Effects of donor-specific blood transfusion on the survival of living related renal grafts.
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Biomedical subjects
Publications and source records attributed to H Sugimoto.
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The mechanism of right-sided traumatic diaphragmatic hernia following blunt trauma was examined. In 13 cases of Traumatic diaphragmatic hernia admitted to the Department of Traumatology Osaka University Hospital, 3 cases were on the right. All cases were associated with severe injuries in the chest, abdomen and pelvis. Rib fractures, hemothorax, and liver injury were seen in the same site of the ruptured diaphragm. So it seemed that there were some differences in the force itself caused diaphragmatic rupture between right-sided and left. We reviewed 40 cases of right-sided traumatic diaphragmatic hernia reported in Japan. The following results were obtained. Main force which caused right-sided diaphragmatic rupture was the blunt impact to the right thoracic wall. In the right-sided diaphragmatic hernia, the most frequently herniated organ was the right lobe of the liver and there was high-frequency of G-I tract herniation in delayed types. Herniation of the abdominal organs seemed to be varied as the time passed.
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Platelets appear to be involved in both the maintenance of homeostasis and the regulation of proliferation of vascular smooth muscle cells. Anomalies of platelet function may be responsible in part for the pathogenesis of vascular disease in experimental and human diabetes. In a search for an appropriate animal model, we have studied platelet function and the properties of platelet cyclic NCL-PDE in rats with streptozocin-induced diabetes, spontaneous diabetes, and human insulin-dependent diabetes mellitus (IDDM). It appears that opposite abnormalities in both aggregation and phosphodiesterase activity exist in the two animal models. In human IDDM, similar abnormalities to those seen in the BB model were observed. Vascular smooth muscle cells in culture can be used as a model for studies of the effect of circulating growth factors in animals and humans. A growth inhibitory factor was found in plasma and serum from STZ and human IDDM but not BB. In humans we observed increased growth-promoting activity of diabetic platelets, but this phenomenon was absent in both animal models. It remains to be evaluated whether these differences may account for the fact that diabetic rats appear resistant to development of vascular complications. It also remains to be established which animal model is the best choice for studying growth abnormalities in diabetes.
A 2-month-old female infant with pancarditis was reported. The patient died after a 26-day clinical course. The autopsy showed pancarditis, including inflammation in all 4 valves and chordae, fibrinoid vasculitis, pharyngolaryngitis and atrophy of the lymph nodes. Microscopic examination revealed proliferative inflammation in the endocardium, valve, myocardium, epicardium and coronary vessels. The histological findings suggested the etiology to be a rheumatic-type reaction at an extremely young age.
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The relationship between abnormality in blood coagulation and Burn Index (B.I.) were examined in 174 patients treated in our department for trauma during past 7 years. Platelet counts decreased rapidly and became minimal at 3rd or 4th hospital day, but PT, APTT, fibrinogen and FDP were abnormal in many cases over 30% BSA only within 24 hours after thermal injury. The platelet counts at 3rd hospital day and PT within 24 hours were well correlated with Burn Index (platelet vs. B.I. r = 0.665, p less than 0.01; PT vs. B.I., r = 0.587, p less than 0.01). And PT was also well correlated with plasma total protein (r = 0.686, p less than 0.01). AT-III, plasminogen and alpha 2 PI had also a tendency of interrelation to plasma protein level. These data suggest that systemic intravascular coagulation does not commonly complicate immediately after thermal injury, although consumption of coagulation factors are mainly occurred at the site of burn and correlated with the loss of plasma protein.
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A series of the title compounds was prepared via condensation of the 3-(aminomethyl)triazolylbenzophenone (5) with N-protected amino acids, followed by deprotection, amination of the 3-[(chloroacetamido)methyl]triazolylbenzophenone (6a,b), or reduction of the relevant azide derivative (6c). Some of the title compounds were also derived directly from the quinazolines 3 or 4 by acid-induced rearrangement, followed by deprotection. These new amino acid amide derivatives of the triazolylbenzophenones (2) were evaluated for central nervous system (CNS) activity. Members of this class of compounds exhibited a high level of CNS activities. For example, 2',5-dichloro-2-[3-[(glycylamino)methyl]-5-methyl-4H-1,2,4-triazol-4-yl] benzophenone (2c) was as active as triazolam, with an ED50 of 0.58 mg/kg (mice, po), against antifighting activity in the foot shock-induced fighting test. Other triazolylbenzophenone derivatives (2a-f) showed similar pharmacological activities.
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Of patients with acute carbon monoxide poisoning admitted to the Trauma Intensive Care Unit of the Osaka University Hospital 39.5% (17/43) manifested hyperamylasemia. Iszyme studies in 16 such patients revealed 87.5% to be of the salivary type. Two patients presented with hyperamylasemia of the pancreatic-salivary type. There was no pancreatic type hyperamylasemia among these patients, negating the possible involvement of the pancreas in hyperamylasemia from carbon monoxide poisoning. There was a statistically significant difference in amylase levels between the arterial and the external jugular venous blood, indicating the salivary gland as the organ mainly responsible for hyperamylasemia in carbon monoxide poisoning. Amylase levels coincided well with the level of consciousness and the base excess. The amylase levels correlated significantly with beta-glucuronidase levels, suggesting the hyperpermeability of cell membranes of the salivary gland as the chief factor in hyperamylasemia secondary to acute carbon monoxide poisoning.