipase C gamma 1, and PDGF-receptor beta chain tyrosine kinase were not changed by epothilone B. However, epothilone B treatment caused a significant decrease in the level of cyclin-dependent protein kinase (CDK) 2, whereas it caused no change in the levels of cyclin E and down-regulated the phosphorylation of retinoblastoma, which plays a critical role in cell cycle regulation. Furthermore, levels of p27, an inhibitor of cyclin E/CDK2 complex, were significantly increased in VSMCs treated with epothilone B, indicating that this might be a major molecular mechanism for the inhibitory effects of epothilone B on the proliferation and cell cycle of VSMCs. These findings suggest that epothilone B can inhibit neointimal formation via the cell cycle arrest by the regulation of the cell cycle-related proteins in VSMCs.</P>
Pulmonary Chondroid Hamartoma With Nontuberculous Mycobacterial Infection: Two Case Reports
Lee, Yong Chul,Moon, Jin Chang,Gang, Su Jin,Park, Seung Yong,Kim, So Ri Wolters Kluwer Health, Inc. All rights reserved. 2015 Medicine Vol.94 No.14
<P>Solitary pulmonary nodules (SPNs) can be manifested in a variety of disorders including neoplasms, infection, inflammation, and vascular or congenital abnormalities. In addition, they are often accompanied with other pulmonary pathologic lesions such as consolidations and several pulmonary disorders present as similar pulmonary nodular lesions simultaneously. Diagnostic workup is important for these SPNs; however, many physicians often miss the second diagnosis for multiple pulmonary lesions with SPNs due to lack of clinical suspicion that each pulmonary nodule or pathologic lesion can have each other's diagnosis. Herein, we report 2 cases of coexistence of pulmonary chondroid hamartoma with nontuberculous mycobacterial (NTM) infection presenting as pulmonary nodules and multiple consolidative lesions. A 60 year-old man was admitted for the evaluation of multifocal pulmonary lesions including SPN with chronic exertional dyspnea. Multiple lung tissues were obtained from each lesion through percutaneous transthoracic needle biopsy (PTNB). At the same time, bacteriologic examination was performed using respiratory samples obtained by bronchoscopy. Based on pathologic and microbiologic results, the patient diagnosed as pulmonary chondroid hamartoma with pulmonary NTM infectious disease. In addition, a 56-year-old woman visited for the evaluation of a small SPN. The SPN was resected surgically for the pathologic examination and turned out to be pulmonary chondroid hamartoma. Interestingly, the diagnostic workup revealed that the patient had Lady Windermere syndrome which is one of features for Mycobacterium avium complex (MAC) pulmonary disease. Both patients were treated with the standard antibiotics against MAC as recommended by the ATS/IDSA guideline. This is the first report of 2 patients, as far as we know, that chondroid hamartoma and NTM disease develop simultaneously in the lung. This report emphasizes that physicians should endeavor to confirm the individual diagnosis for the various pulmonary abnormal lesions detected at the same time, if necessary through multifocal biopsies for each lesion.</P>