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Biomedical subjects

T Tsuboi

Publications and source records attributed to T Tsuboi.

At least 145 records · Page 8Linked to original sources
PubMed1980

Pharmacological evaluation of OP 1206, a prostaglandin E1 derivative, as an antianginal agent.

Effects of OP 1206 were studied on the cardiovascular system and platelet functions to assess OP 1206 as an antianginal agent. OP 1206 given orally at more than 100 micrograms/kg relieved vasopressin-induced ST depression of rat electrocardiogram (ECG), an animal model of angina pectoris, concomitant with slight hypotension. Intra-coronary injection of OP 1206 (1-100 ng/kg) in dogs resulted in a remarkable increase of coronary blood flow without any influence on heart rate, blood pressure, myocardial oxygen consumption and redox potential. Resistance in both large and small vessels of dog coronary artery was decreased by intravenous injection of OP 1206 (1-3 micrograms/kg). Platelet aggregation, adhesiveness, bleeding time, and thrombocytopenia induced by ADP and collagen infusion in guinea-pigs were inhibited by oral administration of OP 1206 at the same doses or doses less than those relieving vasopressin-induced ST depression of ECG. These results suggest that OP 1206 contributes to the improvement of cardiac imbalance between oxygen demand and supply, and suppression of thrombus formation in atherosclerotic heart.

Alprostadil↗
PubMed1979

Aggregation of gel-filtered guinea-pig platelets by lipoproteins.

Very low density lipoproteins (VLDL) and low density lipoproteins (LDL) were isolated from serum of hypercholesterolemic guinea-pigs, and the effect of these lipoproteins on guinea-pig platelets was studied. VLDL (greater than 100 microgram/ml) and LDL (greater than 400 microgram/ml) were found to cause aggregation of gel-filtered platelets (GFP), although the extent of GFP aggregation by LDL was smaller than that by VLDL. In platelet-rich plasma, however, lipoproteins could not induce platelet aggregation. VLDL and LDL even at the low concentrations at which lipoproteins alone could not induce aggregation potentiated ADP-induced aggregation of GFP. VLDL-induced aggregation of GFP was inhibited by apyrase (0.2--1.0 mg/ml) in a concentration-related manner. Prostaglandin E1, dipyridamole, potassium cyanide and ethylenediaminetetraacetic acid inhibited VLDL- and ADP-induced aggregation of GFP in the almost same degree. Inhibitions of VLDL-induced GFP aggregation by acetylsalicylic acid and albumin were slightly stronger than that of ADP-induced aggregation. These findings suggest that lipoproteins modulate platelets so that endogenous ADP can be released from platelets.

Adenosine↗
PubMed1978

Febrile convulsions followed by nonfebrile convulsions: analysis based on a maximum likelihood method and discriminant function.

Two hundred sixty-two nontreated patients with febrile convulsions only and 107 with later nonfebrile convulsions were analyzed based on a maximum likelihood method and discriminant function. The formula for discrimination is as follows: y = 2.9193 x (basic EEG abnormality at the first examination) + 2.2134 x (more than 20 minutes in duration of convulsion) + 1.7358 (fever under 38.4 degrees C before convulsion) + 1.7005 x (specific EEG abnormality at the first examination) + 1.6703 x (more than 5 recurrences) + 1.5610 x (over 4 years of age at the last convulsion) + 1.4921 x (exogenous causes) + 0.3741 x (family histroy of febrile convulsions among second or third relatives)--3.0397. If an item is positive, coefficient x 1 is to be used, and if it is negative, coefficient x 0 is to be applied. When one classifies patients with y greater than 0 as the FCC group, and those with y less than 0 as the FC group, misclassification may be theoretically expected in 18.9% of cases (accuracy in 81.1%).

Age Factors↗
PubMed1977

Genetic aspects of febrile convulsions.

A total of 6706 children 3 years of age (3491 boys, 3215 girls) in a particular geographical area in Fuchu (population approximately 182 000), Tokyo, was investigated. Some 654 children (9.8%; 10.5% for male, 9.0% for female) had had at least one convulsion, and the incidence of febrile convulsions was 6.7% (7.2% for male, 6.2% for female). The 450 FC children with febrile convulsions and 620 randomly selected control children were analyzed on the mode of inheritance. The incidence of the disease among siblings was 21.9% (29.7% after age correction), which rose greatly with increasing numbers of affected family members, and the segregation ratio among siblings was higher (36.5%) with one FC parent, and lower (18.5%) if neither parent had had a seizure. The more severe the illness in FC children, the larger the incidence among siblings. Population and family studies indicated that heredity plays an important role in febrile convulsions and that multifactorial inheritance is most likely.

Child, Preschool↗
PubMed1977

Incidence of seizures and EEG abnormalities among offspring of epileptic patients.

The marriage rate of epileptic patients was 62% in males and 78% in females. Compared with the rates in the general population, the male patients had a 15% lower rate, but there was no difference in females. There were 263 patients with at least one offspring selected for the study. There were 234 sons and 272 daughters (506 total, 1.9 per patient). Distribution by types of seizure was awakening grand mal, absence or myoclonic petit mal in 24%, grand mal with no aura in 21%, grand mal during sleep in 23%, diffuse grand mal in 7%, grand mal with aura in 13%, psychomotor seizure in 9%, and focal seizure in 3%. The probands were composed of 79% idiopathic and 21% symptomatic in pathogenetic classification. An epileptic EEG abnormality was demonstrated in 22% of male and 44% of female probands. The incidence of seizures among offspring was 2.4% (4.2% age-corrected) in a narrow sense (epilepsy) and 9.1% in a broad sense including febrile convulsions. The latter morbidity was 11.0% for the idopathic and 3.2% for the symptomatic group; 11.0% for female and 6.9% for male probands; 10.2% for sons and 8.1% for daughters. The figure was higher for the probands with the age range at onset of seizure of 0--4 years (20.6%) and 20--29 years (12.6%) than for those with other age ranges; higher for those with awakening grand mal, absence, myoclonic petit mal, for those with family history of epilepsy than those without it. Possible correlation of types of seizure between probands and offspring was demonstrated. Thirty-seven percent of offspring exhibited epileptic EEG abnormalities, and the ratio of epileptic EEG abnormalities to clinical manifestation is about 4:1. Possible existence of familial aggregation of EGG abnormalities and of two kinds of families with large or small epileptic predisposition was indicated. The importance of the role of hereditary and environmental factors in epileptic pathogenesis is proved, and the results of an investigation of congenital malformation among offspring of epileptic mothers are presented. These results were considered to be useful for genetic counseling of epileptic patients.

Abnormalities, Drug-Induced↗
PubMed1977

Febrile convulsions followed by nonfebrile convulsions. A clinical, electroencephalographic and follow-up study.

103 patients with febrile convulsions followed by nonfebrile convulsions and 512 patients with febrile convulsions only (FC group) under 5 years of age at the first examination were analyzed from many aspects. A trimodal curve in distribution by age at onset of nonfebrile convulsions was seen: 2--3 years of age with occasional grand mal, 5--6 years of age with absence, and 12 years of age with awakening grand mal. Specific EEG abnormality was observed in 40% at the first examination (29% in FC group). Typical or atypical spike-and-wave complex, polyspikes, or continuous EEG abnormality were characteristic (slow wave burst with spike for FC group). Development from febrile convulsions into nonfebrile convulsions was detected in 17% among male and female patients. To identify an effective sign for the prediction of this development, the ratio between correct and incorrect prediction rates was analyzed. Specific paroxysmal EEG abnormality was increased over 3 years of age. EEG change due to aging and the significance of EEG reexamination were indicated.

Age Factors↗
PubMed1976

Inhibition of human and animal platelet adhesiveness to glass bead columns by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid.

The differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.

Adenosine↗
PubMed1976

Electroencephalographic examination of 50 women with Turner's syndrome.

An EEG study has been made of 50 women with Turner's syndrome, 39 found outside institutions and 11 in institutions for the mentally retarded. We found paroxysmal EEG abnormalities in 23 per cent of the former and in 55 per cent of the latter. We found indications of occipital lobe defects in the mentally retarded Turner women.

Adolescent↗