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Biomedical subjects

S Konno

Publications and source records attributed to S Konno.

At least 199 records · Page 11Linked to original sources
PubMed1985

Inhibitory effect of a novel anticomplementary agent, K-76COONa, on the release of histamine induced by zymosan and compound 48/80.

A novel sesquiterpene anticomplementary agent, K-76COONa, if locally applied, was revealed to have an activity to prevent histamine release from rat connective tissue mast cells not only in a zymosan-induced inflammation of the air pouch type (zymosan-air-pouch inflammation) but also in compound 48/80-induced air-pouch inflammation. Moreover, K-76COONa inhibited in vitro histamine release from rat peritoneal mast cells induced by compound 48/80.

Animals↗
PubMed1985

Analysis of the factor(s) involved in pathogenesis of zymosan-induced inflammation in rats.

The role of mast cell degranulation in increased vascular permeability in zymosan-air-pouch inflammation, an experimental model of inflammation induced by zymosan in rats, was investigated. The complement in the inflammatory pouch fluid was exhausted, and mast cells in the pouch wall subcutaneous tissues were degranulated. The histamine level in the pouch fluid was elevated immediately after application of zymosan in the preformed air-pouch and then quickly declined. Plasma exudation into the pouch fluid changed in close parallel with the change of histamine level. Application of compound 48/80 in the air-pouch also brought about liberation of histamine from mast cells, accompanied with elevation of vascular permeability similar to that observed in the zymosan-air-pouch inflammation. However, the amount of the plasma exudation in the zymosan-air-pouch inflammation was about twice as high as that induced by compound 48/80, though the quantity of histamine liberated in the two cases was almost equal. Rats depleted of histamine and serotonin were incapable of responding to compound 48/80, but zymosan still induced increased vascular permeability. A combination treatment with pyrilamine and methysergide did not abolish plasma exudation caused by zymosan, but brought about complete blockade of the vascular permeability response to compound 48/80. These results suggest that some mechanisms independent of degranulation of mast cells are responsible in part for the initial sudden elevation of vascular permeability in zymosan-induced inflammation.

Animals↗
PubMed1985

Inability of rat anaphylatoxin to induce histamine release in rats.

The role of rat anaphylatoxin in histamine release and increased vascular permeability during the first thirty minute period in zymosan-air-pouch inflammation, an experimental model of inflammation induced by zymosan in an air-pouch prepared on the back of rats, was investigated. Complement depletion by cobra venom factor did not affect the histamine release nor the increased vascular permeability in the inflammation of this type. In spite of apparent anaphylatoxin activity, zymosan activated serum (ZAS) failed to cause any significant release of histamine when infused in the air-pouch on the back. Anaphylatoxin purified from rat serum activated with zymosan in the presence of an inhibitor (epsilon-aminocaproic acid) of anaphylatoxin inactivator gave a single band in both polyacrylamide gel electrophoresis (PAGE) and SDS-PAGE. The molecular weight estimated by SDS-PAGE was approx. 7,000. The purified rat anaphylatoxin failed to induce histamine release nor increased vascular permeability even at 50 micrograms/ml, although it caused contraction of guinea pig ileum at 0.8 micrograms/ml. These results suggest that rat anaphylatoxin does not participate in histamine release and increased vascular permeability in the zymosan-air-pouch inflammation.

Anaphylatoxins↗
PubMed1985

Induction of human HL-60 leukemic cell differentiation by immune interferon is accompanied by an increase in NADase activity and by a decrease in DNA-binding proteins.

The effects of highly purified human immune interferon (IFN-gamma) on the differentiation of human promyelocytic HL-60 leukemic cells have been studied. The addition of 100 units/ml interferon to HL-60 cells for 5 days results in morphological changes characteristic of macrophages. At the biochemical level, there is a 3-fold increase in the specific activity of the enzyme NADase. Kinetic analysis shows that IFN-gamma causes an increase in the Vmax of NADase without affecting the apparent Km. Pulse labeling experiments with [35S] methionine show a marked change in the de novo synthesis of several proteins in the course of interferon treatment. Chromatography on DNA-agarose show that after treatment with interferon for 24 or 48 h, there is a 60-70% decrease in newly synthesized proteins which bind DNA-agarose and can be subsequently displaced from the column with 2% SDS containing buffer (from 7.7-8.7% bound in control cell extracts to 2.6-3.1% bound in interferon treated cell extract).

Cell Differentiation↗
PubMed1983

Induction of zymosan-air-pouch inflammation in rats and its characterization with reference to the effects of anticomplementary and anti-inflammatory agents.

Induction of an experimental inflammation of the air-pouch type with the aid of zymosan (known to activate the alternative pathway of the complement system) was carried out in an attempt to induce a reproducible inflammatory model suitable for quantitative studies. Rats were injected subcutaneously with 8 ml of air on the dorsal surface to make an air-pouch, followed 24h later by 4 ml of 1.6% (w/v) zymosan suspension. This induced inflammatory responses. Treatment with zymosan suspension provoked exudation of fluid, accumulation of polymorphnuclear leukocytes (PMN) in the pouch and the development of granulation tissue as a wall of the pouch. Approximately half of the PMN in the pouch formed a characteristic layer of aggregated cells sticking onto the inner surface of the pouch wall. They were counted after being completely disaggregated by means of incubation with trypsin. In preliminary experiments with potential anti-inflammatory drugs, local application of a novel anti-complementary agent, K-76COONa, inhibited leukocyte accumulation in the pouch, whereas the potent anti-inflammatory agent, dexamethasone, was ineffective. By contrast, exudation of the pouch fluid was effectively inhibited by dexamethasone but not by K-76COONa.

Animals↗
PubMed1983

Protection of the ischemic myocardium with calcium antagonistic drugs.

Ligation of the coronary artery to produce myocardial infarction experimentally was performed in 41 mongrel dogs. The dogs were then treated with niludipine or nifedipine. Niludipine in doses of 0.05 mg/kg/day (niludipine A group) and 0.1 mg/kg/day (niludipine B group) or nifedipine 0.05 mg/kg/day (nifedipine group) was administered for 7 postoperative days. The animals were sacrificed, their hearts removed and extent of myocardial damage studied. 1. The size of infarctions measured by 99mTc-PYP myocardial scintigrams of the isolated heart was significantly smaller in the niludipine A group. 2. The degree of ischemia indicated by LDH isoenzyme patterns was lowest in the niludipine A group followed by nifedipine and niludipine B group in this order. The value for H subunits of LDH isoenzymes on the subepicardial side was higher in the nifedipine group. 3. Histopathological findings varied from specimen to specimen, but in general the niludipine A group showed best improvement. Our results suggest that the calcium antagonistic drugs, niludipine and nifedipine, seem to have myocardium protective properties in dogs. To what degree these findings can be applied clinically needs further studies.

Angiocardiography↗
PubMed1982

Akabane disease in cattle: congenital abnormalities caused by viral infection. Spontaneous disease.

Akabane disease, an infectious disorder causing congenital abnormalities in calves, was studied in naturally affected calves between 1972 and 1974 in Japan. The animals included one three-month fetus from which a strain of Akabane virus (OBE-1) was isolated, and a total of 177 stillborn or premature fetuses and deformed or infirm newborn calves that died within a few days of birth. The three-month fetus had nonpurulent encephalomyelitis in the undifferentiated central nervous system, characterized by necrosis of the nerve tissue and endothelial proliferation in the encephalitic process; and polymyositis in the myotubule phase with parenchymal degeneration and cellular infiltrates in the skeletal muscle. The full-term fetuses and newborn calves had nonpurulent encephalomyelitis in the early stage of the epizootic. In the middle to late stages, a dysplastic muscular change which we call runt-muscle disease was seen simultaneously with a decrease in number of ventral horn neurons in the spinal cord and arthrogryposis in the legs. Cystic cavities and thick vascular walls sometimes were seen in the central nervous system in these stages. Hydranencephaly was prominent in the late stage.

Animals↗
PubMed1982

Akabane disease in cattle: congenital abnormalities caused by viral infection. Experimental disease.

Nonpurulent encephalomyelitis and polymyositis were primary lesions of cattle and goats experimentally infected with Akabane virus. Two caprine fetuses, two months old, were infected placentally and examined 11 days after inoculation; twin caprine fetuses, three months old, were inoculated intramuscularly through the dam's uterus and examined nine days after inoculation. Both lesions were seen in each fetus. Reactive proliferation of immature endothelial cells was a significant encephalitic change. Myositic changes included parenchymal degeneration and cell infiltration in fetuses in the myotubule phase and the beginning of the myofiber phase. Only nonpurulent encephalomyelitis was seen in six calves 14 days to one year old, inoculated intracerebrally and examined six to 47 days after inoculation. Nerve-cell degeneration, neurological mobilization, and perivascular cuffs were typical encephalitic changes in the calves. Five fetuses were infected transplacentally and had polymyositis alone. The four bovine fetuses, two to six months old, were examined nine to 18 days after inoculation, and one caprine fetus, one month old, was examined 11 days after inoculation. Neither encephalomyelitis nor polymyositis was seen in four calves under one year old that were inoculated intravenously.

Animals↗
PubMed1982

Pathological studies on encephalitis in mice experimentally inoculated with bovine coronavirus.

One- to 21-day-old mice were examined pathologically after inoculated intracerebrally or subcutaneously with the Kakegawa strain of bovine coronavirus. In 1- to 4-day-old mice inoculated intracerebrally, the brain contained a small number of neutrophils and lymphocytes having infiltrated diffusely and perivascularly and some degenerative neurons. In mice inoculated intracerebrally at 7 to 21 days of age, severe necrosis of pyramidal cells was shown in Ammon's horn. Perivascular infiltrations of neutrophils and lymphocytes were moderate to severe. Some neurons were degenerative in the cerebral cortex, thalamus and midbrain. Degeneration of some neurons and mild infiltration of neutrophils and lymphocytes were observed in the brain of mice inoculated subcutaneously at 1 to 7 days of age. Perivascular infiltration of neutrophils and lymphocytes was prominent in the cerebral cortex of mice inoculated subcutaneously at 14 days of age. Cellular infiltration was also seen in the thalamus, Ammon's horn, midbrain, cerebellum and medulla oblongata. All the mice, except one, inoculated subcutaneously at 21 days of age were free from neural changes. Electron-microscopically, virus particles were observed in and outside of the degenerative neurons. They had a core 70 nm in diameter and an envelope with spikes.

Aging↗
PubMed1982

Morphology of sulfur granules produced by Staphylococcus aureus and Corynebacterium pyogenes in cows.

Sulfur granules produced by Staphylococcus aureus and Corynebacterium pyogenes were studied by light and electron microscopy. They consisted of bacteria and electron-dense amorphous substance which formed clubs in the periphery of each granule. In those produced by Staph. aureus, cocci were seen at the center of each granule. They were round or pleomorphic. Binary fission was frequently observed. In those produced by Coryn. pyogenes, degenerative bacteria were present at the center of each club. Bacteria found just beneath the club had a thick, electron-less-dense cell wall and electron-dense cytoplasm. Those present at the center of the granule were very long and had a cell wall thin and sometimes undulant, containing ribosomes. The electron-dense amorphous substance surrounded these bacteria and faced the neutrophils or epithelioid cells in the periphery of the granule both species of organisms. They might have been produced by bacteria. Cellular reactions of neutrophils, epithelioid cells, fibroblasts and plasma cells were seen around the sulfur granules produced by both species of organisms.

Animals↗
PubMed1982

Intestinal changes in gnotobiotic piglets experimentally inoculated with porcine rotavirus.

Intestinal lesions were studied in 8 gnotobiotic piglets orally given porcine rotavirus by light microscopy, scanning electron microscopy and transmission electron microscopy. Five of these piglets were killed 6, 12, 18, 24 and 48 hours after inoculation, respectively. Of the other 3 piglets, one died 60 hours and two became moribund 96 and 114 hours after inoculation, respectively. All the infected piglets showed diarrhea between 18 and 24 hours after inoculation. Examination of the small intestine by light microscopy and scanning electron microscopy indicated the extensive degeneration and desquamation of epithelial cells with villi stripped and shortened. Villous degeneration, especially that in the jejunum and ileum, was very severe 24 hours after inoculation. Within 48 hours after inoculation, all the stripped villi were replaced by multiplication of regenerated cuboidal epithelial cells. Transmission electron microscopy revealed many virus particles in the epithelial cells of the small intestine 18 hours after inoculation.

Animals↗
PubMed1981

Successful resection of an aortic arch aneurysm using a temporary trifurcation bypass graft.

Resection of a syphilitic aortic arch aneurysm in a 62-year-old woman was accomplished using a trifurcation temporary bypass system. The bifurcation graft was sutured end-to-side to the ascending thoracic aorta, to the brachiocephalic trunk and to the left common carotid artery, respectively. The attached third limb end was anastomosed end-to-side to the infrarenal abdominal aorta. This technique enabled a large shunt into the abdominal aorta. Occlusion of the iliac arteries proved to be effective in coping with hypotension while attending to the bypass and the volume replacement. The post-operative recovery was uneventful and the patient has remained well after 43 months.

Aorta, Thoracic↗