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Biomedical subjects

H Nagai

Publications and source records attributed to H Nagai.

At least 19 recordsLinked to original sources
PubMed1979

Significance of the quantification and demonstration of hyaluronic acid in tissue specimens for the diagnosis of pleural mesothelioma.

Hyaluronic acid in pleural tissues from patients with mesothelioma, carcinoma, and asbestosis of the lung was quantified by using specific glycosaminoglycan-degrading enzymes. In all cases of pleural mesothelioma, the quantity of hyaluronic acid in mg/g of dry tissue was at least 0.10 mg, whereas carcinomatous pleural tissue and pleura in asbestosis contained 0.02 to 0.03 mg/g of dry tissue.

Asbestosis↗
PubMed1979

Cryoactivation of inactive renin in human plasma.

The mechanism of the increase in renin activity in human plasma which had been kept -5 degrees C for 4 days (cryoactivation) was investigated. From the results of clinical studies, it is likely that the controling mechanism of inactive renin has something in common with that of active renin. The experimental data showed that the increase in renin activity of human plasma by cryoactivation was closely correlated to the increase obtained by incubation with trypsin (r = 0.88, p less than 0.001, n = 10). Soybean trypsin inhibitor, aprotinin and di-isopropylfluorophosphate (DFP) inhibited cryoactivation, indicating that the cryoactivation is due to the action of a trypsin-like serine enzyme. Trypsin which had no effect on plasma renin activity in the presence of the same amount of soybean trypsin inhibitor at 37 degrees C, activated the renin activity during cold incubation, suggesting that the dissociation of the trypsin-inhibitor complex may have taken place at a low temperature. Endogenous trypsin inhibitor is also likely to lose its affinity to endogenous trypsin-like enzyme at a low temperature.

Cold Temperature↗
PubMed1979

Histamine release from rat neutrophils and mast cells as induced by ionophore--a pharmacological approach--.

A comparative study was carried out on the histamine release from rat neutrophils and mast cells by calcium ionohpore A 23 187 (Ionophore). A maximum release of histamine from neutrophils was induced by 10(-6) g/ml Ionophore and that from mast cells was 5 x 10(-6) g/ml. A fairly good correlation was found between the 45Ca incorporation into and the histamine release from both cells. The Ionophore-induced histamine release from both cells was decreased in Ca2+-free Tyrode's solution and by pretreatment with 0.05 M EDTA. Effects of different drugs on Ionophore-induced histamine release from neutrophils were similar to those seen in mast cells. Dibutyl cyclic adenosine monophosphate, theophylline, isoproterenol and prostaglandin E1 had not or only a slight inhibition on the release. The dose dependent inhibition of release was observed with disodium cromoglycate, N-(3',4'-dimethoxycinnamoyl) anthranilic acid and disodium baicalein phosphate, in experiments using both cells. Colchicine did not inhibit the reaction in these cells, however phosphatidylserine enhanced the reaction. On the other hand, the effect of concanavalin A was different in each type of cells, the release from mast cells was inhibited while the release from neutrophils was potentiated. These findings suggest the similarity of biochemical events in Ionophore-induced histamine release from neutrophils and mast cells.

Animals↗
PubMed1979

A biological study on hot-water extract from delipidated Mycobacterium bovis strain BCG.

The biological activity of a hot-water extract from delipidated BCG, designated as HSA (Hot-water Soluble Adjuvant), was investigated. The HSA did not induce hyperreactivity to bacterial endotoxin. The hot-water extract from which nucleic acids had been removed by streptomycin (SM-HSA) was found to enhance the delayed-type hypersensitivity as evidenced by the results of footpad reaction of mice. The HSA and SM-HSA could be injected to mice by an intraperitoneal route for 20 consecutive days without undesirable side effects. A comparative study was made on the effects of HSA in relation to the duration and doses of treatment with HSA using the ddI mice inoculated with Sarcoma-180. The most remarkable effect was observed when 0.25 mg of HSA had been injected for 20 consecutive days. Also SM-HSA was found to exert antitumor activity when applied in the same manner as above. These results suggest that the presence of nucleic acids is not related to the biological and antitumor activities of the hot-water extract.

Adjuvants, Immunologic↗
PubMed1979

[Intraventricular hemorrhage with hepatic insufficiency--report of a case (author's transl)].

Authors report a case of intraventricular hemorrhage with hepatic insufficiency. A 36-year-old man was admitted following the sudden onset of coma. For 10 years before admission he had suffered general fatigue and jaundice, which were treated with medication as acute hepatitis. On the day of admission he began to suffer from a severe headache. Within one hour he was comatose and began to have vomiting, followed by seizures characterized by tonic movement of the right extremities. Lumbar puncture showed an initial pressure over 400 mmH2O, with grossly bloody spinal fluid. Numerous hemorrhages were noted in both optic fundi. Bilateral carotid angiography demonstrated slight enlargement of left lateral ventricle. Computerized tomography revealed that the lareral, third and fourth ventricles were dilated. There were discrete areas of increased absorption coefficient with values measuring between 30 to 35 in the Hounsfield scale in all ventricles. Two burr holes in both frontal areas were performed. About 50ml of blood clot at left ventricle and 30 ml of blood clot with liquor at right ventricle were removed. The patient died 7 days after operation. Autopsy revealed clotted blood in the whole ventricular system, mainly in right anterior horn of lateral ventricle, and a markedly cirrhotic liver with hepatoma. In our review of the literature, the relationship between intraventricular hemorrhage and bleeding tendency caused by hepatic insufficiency was discussed.

Adult↗
PubMed1978

Cryoactivation of plasma renin.

1. The mechanism of increased renin activity after human plasma had been kept at -5 degrees C for 4 days (cryoactivation) was investigated. 2. The increase in renin activity of human plasma by cryoactivation was closely correlated to the increase obtained by incubation with trypsin (r = 0.88, P less than 0.001, n = 10). 3. An inhibitor of thiol enzyme, N-ethylmaleimide did not inhibit cryoactivation. 4. Soyabean trypsin inhibitor and di-isopropylflurophosphate (DFP) inhibited cryoactivation, suggesting that the cryoactivation may be due to the action of a trypsin-like serine enzyme. 5. In an experiment in the rat haemorrhagic shock caused parallel and cryoactivated plasma, the renin activity being about two times higher in the latter. No significant differences were found in the concentrations of renin and renin substrate between the non-cryoactivated and cryoactivated plasma samples. 6. The results may indicate that a destruction of an inhibitor of the renin-renin substrate reaction is responsible for the increase of renin activity after exposure of rat plasma to low temperature. A trypsin-like enzyme in plasma might have destroyed the inhibitor during this procedure.

Animals↗
PubMed1978

The analysis of the intracranial pressure by the concept of the driving pressure from the vascular system.

In order to understand the pathogenesis of intracranial hypertension, the intracranial pressure (ICP) has usually been studied with the concept of volumetric pressure. In other words, the ICP is held to derive from the volume of the intracranial elements (e.g., brain, blood and cerebrospinal fluid). In this paper, the authors propose a new concept of the so-called driving pressure and apply it to both clinical and experimental studies. The driving pressure (DP) consists of the combined pressure continuously exerted on the ICP by the arterial pressure (ADP) and venous pressure (VP) systems.

Adolescent↗
PubMed1978

Antigen-, anti-F(ab')2- and anti-IgE-induced histamine release from rat mast cells.

The existence of IgE antibody molecules on peritoneal mast cells from rats immunized with dinitrophenylated ascaris extract was demonstrated by double antibody immunofluorescence staining and by histamine release induced by anti-IgE antibodies. Cross-linking of the IgE molecules, which are fixed to mast cells, by interaction with either the homologous antigen or with antibodies to the Fab or Fc regions of IgE, triggered in the presence of calcium ions a chain of intracellular reactions which involve cyclic nucleotide modulation and energy-requiring processes leading ultimately to the release of histamine from the granules of these cells. Although there was no apparent difference in the mechanism(s) underlying the reactions triggered by any of these three agents, the extent of histamine release caused by antibodies to the Fc region of the IgE was significantly lower than that induced by cross-linking of IgE molecules through their Fab regions by reactions with either anti-Fab antibodies or antigens.

Animals↗
PubMed1978

The inhibition of histamine release by antiallergic drugs.

Three new antiallergic drugs, Doxantrazole, PRD-92 and N5', as well as disodium cromoglycate, inhibited the IgE-mediated PCA reaction in the rat triggered by the homologous antigen, but did not have an antagonistic effect on histamine itself. Moreover, all the drugs examined caused in vitro inhibition of antigen-mediated histamine release from peritoneal mast cells and chopped lung tissue of sensitized rats producing IgE antibodies. Doxantrazole had a synergistic effect on the inhibition of histamine release by isoproterenol, whereas the other drugs were devoid of this capacity. PRD-92 and N5' inhibited the ionophore A23,187 induced histamine release, but did not have any effect on the D2O-enhanced histamine release which was triggered by antigen.

Animals↗