Effects of saikosaponins on liver tyrosine aminotransferase activity induced by cortisone in adrenalectomized rats.
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Biomedical subjects
Publications and source records attributed to H Okuda.
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This study was designed to obtain basic information about the mechanism of the occurrence of muscular disorders after exposure to vibration. The hind legs of rats were exposed to acute and chronic local vibration at frequencies of 30, 60, 120, 240, 480, and 960 Hz with a constant acceleration of 50 m/sec2. The exposure time was four hours for acute, and four hours a day for two weeks continuously for chronic exposure. Blood was collected after exposure to measure plasma creatine phosphokinase (CPK) activity. In both exposure groups the activity of plasma CPK was significantly higher at 30, 60, 120, 240, and 480 Hz compared with the control group and was especially high at 30 Hz; there was no significant change at 960 Hz. As a result of an analysis of the CPK isoenzymes, the increase in plasma CPK activity was shown to be due to the activity of the plasma CPK-MM fraction, originating in the skeletal muscle. Plasma CPK activity showed a tendency to decrease gradually with the increase in vibration frequency during acute exposure but showed no such tendency during chronic exposure. There was no remarkable pathohistological change in muscle preparations from the hind legs, hence it was presumed that the increase in plasma CPK activity was caused not by the morphological changes of muscle but by other mechanisms, such as an increase in the permeability of the cell membrane.
Effects of respiratory and metabolic acidosis (pH approximately 6.8) on myocardial function were studied in the newborn and adult rabbits. Mechanical function was studied in the isolated arterially perfused heart preparation. Acidosis was induced either by increase of the perfusate PCO2 or by decrease of the bicarbonate content. During respiratory acidosis, developed tension (DT) decreased to 43 +/- 3% of control (n = 18) in the adult and this depression was significantly greater than in the newborn (DT = 92 +/- 4%, n = 6). Depression of DT by respiratory acidosis was observed even at high extracellular Ca. During metabolic acidosis, mechanical function decreased gradually and DT at 30 min into acidosis in the adult was 78 +/- 3% of control (n = 6). This depression of DT in the adult was significantly greater than in the newborn (DT at 30 min = 96 +/- 1% of control, n = 6). Statistical analysis using paired t test showed that respiratory acidosis, but not metabolic acidosis, caused significant negative inotropism in the newborn. Myofibrils were isolated and the ATPase was measured at 10(-8) to 10(-4) M Ca and at pH of 7.1 (control), 6.5, and 6.0. Reducing pH depressed the ATPase activity similarly in the newborn and adult. Intracellular buffer capacity was determined by titrating muscle homogenate with HCI. Although the initial pH was not different, addition of HCl to the homogenate caused less decrease in pH in the newborn. These data indicate that contractile function in the newborn heart is more resistant to acidosis and this may be due partly to the greater intracellular buffer capacity.
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The total post-heparin lipolytic activity (PHLA) and hepatic triglyceride lipase (HTGL) and lipoprotein lipase (LPL) activities in post-heparin plasma of patients with various cancers were measured. In patients with cancers, PHLA was similar to that of controls, but the HTGL activity was decreased and the LPL activity was increased. Thus, in cancer patients the ratios of HTGL to PHLA were lower, and the ratios of LPL to PHLA were higher than in controls. No correlation was found between the plasma lipid level and HTGL or LPL activity.
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Hepatic triglyceride lipase was obtained from post-heparin plasma of rats in an electrophoretically homogeneous form. The enzyme had an isoelectric point at pH 4.9 and molecular weight of 65,000. The relation between the "lipase" and "esterase" activities of the enzyme was studied using emulsified triolein and water-soluble methyl butyrate (80 mM) as substrates. The same enzyme protein catalyzed the hydrolyses of both emulsified triolein and water-soluble methyl butyrate. The relation of activity to the methyl butyrate concentration differed from those for pancreatic lipase and liver esterase. During purification, the ratio of methyl butyrate to triolein-hydrolyzing activity of the enzyme increased. On digestion of the enzyme with trypsin, the "lipase" activity was retained. However, the trypsin-treated enzyme was adsorbed to a heparin-Sepharose column and eluted with 0.75 M NaCl, like the untreated enzyme. These results suggest that rat hepatic triglyceride lipase contains a so-called "hydrophobic recognition site" that is destroyed by trypsin treatment and is distinct from the heparin-binding and catalytic sites.
Soluble elastin, prepared from insoluble elastin by treatment with oxalic acid or elastase, was found to inhibit the formation of thromboxane B2 both from [1-14C]arachidonic acid added to washed platelets and from [1-14C]arachidonic acid in prelabeled platelets on stimulation with thrombin. In both systems, the formation of 12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE) was accelerated. Oxalic acid-treated soluble elastin at 1 and 10 mg/ml inhibited the formation of thromboxane B2 from exogenously supplied arachidonic acid 21 and 59%, respectively, and the formation of thromboxane B2 in prelabeled platelets stimulated by thrombin 44 and 94%, respectively. These concentrations of elastin increased the formation of 12-HETE from exogenously supplied arachidonic acid about 3.4- and 7.3-times, respectively. Almost all the added arachidonic acid was converted to metabolites. In prelabeled platelets, soluble elastin at 1 and 10 mg/ml increased the formation of 12-HETE stimulated by thrombin about 1.3- and 2.8-times, respectively, and inhibited the thrombin-induced total productions of thromboxane B2 (12-hydroxy-5,8,10-heptadecatrienoic acid (12-HETE) and free arachidonic acid by 26 and 25%, respectively. Elastase-treated digested elastin also inhibited the formation of thromboxane B2 and stimulated the formation of 12-HETE in prelabeled platelets stimulated by thrombin. This inhibitory action of elastin was not replaced by desmosine. The level of cAMP in platelets was not affected by soluble elastin. Soluble elastin was also found to inhibit platelet aggregation induced by thrombin. However, the inhibitory action of soluble elastin on platelet aggregation cannot be explained by inhibition of thromboxane B2 formation by the elastin.
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A survey of 2985 apparently healthy Taiwanese in southern Taiwan revealed a high prevalence (18.2%) of hepatitis B surface antigen (HBsAg). It was significantly higher in males (22.3%) than in females (13.6%), but no correlation with family origin, socioeconomic status or residence was established. About one-third of the breeding female HBsAg carriers were HBeAg-positive, and these may be an important source in the spread of HBV. Subtyping of HBsAg in 63 subjects showed adw to be dominant in this area, and 8 subjects with suspicious results had overlapping heterotypic HBV's (7 adwr and 1 adyw) in addition to 2 subjects in which coexistence of HBsAg and anti-HBs was recognized. The association between HBsAg positivity and serum transaminase elevation was significant, especially in the older groups who had a higher abnormal rate. Hepatitis A virus infection was serious too, with nearly 100% of people above 20 years of age being anti-HA antibody positive.
To determine how centrum abnormalities in medaka could be used to indicate the degree of water pollution, several rearing experiments were carried out. Medaka eggs were placed at certain points on a stream flowing from an area in which fenitrothion emulsion (organophosphorous pesticide--MEP) was being applied aerially. There was sufficient probability that the eggs were exposed to the MEP. They were brought to the laboratory, and reared in dechlorinated water to adulthood. The external forms and vertebral centra of each adult fish were closely observed. It was found that the incidence of centrum-damaged fish in the exposure experiment groups was significantly higher than in the control and blank experiments, and the influence of the aerial application of MEP was clearly indicated in this manner. Consequently, it was confirmed that centrum abnormalities in medaka may be used as a biological index for indicating the degree of water pollution by agricultural chemicals.
The ascites fluids from patients with hepatoma or ovarian tumor and the pleural fluid from patients with malignant lymphoma elicited fatty acid release in slices of rat adipose tissue in vitro. The lipolytic factor, named toxohormone-L, was isolated from the ascites fluid of patients with hepatoma. The isolated preparation gave a single band on both disc gel electrophoresis and sodium dodecyl sulfate (SDS)-acrylamide gel electrophoresis in the presence of beta-mercaptoethanol. Its molecular weight was determined to be 70,000-75,000 and 65,200 by SDS-acrylamide gel electrophoresis and analytical ultracentrifugation respectively. Injection of toxohormone-L into the lateral ventricle of rats significantly suppressed food and water intakes. There was at least a 5-hr delay between its injection and the appearance of its suppressive effect.
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