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Biomedical subjects

M Tsuchiya

Publications and source records attributed to M Tsuchiya.

At least 361 records · Page 20Linked to original sources

Microcirculatory disturbances of oral mucosa and periodontal disease in patients with liver cirrhosis.

This study showed: (1) The bone score in cirrhotic patients was significantly lower than that in the control group. (2) In liver cirrhosis, capillaries were decreased in number and they were dilated compared to that in the control. In particular, the capillaries in cirrhotic patients with ascites or oesophageal varices were dilated compared to those without. (3) Blood flow of the mucogingival junction was significantly decreased in patients with liver cirrhosis in comparison with the control group. These results suggest that microcirculatory disturbances of oral mucosa are important in the progress of periodontal disease in patients with liver cirrhosis.

Female↗

[Let's study pharmacokinetics related to anesthesiology by using computer graphics: intravenous drugs].

The pharmacokinetics of intravenous drugs used during anesthesia provides us important information for patients' care. The pharmacokinetic data are usually shown in a graphic expression together with numerical values. The numerical values are only convenient for investigators in exchanging their knowledge and information. The graphic data contain, however, whole and real information obtained in a pharmacokinetic study. The authors demonstrated a way to derive information from graphic data, which is practically applicable for patients' care. We also showed a way to calculate numerical values from graphic data by using "graphnote" by Fukutake Pub. Co. We believe that our manual way to calculate numerical values from graphic data, with an aid of computer graphics combined with scientific calculator, helps us to understand the invisible processes performed inside "a black box" or a computer installed with a commercially available soft ware for the pharmacokinetics.

Anesthesia, Intravenous↗

[Case of skeletal open bite treated with orthognathic surgery, with special reference to morphological and functional analysis of the tongue].

Malfunction and abnormal posture of the tongue has been thought to be one of etiological factors for skeletal open-bite at length. In this study, an adult female patient with anterior open-bite is reported, who has been treated by means of posterior maxillary osteotomy and has obtained a good occlusion and profile, which is stable throughout the retention period. Electromyography was obtained from the tongue muscles by surface electrodes and the tongue muscle activity during deglutition was measured before and after surgery. The tongue posture was also analyzed on the basis of the roentgen cephalogram with the mandible at the rest position. Larger tongue muscle activities during swallowing was revealed compared to the control subjects. In addition, anteriorly and superiorly positioned tongue was seen in the initial stage. The amplitudes of the tongue muscle had decreased and tongue posture had shifted posteriorly and inferiorly following surgery, which approximated to the those observed in the control subjects. These improvements of the abnormal activity and posture of the tongue and the stability of occlusion after surgery confirmed that posterior maxillary osteotomy is an effective surgical operation for the anterior open-bite patients in terms of prognosis.

Adolescent↗

[An experimental study on the severe type of alcoholic liver disease--a pathogenetic role of potentiated activation of complement system by endotoxin after chronic ethanol consumption].

Endotoxemia frequently appears in severe type of alcoholic liver disease. However, we have little knowledge how endotoxin influences the progression of alcoholic liver injury. Thus, to study the causal mechanism for the progression to the severe type of alcoholic liver diseases, endotoxin (0.2 mg/100 g BW, E. Coli O26:B6) was intravenously injected in chronic ethanol-fed rats and controls, and then, rats were sacrificed after 16 hours of endotoxin treatment. The elevation of serum GOT and GPT activities induced by endotoxin was significantly higher in chronic ethanol-fed rats than controls, and these biochemical changes were well correlated with the grade of necrosis of liver histology. Furthermore, in chronic ethanol-fed rats, endotoxin treatment tremendously increased blood BUN and creatinine levels and produced the degeneration of renal tubuli with neutrophil infiltration into glomerulus. These experimental findings are very similar to the severe type of alcoholic liver disease. On the other hand, endotoxin significantly decreased serum values of CH50 in chronic ethanol-fed rats, but not in controls. Such alterations of CH50 induced by endotoxin were well correlated with the several parameters indicating the injury of liver and kidney. Therefore, the present study may indicate that chronic ethanol ingestion aggravates endotoxin-induced organ injury, and that the activation of complement system may associate with such progression of organ injury.

Animals↗

[Effect of combined administration of HBs antigen and anti-HBs antibody on induction of anti-HBs antibody production in vitro and in vivo].

It was considered that nonresponsiveness to hepatitis B surface antigen was in part due to a failure in the antigen recognition (i.e., antigens' phagocytosis, processing and presentation by accessory cells). In order to enhance the capture of antigens, we investigated the effect of simultaneous administration of HBs antigen and anti-HBs IgG on antibody responses in vitro and in vivo. As a result, in vitro sensitization of mononuclear cells from anti-HBs-positive subjects with HBs antigen and anti-HBs IgG induced significant amounts of anti-HBs IgG production in 5 of 6 cases, whereas sensitization with HBs antigen alone failed to induce the antibody production in most cases. In vivo administration of HBs vaccine and anti-HBs immunoglobulin to non-responders to the vaccine triggered active anti-HBs antibody responses in 3 of 7 cases in vivo and in 5 of 7 cases in vitro.

Hepatitis B Antibodies↗

Halothane, an inhalation anesthetic, activates protein kinase C and superoxide generation by neutrophils.

The rate of superoxide generation of guinea pig intraperitoneal neutrophils by a chemotactic peptide or 12-O-tetradecanoylphorbol-13-acetate (TPA) was increased by 2-bromo-2-chloro-1,1,1,-trifluoroethane (halothane), an inhalation anesthetic. This increase was inhibited by 1-(5-isoquinolinesulfonyl)methylpiperazine dihydrochloride (H-7), a specific inhibitor of Ca2+- and phospholipid-dependent protein kinase C (PKC). Halothane was found to significantly activate partially purified PKC. The activation required phosphatidylserine (PS) and Ca2+. Dioleoylglycerol- or TPA-activated PKC activity was further increased by halothane. The cytoplasmic proteins of guinea pig neutrophils phosphorylated by halothane-activated PKC were similar to those phosphorylated by PMA-activated PKC. The phosphorylation of a 48 kDa protein, a phosphorylated protein required for NADPH oxidase activation, was also increased by halothane. These data suggest that the increase of superoxide production by halothane is correlated with its activation of PKC.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Luminol-dependent photoemission from single neutrophil stimulated by phorbol ester and calcium ionophore--role of degranulation and myeloperoxidase.

Luminol-dependent photonic burst from phorbol ester-treated single neutrophil was visually investigated by using an ultrasensitive photonic image intensifier microscope. Neutrophils stimulated by phorbol myristate acetate (0.1 microgram/ml) alone produced a negligible level of photonic activities in the presence of luminol (10 micrograms/ml). The additional application of 0.1 microM Ca2+ ionophore A23187 induced explosive changes of photonic burst corresponding to the distribution of neutrophils, and these photonic activities were gradually spread to extracellular space. Sodium azide, which prevents myeloperoxidase activity, inhibited Ca2+ ionophore-induced photonic burst from phorbol ester-treated neutrophil. These findings suggest a prerequisite role of degranulation and myeloperoxidase release in luminol-dependent photoemission from stimulated neutrophils.

Azides↗

Preferential ADP-ribosylation of arginine-3 in synthetic heptapeptide Leu-Arg-Arg-Ala-Ser-Leu-Gly.

Hen liver nuclear ADP-ribosyltransferase modified the synthetic heptapeptide Kemptide (Leu-Arg-Arg-Ala-Ser-Leu-Gly) at arginine-2 and/or arginine-3. Trypsin treatment of ADP-ribosyl-Kemptide revealed that the ADP-ribosylation of arginine-3 was constantly more abundant than that of arginine-2. ADP-ribosylation of Kemptide suppressed the subsequent phosphorylation by cyclic AMP-dependent protein kinase.

Adenosine Diphosphate↗

ADP-ribosylation suppresses phosphorylation of the L-type pyruvate kinase.

L-type pyruvate kinase (EC 2.7.1.40) purified from pig liver was ADP-ribosylated by incubation with NAD and ADP-ribosyltransferase purified from hen liver nuclei. Maximal incorporation of the ADP-ribose moiety from NAD into the L-type pyruvate kinase was 0.98 mol/mol of subunit. The Km values for NAD and L-type pyruvate kinase were 0.17 mM and 9.7 microM, respectively. ADP-ribosylation of the L-type pyruvate kinase resulted in suppression of the subsequent phosphorylation catalyzed by cAMP-dependent protein kinase. The ADP-ribosylation-induced suppression of phosphorylation of the L-type pyruvate kinase also resulted in suppression of the phosphorylation-induced inactivation. Amino acid analysis, after exhaustive sequential digestion of ADP-ribosyl-L-type pyruvate kinase with pepsin, aminopeptidase M and carboxy-peptidase B showed arginine to be the ADP-ribose-accepting amino acid. These results together with finding of the ADP-ribosyltransferase activity in mammalian liver cytosol (Moss, J. and Stanley, S.J. (1981) J. Biol. Chem. 256, 7830-7833) suggest that ADP-ribosylation may participate in the regulation of the L-type pyruvate kinase activity through changes in the rate of phosphorylation.

Adenosine Diphosphate Ribose↗

Alterations in gastric mucosal microvascular endothelium in a stressed condition--relevance to gastric ulcerogenesis.

The present paper describes the morphological and functional alterations of the gastric mucosal microvascular endothelium under restraint-stressed condition. On the basis of the direct cholinergic innervation of capillaries and non-muscular venules in the gastric mucosa, these endothelial changes would be caused by the stress-induced overstimulation of the cholinergic nerves and modified by the degranulation of mast cells, contributing to the stress-induced ulcer formation as schematically illustrated in Fig. 10.

Aged↗

Active oxygen species generated by monocytes and polymorphonuclear cells in Crohn's disease.

Chemiluminescence (CL) analysis of monocytes and polymorphonuclear cells (PMNs) was performed on 13 patients with Crohn's disease (CD) and 10 healthy volunteers. The percentages of monocyte populations in mononuclear cells obtained from the patients with CD were greater than those from the healthy volunteers, but the numbers of PMNs were not different between the two groups. The peak level of phorbol myristate acetate (PMA)-induced CL activity generated by diluted whole blood from the patients with CD was more significantly elevated than that from the healthy volunteers, whereas the peak levels of opsonized zymosan-induced CL activity did not differ between the two groups. In monocytes, the peak levels of both PMA- and opsonized zymosan-induced CL activity were significantly higher in the patients with CD than in the healthy volunteers. CL in PMNs, however, showed no significant difference between CD and controls. It is suggested that monocytes of CD have a large capacity to generate active oxygen species. The present study suggests that excessive active oxygen species released by monocytes and perhaps macrophages may play an important role in formation of the intestinal lesions in CD.

Adult↗

Autoradiographic demonstration of gastrin-releasing peptide-binding sites in the rat gastric mucosa.

The location of [125I]iodotyrosyl gastrin-releasing peptide-binding sites in the rat fundic mucosa was studied. Peptide specificity was demonstrated by competitive binding studies using the addition of a large amount of cold gastrin-releasing peptide or substance P. Autoradiography of the stomach tissue was carried out by freeze-drying, embedding in Epon, wet-sectioning with ethylene glycol, and dry-mounting the emulsion film by the wire-loop method to prevent loss of the labeled substance. Specific binding sites of gastrin-releasing peptide were found on D cells, surface mucus cells, and parietal cells, whereas few binding sites were seen on the chief or mucus neck cells.

Animals↗

ADP-ribosylation of bradykinin and effects on its biological activities.

We investigated the ADP-ribosylation of bradykinin by hen liver nuclear ADP-ribosyltransferase. Two Arg residues of the peptide were modified by this enzyme. Arg1 was preferentially modified as compared to Arg9; the Vmax/Km for Arg1 was 3 times higher than that for Arg9. These results were given support by data observed in experiments with des-Arg1 and des-Arg9 bradykinin; the Vmax/Km for des-Arg9 bradykinin was 3 times that for des-Arg1 bradykinin. ADP-ribosylation suppressed the biological activity of bradykinin, as related to both binding and contractile activities. The extent of ADP-ribosylation-induced suppression of both activities was higher in the case of the modification of Arg1 than that of Arg9. In view of the observation of ADP-ribosyltransferase activity in skeletal, cardiac, and smooth muscles (Soman, G. et al. (1984) Biochem. Biophys. Res. Commun. 120, 973-980; Shimoyama, M. et al. (1987) in The 8th International Symposium on ADP-Ribosylation, Texas, abstract p. 13), bradykinin functioning in the contraction of smooth muscle may be modified in this way in vivo.

ADP Ribose Transferases↗

Involvement of autonomic nervous system in gastric mucosal defense mechanism.

This article describes the histochemical, immunohistochemical, radioautographic, and ultrastructural localizations of aminergic and peptidergic nerves, neurotransmitter receptors, and their binding sites in the stomach wall. Cholinergic and vasoactive intestinal polypeptide (VIP)-ergic nerve fibers are distributed along the gastric microvasculature, within the myenteric and submucosal plexuses, and in the muscularis mucosae and circular muscle layer. In the mucosa, both nerve fibers evenly extend along the capillaries in association with the epithelial cells up to the mucosal surface. In particular, cholinergic nerves are proved to doubly innervate the mucosal capillaries and nonmuscular venules as well as the parietal cells. Adrenergic and neuropeptide Y (NPY)-containing nerves are distributed primarily along the arterioles of the gastric microvasculature, within the myenteric plexuses, and in the circular muscle layer. These nerve fibers extend up to the basal portion of the mucosa in close association with small arterioles, capillaries, and epithelial cells. Some of the adrenergic nerve axons are coexistent with the cholinergic nerve axons within the Schwann cell. Histamine H1 receptors are widely located on the walls of arterioles, capillaries and venules, while H2 receptors are evident not only on the parietal cells but also on the walls of the collecting venules and surrounding capillaries in the mucosa. Dopamine D1 receptors are predominantly located on the smooth muscle cells of the arterioles near the muscularis mucosae, while D2 receptors are present on the walls of postcapillary venules and collecting venules. Functional coordination of both intramural peptidergic nerves as intrinsic origin and aminergic nerves as extrinsic origin is considered to be essential for maintaining the gastric mucosal defense mechanism against a variety of aggressive factors.

Animals↗