BACKGROUND AND OBJECTIVES: Doppler indexes of pulmonary venous flow (PVF) have been recognized to be useful in defining left ventricular filling characteristics, but their long-term prognostic value in patients with acute myocardial infarction (AMI) is not clear. The purpose of this study was to determine the prognostic significance of Doppler indexes of PVF after AMI. SUBJECTS AND METHODS: Doppler echocardiographic examination was performed in 122 patients with AMI between 7 to 10 days after attack, and followed for 30 months. Peak systolic velocity (PVs), peak diastolic velocity (PVd), and peak reverse flow velocity associated with atrial contraction (PVa) of PVF were measured by transthoracic echocardiography. End-points were cardiac death or readmission due to congestive heart failure (re-CHF). RESULTS: There were 9 deaths (7.4%) and 13 patients with re-CHF (10.7%) during the follow-up period. Patients with events had higher PVa (p=0.039). Subgroup analysis of patients with E/A ratio > 1 showed that they had lower PVs/PVd ratio (p=0.029) and higher PVa (p=0.069). Event-free survival was significantly lower in patients with PVs/PVd ratio < 1.3 (30-month survival rate 74% vs. 100% in those with PVs/PVd ratio > or =1.3). Multivariate Cox analysis revealed that Killip class II, and EF <50% were independent predictors of cardiac events; and PVa > or =25 cm/sec as well as age > or =65 years were independent predictors of cardiac mortality in patients with E/A ratio >1. CONCLUSION: PVa and PVs/PVd ratio of PVF were helpful indexes in predicting the prognosis in patients with AMI and an E/A ratio of >1.
Death ; Disease-Free Survival ; Echocardiography ; Follow-Up Studies ; Heart Failure ; Humans ; Mortality ; Myocardial Infarction* ; Prognosis ; Pulmonary Veins ; Survival Rate

The infant kidney is more vulnerable to infections than the adult kidney. It is common that acute pyelonephritis (APN) during infancy and early childhood manifests growth retardation of kidney, ultimately leading to chronic renal failure. However, little is known about the pathogenesis of renal growth retardation in APN in youth. To understand the mechanism underlying the cortical lesions, urinary tract infection was induced in infant rats. To induce ascending APN, saline solution containing Escherichia coli (ATCC No. 25922) 107 bacteria/ml was infused into the bladder through the 16 gage silicone cannula in three-week-old weaning Sprague Dawley rats (weight 50~60 g, n=66). In the normal control group (n=20), saline was infused. Experimental groups were divided according to the treatment into the APN group (APN without any treatment, n=23) and TRX group (APN with ceftriaxone treatment, n=23). After performing the histopathologic examination, including inflammatory score, fibrosis score, and tubular atrophy score, we measured the apoptosis index in the tubular cells of noninflammatory cortical area at post-infection week 1 and 3 by the in situ TUNEL method. Kidney weight was significantly decreased in the APN group compared with the normal group at postinfection week 1 and 3. In the APN group, tubulointerstitial inflammation with heavy neutrophilic infiltration was found mainly in the upper and lower poles of the kidney in both the first and third week groups. Fibrosis was dominant in the third week of the APN group. However, inflammation and fibrosis were not significantly improved by TRX treatment. The apoptotic index of tubular cells was significantly increased in noninflammatory cortical area in the first week of both APN and TRX groups. It decreased near the normal control value in the third week. TGF-beta1 protein expression was localized in the inflammatory area. There was no TGF-beta1 expression in the tubules of the noninflammatory area. These findings suggest that renal growth retardation in experimentally induced APN in infant rats is related not only with the inflammatory reaction itself but also with the increased apoptosis of tubular cells in noninflammatory area. Ceftriaxone alone does not eliminate the inflammation nor prevent growth retardation effectively.
Adolescent ; Adult ; Animals ; Apoptosis* ; Atrophy ; Catheters ; Ceftriaxone ; Escherichia coli ; Fibrosis ; Humans ; In Situ Nick-End Labeling ; Infant* ; Inflammation ; Kidney ; Kidney Failure, Chronic ; Neutrophils ; Pyelonephritis* ; Rats* ; Rats, Sprague-Dawley ; Silicones ; Sodium Chloride ; Transforming Growth Factor beta1 ; Urinary Bladder ; Urinary Tract Infections ; Weaning

No Abstract Available.
Fas Ligand Protein* ; Keratoconus*

BACKGROUND: Platelet function is directly influenced by lipoproteins, and platelets from hypercholesterolemic patients display increased reactivity which is related to initiation, progression, and development of thromboembolic complications in atherosclerosis. But the exact mechanism of this effect is unclear. METHODS: In this study, total and activated numbers of platelet glycoprotein (Gp) IIb/IIIa were evaluated in twenty patients (7 men; age, 55.4+/-8.7 years) with hypercholesterolemia (plasma total cholesterol level over 240 mg/dL and normal triglyceride level) and twenty one subjects (8 men; 51.1+/-13.7 years) with normal plasma cholesterol and triglyceride levels. Flow cytometry was used to detect the binding of fluorescein isothiocyanate (FITC)-conjugated anti-CD41 or PAC1 to platelet Gp IIb<1/4>/<1/4>IIIa in whole blood. When whole blood was incubated with PAC1, platelets were also activated with adenosine diphosphate (ADP) or thrombin. RESULTS: PAC1 was more bound to unstimulated platelets from patients with hypercholesterolemia (p<0.005), and binding of PAC1 correlated significantly with plasma total cholesteol (r=0.48, p=0.002) and LDL-cholesterol (r=0.47, p=0.002) levels. Binding of PAC1 to unstimulated platelets increased as binding of anti-CD41 increased (r=0.40, p=0.01). On multivariate linear regression analysis, plasma total cholesterol level and binding of anti-CD41 were independent variables that determined binding of PAC1. After ADP- or thrombin-stimulation, binding of PAC1 to platelets and percentage of antibody positive cells were also greater in patients with hypercholesterolemia (p<0.05). There was a significant positive correlation between mean platelet volume and binding of anti-CD41 to unstimulated platelets (r=0.46, p<0.0050), but the latter was not different between hypercholesterolemia and control groups. CONCLUSION: Unstimulated platelets from patients with hypercholesterolemia had similar total number of Gp IIb/IIIa to those from control subjects, but had more activated Gp IIb/IIIa. After ADP- or thrombin-stimulation, platelet Gp IIb/IIIa was also more activated under hypercholesterolemia.
Adenosine Diphosphate ; Atherosclerosis ; Blood Platelets* ; Cholesterol ; Flow Cytometry ; Fluorescein ; Glycoproteins* ; Humans ; Hypercholesterolemia ; Linear Models ; Lipoproteins ; Male ; Mean Platelet Volume ; Plasma ; Thrombin ; Triglycerides

Menetrier's disease is characterized by enlarged gastric folds with foveolar hyperplasia and cystic dilatation of gastric glands. The additional biochemical features of hypoproteinemia, hypochlorhydria, and increased gastric mucus are often encountered. The pathogenesis and etiologic factors have not been clearly defined. In this report, we present two cases of Menetrier's disease in the stomach, one occurring in a 38-year-old male, associated with massive hematemesis, and the other in a 39-year-old male. Grossly, both cases showed marked giant gastric rugal folds resembling cerebral convolutions, sparing the antral portion. Microscopically, the giant gastric rugal folds consisted of the striking foveolar hyperplasia accompanied by an occasional presence of the smooth muscle fibers from the muscularis mucosa. The immunohistochemical stain revealed an intense positive reaction for transforming growth factor-alpha (TGF-alpha) and epidermal growth factor receptor (EGF-R) in the majority of mucous cells throughout the gastric mucosa and parietal cells, but did not reveal for epidermal growth factor (EGF). We suggested that TGF-alpha and EGF-R might be involved in the pathogenesis of Menetrier's disese.
Achlorhydria ; Adult ; Dilatation ; Epidermal Growth Factor ; Gastric Mucosa ; Gastritis, Hypertrophic* ; Hematemesis ; Humans ; Hyperplasia ; Hypoproteinemia ; Immunohistochemistry ; Male ; Mucous Membrane ; Mucus ; Muscle, Smooth ; Rabeprazole ; Receptor, Epidermal Growth Factor ; Stomach ; Strikes, Employee ; Transforming Growth Factor alpha

BACKGROUND AND OBJECTIVES: Regular aerobic exercise plays a role in the prevention of cardiovascular diseases, but the risk of primary cardiac arrest transiently increases during vigorous exercise, particularly in sedentary men. There has been a controversy regarding the effect of exercise on platelet functional behavior, which is related to the pathogenesis of coronary ischemia. We evaluated the cytoplasmic free calcium concentration of platelets in healthy men after treadmill exercise. MATERIALS AND METHOD: Five physically active (group I: age, 24.2+/-2.3 years) and five sedentary men (group II: age, 22.4+/-1.4 years) were included in this study. Platelet calcium was measured with fluorescent dye, quin2 before and after treadmill exercise. RESULTS: Platelet calcium levels were increased from 86.8+/-11.8 nM to 128.8+/-15.0 nM in group I (p<0.05) and from 102.6+/-14.4 nM to 162.4+/-26.5 nM in group II (p<0.05) immediately after exercise. Thereafter, platelet calcium levels were decreased in group I, but continuously increased in group II. At fifteen minutes after exercise, platelet calcium concentrations were significantly higher than baseline values in group II (205.8+/-53.9 nM vs 102.6+/-14.4 nM: p<0.05), but not in group I (115.2+/-15.7 nM vs 86.8+/-11.8 nM). CONCLUSION: Cytoplasmic free calcium concentration in platelets were continuosly increased after treadmill exercise in sedentary men but not in physically active men.
Blood Platelets* ; Calcium* ; Cardiovascular Diseases ; Cytoplasm* ; Exercise ; Heart Arrest ; Humans ; Ischemia ; Male*

BACKGROUND AND OBJECTIVES: Regular aerobic exercise plays a role in the prevention of cardiovascular diseases, but the risk of primary cardiac arrest transiently increases during vigorous exercise, particularly in sedentary men. There has been a controversy regarding the effect of exercise on platelet functional behavior, which is related to the pathogenesis of coronary ischemia. We evaluated the cytoplasmic free calcium concentration of platelets in healthy men after treadmill exercise. MATERIALS AND METHOD: Five physically active (group I: age, 24.2+/-2.3 years) and five sedentary men (group II: age, 22.4+/-1.4 years) were included in this study. Platelet calcium was measured with fluorescent dye, quin2 before and after treadmill exercise. RESULTS: Platelet calcium levels were increased from 86.8+/-11.8 nM to 128.8+/-15.0 nM in group I (p<0.05) and from 102.6+/-14.4 nM to 162.4+/-26.5 nM in group II (p<0.05) immediately after exercise. Thereafter, platelet calcium levels were decreased in group I, but continuously increased in group II. At fifteen minutes after exercise, platelet calcium concentrations were significantly higher than baseline values in group II (205.8+/-53.9 nM vs 102.6+/-14.4 nM: p<0.05), but not in group I (115.2+/-15.7 nM vs 86.8+/-11.8 nM). CONCLUSION: Cytoplasmic free calcium concentration in platelets were continuosly increased after treadmill exercise in sedentary men but not in physically active men.
Blood Platelets* ; Calcium* ; Cardiovascular Diseases ; Cytoplasm* ; Exercise ; Heart Arrest ; Humans ; Ischemia ; Male*

Numerous cause of the carpal-tunnel syndrome have been reported, but we could not find a reference for tuberculosis of the median nerve causing this syndrome. Therefore, we are presenting the case report of this rare condition as another cause of the carpaltunnel syndrome.
Carpal Tunnel Syndrome ; Median Nerve ; Tuberculosis

BACKGROUND/AIMS: The purpose of this study was to evaluate the effectiveness of lamivudine treatment in patients with chronic liver disease caused by chronic infection of hepatitis B virus (HBV). METHODS: Thirty-ive patients with chronic infection of HBV were included in this study who were diagnosed at Hanyang University Hospital from January 1998 to January 1999. They received 150mg of lamivudine per oral once daily for 6 months with follow-p of liver function test, serum HBV DNA and serologic markers for hepatitis B virus every two months. Lamivudine was well tolerated. Eight patients underwent liver biopsies before entering the study and follow-p biopsies were done at 5 patients. RESULTS: Out of all 35 patients, chronic hepatitis patients histologically confirmed were 8, chronic hepatitis patients clinically diagnosed were 25 and liver cirrhosis patients clinically diagnosed were 2. The mean age was 35.7 years. Male-female ratio was 2.2:1. There was no hepatitis B surface antigen (HBsAg) negative seroconversion. The HBeAg loss rate was 26.9%(7/26) and HBeAg seroconversion rate was 10.7%(3/28) at the end of follow-p. Ten patients were anti-Be positive prior to treatment, 3 of them became anti-Be negative at the end of follow-p. Five patients underwent follow-p liver biopsies, in which histologic improvements were shown in 4 cases. Serum replicative HBV DNA by bDNA assay was decreased in all patients and HBV DNA was undetectable in 52.9%(9/17) at the end of treatment. Out of the 15 patients with abnormal alanine aminotransferase (ALT) levels at baseline, ALT level in 7 patients(46.7%) was normalized at treatment completion. Pretherapy ALT level was the only predictive factor for loss of HBeAg by stepwise logistic regression analysis(odds ratio : 1.0208) (95% Confidence Interval : 1.0023 ~ 1.0396) (p value=0.0271). CONCLUSIONS: Lamivudine induced sustained suppression of HBV replication during treatment in all patients. In treating patients with lamivudine, who had chronic liver disease due to chronic infection of HBV, the improvement of liver function test and suppression of viral replication appeared early and was sustained during the 6months treatment. This, in turn, may induce histological improvement as well. Pretherapy ALT level was the only predictive determinant for HBeAg loss during lamivudine therapy, and that should be kept in mind in selecting patients for treatment.
Alanine Transaminase ; Biopsy ; Branched DNA Signal Amplification Assay ; DNA ; Hepatitis B e Antigens ; Hepatitis B Surface Antigens ; Hepatitis B virus ; Hepatitis B* ; Hepatitis* ; Hepatitis, Chronic ; Humans ; Lamivudine* ; Liver ; Liver Cirrhosis ; Liver Diseases ; Liver Function Tests ; Logistic Models ; Prospective Studies*

No abstract available.
Antibodies* ; Hemorrhagic Fever with Renal Syndrome* ; Humans* ; Immunization*