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Biomedical subjects

M Ikezaki

Publications and source records attributed to M Ikezaki.

15 recordsLinked to original sources
PubMed1983

Development of sensitivity to different secretagogues in the rat stomach.

Acid and pepsin secretion and gastric mucosal histidine decarboxylase activity were measured in rats of various ages between 5 and 40 days after injection of saline, pentagastrin, histamine, or carbachol. Basal acid secretion first appeared on day 15. At this time carbachol significantly stimulated both acid and pepsin secretion. Gastrin and histamine did not stimulate acid or pepsin secretion until day 20. Histidine decarboxylase activity first appeared on day 10 and was first increased by pentagastrin on day 18. Injection of 8-day-old rats with corticosterone prematurely induced acid secretion on day 12 in response to all three stimulants and pepsin secretion in response to carbachol only. These studies provide a comprehensive picture of the development of gastric mucosal sensitivity to the three naturally occurring stimulants and indicate that adrenal glucocorticoids play an important role in that development.

Aging↗
PubMed1979

Lipid peroxidation and lysosomal enzymes in D-galactosamine hepatitis and its protection by vitamin E.

Role of lipid peroxidation on lysosomal instability in liver tissue was investiaged in an experimental model of D-galactosamine hepatitis in rats fed on vitamin E (V.E) deficient diet. Administration of D-galactisamine to V.E deficient rats resulted in a sudden increase of serum glutamic oxaloacetic transaminase (sGOT), glutamic pyruvic transaminase (sGPT), lipid peroxide value, as well as beta-glucuronidase and acid phosphatase activity examined as markers of lysosomal enzymes, when compared with control rats fed on V.E supplemented diet. Lipid peroxide in the liver tissue also showed significant increase in V.E deficient rats. In contrast, beta-glucuronidase and acid phosphatase in the liver tissue were found to decrease in V.E deficient rats by the administration of D-galactosamine, indicating that the enzymes in the lysosome were entirely released outside the liver cells as a result of cell destruction. It is concluded that the increase of lipid peroxide causes the instability of lysosomal membranes and releases various kinds of hydrolytic enzymes to lead further to cell damage. V.E might act on inhibiting lipid peroxidation to stabilize lysosomal membranes.

Acid Phosphatase↗
PubMed1979

Cold activation of complement and kinin.

Differences between serum and plasma complement, which now is called as the cold activation of complement, was investigated in relation with the phenomenon reported as the cold promoted activation of factor VII, to which kallikrein and Hageman factor are known to participate. Despite the presence of several similarities in these two phenomena, it is concluded that the cold activation of complement is not related to the coagulation nor the kinin system. Evidence that tranexamic acid, a potent antiplasmin compound, provided an inhibitory effect on the cold activation of complement, suggested that the phenomenon could not be explained by a single mechanism, and plasmin might be involved in the phenomenon in a limited case.

Cold Temperature↗
PubMed1979

Effect of a streptococcal preparation on the complement system.

Streptococcal preparation OK-432 (Picibanil), clinically being used as an immunopotentiator, has been shown to activate the complement system either through the classical or the alternative pathway in vitro [15]. In this experiment, OK-432 was found to increase serum complement level in guinea pigs, and in human without malignancy, when investigated by hemolytic assay using sensitized sheep erythrocytes (EA) for the classical pathway activity and unsensitized rabbit erythrocytes (RaE) for the alternative pathway activity. Assay of complement components revealed a significant increase in C3, but decrease in Clq, while no specific tendency was observed in C4, C5, C9, properdin, C3 activator and Cl-inhibitor. These evidences suggested that OK-432 might potentiate immune response of the host by elevating serum complement level, in addition to activate the complement system.

Aged↗
PubMed1978

A case of Menetrier's disease associated with protein-losing gastropathy and abnormal serum complement profile.

A 44-year-old man with Menetrier's disease associated with protein-losing gastropathy and with abnormal serum complement profile is reported. He was treated by an antifibrinolytic compound tranexamic acid (trans-AMCHA) since he was found to have elevated fibrinolytic activity in the biopsied gastric mucosa. The therapy brought his serum protein from 3.8 g/dl to 5.6g/dl, however could not reduce his mucosal disorder. Substitution of a placebo for trans-AMCHA resulted in marked depression of his serum protein to 3.7 g/dl. It was concluded that trans-AMCHA was effective in raising his serum protein to a certain extent but failed to block the vicious circle of "mucosal disorder", "increased tissue fibrinolysis" and "hypoproteinemia" (Kondo, M. et al. Gastroenterology 70, 1045, 1976). Abnormal serum complement profile seen in this patient was found to be due to cold activation of the classical complement pathway (Kondo, M. et al. J. Immunol. 117, 486, 1976). Although no correlation between the phenomenon and Menetrier's disease has been clarified yet, the appearance of wheezing as in asthma when exposed to cold suggested that cold activation of complement occurred in vivo and resulted in increasing of the vascular permeability in the lungs.

Adult↗
PubMed1978

Anti-fibrinolytic therapy of giant hypertrophic gastritis (Menetrier's disease).

In five cases of giant hypertrophic gastritis (Menetrier's disease) biopsied gastric mucosa was examined for fibrinolytic activity; in all cases there was marked elevation of the activity due mainly to tissue plasminogen activator. The patients were given antifibrinolytic therapy with oral tranexamic acid (trans-4-aminomethyl cyclohexane carboxylic acid; trans-AMCHA), and four of the patients showed marked improvement of their hypoproteinemia as well as their mucosal disorders. One patient, who showed moderate increase of serum protein level but no reduction of the mucosal disorder, finally received gastrectomy. It was concluded that antifibrinolytic therapy seemed to block the vicious circle of 'membrane disorders', 'increased tissue fibrinolysis', 'increased vascular permeability' and 'hypoproteinemia' in Menetrier's disease.

Adult↗
PubMed1975

Streptococcal preparation as an activator of host-mediated immune response: cellular immunity and alternate pathway of complement.

Streptococcal preparation, OK-432, was examined for its ability to initiate a host-mediated immune response. Aged individuals with negative skin response to phytohemagglutinin (PHA), as well as reduced in vitro blastoid transformation of lymphocytes, were treated with OK-432, and the response to PHA appeared in two out of three cases. The preparation was also demonstrated to convert C3 proactivator of complement when incubated with fresh human serum, as tested by immunoelectrophoresis, indicating the possibility that OK-432 might activate the alternate pathway of complement.

Aged↗