Biomedical subjects
Publications and source records attributed to H Shio.
Prostaglandin E(1) (10(-8) to 1O(-7) molar) is effective in improving the preparation of human platelet concentrates from plasma rich in platelets and from whole blood. A procedure has been developed for the use by blood banks, on a trial basis.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Platelet aggregation in the post-acute phase of 48 patients with cerebral thrombosis was measured to see if any specific type of cerebral infarction is associated with enhanced platelet aggregation. All patients were examined with cerebral angiography and computed tomography (CT). Stenotic lesions in major cranial arteries were analyzed by measuring the apparent diameter. Severe stenosis was defined as 75 per cent constriction or more. Enhanced aggregation of platelets (secondary aggregation at 1 microM ADP or less) was present in 5 of 25 patients (20%) who had severe vessel stenosis or occlusion. CT examination frequently revealed both cortical and deep involvement. On the other hand, 13 of 23 patients (57%) with less stenotic lesions showed enhanced aggregation and that was statistically significant (p less than 0.05). Many patients of this group had persistent hypertension and small deep infarctions. Platelet aggregation was also measured in 20 hypertensive control subjects without stroke. Four of them (20%) showed enhanced aggregation. These findings suggest that a combination of enhanced platelet aggregation and hypertension increases the risk of small deep infarctions accompanied by mild stenotic changes of the major cranial arteries.
The effect of superoxide anions (O2-) on red blood cells (RBC) deformability and membrane proteins was investigated using hypoxanthine-xanthine oxidase system. Exposure of RBC to O2- caused a marked decrease in RBC deformability with a concomitant increase in cell volume and shape changes. The RBC exposed to O2- also displayed pronounced degradation of membrane proteins such as band 3 protein and spectrin; new bands of low molecular weight products appeared as the original membrane proteins tended to diminish, without the appearance of high molecular weight products. Since the membrane proteins are involved in processes regulating membrane properties such as permeability and viscoelasticity, the decreased deformability induced by O2- may be attributable to changes in membrane proteins. Interestingly, resealed ghosts exposed to O2- did not show any significant change in membrane proteins, which suggests the existence of further generation of O2- and subsequent production of other active oxygen species mediated by O2(-)-initiated autoxidation of hemoglobin in intact RBC. Furthermore, electrophoretic analysis suggested that active oxygens increased the endogenous proteolytic susceptibility of RBC. In conclusion, a close linkage was suggested between RBC deformability and the membrane proteins.
Although a decrease in the deformability of red blood cells (RBCs) has been suspected in Heinz body-forming hemolytic anemia, it remains uncertain whether the formation of Heinz bodies themselves impairs RBC deformability or not. To elucidate this question, we used RBCs treated with phenylhydrazine and RBCs from patients with unstable hemoglobin (Hb) disease (Hb Yokohama) to investigate the effect of Heinz body formation on deformability in terms of RBC filterability through nickel mesh and viscosity of the RBC suspension. The phenylhydrazine-treated RBCs exhibited a marked decrease in deformability in a dose-dependent manner. The Heinz body-forming RBCs from the patients also showed a marked decrease in deformability. Thus we confirmed that Heinz body formation impairs RBC deformability. Further, both phenylhydrazine-treated RBCs and RBCs from the patient showed a degradation of spectrin without any cross-linking of membrane proteins, thereby suggesting that the impaired deformability is associated with the oxidative degradation of the cytoskeletal framework. In summary, this study supports the conclusion that RBC deformability is impaired by the presence of Heinz bodies as well as the related oxidative damage involved in their formation.
Explore the source record for details and available documents.