Fractional time intervals during cardiac cycle were determined by means of the analyses of mechanocardiograms in 100 male patients with hypertension and 100 healthy males, which served as controls. The mechanocardiograms anyalyzed in this study were simultaneously recorded electrocardiograms, phoocardiograms, apexcardiograms and carotid pulse tracings. Of various time intervals during systolic in patients with hypertension, the mechanical systole(both C-D and C-A2 intervals), the isovolumic contraction time, the initial phase of ventricular contraction and the ventricular pressure elevation time were significantly prolonged, whereas the protodiastole was significantly shortened. The prolongation of the mechanical systole was caused primarily by the lengthening of the isovolumic contraction time, which resulted from the prolongation of the components of the latter, namely the initial phase of ventricular contraction and the ventricular pressure elevation time. During diastole, there were significant prolongation of the isovolumic relaxation time and the rapid ventricular filling period, and a significant shortening of the slow ventricular filling period. Among these time intervals, the mechanical systole(C-A2 inlerval), the isovolumic contraction time, the ventricular pressure elevation time and the isovolumic relaxation time showed significant positive correlation with blood pressure. On the other hand, the slow ventricular filling period was significantly negatively correlated with blood pressure. These facts suggested that the changes in these time intervals were related to increased afterload and/or resultant myocardial or hemodynamic alterations.
Blood Pressure ; Diastole ; Electrocardiography ; Hand ; Hemodynamics ; Humans ; Hypertension* ; Male ; Relaxation ; Systole ; Ventricular Pressure

Fractional time intervals during cardiac cycle were determined by means of the analyses of mechanocardiograms in 100 male patients with hypertension and 100 healthy males, which served as controls. The mechanocardiograms anyalyzed in this study were simultaneously recorded electrocardiograms, phoocardiograms, apexcardiograms and carotid pulse tracings. Of various time intervals during systolic in patients with hypertension, the mechanical systole(both C-D and C-A2 intervals), the isovolumic contraction time, the initial phase of ventricular contraction and the ventricular pressure elevation time were significantly prolonged, whereas the protodiastole was significantly shortened. The prolongation of the mechanical systole was caused primarily by the lengthening of the isovolumic contraction time, which resulted from the prolongation of the components of the latter, namely the initial phase of ventricular contraction and the ventricular pressure elevation time. During diastole, there were significant prolongation of the isovolumic relaxation time and the rapid ventricular filling period, and a significant shortening of the slow ventricular filling period. Among these time intervals, the mechanical systole(C-A2 inlerval), the isovolumic contraction time, the ventricular pressure elevation time and the isovolumic relaxation time showed significant positive correlation with blood pressure. On the other hand, the slow ventricular filling period was significantly negatively correlated with blood pressure. These facts suggested that the changes in these time intervals were related to increased afterload and/or resultant myocardial or hemodynamic alterations.
Blood Pressure ; Diastole ; Electrocardiography ; Hand ; Hemodynamics ; Humans ; Hypertension* ; Male ; Relaxation ; Systole ; Ventricular Pressure

We report a case of acute transient encephalopathy with mental alteration, myoclonic jerks, and periodic triphasic wave electroencephalographic patterns caused by a therapeutic dose of baclofen. The clinical and electroencephalo-graphic abnormalities improved to a normal range shortly after baclofen was discontinued. We discuss the pathogenesis and review the literature about baclofen-induced encephalopathies.
Baclofen ; Myoclonus ; Reference Values

Interleukin-6(IL-6) stimulate osteoclast differentiation. 17beta-estradiol, 1,25-dihydroxyvitamin D3(1,25-(OH)2D3) and interleukin-1beta inhibit or stimulate osteoclast differentiation by decreasing or increasing the synthesis of interleukin-6(IL-6) from stromal/osteoblastic cells, respectively. Periodontal ligament(PDL) cells reside between the alveolar bone and the cementum and have osteoblastic characteristics. To estimate the effect of 17beta-estradiol and 1,25(OH)2D3 on IL-6 production of PDL cells, PDL cells were treated with 17beta-estradiol or 1,25-(OH)2D3 in the absence or the presence of IL-1beta. The concentration of IL-6 produced form PDL cells was determined by enzym linked immunosorbent assay(ELISA). In unstimulated PDL cells, we detected constitutive production of IL-6 at 1st and 2nd day. IL-1beta increased IL-6 synthesis at 1st day and 2nd day. 17beta-estradiol had no significant effect on the secretion of this cytokine, either constitutively or after stimulation with IL-1beta(0.05 ng/ml). 1,25-(OH)2D3(10(-8)M) decreased not only constitutive IL-6 production but also IL-1beta-induced IL-6 production at 2nd day. These results suggest that 1,25-(OH)2D3 may control IL-1beta-induced osteoclast differentiation by decreasing IL-1beta-induced IL-6 secretion of PDL cells.
Calcitriol* ; Dental Cementum ; Interleukin-1beta ; Interleukin-6* ; Osteoblasts ; Osteoclasts ; Periodontal Ligament*

Effects of thoracentesis on thoracic impedance and cardiac performance were studied in patients with uncomplicated unilateral tuberculous pleural effusion. The speed of the removal of the pleural effusion in thoracentesis was essentially similar to that of a generally used for therapeutic purpose in daily practice. Thoracic impedance was measured in 23 cases before, 4 and 10 minutes after thoracentesis to the amount of pleural effusion aspirated was observed. In 11 cases out of 23, the changes in cardiac performance as assessed by stroke volume, cardiac output, heart rate, heather index and ratio of pre-ejection period to left ventricular ejection time(PEP/LVET) were observed 4 minutes after 150 ml to 1,000 ml of thoracentesis. In these cases, stroke volume, cardiac output, and Heather index were determined from impedance cardiograms, and PEP/LVET from mechanocardiograms recorded simultaneously with the former. A significant increase in thoracic impedance was observed both 4 and 10 minutes after thoracentesis. There was a slight but a significant correlation between the changes in thoracic impedance and the amount of pleural fluid aspirated only 4 minutes after thoracentesis. Thoracentesis showed no consistent influence on cardiac performance as reflected to stroke volume, cardiac output, heart rate, heart index and PEP/LVET. These facts suggest that measurement of thoracic impedance may be a useful method reflecting alterations in pleural fluid volumes, particularly when it occurs in a relatively short period of time, and the effects of thoracentesis of less than one liter on the cardiac functions as determined by the above-mentioned parameters were variable.
Cardiac Output ; Electric Impedance* ; Heart ; Heart Rate ; Humans ; Pleural Effusion ; Stroke Volume

Twenty-one cases of mitral valve prolapse (MVP) diagnosed by M-mode echocardiograms were studied in regard to the underlying or associated conditions, types of MVP, and dimensions of the cardiac structures and parameters reflecting cardiac performance determined by echocardiograms. In 9 cases, MVP was thought to be idiopathic origin. Associated conditions in the remainder were 5 cases of congenital heart disease, 2 cases of rheumatic myocarditis, 1 case each of aortic valve disease, ischemic heart disease and hyperthyroidism, and 2 cases of undiagnosed cardiac conditions. There were 2 cases of buckling type of MVP and in the remainder hammock type. In these 2 patients with hammock type of MVP, mitral valve echoes were seen in the left atrium during systole in 1 case, and diastolic anterior displacement of posterior mitral leaflet in the other. In 9 cases of idiopathic MVP, cardiac dimensions and parameters reflecting cardiac performance as determined from echocardiograms showed no significant differences from those of 27 normal controls.
Aortic Valve ; Echocardiography* ; Heart Atria ; Heart Defects, Congenital ; Humans ; Hyperthyroidism ; Mitral Valve Prolapse* ; Mitral Valve* ; Myocardial Ischemia ; Myocarditis ; Systole

Almost all advanced glomerular diseases have glomerular sclerotic changes to varying degrees whatever causes their primary glomerular disease are. Pathogenesis of these sclerosis has been thought of as the hyperfiltration in the primary glomerulosclerosis due to development of glomerular hypertension in each insulted glomeruli. This background gave the theoretical bases for antihypertensive therapies for supporting chronic renal insufficient patients. Angiotensin converting enzyme (ACE) inhibitor, one of the antihypertensive drugs, has received attention recently for its effectiveness. The aims of this study determined the effects and mechanism of the ACE inhibitor, enalapril, on the glomerulosclerosis in FGS/NgaKist mice, which was an animal model of chronic renal failure by generating spontaneously heavy proteinuria and progressive glomerulosclerosis. Five-week-old FGS/NgaKist mice (n=38) were assigned to four groups. Group 1a (n=6) and group 2a (n=8) fed with a vehicle, were sacrificed at the end of 10 weeks and 15 weeks, respectively. Group 1b (n=12) and 2b (n=12) received enalapril (100 mg/L) in drinking water for 5 weeks and 10 weeks from 6th week of age respectively, and were sacrified on the same day as the control groups. Doses of enanapril were maintained to 2 mg/kg/day by measuring the amount of water consumption. In enalapril groups 1b and 2b, systemic blood pressure (74.7 14.0 mm Hg, 74.3 15.9 mmHg) were significantly lower than control group 2a (116.1 4.6 mmHg, P<0.001). Similarly, degree of proteinuria lowered in enalapril group 2b versus control group 2a (0% and 50.0%, P<0.001). Glomerulosclerosis percentage significantly decreased (P<0.001) (group 1b and 2b; 1.9 6.5, 5.6 7.0 vs control 1a and 2a; 32.8 15.5, 31.4 13.8). Glomerulosclerosis score also decreased (P<0.001) (group 1b and 2b; 0.02 0.08 vs control 1a and 2a; 0.48 0.12, 0.30 0.14). The immunofluorescent staining of enalapril groups showed negative for mesangial deposition of IgG, IgA, IgM, and C3 which were positive in control groups. Immunohistochemical staining with TGF-beta1 was negative in enalapril groups and sclerotic glomeruli both enalapril groups and control groups. These results support that the ACE inhibitor has a renoprotective effect on glomerulosclerosis not only by decreasing the blood pressure but also by suppressing the immune deposits on glomeruli.
Angiotensins* ; Animals ; Antihypertensive Agents ; Blood Pressure ; Drinking ; Drinking Water ; Enalapril ; Humans ; Hypertension ; Immunoglobulin A ; Immunoglobulin G ; Immunoglobulin M ; Kidney Failure, Chronic ; Mice ; Models, Animal ; Peptidyl-Dipeptidase A* ; Proteinuria ; Sclerosis* ; Transforming Growth Factor beta1

No abstract available.
Lung Neoplasms* ; Lung* ; Neoplasm Metastasis* ; Toes*

No abstract available.
Bronchoscopes*

No abstract available.
Eosinophilic Granuloma* ; Eosinophils* ; Lymph Nodes*