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Biomedical subjects

T Matsuda

Publications and source records attributed to T Matsuda.

At least 1,585 records · Page 88Linked to original sources
PubMed1981

Thiamine as an integral component of brain synaptosomal membranes.

Synaptic plasma membranes were prepared from rat cerebral cortex to determine if thiamine was localized in the membranes. The synaptosomes, prepared by discontinuous sucrose gradient centrifugation, were subjected to osmotic shock at pH 9.5 for 10--15 min and subfractionated on a discontinuous sucrose gradient. The two membrane fractions that were obtained were free of contamination by mitochondrial membrane and soluble fractions. In order to ensure specificity, thiamine was assayed fluorometrically before and after the addition of thiaminase I (thiamin:base 2-methyl-4-aminopyrimidine-5-methenyltransferase, EC 2.5.1.2). The thiamine content of the two membrane fractions was 9 and 10 pmol/mg protein.

Animals↗
PubMed1981

Prophylactic intubation and continuous positive airway pressure in the management of inhalation injury in burn victims.

Burn mortality statistics are influenced by age and degree of total surface body burn. The addition of an inhalation injury to a cutaneous burn results in a significant increase in mortality rate. Nine hundred fourteen patients with acute thermal injury were screened for positive history of burn in a closed space, facial or oropharyngeal burn, singed nasal vibrisae, carbonacious sputum, and clinical signs of upper airway involvement. On admission, 84 patients (9.2%) had more than one of the previously mentioned factors. They were prophylactically intubated and placed on optimum level of continuous positive airway pressure (CPAP) and intermittent mandatory ventilation (IMV). The mortality rate among patients without inhalation injury was 7.1%, while 54.7% of patients with inhalation injury died. Comparison of burn patients with inhalation injury to those without pulmonary involvement at the same age group and with the same percentage of burn showed significantly higher mortality rate in patients with inhalation injury. The main cause of death in the first 72 h postburn (stage 1) in patients without inhalation injury was peripheral shock (10.1%) and in patients with inhalation injury was peripheral shock (15.2%) and cardiac failure (10.8%). No pulmonary related death occurred in this stage. In 3-10 days postburn period (stage 2), burn wound sepsis (10.1%) and cardiac failure (11.8%) were the major causes of death in patients with inhalation injury. In patients with inhalation injury, pulmonary sepsis (26%) was the major cause of death in this stage. Major causes of death after 10 days postburn (stage 3) in patients without inhalation injury were pulmonary sepsis (20%) and burn wound sepsis (22%). In patients with inhalation injury, burn wound sepsis (21.7%) was the main cause of death. These data suggest that prophylactic intubation and CPAP therapy in burn patients with suspected inhalation injury prevent pulmonary related death in early stage of burn. Irrespective of presence of inhalation injury, sepsis originating from the wound or respiratory tract is the main cause of death in the late stage of burn.

Adolescent↗
PubMed1981

Disseminated intravascular coagulation in the aged complicated by acute myocardial infarction.

The incidence and pathologic features of cardiac lesions in 184 autopsied aged patients with disseminated intravascular coagulation (DIC) were reported. Coronary thrombosis was noted in 31 (16.8%), fresh myocardial necrosis in 60 (32.6%) and massive myocardial hemorrhage in 49 (26.6%) of these patients. Fresh myocardial infarction was present in 16 (8.7%) patients, 13 of whom manifested coronary thrombosis. The site of thrombi deposition was closely related to preexisting stenotic lesions of the coronary arteries. Only 3 of 16 patients with disseminated intravascular coagulation and acute myocardial infarction had typical cardiac symptoms. In most patients, the electrocardiographic changes were equivocal or not diagnostic for the diagnosis of acute myocardial infarction. We suggest the possibility that coronary thrombi in disseminated intravascular coagulation may gradually increase in extent and severity, leading to confluent areas of myocardial necrosis. The possibility of death due to heart failure, arrhythmia or cardiac rupture, points to the importance of recognizing the frequent cardiac involvement in aged patients with disseminated intravascular coagulation.

Aged↗
PubMed1981

[Clinical effect of acetylspiramycin on primary atypical pneumonia in children (author's transl)].

Clinical effect of acetylspiramycin, one of macrolide antibiotics, primary atypical pneumonia and serologically proven Mycoplasma pneumonia in children was studied. Twenty-four cases of these pneumonia (PAP 11, MP 13) in children were selected and acetylspiramycin was given in dose of approximately 30 mg/kg/day orally. Clinical response was evaluated in terms of improvement in fever, cough and chest X-ray. Clinical response was excellent in 4, good in 5, fair in 14 cases and none in 1 case. No definite adverse effect was observed, however 3 cases showed skin rashes. Two cases showed evanescent small erythematopapulous rash and 1 case developed urticaria on the 2nd to 4th day after this drug was given. These skin rash seemed one of the manifestation of Mycoplasma infections, rather than adverse side effect. One case showed elevated transaminase activity before acetylspiramycin was given and improved on the 2nd week, although this drug was continued. No other side effect was observed. We were able to use acetylspiramycin only in the form of 200 mg tablet and difficulty of the administration was encountered in children under 5 years of age. Other form (dry syrup, etc.) of this drug should be considered for the clinical use in children. In conclusion, acetylspiramycin was effective and safe for the treatment of primary atypical pneumonia and Mycoplasma pneumonia.

Adolescent↗
PubMed1980

Effect of cyclic nucleotide derivatives on the release of ACh from cortical slices of the rat brain.

Atropine (5 nM to 5 muM), but not D-tubocurarine or hexamethonium, enhanced the release of acetylcholine (ACh) from rat brain cortical slices exposed to high K+. The enhancement was dose-dependent, and it could be partially antagonized by oxotremorine (50-500 muM) or by dibutyryl or 8-bromo-cyclic GMP (1 mM), but not by tetrodotoxin (200 nM) or by dibutyryl cyclic AMP (1 mM). The effects of oxotremorine and the cyclic GMP derivatives were not due to diminished ACh synthesis, since these compounds did not influence the reduction of tissue ACh resulting from treatment with K+ and atropine. These results suggest that cyclic GMP may mediate the regulation of ACh release by presynaptic muscarinic receptors.

Acetylcholine↗