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Biomedical subjects

Y Kori

Publications and source records attributed to Y Kori.

36 records · Page 2Linked to original sources
PubMed1987

[Risk factors in the surgical repair of tetralogy of Fallot: analysis of preoperative factors by stepwise regression].

Fifty-one patients undergoing total repair of tetralogy of Fallot between November 1977 and June 1985 were analyzed with respect to determinants of operative mortality and postoperative right to left ventricular peak systolic pressure ratio (RV/LV). The risk factors were age, sex (Sex), previous shunting operation (Shunt), extent of right ventricular outflow tract patch (Patch), various PA-indexes, maximal left atrial volume/BSA (LA/BSA), left ventricular end diastolic volume index (LVEDVI), LVEDVI/normal-LVEDVI, RV/LV, Hb, BSA and weight. Univariate analysis indicated that RV/LV and LA/BSA were associated with operative death. A model for operative mortality with three variables emerged from the multiple stepwise regression analysis: Patch, Shunt and Sex (R = 0.421, R2 = 0.177, F = 3.37). A model for predicted RV/LV with five variables: Weight, Shunt, BSA, Patch and Sex (R = 0.602, R2 = 0.363, F = 5.12). However, it was thought difficult to predict operative mortality and postoperative RV/LV by the preoperative variables. Intra- and postoperative factors might have larger influences on operative mortality and RV/LV than the preoperative ones.

Analysis of Variance↗
PubMed1986

[Clinical study of chemotherapy (PPM therapy) with cisplatin, peplomycin and mitomycin C in squamous cell lung cancer].

The effect of PPM therapy, consisting of cisplatin, peplomycin and mitomycin C, was evaluated in 15 cases of squamous cell lung cancer. Ten partial responses were achieved in primary cases and the response rate was 66.7%. Nephrotoxicity was well controlled with a continuous infused drip and FOM. The nausea and vomiting were reasonably well controlled with methylprednisolone and metoclopramide. Severe interstitial pneumonitis occurred in 5 cases (33.3%). PPM therapy is considered to be a very useful combination chemotherapy for squamous cell lung cancer but careful attention must be paid to pulmonary toxicity.

Aged↗
PubMed1983

Studies on the effects of hyperkalemia on serum and myocardial digoxin concentration in dogs.

The effects of hyperkalemia on serum and myocardial digoxin (DX) concentration was studied in conjunction with hemodynamic changes in 31 normal dogs. The myocardial DX concentration in the hyperkalemic (HK) group was significantly lower than that in normokalemic (NK) group, despite a significantly higher serum DX concentration in the HK group. In the HK group, the myocardial sodium concentration was significantly lower than in the NK group. Coincident with these biochemical changes, no increase of LV max dP/dt after DX administration was observed in the HK group. These results suggest that there might be competitive antagonism between myocardial uptake of potassium and DX.

Animals↗
PubMed1980

Immaturity of the enzyme activity and the response to inducers of rat liver cysteine dioxygenase during development.

Cysteine dioxygenase activity was not detected in the liver of either fetal or 2-day-old rat. The enzyme activity of neonatal rat liver gradually increased between the 4th and 12th postnatal days and then sharply increased to reach the adult level by the 28th postnatal day. No cysteine dioxygenase activity was observed in the fetal liver at the 18th day of gestation from a dam injected with hydrocortisone. Hydrocortisone-mediated induction was first observed in the livers of 4-day-old rats. The duration of hydrocortisone-mediated induction was much longer in the livers of 4- to 12-day-old rats than in those of adult rats. The enzyme half-life in livers of 10- and 20-day-old rats was 6.4 and 3.7 h, respectively. The half-life of the enzyme in 20-day-old rat liver was increased to 6.2 h by L-cysteine injection.

Aging↗
PubMed1978

Rat liver cysteine dioxygenase (cysteine oxidase). Further purification, characterization, and analysis of the activation and inactivation.

Rat liver cysteine dioxygenase has been purified to homogeneity. It is a single subunit protein having a molecular weight of 22,500 +/- 1,000, with a pI of 5.5. The enzyme purified was catalytically inactive and activated by anaerobic incubation with either L-cysteine or its analogues such as carboxymethyl-L-cysteine, carboxyethyl-L-cysteine, S-methyl-L-cysteine, D-cysteine, cysteamine, N-acetyl-L-cysteine, and DL-homocysteine. The enzyme thus activated with L-cysteine was rapidly inactivated under aerobic condition. This rapid inactivation was observed at 0 degrees C where no formation of either the reaction product cysteine sulfinate or the autoxidation product of cysteine, cystine, was detected. Further analysis shows that the inactivation of the activated enzyme was due to oxygen but unrelated to either the presence of substrate, enzyme turnover or accumulation of inhibitor produced during assay. A distinct rat liver cytoplasmic protein, called protein-A, could completely prevented the enzyme from the aerobic inactivation. The loss of activity during assay in the absence of protein-A was shown to be a first order decay process. From the plots of log(deltaproduct/min) versus time, the initial velocity (VO) and the velocity at 7 min (V7) were obtained. The apparent Km value for L-cysteine in the absence of protein-A was calculated from the initial velocity as 4.5 X 10(-4)M. Protein-A did not alter the apparent Km value for L-cysteine. The chelating agents such as o-phenanthroline, alpha,alpha'-dipyridyl, bathophenanthroline, 8-hydroxyquinoline, EGTA, and EDTA strongly inhibited the enzyme activity when these chelating agents were added before preactivation. The purified cystein dioxygenase contains 1 atom of iron per mol of enzyme protein. By the activation procedure, the enzyme became less susceptible to the heat denaturation, the inhibitory effects of chelating agents and the tryptic digestion.

Animals↗
PubMed1978

Decrease of rat liver cysteine dioxygenase (cysteine oxidase) activity mediated by glucagon.

The hepatic cysteine dioxygenase activity of rats was markedly decreased by the intraperitoneal administration of glucagon. The enzyme activity was also decreased by either dibutyryl cyclic AMP or theophylline. The prior administration of actinomycin D completely blocked the glucagon-mediated decrease of enzyme activity, while administrations of this inhibitor of protein synthesis after glucagon injection did not block the decrease of enzyme activity. A single administration of actinomycin D resulted in a slight increase of cysteine dioxygenase activity in the rat liver. On the other hand, the injection of cycloheximide resulted in a rapid decrease of the hepatic cysteine dioxygenase with a half-life of 2.5 h. The half-life of the enzyme in rat liver after glucagon administration was one hour. The administration of hydrocortisone or insulin had no effect on the glucagon-mediated decrease of cysteine dioxygenase of rat liver. The enzyme activity of alloxan diabetic rat liver was almost the same as that of the intact rat liver. The evidence obtained here suggests that enhancement of degradation or inactivation of cysteine dioxygenase is responsible for the glucagon-mediated decrease of the enzyme activity in rat liver.

Adrenal Glands↗