1.Change of Serum Levels of C-Reactive Protein After Coronary Angioplasty and Its Effects on Clinical Restenosis.
Jong Seon PARK ; Gu Ru HONG ; Chae Hoon LEE ; Dong Gu SHIN ; Young Jo KIM ; Bong Sup SHIM
Yeungnam University Journal of Medicine 2001;18(2):215-225
BACKGROUND: There are many evidences that inflammation is an important determinant of the development of atherosclerosis and one of the systemic markers of inflammation, C-reactive protein(CRP), is associated with extent of coronary artery disease and risk of coronary events. We assessed the time response of CRP response after coronary angioplasty and it's influence on the clinical restenosis in angina patients. MATERIALS AND METHODS: Patients included 36 angina patients undergoing single vessel angioplasty. Levels of CRP were measured before and 12, 24, 48, and 72 hours after angioplasty. Clinical restenosis was assessed at 6 months after procedure. RESULTS: Baseline CRP level was 0.30+/-0.01 mg/dL in stable and 0.46+/-0.28 mg/dL in unstable angina patients(p<0.05). After angioplasty, CRP level was increased with peak at 24 hour and persisted to 72 hours after angioplasty. At 24 hour after angioplasty, the magnitude of CRP change was 0.32+/-0.31 mg/dL in stable and 0.79+/-0.73 mg/dL in unstable angina patient(p<0.05). The change of CRP level was not associated with troponin-T after angioplasty. In unstable angina patients, clinical restenosis was developed in 8% of patients with low baseline CRP levels and in 50% of those with high baseline CRP levels more than 0.6 mg/dL(p<0.05). CONCLUSION: In unstable angina patients, inflammatory response is more increased than stable angina patients, and increased inflammatory response effects on the restenosis after coronary angioplasty.
Angina, Stable
;
Angina, Unstable
;
Angioplasty*
;
Atherosclerosis
;
C-Reactive Protein*
;
Coronary Artery Disease
;
Humans
;
Inflammation
;
Troponin T
2.Expressions of Epidermal Growth Factor Receptor, c-erbB-2 and p53 Protein as Useful Markers of Malignant Potential in a Transitional Cell Carcinoma of the Urinary Bladder.
Gu KONG ; Ki Yong SHIN ; Sun Jin KIM ; Young Hyeh KO ; Hae Young PARK ; Young Nam WOO ; Jung Dal LEE
Korean Journal of Pathology 1997;31(1):51-58
Transitional cell carcinoma(TCC) of the urinary bladder shows marked heterogeneity in biological behaviors. Evidence has accumulated that biological markers may provide significant information to predict the potential aggressiveness of TCC. We have assessed the expression of the epidermal growth factor receptor (EGF-R), c-erbB-2 and p53 proteins in 56 cases of TCC to investigate the prognostic significance of differential expression of these oncoproteins using an immunohistochemical method. We analysed the expression patterns of these oncoproteins according to tumor stage and grade. And we assessed the probability of progression-free survival in stage T1 tumors according to their expressions. Positive rates of EGF-R (>+3 staining intensity), c-erbB-2 (intense membrane staining) and p53 proteins (>20% positive cells) were 73.2%, 37.5% and 42.9%, respectively. Invasive tumors had significantly higher positive rates of all three factors than did superficial tumors (p<0.005 for EGF-R and c-erbB-2, p<0.05 for p53). High grade tumors had significantly higher positive rates of c-erbB-2 and p53 proteins (p<0.005). In superficial tumors, T1 tumors had higher positive rate of p53 protein compared with Ta tumors (p<0.05). Twelve cases of superficial tumors (34.3%) were positive for EGF-R and negative for c-erbB-2 and p53 proteins. Nine cases of superficial tumors(25.7%) were negative for all three factors. In invasive tumors, however, 42.5% of the cases were positive for all three factors. The overexpression of p53 protein was the only useful marker to predict the rapid progression in stage T1 tumors (p<0.05, log-rank test). These results suggest that the differential overexpression of EGF-R, c-erbB-2 and p53 proteins could be useful to depict tumor aggressiveness of TCC of the urinary bladder. And, the overexpression of a p53 protein may be a useful marker to predict the possibility of rapid progression in stage T1 tumors.
Biomarkers
;
Carcinoma, Transitional Cell*
;
Disease-Free Survival
;
Epidermal Growth Factor*
;
Immunohistochemistry
;
Membranes
;
Oncogene Proteins
;
Population Characteristics
;
Receptor, Epidermal Growth Factor*
;
Staphylococcal Protein A*
;
Urinary Bladder*
3.Evaluation of left artial appendage function by transesophageal echocardiography.
Hyun Chul SHIN ; Seung Ho KANG ; Dong Gu SHIN ; Young Jo KIM ; Bong Sup SHIM ; Hyun Woo LEE
Journal of the Korean Society of Echocardiography 1993;1(1):109-118
No abstract available.
Echocardiography, Transesophageal*
4.A Case of the Membranous Type of Prepyloric Gastric Atresia.
Young Soon SHIN ; Byeng Gu MIN ; Kyeong Sook CHO ; Jong Dai JO
Journal of the Korean Pediatric Society 1990;33(9):1276-1280
No abstract available.
5.Analysis of 35 cases of microsurgical resection and anstomosis in the management of the patjologic tubal occlusion.
Noh Hyeon PARK ; Young Chul YOO ; Chang Jae SHIN ; Jung Gu KIM ; Yoon Seok CHANG
Korean Journal of Obstetrics and Gynecology 1991;34(5):739-746
No abstract available.
Sterilization, Tubal*
6.The relationship between changes in serum insulin-like growth factor profiles and changes in bone mineral density in postmenopausal women receiving hormone replacement therapy.
Seok Hyun KIM ; Young Min CHOI ; Chang Suk SUH ; Jung Gu KIM ; Chan Soo SHIN
Korean Journal of Obstetrics and Gynecology 2000;43(1):26-31
PURPOSES: To evaluate the effect of hormone replacement therapy(HRT) on serum insulin-like growth factors(IGFs) levels and to investigate if changes in serum IGFs reflect changes in BMD after HRT in postmenopausal women. MATERIAL & METHODS: IGF-I and IGF-II were measured by radioimmunoassay after Bio-spin P-10 seperation in sera obtained every 3 months from postmenopausal women who was taking premarin alone (premarin group; n=17) or premarin-medroxyprogesterone acetate(MPA group; n=42) for 1 year. Also, bone mineral density(BMD) were determined before and 1 year after HRT by dual energy X-ray absorptiometry(DEXA). All statistics were performed by Paired t-test, student's t-test, repeated measures ANOVA test, Pearson's coefficient. RESULTS: HRT increased BMD of the lumbar spine and proximal femur in both premarin group and MPA group, but any difference in degreee of increase in BMD was not noted between premarin group and MPA group. Compared with pretreatment levels, serum IGF-I levels decreased at 3, 6 and 12 months after therapy only in latter group whereas serum IGF-II levels increased at 6 and 12 months after HRT in both groups. Changes in serum IGF-I and IGF-II levels during therapy did not show any difference by the bone response to HRT. Changes in serum IGF-II levels after HRT did not correlated with the 1 year changes in BMD at any skeletal sites studied, but changes in serum IGF-I levels from pretreatment to 6 months after HRT was negatively correlated with change in BMD of Ward's triangle. CONCLUSION: HRT influences serum IGF levels in postmenopausal women and changes in serum IGF-I levels may predict the changes in BMD of Ward's triangle after HRT.
Bone Density*
;
Estrogens, Conjugated (USP)
;
Female
;
Femur
;
Hormone Replacement Therapy*
;
Humans
;
Insulin-Like Growth Factor I
;
Insulin-Like Growth Factor II
;
Postmenopause
;
Radioimmunoassay
;
Spine
7.A Case of Neurofibromatosis with Bilateral Pheochromocytoma.
Hong Seung KIM ; Young Gu SHIN ; Il Hoi KIM ; Yun Mee KIM ; Mee Yeon CHO
Journal of Korean Society of Endocrinology 1997;12(3):478-484
Pheochromocytoma is originated from chromaffin cell of sympathetic nervous system and associated with other disease, such as neurofibromatosis, duodenal carcinoid, medullary thyroid cancer and parathyroid adenoma. Especially, pheochromocytoma is developed more than 50% in neurofibromatosis associated with hypertension. In such cases, several clinical features documented as more frequent bilateral phochromocytoma, more associated with other neuroendocrine tumors and thus more poor prognosis. We can observe the sustained hypertension despite of surgical resection of tumors in pheochromocytoma cases. One of the possible reason of post operative sustained hypertension is the pheochromocytoma originated from minor organ of Zukerkandl that was not resected during operation. Untreated or delayed treated cases with pheochromocytoma were often expired by complication of hypertension such as cerebrovascular hemorrhage, myocardial infarction, etc. Thus, in neurofibromatosis with hypertension, screening of pheochromocytorna is very important for the early detection of tumor and more favorable prognosis. Recently, We experienced a case of neurofibromatosis associated with bilateral pheochromocy-toma expired by cerebral hemorrhage during operation, so we report the case with literature review.
Carcinoid Tumor
;
Cerebral Hemorrhage
;
Chromaffin Cells
;
Hemorrhage
;
Hypertension
;
Mass Screening
;
Myocardial Infarction
;
Neuroendocrine Tumors
;
Neurofibromatoses*
;
Parathyroid Neoplasms
;
Pheochromocytoma*
;
Prognosis
;
Sympathetic Nervous System
;
Thyroid Neoplasms
8.The Predictors of Mitral Regurgitation in Percutaneous Mital Commussurotomy Using Inoue Balloon.
Jong Seon PARK ; Dong Gu SHIN ; Young Jo KIM ; Bong Sup SHIM
Korean Circulation Journal 2000;30(9):1125-1132
BACKGROUND AND OBJECTIVES: Percutaneuous transvenous mitral commissurotomy(PTMC) has been performed as an effective non-surgical treatment modality of rheumatic mitral stenosis. Mitral regurgitation(MR) as a complication of the procedure occur in 20-53% of the patients. The moderate to severe mitral reguargitation, created by the PTMC, sometimes leads to the requirement for mitral valve replacement, but most of the MR limits the optimal dilation of mitral commissure due to the worry about the progression of the MR. This study was designed to evaluate the occurrence of mitral regurgitation and predictive factors for the moderate to severe mitral regurgitation(grade> or =2) induced by PTMC. METHODS: This study enrolled 46 patients(female 42, mean age 45 years) who have performed PTMC in Yeungnam University Hospital from May 1996 to May 1999. We analyzed the occurrence rate of mitral regurgitation(MR) and predictive factors for MR grade> or =2 after procedure. RESULTS: MR was detected in 35% of the patients prior PTMC, and in 56% after the procedure(grade 1, 30%; grade 2, 15%; grade 3, 11%). 21 cases of the MR was commissure MR as a grade< or =2. MR grade 3, occured in 5 patients, was non-commissure MR caused by the unilateral rupture of the lateral commissure in 4 patients and tearing of the annulus in one patient. On the univariate analysis, patients with MR grade> or =2 showed more frequent atrial fibrillation, mitral regurgitation and fluoroscopic calcification, and had more severe symptoms than patients with MR grade<2 before the procedure. On the analysis of the calcification, there was no significant difference of the leaflet calcification score, but the commissure calcification score was significantly higher in MR> or =2 group than MR<2 group(1.5+/-0.54 vs 2.5+/-0.96, p=.02). On the multivariate logistic regression analysis, independent predictor of MR grade> or =2 was fluoroscopic mitral calcification(OR 6.38, p=.048). CONCLUSION: Mild to moderate commissure MR was observed in most of the patients after PTMC. Commissure calcification have more influence on the development of MR grade> or =2 than valvular calcification, and the fluoroscopic mitral calcification can predict the occurrence of MR grade> or =2 mitral regurgitation after PTMC.
Atrial Fibrillation
;
Humans
;
Logistic Models
;
Mitral Valve
;
Mitral Valve Insufficiency*
;
Mitral Valve Stenosis
;
Rupture
9.Correlation of Tumor Angiogenesis and nm23-H1 Expression with Lymph Node Metastasis in Proper Muscle Gastric Cancer.
Eun Sook NAM ; Gu KANG ; Hyung Sik SHIN ; Young Eui PARK
Korean Journal of Pathology 1997;31(5):410-416
We studied clinicopathologic features of 44 cases of PM (proper muscle) gastric cancer, correlated the lymph node metastasis and found the result of immunohistochemical staining for tumor angiogenesis using antibodies to Factor VIII-related antigen and nm23-H1, known as meatastasis inhibitory substance. The results were as follows: 1) The average age of these 44 cases of PM gastric cancer was 55.1 years old (range 35-81). The ratio of male to female was 2.2 : 1. The tumor was located at the antrum of stomach in 72.7% of the cases. The average size of the tumor was 4.1 cm (range 0.6-9). The gross features were comprised of Borrmann type I (6.8%), II (29.6%), III (56.8%), IV (6.8%), respectively. The microscopic type was a diffuse type in 70.5% and an intestinal type in 29.5%. There were lymph node metastasis in 25 of the 44 cases (56.8%). 2) The microvessel count was higher in the lymph node positive group (average 69.3) than in the lymph node negative group (average 45.6) (P=0.004). There was a higher microvessel density in diffuse type, over 4 cm of tumor size, proximally located tumor, older than 50 years, Borrmann type II and IV, but there was no statistically significant correlation. 3) The more decreased expression of nm23-H1 was found in the lymph node positive group (56.0%) than in the lymph node negative group (31.6%), but showed no statistical significance (P=0.0142). There was no significant correlation between the expression of nm23-H1 and the other clinicopathologic factors. We suggest that the microvessel count of the tumor angiogenesis may be a prognostic factor for predicting lymph node metastasis and also help to determine the therapeutic modalities of PM gastric cancer.
Antibodies
;
Female
;
Humans
;
Lymph Nodes*
;
Male
;
Microvessels
;
Neoplasm Metastasis*
;
Stomach
;
Stomach Neoplasms*
;
von Willebrand Factor
10.The Role of the Adenosine Receptor Subtypes and Protein Kinase C in Ischemic Preconditioning in the in Vivo Cat Heart.
Young Jo KIM ; Dong Gu SHIN ; Jong Seon PARK ; Kyo Won CHOI ; Bong Sub SHIM
Korean Circulation Journal 1996;26(5):1038-1047
BACKGROUND: It is well known that ischemic preconditioning protects the heart against infarction or arrhythmias from a subsequent ischemic injury. Recent laboratory data indicate that the adenosine during the ischemic period may trigger protection via A1 or A3 adenosine receptor and also protein kinase C(PKC) plays a central role. This study was designed to determine the role of adenosine receptor subtypes and PKC in the preconditioning protection. METHODS: All cat heart groups were subjected to 40min ischemia and 30min reperfusion. The preconditioning protocol consists of 4min ischemia and then 10min of reperfusion 4 times. The effects of ischemic preconditioning, nonselective adenosine receptor blocker(SPT), an A1 specific antagonist(DPCPX) and protein kinase C inhibitor(Polymyxin B), on ischemic preconditioning were determined by infarction size. There were 5 groups : (1) control group (Group 1, n=10)(2) Ischemic preconditioned group(Group 2, n=9)(3) DPCPX pretreatment group(Group 3, n=6)(4) SPT preteatment group(Group 3, n=6)(5) Polymyxin B pretreatment group(Group 5, n=6). SPT and DPCPX were given intravenously 5 min before ischemic preconditioning. Polymyxin B was administered to cats for 30min during ischemic preconditioning period. RESULTS: Ischemic preconditioning only or pretreatment with DPCPX prior to preconditioning demonstrated a significant reduction in infarct size(22.6+/-1.5, 25.4+/-0.9% infarction of the risk zone, respectively, p<0.05) with respect to control, SPT-pretreatment, and polymyxin B-pretreatment groups(44.0+/-1.7, 43.0+/-2.0 and 40.3+/-0.4% infarction of the risk zone, respectively). CONCLUSIONS: Ischemic preconditioning protects heart from subsequent ischemia. Protection was blocked by SPT and protein kinase C inhibitor(polymyxin B), but not by A1 antagonist DPCPX. The cardioprotective effects by ischemic preconditioning in the in vivo cat heart appear to be dependent on A3 adenosine receptors and activation of protein kinase C.
Adenosine*
;
Animals
;
Arrhythmias, Cardiac
;
Cats*
;
Heart*
;
Infarction
;
Ischemia
;
Ischemic Preconditioning*
;
Polymyxin B
;
Polymyxins
;
Protein Kinase C*
;
Protein Kinases*
;
Receptors, Purinergic P1*
;
Reperfusion