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Biomedical subjects

M Kubo

Publications and source records attributed to M Kubo.

At least 541 records · Page 30Linked to original sources
PubMed1986

[Clinical study of HCFU in combination with irradiation therapy in squamous cell carcinoma of the head and neck].

Sixty-two patients with squamous cell carcinoma of the head and neck were administered a mean total dose of 75.9 g carmofur (HCFU) in combination with a mean total dose of 49.0 Gy irradiation therapy. The primary sites of cancer were: larynx 29 cases, oral cavity 11 cases, nasal and paranasal cavity 7 cases, hypopharynx 5 cases, nasopharynx 5 cases, epipharynx 3 cases, and others 2 cases. The clinical stages were: stage I II cases, stage II 15 cases, stage III 17 cases, and stage IV 19 cases. In 57 evaluable patients having measurable lesions, overall response rate, including 26 complete responses (CR) and 16 partial responses (PR), was 73.7%. Average doses of HCFU were 13.1 g at PR, 27.8 g at CR, and those of irradiation were 27.7 Gy at PR, 48.5 Gy at CR. The median duration of PR was 44.8 weeks and that of CR was 47.0 weeks, the overall response interval being 47.7 weeks. Of the 62 patients, 25 (40.3%) complained of side effects including pollakisuria (9 cases), appetite loss (6 cases), stomatitis (5 cases), and so on.

Antineoplastic Agents↗
PubMed1986

[Severity and non-uniformity of regional wall motion in dilated cardiomyopathy evaluated by two-dimensional echocardiography].

A two and a half year follow-up study of segmental left ventricular wall motion was performed by two-dimensional echocardiography for 26 patients with dilated cardiomyopathy (DCM). Segmental analysis of left ventricular wall motion abnormalities (WMA) was performed using 11 segments obtained by short- and long-axis views of the left ventricle. Wall motion in each segment was classified and assigned a numerical score as normal (0), hypokinetic (1), severely hypokinetic (2), and akinetic or dyskinetic (3). Based on this categorization, a wall motion abnormality index (WMAI) was derived as an overall assessment of left ventricular asynergy. The intersegmental standard deviation of the wall motion abnormality score was used as an index of left ventricular asynergy (non-uniformity index: NUI). During the follow-up period, the wall motion abnormality index increased in all of the 26 patients (from 1.23 to 1.82, p less than 0.001), but the non-uniformity index did not change (from 0.72 to 0.73). When comparing the non-uniformity index among three groups classified according to the grade of wall motion abnormality, both at the initial and during follow-up studies, the moderate wall motion abnormality group (1.0 less than or equal to WMAI less than 2.0) had larger non-uniformity indexes (0.83, 0.84) than the other groups, and the severe non-uniformity index (greater than or equal to 0.9) was observed solely in the moderate group. In the follow-up study, these 26 patients were categorized in two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Malignant familial cardiomyopathy with sudden death, typical asymmetric septal hypertrophy and dilated cardiomyopathy-like features].

Twenty-one members of a family were traced for three generations including the propositus, who had typical dilated cardiomyopathy (DCM)-like features. Clinical, radiological, electrocardiographic and echocardiographic examinations were performed for 13 of 16 still living. Five of 21 members died including three of sudden death. Among living 16 members, five had congestive heart failure, greater than grade III of the NYHA, and cardiomegaly on chest radiography in five. Left ventricular hypertrophy, abnormal Q waves, and ST-T changes were observed on electrocardiography in two, five and eight members, respectively. Echocardiography revealed asymmetric septal hypertrophy (ASH) in four, two of whom had systolic anterior motion (SAM) of the mitral valve. Two had features simulating DCM, and five had mitral valve prolapse. Among six patients with ASH or features simulating DCM, four had cardiac catheterization, coronary angiography and endomyocardial biopsy. None had significant coronary stenosis, but all had high left ventricular end-diastolic pressure (LVEDP) (23 +/- 7 mmHg). Endomyocardial biopsy showed moderate myocardial cellular hypertrophy, interstitial myocardial fibrosis, nuclear changes and myocardial disarrangement, with features characteristic of HCM. In this family with malignant HCM, patients had various clinical features including typical HCM, simulated DCM, DCM coexisted with mitral valve prolapse, and sudden death occurred frequently.

Adolescent↗
PubMed1985

Mechanism of cationic amphiphilic drug inhibition of purified lysosomal phospholipase A1.

Cationic amphiphilic drugs like chlorpromazine, propranolol, and chloroquine inhibit lysosomal phospholipase A in vitro. Some workers have proposed that cationic amphiphilic drugs inhibit the activity of phospholipase A1 by forming substrate-drug complexes which cannot be degraded while others have reported competitive inhibition implying drug effects on the enzyme. To analyze the mechanism of inhibition, we examined the binding ability of these drugs to unilamellar vesicles of dioleoylphosphatidylcholine and correlated these results with a detailed kinetic analysis of phospholipase A. Chlorpromazine and propranolol bound to small unilamellar liposomes of dioleoylphosphatidylcholine substrate in a positive cooperative way consistent with two binding sites: a high-affinity site with low capacity and a low-affinity site with high capacity. The affinity of chlorpromazine for the high-affinity site was 2 times greater than that of propranolol (KA = 13 807 +/- 1722 vs. 8481 +/- 1078 M-1), and the saturation number for chlorpromazine was 3 times greater than for propranolol (N = 0.20 +/- 0.004 vs. 0.07 +/- 0.02 mol of drug/mol of phosphatidylcholine). Chloroquine did not bind to unilamellar liposomes of dioleoylphosphatidylcholine. We carried out detailed kinetic studies using purified lysosomal phospholipase A1 from rat liver. In the case of chloroquine inhibition, the Lineweaver-Burk double-reciprocal plots showed straight lines, but the slope replots were curved, indicating the formation of complexes having 2 mol of chloroquine/mol of enzyme (EI2 complexes). Thus, chloroquine is a competitive inhibitor which forms EI2 complexes with phospholipase A1. However, in the case of chlorpromazine and propranolol, the observed kinetic data do not fit to the same equilibrium used for the case of chloroquine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effect of dexamethasone on growth hormone (GH) response to growth hormone releasing hormone in acromegaly.

The effect of dexamethasone on the GH response to GH-releasing hormone (GHRH) was studied in vivo in six patients with acromegaly as well as in vitro in monolayer cultures of GH-secreting pituitary tumor cells obtained from three of these patients. Oral administration of 9 mg/day dexamethasone for 2 days decreased plasma GH responses to iv injection of 100 micrograms GHRH-(1-44 amide) in all six patients. Blood glucose levels were significantly increased, while plasma somatomedin-C levels were significantly decreased by this regimen of dexamethasone treatment. On the other hand, 2-day pretreatment with 50 nM dexamethasone of monolayer cultures of pituitary adenoma cells potentiated GH release basally and/or in response to 100 pM to 1 nM GHRH in vitro. These results indicate that the potentiating action of 2-day treatment of dexamethasone in vitro is overwhelmed in vivo by some extra-pituitary action, probably on the central nervous system, of glucocorticoids in patients with acromegaly.

Acromegaly↗