This study was undertaken to observe the mutagenic occurrence in urine excreted after the ingestion of roast beef. Two healthy nonsmoker persons of both sex were selected for this test, employing two strains (TA98, TA100) of Salmonella typhimurium according to Ames' method. The mutagenic activity began to appear in urine of both sex three hours after ingestion of 300 g of roast beef, gradually increasing until 6 hours and declining thereafter.
Eating* ; Humans* ; Methods ; Red Meat* ; Salmonella typhimurium

Behcet's disease was originally described as a triple symptom complex of oral aphthous ulceration, genital ulceration, and hypopyon iritis. It is now known to have a wide systemic manifestations. Among them, the central nervous system involvement should be diagnosed earlier because of it's lethal potential. Recently the authors experienced a case of Behcet's disease with CNS involvement. A 51-year-old female patient was admitted due to deterioration of mentality and generalized ache since 2 years prior to admission. The findings on physical examination were compatible with Behcet's disease, but without cerebrospinal pleocytosis. The manifestations were improved with medications of prednisolone, chlorambucil, colchicines, but relapsed relapsed 2 months later during subsequent tapering of prednisolone and chlorambucil. The patient is now on medication again. A case of Behcet's disease with CNS manifestations is reported with review of literature.
Behcet Syndrome ; Central Nervous System ; Chlorambucil ; Female ; Humans ; Iritis ; Leukocytosis ; Middle Aged ; Physical Examination ; Prednisolone ; Stomatitis, Aphthous ; Ulcer

No abstract available.

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

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

BACKGROUND: It is well known that ischemic preconditioning protects the heart against infarction or arrhythmias from a subsequent ischemic injury. Two phases of the effect of preconditioning has been explored, early protection and second window of protection at 24 hours. The late protection was seen in some animal model, but the precise mechanism is controversal. This study was designed to evaluate the late cardioprotective effect and role of HSP70 in ischemic preconditioning of cat heart. METHODS: Two groups of cats were studied. Control animals were subjected to an episode of 40-min coronary artery occlusion followed by 30-min reperfusion. Experimental animals were subjected to ischemic preconditioning before the 40-min ishcemia/reperfusion. The preconditioning protocol was comprised of three 5-min episodes of ischemia interspersed by 10-min episodes of reperfusion. After sustained ischemia and reperfusion, left ventricular risk area and infart area were measured by injection of Evans blue bye and triphenyltetrazolium staining, and myocardial HSP70 mRNA was examined in risk(left ventricular anterior wall) and nonrisk(left ventricular posterior wall) area using northern blot hybridization. HSP70 mRNA expression was quantified as a percent of GAPDH. The late cardioprotective effects of ischemic preconditioning were determined by infarct size (% area at risk). RESULTS: Infarct size was markedly limited by ischemic preconditioning when compared with the control group (18.5+/-6.9% vs 38.5+/-11.1%; p<0.001). HSP70 mRNA expression in risk area was much higher in preconditioning group than control group(78+/-12% vs 41+/-11%; p<0.01). But, there was no significant difference of HSP70 mRNA expression in the posterior wall between control and ischemic preconditioning group. CONCLUSIONS: These data suggest that ischemic preconditioning have delayed myocardial protective effect from ischemia. The increase in myocardial HSP70 mRNA may be one of the contributing factors to the delayed cardioprotective effects of ischemic preconditioning in cats.
Animals ; Arrhythmias, Cardiac ; Blotting, Northern ; Cats* ; Coronary Vessels ; Evans Blue ; Heart* ; Heat-Shock Proteins* ; Hot Temperature* ; HSP70 Heat-Shock Proteins ; Infarction ; Ischemia ; Ischemic Preconditioning* ; Models, Animal ; Reperfusion ; RNA, Messenger

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

Sudden cardiac death (SCD) remains a preeminent public health problem. Identification of high-risk patients, susceptible to SCD, is essential for the successful prophylactic therapy. The majority of such sudden deaths are preceded by fatal ventricular arrhythmias, mainly as a result of ischemic heart diseases. This article is intended to describe the methods of prediction, the results and limitations of the currently used methods. The current measures available for screening of high-risk patients, such as demographic variables, left ventricular contractile function, ventricular ectopy by Holter monitoring, late potentials by signal-averaged ECG, heart rate variability, QT dispersion and even electrophysiologic testing, have limited sensitivity, and specificity, and are only helpful in a minority of patients already at high-risk. The predictive value of each method is modest, even when several predictors are combined. As a result, the effect on the cumulative incidences of SCD, in the population at large, have been relatively small, as the majority of SCD occurs in patients who do not have the characteristics leading to their inclusion in trials of implantable defibrillators. A challenge for the future will be the development of new approaches, or techniques, which will allow screening for markers of increased risk of fatal ventricular arrhythmias in large general populations, of which the relative risk is low, but the number of deaths, due to arrhythmias, are high. Incidences of coronary artery diseases, one of the most important causes of sudden cardiac death, including acute myocardial infarction, have recently grown exponentially in Korea. Therefore, there is a need to develop our own risk stratification strategy by searching for new tools for the prediction, and refinement, of existing tools.
Arrhythmias, Cardiac ; Coronary Artery Disease ; Death, Sudden ; Death, Sudden, Cardiac* ; Defibrillators, Implantable ; Electrocardiography ; Electrocardiography, Ambulatory ; Heart Rate ; Humans ; Incidence ; Korea ; Mass Screening ; Myocardial Infarction ; Myocardial Ischemia ; Public Health ; Risk Assessment ; Sensitivity and Specificity ; Ventricular Function

The 8 cases of left ventricular thrombus detected by the 2 D echocardiography or left ventriculography, after acute transmural anterior myocardial infarction were effectively lysed by the thrombolytic agents and heparin therapy. The thrombolytic agents were either urokinase or tissue plasminogen activator. Urokinase was infused intravenously at a dose of 1.0 million unit for three days. And tissue plasminogen activator was infused at a dose of 100mg for a day. In all cases, the thrombi were completely lysed. At follow up, no recurrence of left ventricular thrombus was found. We have experienced 2 cases of peripheral embolization in which, left ventricular thrombi were protruding nonmobile type. The one was the embolic cerebral infarction, the other was transient hoarseness and paresthesia on the left foot, which may be transient ischemic attack. These results show that left ventricular thrombi can be treated by intravenous thrombolytic agents without life-threatening complication. However, for the better establishment of the risk and benefit of therapy further investigation is needed.
Cerebral Infarction ; Echocardiography ; Fibrinolytic Agents ; Follow-Up Studies ; Foot ; Heparin ; Hoarseness ; Ischemic Attack, Transient ; Myocardial Infarction* ; Paresthesia ; Recurrence ; Thrombolytic Therapy* ; Thrombosis* ; Tissue Plasminogen Activator ; Urokinase-Type Plasminogen Activator

No abstract available.
Papillary Muscles* ; Tachycardia, Ventricular*