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Biomedical subjects

K Takebe

Publications and source records attributed to K Takebe.

At least 163 records · Page 9Linked to original sources
PubMed1986

Renal kallikrein in diabetic patients with hypertension accompanied by nephropathy.

We measured the 24-h excretion of urinary kallikrein in 27 patients with Type 2 (non-insulin-dependent) diabetes and in 10 normal control subjects. Mean (+/- SD) kallikrein excretion in diabetic patients with nephropathy (6.2 +/- 2.4 naphthyl units (NU)/day, n = 13) was significantly lower than in control subjects (12.8 +/- 3.4 NU/day, p less than 0.01) and in diabetic patients without nephropathy (9.4 +/- 3.4 NU/day, n = 14, p less than 0.05). Kallikrein excretion in hypertensive diabetic patients with nephropathy (5.1 +/- 1.6 NU/day, n = 8) was significantly lower (p less than 0.05) than in normotensive patients with nephropathy (8.3 +/- 2.1 NU/day, n = 5). There were no significant differences in kallikrein excretion rate (24-h excretion of urinary kallikrein/24-h creatinine clearance) among control subjects (9.9 +/- 4.3 NU/ml), diabetic patients with (9.0 +/- 3.2 NU/ml) and without (9.3 +/- 3.5 NU/ml) nephropathy. However, kallikrein excretion rate in hypertensive diabetic patients with nephropathy (7.7 +/- 3.3 NU/ml) was significantly lower (p less than 0.05) than in normotensive diabetic patients with nephropathy (11.8 +/- 2.0 NU/ml, n = 10). Respective basal and post-stimulated (with intravenous furosemide 40 mg plus 60 min ambulation) plasma aldosterone concentrations measured in control subjects and in hypertensive diabetic patients with nephropathy were similar and increased to the same extent in the 2 groups (5.5 +/- 3.2 versus 5.3 +/- 3.2 and 9.3 +/- 2.6 versus 10.5 +/- 3.4 ng/ml), although the respective plasma renin activity tended to be lower in diabetic patients than in control subjects (0.7 +/- 0.6 versus 1.3 +/- 0.9 and 1.8 +/- 1.8 versus 3.0 +/- 2.6 ng-1 . ml-1 . h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Renal effects of nicardipine in patients with mild-to-moderate essential hypertension.

We studied the renal effects of nicardipine, a calcium entry blocker, in seven patients with mild-to-moderate essential hypertension. Glomerular filtration rate (GFR) and renal blood flow (RBF) were measured by means of thiosulfate and para-aminohippurate, respectively. Intravenous administration of nicardipine hydrochloride (0.5 mg) increased RBF by 26.8 +/- 5.8% (mean +/- SEM, p less than 0.01), GFR by 35.4 +/- 12.4% (p less than 0.05), and urinary excretion of sodium by 56.4 +/- 10.7% (p less than 0.05) with a significant (p less than 0.01) reduction in systolic and diastolic blood pressure as compared to control values. Nicardipine decreased total renal vascular resistance by 30.0 +/- 3.2% (p less than 0.05) from the control value, while filtration fraction remained unchanged. Our results indicate that nicardipine has several favorable renal effects with a concomitant hypotensive action in patients with mild-to-moderate essential hypertension.

Adult↗
PubMed1986

Plasma renin activity, active and inactive renin concentrations, and their responses to beta 1-adrenoceptor blockade with metoprolol in hyperthyroidism.

Plasma renin activity (PRA), plasma renin concentration (PRC), inactive renin concentration (IRC) and total renin concentration (TRC) were measured in 31 normal controls and in 8 patients with hyperthyroidism. TRC was determined as angiotensin I generated with sheep renin substrate after an acid activation of plasma. The angiotensin I of non-acidified plasma was expressed as PRC. IRC was calculated as TRC minus PRC. The mean values for PRA, PRC, IRC and TRC were significantly (P less than 0.05 to P less than 0.01) higher in the hyperthyroid patients than in the normal or euthyroid controls. The administration of a beta 1-adrenergic blocker, metoprolol (120 mg/day for 14 days), produced a significant (P less than 0.05 to P less than 0.01) fall in levels of T4, PRA and TRC, and reduced the active renin ratio calculated from PRC/TRC significantly (P less than 0.025), as compared to the pretreatment values. Our observations support the idea that the higher PRA in hyperthyroidism is due to an increased secretion of renin. Furthermore, the results may indicate that the conversion of inactive to active renin is accelerated in hyperthyroidism, possibly by an increased sympathetic activity.

Adult↗
PubMed1986

Pure dysarthria due to anterior internal capsule and/or corona radiata infarction: a report of five cases.

Five cases with a sudden onset of dysarthria in the setting of hypertension are presented. No case had limb weakness or other neurological deficits. Computed tomographic scan demonstrated a small low density lesion in the anterior part of the internal capsule or the adjacent corona radiata. All cases showed a good recovery from dysarthria within two to four weeks.

Afferent Pathways↗
PubMed1986

Renal effects of nicardipine, a calcium entry blocker, in hypertensive type II diabetic patients with nephropathy.

We studied the renal effects of nicardipine, a calcium entry blocker, in eight patients with essential hypertension (group A, WHO I or II), six hypertensive type II diabetics with mild-to-moderate nephropathy (group B, urinary albumin 200-789 mg/day), and six hypertensive type II diabetics with severe or advanced nephropathy (group C, urinary albumin 1,596-4,300 mg/day). The patients received an intravenous dose of nicardipine hydrochloride (0.5 mg) or saline placebo in a random order. Glomerular filtration rate (GFR) and renal blood flow (RBF) were measured by means of thiosulfate sodium and p-aminohippurate, respectively, during the 30 min after the nicardipine or saline injection. Blood pressures were serially monitored during the study. Nicardipine reduced both systolic and diastolic blood pressures significantly (P less than .05 to .01) at all measurement periods in all study groups compared with the respective placebo. Nicardipine increased RBF (P less than .01), GFR (P less than .05), and urinary Na+ excretion (P less than .01) and decreased total renal vascular resistance (P less than .01) in groups A and B, but these parameters remain unchanged in group C. The filtration fraction remained unaltered in all groups. The results indicate that nicardipine has several favorable renal effects with a concomitant hypotensive action in hypertensive type II diabetics with mild-to-moderate nephropathy, as observed in patients with uncomplicated essential hypertension, and the renal pharmacological responsiveness appears to be related to the severity of nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[A phase II study of intravenous VP-16-213 in small cell and non-small cell carcinoma of the lung].

A phase II clinical trial of VP-16-213 was carried out in 71 patients with small cell and non-small cell carcinoma of the lung. Forty-eight evaluable cases consisted of 36 small cell carcinomas, 7 epidermoid carcinomas, 4 adenocarcinomas and one unclassified carcinoma. VP-16-213 was administered by drip infusion at dosages of 60-100mg/m2/day for 5-consecutive days at 3-4 week intervals. Twelve of 36 (33.3%) small cell carcinomas had partial responses, while no responses were obtained in non-small cell carcinomas. Median duration of responses was 46 days (range 31-133 days). The dose limiting toxicity was leukopenia. Median number of days to nadir was 14 days and median numbers of days for recovery was 11 days. Nausea (38%), vomiting (12%), anorexia (45%) and alopecia (74%) were major clinical toxicities although these were mild or reversible. We concluded that VP-16-213 was useful in the treatment of small cell lung cancer and the dose schedule used in this study was recommendable with small dose reduction for further trial of combination chemotherapy.

Adult↗
PubMed1986

[In vivo antibacterial activity of cefbuperazone. Synergy of cefbuperazone for bactericidal effect with human polymorphonuclear leukocytes].

Studies were done utilizing E. coli No. 59 which are resistant against human and mouse serum, and the following results were obtained. The therapeutic effect of cefbuperazone (CPBZ) against systemic infections of mice was much higher than that of cefmetazole (CMZ), cefotetan (CTT), latamoxef (LMOX) and cefoperazone (CPZ). Synergistic bactericidal effect with human polymorphonuclear leukocytes was more marked for CBPZ than CMZ.

Animals↗
PubMed1986

[Disulfiram-like reactions resulting from the administration of cephem antibiotics with methyltetrazolethiol moiety examined by using different doses].

The disulfiram-like reactions following the treatment of cephem antibiotics with methyltetrazolethiol moiety (latamoxef (LMOX) and cefoperazone (CPZ) was studied by using large (500 mg/kg) and small (50 mg/kg) doses of the drugs. Normal and fatty liver rats were injected intraperitoneally with the cephem antibiotics. After overnight fasting blood samples were obtained following an administration of 20% ethanol (2g/kg). Blood ethanol and acetaldehyde concentrations, and liver acetaldehyde dehydrogenase activity were determined. Blood ethanol concentration upon the small dose was similar to that obtained upon the large dose in both groups of normal and fatty liver rats. Blood acetaldehyde concentration upon the large dose was higher than that upon the small dose; 2-fold increase in normal rats and 2.6-4.7-fold increase in fatty liver rats were observed after administering LMOX, while 3.7-fold increase in normal rats and 5-5.7-fold increase in fatty liver rats upon administering CPZ. Additionally, liver acetaldehyde dehydrogenase activity (Enzyme 1) observed upon the large dose was lower than that observed upon the small dose; the degree of reduction was 33% in normal and 19% in fatty liver rats upon the administration of LMOX, while 37% in normal and 45% in fatty liver rats upon the administration of CPZ.

Acetaldehyde↗
PubMed1986

[Histydyl-proline diketopiperazine (HPD), a metabolite of thyrotropin-releasing hormone (TRH), improves the ataxic gait in 3-acetylpyridine (3-AP) treated rats].

Histidyl-proline diketopiperazine (HPD) is the active metabolite deriving from thyrotropin-releasing hormone (TRH). However, its regional distribution in the central nervous system is quite different from TRH. Above all, it is to be noted that cerebellum is one of the richest region of HPD. In rat cerebellum, for example, the concentration of HPD is 20 times higher than that of TRH. This indicates the probable action of HPD within cerebellar system. Recently, a fascinating hypothesis has been proposed by Prasad et al that some activities of TRH are based on its conversion to HPD. The purpose of this experiment is to clarify whether the hypothesis may also be appropriate for the action in the cerebellar system. Twenty four Wistar rats treated with 3-acetylpyridin (3-AP) intraperitoneally were used in our experiment. Before 3-AP administration, those rats were conditioned by electric stimulation to run forward. The 3-AP treated rat is established so as to make an ataxic rat along with a selective degeneration of the inferior olive nucleus. Those ataxic rats were divided into 3 groups according to the test drugs, that is, the group of HPD, TRH (5 mumole/kg each), and saline [the same volume (3.6 ml/kg)] control. Eight rats of each group received an intraperitoneal injection once a day from 5th to 9th day after 3-AP treatment. The behavioral tests were carried out at the 5th, 7th, and 9th day after 3-AP treatment. The ataxic gaits were observed every 30 minutes over 4 hours in succession.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Adrenocortical carcinoma with Cushing's syndrome presenting unusual urinary 17-ketosteroid fractionation.

A case of adrenal carcinoma with Cushing's syndrome was presented. Endocrinological and morphological investigations disclosed the presence of a functional adrenal carcinoma. This case was characterized by its unusual urinary 17-ketosteroid (17-KS) fractionation, i.e. a marked elevation of 17-KS was accompanied by the increments of etiocholanolone, but not of dehydroepiandrosterone (DHEA) or androsterone. Measurements of the plasma adrenocorticosteroids revealed normal DHEA and DHEA-S (sulfate) levels, moderately increased 17-OH-pregnenolone, and markedly increased (less than 100 times the normal) 11-deoxycortisol (cpd S). Therefore, it seems plausible that the normal urinary DHEA level in this patient would have occurred as a result of remarkably low C17-20 lyase activity sufficient to hamper DHEA production, and that markedly increased etiocholanolone might possibly have been converted from cpd S as well as from DHEA and androstenedione through 5 beta-reduction.

17-Ketosteroids↗