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Biomedical subjects

Y Sasai

Publications and source records attributed to Y Sasai.

At least 163 records · Page 9Linked to original sources
PubMed1983

Acid hydrolases in the initiation of ischemic myocardial necrosis.

Alterations in myocardial acid hydrolases in acute ischemia were studied in relation to the evolution of cardiac cellular necrosis by the determination of cathepsin D, acid phosphatase (AcPase), and beta-glucuronidase activities of the myocardial fractions and by electron microscopic cytochemical studies on AcPase in the canine heart. In the normal myocardium, the same level of activity of acid hydrolases was found in sarcoplasmic reticulum (SR) as in the lysosome fraction. In electron microscopy, AcPase reaction products were observed markedly in SR and moderately in lysosomes, in residual bodies, and in Golgi apparatus. In the ischemic myocardium, at 20 to 30 min after coronary ligation, activation of these enzymes was observed in both SR and lysosomes, and at 60 to 90 min they were decreased in the particles and, in turn, increased in the cytoplasm accompanying the ischemic fine structural changes. At 2 to 3 hr those acid hydrolase activities in the cytosol were decreased, indicating the loss of enzymes from necrotic myocardial cells. Acid hydrolases are the most important factor for the evolution of ischemic myocardial necrosis by being activated not only in lysosomes but also in SR and by being released to the cytoplasm to disintegrate the cellular structures.

Acid Phosphatase↗
PubMed1983

Sialomucin in Paget cells of extramammary Paget's disease.

The cytoplasmic sialomucin in Paget cells of extramammary Paget's disease was examined by means of a battery of histochemical techniques. The staining methods used involved an electrolyte--Alcian Blue (pH 5.8), periodic acid--Schiff and azure A at selected pH levels. Methylation, saponification, borohydride reduction, acid hydrolysis, and digestion with diastase, neuraminidase (Vibrio cholerae) or chondroitinase ABC, were also employed. The cytoplasmic mucin was found to exhibit positive reaction for the above staining which were variously altered by the chemical modification procedures and diminished in intensity or abolished by digestion with neuraminidase. These results suggest that the cytoplasmic mucin is sialomucin without side-chain substituent in extramammary Paget's disease located in axillary or genital area, and with a substituent at C7 in the disease located in perianal area.

Histocytochemistry↗
PubMed1983

Cytofluorometric study of nuclear DNA in experimentally induced epidermal hyperplasia.

The rate of cell proliferation in the basal cell layer by epidermal hyperplasia of guinea pig ear was investigated with cytofluorometric method. Epidermal hyperplasia was caused by tape stripping or the application of n-hexadecane or retinoic acid. In non-treated epidermis, the mean of the relative numbers of cell in each phase to the total cell number was 62.8% (G1), 34.6% (S) and 2.6% (G2 + M), respectively. In the case of tape stripping, growth in the relative number of S phase cells showed approximately the same proportions at 3 to 12 h. At 24 h, the relative number of S phase cells was lower than that in non-treated epidermis. By the application of n-hexadecane, the relative number of S phase cells was highest at 6 h. It was highest at 3 h by the retinoic acid application. On the other hand, the value of nuclear protein in G1 cells was highest at 6 h by both tape stripping and n-hexadecane application, while the value by retinoic acid was similar to that in non-treated epidermis.

Alkanes↗
PubMed1983

Electron microscopic cytochemical studies on acid phosphatase activity in acute myocardial ischemia.

Alterations in the localization and the intensity of acid phosphatase activity were studied electron microscopically in acute ischemic myocardial cells in the dog, in relation to processes of cellular degradation. In normal myocardial cells, the acid phosphatase activity was concentrated in the terminal cisternae, the longitudinal elements and the subsarcolemmal cisternae of the sarcoplasmic reticulum and the primary lysosomes. Activity was moderate in the secondary lysosomes, residual bodies and Golgi apparatus. As early as 15 min after coronary ligation the intensity of acid phosphatase activity increased in the enlarged lysosomes and the sarcoplasmic reticulum of the ischemic myocardial cells. Fine deposits of the reaction product were distributed in the sarcoplasm around lysosomes and the sarcoplasmic reticulum after 30 min, and the activity began to decrease in lysosomes and in the sarcoplasmic reticulum. One to 3 hours after ligation, intramitochondrial dense deposits appeared, and the reaction product decreased both in lysosomes and the sarcoplasmic reticulum. The fine reaction product, which leaked from lysosomes and the sarcoplasmic reticulum, was scattered in the sarcoplasm and was accompanied by fine structural changes indicating cellular necrosis. From these findings it is strongly suggested that acid hydrolases in lysosomes and the sarcoplasmic reticulum are closely related to the necrotic process in ischemic myocardial cells.

Acid Phosphatase↗
PubMed1982

Polymorphonuclear leukocyte chemotaxis in sporotrichosis.

A lesion of sporotrichosis shows a characteristic arrangement of the infiltrate in three zones: the central suppurative zone composed of polymorphonuclear leukocytes, the tuberculoid zone and the round cell zone. For investigating the pathomechanism of the suppurative zone formation, polymorphonuclear leukocyte chemotaxis to sporotrichin was assayed with the agarose plate method. Polymorphonuclear leukocytes in the patients with sporotrichosis showed an enhanced chemotactic index in comparison with that in the control subjects. However, there was no difference in non-specific chemotaxis to bacteria-derived substance between the patients and the control subjects.

Aged↗
PubMed1982

Studies on intracardiac acid hydrolases in the ischemic myocardial necrosis.

Activities and subcellular distributions of acid hydrolases, cathepsin D, acid phosphatase and beta-glucuronidase in myocardial subfractions were determined serially with reference to the initiation of myocardial necrosis in dog hearts with acute ischemia. The following results were obtained: 1) In the normal myocardium, respectable activities of three enzymes were obtained either in the sarcoplasmic reticulum or in the lysosome-containing fraction. 2) Thirty min after coronary ligation, an increase in the activities was observed in both lysosome and sarcoplasmic reticulum fractions of the ischemic heart muscle. After 60 to 90 min these activities were decreased rapidly in both fractions to about 70% of those of the normal myocardium with an increase in the cytosolic activity. Two to 3 hours after ligation, the reduction in the cytosolic activity was noted, indicating an escape of the enzymes from the necrotic myocardium. The subcellular distribution of these enzymes was further altered in the ischemic heart muscle for 12 to 14 hours reflecting an infiltration of the interstitial cells. These findings suggest that activation and release of acid hydrolases not only in lysosomes but also in the sarcoplasmic reticulum are one of the primary and the earliest factors for the evolution of ischemic myocardial injury which leads to necrosis.

Acid Phosphatase↗
PubMed1981

Development of experimental sporotrichosis in normal and modified animals.

The development of experimental sporotrichosis was examined in immunologically-disturbed mice. In the case of intracutaneous inoculation, the lesion in cyclophosphamide-treated mice enlarged strikingly up to 6 days, but at 12 days it was similar in size to that in non-treated mice. The lesion in irradiated mice developed slowly up to 12 days, but thereafter it developed promptly. In nude mice, the lesion was smallest during the development of the lesion. Histological examination showed that numerous organisms were present in the lesion of nude and irradiated mice. Intraperitoneal inoculation showed that dissemination of spores were easily induced in nude mice as compared with littermate mice. These results indicate an important role of cellular immunity in the defence mechanism of sporotrichosis.

Animals↗
PubMed1981

The cytoplasmic mucin in Paget cells of extramammary Paget's disease.

The cytoplasmic mucin in the Paget cells of extramammary Paget's disease was examined with a battery of histochemical techniques. The staining methods used were alcian blue, azure A and periodic acid-Schiff. In a further attempt to identify various polyanions, staining was carried out with alcian blue containing various concentrations of electrolyte. Methylation, saponification, borohydride reduction, acid hydrolysis, and digestion with diastase, sialidase, chondroitinase ABC, or nucleases were also employed. The results obtained suggest that the cytoplasmic mucin in the Paget cells is sialomucin without side-chain substituent.

Alcian Blue↗
PubMed1981

Studies on the Na+-K+-ATPase in myocardial infarction.

Changes in the cardiac sarcolemma in myocardial infarction were studied by both determination of Na+-K+-ATPase activity and SDS gel electrophoretic analysis of sarcolemmal proteins in the canine heart. Ninety minutes after coronary ligation, Na+-K+-ATPase activity in ischemic myocardium was decreased significantly to approximately 36% of that of non-ischemic myocardium, and it remained at the lower level for 28 days. By SDS gel electrophoresis, reduction of the protein band with molecular weight of 111,000, which is suggestive of the main component of ATPase, was observed simultaneously with the reduction of Na+-K+-ATPase activity. These results indicate that ischemia for 90 minutes produces substructural changes in the sarcolemma indicating irreversible myocardial changes.

Animals↗
PubMed1981

Alterations in cardiac troponin subunits in myocardial infarction.

1. Alterations in troponin subunits in myocardial infarction were studied in the dog heart by the analysis of troponin-tropomyosin complex, i.e, native tropomyoin, of total structural proteins in SDS gel electrophoresis, and by the measurement of degree of activation of actomyosin-ATPase by Ca++. 2. At 12 to 24 hours after coronary ligation, reductions in TN-C and tropomyosin were observed followed by a decrease in TN-I at 48 hours. The relative contents of these subunits were the lowest at 72 hours to 7 days falling to less than 10% of those in the non-ischemic myocardium. On the contrary, TN-T was preserved through the course of myocardial infarction. 3. Actomyosin-ATPase activity was increased at 12 to 24 hours after coronary ligation and then reduced rapidly at 24 to 48 hours together with the degradation of myosin. However, the activation of actomyosin-ATPase by Ca++-troponin-tropomyosin was reduced already at 12 hours simultaneously with the reduction in TN-C, and almost completely lost at 48 hours. 4. Troponin subunits and actomyosin-ATPase activity returned to those of the control myocardium at 28 days after coronary ligation indicating the recovery of infarcted tissue.

Adenosine Triphosphatases↗