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N Kohashi

Publications and source records attributed to N Kohashi.

At least 19 recordsLinked to original sources
PubMed1995

[The reliability and validity of a new self-completed questionnaire (QUIK)].

In order to evaluate the reliability and validity of a self-completed questionnaire (QUIK), devised to measured QOL, we examined the QUIK scores of elderly who visited the Kumamoto Health Administrative Center for a medical check-up in March 1994. The QUIK questionnaire, which is a close-ended and disease non-specific questionnaire, covered four domains such as physical functioning, emotional adjustment, interpersonal relationships, and attitudes toward life, interacting reciprocally. The mean and standard deviation on QUIK were much better in terms of total score (5.1 +/- 5.4), for each domain score in comparison with the patient group, and even in comparison with the non-patient group. The distribution of total scores on QUIK were as follows: excellent 15%, good 35%, fair 36%, poor 11%, very poor 2% and grossly impaired 0% according to a six-tiered rating scale. The internal consistency in terms of total score was alpha = 0.86. Very close correlation were seen among score, each domain score and satisfaction, being healthy and present state of feeling. If the cut-off points of total score were set between 9 and 10, the sensitivity were 0.65, specificity was 0.65 for the age index, sensitivity 1.00, validity 0.29 for the satisfaction index, while, sensitivity was 0.85 and validity 0.48, for the feeling index. There was a very close reciprocal correlation among the four domains, except for the relation between physical functioning and interpersonal relationship using multiple regression analysis. Further, significant correlations were obtained between the score in each domain and the score based on subtracting each domain score from the total score.

Aged↗
PubMed1992

[Quality of the life in hypertensive outpatients].

In order to evaluate the quality of life (QOL) in hypertensive outpatients, we selected 78 patients with hypertension of various degrees of severity (WHO Classification I: 29 cases, II: 15, III: 34), 59 not ill healthy persons (N1) and 22 normotensive outpatients (N2) aged at 50 years and over, using the self-completed questionnaire (QUIK) which we developed. QUIK covers four domains including physical functioning (20 questions), emotional adjustment (10), interpersonal relationships (10) and attitudes toward life (10) totaling 50 questions. In this study the internal consistency of QUIK was alpha = 0.95 by the Kuder-Richardson formula 20 and it's repeatability was r = 0.89 by the Spearman-Brown formula. The QOL in hypertensive outpatients was definitely worse in terms of total score (N1 5.1 +/- 4.4 vs WHO II 9.3 +/- 7.2 and III 12.1 +/- 5.6, p < 0.05), for physical functioning (N1 2.5 +/- 2.1 vs WHO I 3.7 +/- 2.8, II 4.7 +/- 3.8, III 5.4 +/- 2.8 p < 0.05), for emotional adjustment (N1 1.2 +/- 1.4 vs WHO III 2.3 +/- 1.7, p < 0.01), for interpersonal relationships (N1 0.8 +/- 1.3 vs WHO III 1.6 +/- 1.5, p < 0.01) and for attitudes toward life (N1 0.7 +/- 1.2 vs WHO III 2.7 +/- 2.0 p < 0.01). The total QUIK score increased according to the severity of symptoms (WHO I 5.8 +/- 4.4, WHO II 9.3 +/- 7.2 and WHO III 12.1 +/- 5.6), respectively. The total score of WHO I was significantly lower compared with that of WHO III (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Regulation of aldosterone receptor in rat kidney cytosol by atrial natriuretic factor.

We investigated the effect of atrial natriuretic factor (ANF) on aldosterone receptors in the kidney cytosol, because the binding of aldosterone to aldosterone receptors in the cytosol is considered a critical step of its action. Rat atriopeptin III was injected into male Sprague-Dawley rats (200-250 g) via the femoral vein while under pentobarbital anesthesia, and aldosterone receptors in the kidney cytosol were determined. The maximum binding capacity and dissociation constant were calculated by the Scatchard analysis. Maximum binding capacity of both types of aldosterone receptor (Type I, high affinity and low binding capacity and Type II, low affinity and high binding capacity) gradually decreased after ANF injection, reached the lowest level after 2 hours, and then slightly recovered. When more than 2.5 micrograms/kg of rat atriopeptin III was injected, the density of aldosterone receptors significantly decreased. Injection of 12.5 micrograms/kg of rat atriopeptin III decreased maximum binding capacity of Type I receptor from 42.3 +/- 2.4 (mean +/- SD, n = 6) to 22.8 +/- 3.2 femtomole/mg protein (n = 6) (p less than 0.01), and that of Type II receptor decreased from 388 +/- 46 to 285 +/- 30 fmol/mg protein (p less than 0.01). Dissociation constant of both types of receptors did not change significantly after ANF injection. Plasma aldosterone concentration showed no significant change after ANF injection, and a significant change was noted after ANF administration on aldosterone receptors in the experiments on adrenalectomized rats 7 days after operation. Furosemide had no significant effect on aldosterone receptors in both normal and adrenalectomized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1983

Decrease of urinary taurine in essential hypertension.

In order to evaluate how taurine relates to the pathogenesis of essential hypertension, the taurine content of plasma, whole blood and urine was measured in 18 normals and in 79 hypertensive patients. The patients included 32 untreated cases of essential hypertension, 32 treated cases and 15 cases with labile hypertension. There were no statistically significant differences between normals and essential hypertensives in either plasma or whole blood taurine content. However, in comparison to urinary taurine excretion in normals, 1594.0 +/- 143.7 mumol/day (mean +/- SE), that for untreated essential hypertensives, 708.1 +/- 57.1 mumol/day (p less than 0.001), and for treated essential hypertensives, 953.6 +/- 94.3 mumol/day (p less than 0.001), were significantly lower. Those with labile hypertension showed almost the same value, 1478.3 +/- 134.3 mumol/day, as normals. Taurine clearance and the taurine/creatinine ratio were also markedly decreased in essential hypertensives without treatment. For all subjects, taurine clearance had a positive correlation (r = 0.327, p less than 0.01) with creatinine clearance, but there were significant negative correlations between systolic blood pressure and daily urinary taurine excretion (r = -0.472, p less than 0.01) and between diastolic blood pressure and daily urinary taurine excretion (r = -0.382, p less than 0.01). There were also significant positive correlations between daily urinary taurine excretion and serum high-density lipoprotein cholesterol (r = 0.559, p less than 0.01) and between the former and cardiac index (r = 0.547, p less than 0.01). These results suggest that a deficiency of taurine plays an important role not only in elevating blood pressure in essential hypertension but also in atherogenesis as well.

Adult↗
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↗
PubMed1976

Purification and some properties of rat liver cysteine oxidase (cysteine dioxygenase).

Cysteine oxidase (cysteine dioxygenase, EC 1.13.11.20) was purified approximately 1000-fold from rat liver. The purified enzyme (protein-B) was obtained as an inactive form, which was activated by anaerobic preincubation with L-cysteine. The active form of protein-B was inactivated during aerobic incubation to produce cysteine sulfinate. This inactivation of protein-B was protected by a distinct protein in rat liver cytoplasm, namely stabilizing protein (protein-A). The Ka and Km values for L-cysteine were 0.8-10(-3) M and 1.3-10(-3) M respectively. The enzyme was strongly inhibited by Cu+ and/or Fe2+ chelating agents but not by Cu2+ chelating agent. The optimum pH of enzyme reaction was 8.5-9.5 while that of enzyme activation was 6.8-9.5, with a broad peak.

Animals↗
PubMedDate not supplied

Rat atrial natriuretic peptides inhibit oxygen consumption by rat kidney.

The inhibitory effect of high and low molecular weight native and synthetic rat atrial peptides on oxygen consumption in isolated rat kidney mitochondria and slices was measured. Oxygen consumption by mitochondria was measured in the presence of succinate and/or adenosine diphosphate, furosemide, and low and high molecular weight native and synthetic rat atrial peptides. After the addition of succinate, adenosine diphosphate limiting respiration (State 4) increased in the presence of low, but not high, molecular weight native rat atrial peptides. Furosemide caused a significant decrease in State 4 respiration (p less than 0.001). Angiotensin II and arginine vasopressin did not alter State 4 respiration. The rate of oxygen consumption after the addition of saturating adenosine diphosphate in the presence of saturating succinate (State 3 respiration) was reduced by low and high molecular weight native rat atrial peptides. Furosemide completely blocked oxygen consumption after the addition of adenosine diphosphate. Oxygen consumption was unchanged by trypsin treated (natriuretically inactive) low molecular weight rat atrial peptides and ventricular protein extracts of high and low molecular weight native rat atrial peptides. Synthetic and low molecular weight native rat atrial peptides had similar effects on mitochondrial oxygen consumption. Low molecular weight native and synthetic rat atrial peptides decreased the adenosine diphosphate to oxygen ratio, and these peptides, as well as furosemide, also induced mitochondrial swelling; none of the other rat atrial peptide combinations nor angiotensin II produced this effect. In kidney slices, basal oxygen consumption (without substrates) was stimulated by succinate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗