No abstract available.
Depression* ; Humans

Heart failure is a recognized, although uncommon, cause of massive liver cell necrosis, the clinical consequence of which are intermingled with those of cardiac insufficiency in most case. But, hepatic coma is rerely caused by hepatic congestion only. We report the three cases with heart failure resulted in massive liver cell necrosis and fulminant hepatic failure. The manifestations of fulminant hepatic failure were hepatic encephalopathy, jaundice, marked increase of prothrombin time and serum transaminase and there were no evidences of viral hepatitis and toxic hepatitis as a cause of liver failure.
Drug-Induced Liver Injury ; Estrogens, Conjugated (USP)* ; Heart Failure* ; Hepatic Encephalopathy ; Hepatitis ; Jaundice ; Liver ; Liver Failure ; Liver Failure, Acute* ; Necrosis ; Prothrombin Time

The immunocompetence is important not only to kill the neoplastic cells but also to keep the neoplastic cells from growing further. T lymphocyte is plays the most important role in maintaining the tumor immunity efficiently. T lymphocyte has its specific functions depending in the subset of T lymphocytes. The author analyzed the T lymphocyte subsets in 31 brain tumor patients using anti-CD3, anti-CD4, anti-CD8 monoclonal antibodies and flow cytometry to determine the immunological status of brain tumor patients. All CD3, CD4 and CD8 subsets were reduced in both benign and malignant brain tumor patients but more signigicantly reduced in malignant tumor group. But in benign tumor group, the subtypes of T lymphocytes were not so different from those of normal healthy controls except the pituitary tumor patients, who showed the significant decrease in all the subtypes. In malignant tumor group, each subtype was signigicantly reduced and CD8 subtypes was markedly reduced in metastatic tumor patients, These analyses were considered to have the possibility to be contributable to planning the further immunotherapy and also the possibility to moniter the brain tumor patients clinically.
Antibodies, Monoclonal ; Brain Neoplasms* ; Brain* ; Flow Cytometry ; Humans ; Immunocompetence ; Immunotherapy ; Lymphocytes ; Pituitary Neoplasms ; T-Lymphocyte Subsets* ; T-Lymphocytes*

No abstract available.
Eustachian Tube*

Guyons canal syndrome is an uncommon disease characterized by ulnar nerve compression symptoms within Cuyon s canal. The symptoms vary with the level of compression, and the cause of compression may be extrinsic or intrinsic. We have had experience with a case of the syndrome that was caused by a ganglion in the canal.
Ganglion Cysts ; Ulnar Nerve Compression Syndromes

Identification of patients with combined valvular prolapse has important clinical imlications, because such patients appear to be early surgical candidates. Detection of combined valvular prolapse became more feasible with development of 2-dimentional echocardiography and the incidence of combained mitral and valve prolapse is reported to be variable from 3% to 24%. The authors found a case of combined mitral and aortic valve prolapse detected by 2-dimensional echocardiography. This 30-years-old male patient who admitted because of peptic ulcer bleeding revealed a prolapse of anterior mitral leaflet with regurgitation and also a prolapse of the right coronary cusp into the left ventricular outflow tract but without evidence of aortic regurgutation by Doppler echocardiogram. he discharged without surgical intervention and needs further observation.
Aortic Valve Prolapse* ; Aortic Valve* ; Echocardiography ; Hemorrhage ; Humans ; Incidence ; Male ; Mitral Valve ; Peptic Ulcer ; Prolapse

No abstract available.
Leg*

The authors reported here a 23 years-old female patient with acute renal failure and anaphylaxis induced by rifampicin, who was suffered from exudative pericarditis. The diagnosis was made by its reproducibility with rifampicin. The pathogenesis of acute renal failure and anaphylaxis in this case was thought to be immunologic mechanism, because of elevated IgE and depressed complements. Relevant literature was also reviewed.
Acute Kidney Injury* ; Anaphylaxis* ; Complement System Proteins ; Diagnosis ; Female ; Humans ; Immunoglobulin E ; Pericarditis ; Rifampin ; Young Adult

In single atrial and ventricular cells isolated from the guinea-pig and the rabbit heart, action potentials and membrane currents were recorded by using the whole cell voltage clamp technique. In rabbit atrial cells the repolarization showed two distinctive phases, referred as the early and late phases(early and late plateau phase), but in guinea-pig atrial cells there was a maintained plateau and less distinctive two phases of repolartization. Increasing intracellular sodium or reducing external sodium by replacement with lithium suppressed the late phase of the action potential in rabbit atrial cells and shortened the plateau of action potential in rabbit ventricle and guinea-pig atrial cells. Reducing external sodium decreased Ca-current and late inward current in voltage clamp. Ouabain in the concentration of 10(-5)M shortened the duration of action potential and shifted the holding current level to outward direction, decreased Ca-current and moved late inward current to outward direction. Ryanodine 10(-6)M which is known to be an inhibitor of Ca-release in the intracellular store, suppressed the late phase of action potential in rabbit atrial cells and shortened the plateau of action potential in rabbit ventricular cells. Ryanodine also decreased Ca-current and shifted late inward current to outward direction. It is concluded that an inward current activated by intracellular calcium contributes to the late Phase of the action potential in rabbit atrial cells and to the late plateau in rabbit ventricular cells and in guinea-pig atrial cells. It may be carried by the Na-Ca exchange precess and/or by calcium-activated non-specific channels but preferably Na-Ca exchange machanism.
Action Potentials* ; Calcium ; Heart* ; Lithium ; Membranes* ; Myocytes, Cardiac ; Ouabain ; Ryanodine ; Sodium

Left ventricular hypertrophy is a compensatory response to hemodynamic overload secondary to an increased systemic resistance. This increase, however, is not the only cause of hypertrophy, and there are other factors which can have a significant effect on its incidence. To determine whether chronic antihypertensive therapy by enalapril modifies the cellular and subcellular changes of left ventricular hypertrophy observed in spontaneously hypertensive rats(SHR), 20-weeks-old SHR were treated for 22 weeks with enalapril(2mg/kg) and compared with normotensive Wister-Kyoto rats and not-treated SHR. Systolic blood pressure in enalapril-treated SHR was significantly lowered after 22 weeks compared with that of untreated control SHR group. Myocytes were reduced in size and fibrination seen in cardiac muscle fibers of control SHR was decreased in treated SHR group. Myofibrils appeared to be irregular in shape and myofilaments are decreased in control SHR but in enalapril-treated SHR the diameter and length of the myofilament became turned to regular forms. These results suggest that, enalapril, angiotensin converting enzyme inhibitor, may regress hypertrophy and some subcellular changes may be modified by enalapril.
Animals ; Blood Pressure ; Enalapril* ; Fibrin ; Hemodynamics ; Hypertrophy ; Hypertrophy, Left Ventricular* ; Incidence ; Muscle Cells ; Myocardium ; Myofibrils ; Peptidyl-Dipeptidase A ; Rats ; Rats, Inbred SHR*