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Biomedical subjects

N Takayanagi

Publications and source records attributed to N Takayanagi.

At least 91 records · Page 5Linked to original sources
PubMed1984

Neosurugatoxin, a specific antagonist of nicotinic acetylcholine receptors.

Neosurugatoxin (NSTX) (3 nM-30 nM), recently isolated from the Japanese ivory mollusc (Babylonia japonica) exerted a potent antinicotinic action in the isolated guinea pig ileum. Specific [3H]nicotine binding to rat forebrain membranes was saturable, reversible, and of high affinity. Nicotinic cholinergic agonists exhibited a markedly greater affinity for [3H]nicotine binding sites than a muscarinic agonist, oxotremorine. Although alpha-bungarotoxin had no effect on [3H]nicotine binding, low concentrations (1 nM-1 microM) of NSTX inhibited [3H]nicotine binding in the forebrain membranes and its IC50 value was 69 +/- 6 nM. On the other hand, NSTX did not affect muscarinic receptor binding in the brain. These data indicate that NSTX may be of appreciable interest as a neurotoxin with a selective affinity for ganglionic nicotinic receptors.

Animals↗
PubMed1984

Pathological study on livers with noncirrhotic portal hypertension and portal venous thromboembolic occlusion: report of seven autopsy cases.

Seven adult autopsied cases with noncirrhotic portal hypertension and thromboembolic occlusion of the large extra- and intrahepatic portal veins are presented. There were two types of portal venous occlusion: old thromboembolic occlusion (group A, two cases) and fresh thromboembolic occlusion (group B, five cases). In group A the occlusion was complete and the affected veins, which were identified clearly by elastic fiber stains, were characteristically shrunk to cause a long-standing portal hypertension. Extra- and intrahepatic collaterals were prominent. In group B the extra- and, sometimes, intrahepatic larger portal veins with fresh thromboemboli revealed variable degrees of phlebosclerosis, probably resulting from organization of repeated portal venous thromboemboli. These sclerotic changes further extended into the medium-sized and smaller intrahepatic portal veins. The latter and other hepatic morphology resembled those of idiopathic portal hypertension without larger portal venous occlusion (group C). Thus, in group B the widespread involvement of the portal venous system by thromboembolic events, particularly the smaller ones, might be important not only for the development of portal hypertension but also for understanding the hepatic pathology of idiopathic portal hypertension.

Adult↗
PubMed1983

[Increase in pulmonary resistance induced by Forssman antiserum in guinea pigs].

Intravenous injection of Forssman antiserum produced a diphasic increase in pulmonary resistance in guinea pigs. The first increase (phase I) occurred with 20 sec latency after injection of Forssman antiserum. The second increase (phase II) occurred immediately thereafter, and this lasted more than 30 min and was irreversible. In the lung, hemorrhages and edema were evident. Hemorrhagic fluid was noted in the bronchiole and the alveoli. Polymorphonuclear leucocytes aggregated in the capillary lumen. The endothelial lining of the venule had been destroyed. Phases I and II were not blocked by DSCG. These were completely blocked by cobra venom factor and carrageenin. Isoproterenol, salbutamol and aminophylline selectively blocked phase I. Also, aminophylline weakly blocked phase II. Cyproheptadine blocked phase I, but chlorpheniramine did not. In contrast, indomethacin and aspirin selectively blocked phase II. Superoxide dismutase significantly blocked phase II, but inactivated superoxide dismutase and catalase did not. The present findings suggest that activation of the complement system appears to be essential for the induction of the increase in pulmonary resistance mediated by Forssman antiserum. Phase I is probably due to the contraction of the respiratory tract. Serotonin may be one of the substances for this contraction. In contrast, phase II is due to disintegration of the endothelial lining and extravasation of hemorrhagic exudates into the respiratory tract. Prostaglandins and/or superoxide radical may take part in the phase II response.

Airway Resistance↗
PubMed1983

[Anti-inflammatory effect of Cu-Zn superoxide dismutase on carrageenin-induced arthritis in rabbits].

Anti-arthritic action of superoxide dismutase (SOD) was studied in rabbits. Arthritis was induced by intraarticular injections of lambda-carrageenin (1%, 1 ml) into the knee joint weekly for two weeks. In this experimental arthritis, acid phosphatase activity, quantities of protein, uronic acid and lipid peroxide, and leukocyte counts in the synovial fluid increased; and the quantity of uronic acid in the articular cartilage decreased. Microscopic findings of the synovial membrane showed a proliferative synovitis. The responses of the left and right knee joint to carrageenin were much to the same in degree, so that the anti-arthritic action of SOD by intraarticular injections was evaluated on one knee joint, referring to the other joint as a control (saline injections). Two injections of SOD (350 SOD unit = 0.1 mg), one a week, suppressed the inflammatory changes in the biochemical parameters of the synovial fluid and the articular cartilage; particularly, significant inhibitory effects on acid phosphatase, lipid peroxide and leukocyte were observed. The microscopic findings of the synovial membrane also revealed that SOD was efficacious. On the other hand, 0.1 mg of denatured SOD, prepared by reducing the S-S bond or heating under an alkaline condition, did not show any anti-arthritic activity. These results suggest that the anti-arthritic action of SOD actually depends on the enzymatic activity of superoxide dismutase.

Acid Phosphatase↗
PubMed1983

[Antihypertensive action of elcatonin].

Subcutaneous injections of elcatonin, a synthetic analogue of eel calcitonin, lowered the blood pressure in DOCA/saline-hypertensive and spontaneously hypertensive rats (SHR), but not in normotensive Wistar rats. The hypotensive effect was more prominent in the DOCA hypertensive rats. Daily injections of elcatonin (10-30 U/kg/day for 21 days) resulted in maximum hypotension on the 4th day in DOCA hypertensive rats and on the 14th day in SHR, and the reduced level of blood pressure was maintained. After the cessation of elcatonin injections, the pressure started to elevate gradually towards the control level. In normotensive rats, elcatonin did not significantly alter the blood pressure for 6 weeks. Daily injections of elcatonin significantly prevented the development of DOCA-induced hypertension and spontaneously-occurring hypertension. Elcatonin-induced hypotension did not differ in the control and parathyroidectomized DOCA hypertensive rats. Elcatonin did not alter the pressor response to noradrenaline, vasopressin and angiotensin II nor the depressor response to isoproterenol, acetylcholine and histamine in DOCA hypertensive rats. It is concluded that the antihypertensive effect of elcatonin is not associated with the release of parathyroid hormone nor with the blockade of alpha, beta, angiotensin II and vasopressin receptors.

Animals↗
PubMed1981

Uridine diphosphate galactose 4-epimerase deficiency.

A case of uridine diphosphate galactose (UDP-Gal) 4-epimerase deficiency was discovered by mass screening of newborn infants. UDP-Gal 4-epimerase activity of red blood cells from the patient was found to be remarkably low, i.e., 7.5% of the level in normal controls at comparable ages. The parents showed intermediate values between those of the patient and controls. The enzyme activity in a specimen of liver tissue obtained from the patient by needle biopsy revealed a normal value. Subsequently, two other families with the condition were found by mass screening and these individuals were found to be heterozygotes.

Carbohydrate Epimerases↗
PubMed1976

Inoculation experiment of Marek's disease vaccine contaminated with a reticuloendotheliosis virus.

Two-day-old chicks were inoculated with one or ten doses of Marek's disease (MD) vaccine originated from the herpesvirus of turkeys (HVT) and contaminated with a reticuloendotheliosis virus (REV). As a result, they presented such symptoms as abnormality in the vane of remiges, undergrowth, anemia, and leg paralysis. These symptoms were the same as those induced by the same vaccine among chicks in the field. Control chicks which had been placed in the same house as those inoculated with the vaccine exhibited no abnormal signs. A persistent infection with REV was noticed in the vaccine-inoculated group. A horizontal infection with REV was the highest in the control group, which was followed by the group inoculated with one dose and that inoculated with ten doses in the order listed. The antibody response of chicks to HVT and MD virus was also inhibited by REV.

Animals↗
PubMed1975

Study of the variation of urinary protein patterns referring to the histopathological changes in renal diseases.

Protein constituents of the concentrated urine prepared from 131 patients with various renal diseases were analysed by the use of electrophoretic and immunochemical methods, referring to histopathological findings of the kidney obtained from biopsy or autopsy. Excretion of macromolecular serum proteins in the urine would be promoted not only by the lesion in glomerular filtration but also by the damage in tubular structure due to severe inflammatory change. From the evaluation of levels of immunoglobulins and various autoantibodies in the blood and urine, there could be found that their increase in the urine was mostly associated with chronic persistent inflammatory reactions followed by destructive changes in parenchymal tissue of the kidney. Investigation of the features of urinary protein and activities of autoantibodies in the urine is likely to be advantageous for the differentiation or renal disease and the decision of condition in individual patient. However, it must be noted that variation of the urinary patterns is caused by more complicated pathologic changes in whole kidney rather than the disturbance of glomerular filtrating mechanism.

Adult↗