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Biomedical subjects

E Masuda

Publications and source records attributed to E Masuda.

49 records · Page 3Linked to original sources

Age-related change in human gastric mucosal energy metabolism.

Many investigators have reported a decrease in mucosal blood flow resulting in impairment of gastric mucosal energy metabolism in animal experiments. Recently, endoscopic studies using reflectance spectrophotometry and laser Doppler flowmetry have indicated that gastric mucosal blood flow in humans decreases with age. However, changes in energy metabolism in human gastric mucosa with age remains obscure. In this study, we measured adenine nucleotides in biopsy samples from human gastric mucosa, using high-performance liquid chromatography, and investigated changes in energy metabolism with age in subjects proven normal endoscopically. Energy charge (EC = (ATP + 1/2 ADP)/ATP + ADP + AMP) in the gastric antral and body mucosa showed decrease with age. When the subjects were divided into two groups, less than and more than 65 years old, the EC level was significantly lower in the latter than the former in both antral and body mucosa (0.65 +/- 0.06 versus 0.74 +/- 0.03 in the antrum, 0.73 +/- 0.04 versus 0.79 +/- 0.04 in the body) and significantly less in the antral mucosa than in body mucosa in both groups. The adenosine triphosphate (ATP) level in the older group showed a significant decrease (6.48 +/- 1.14 versus 9.63 +/- 1.92 in the antrum, 8.59 +/- 1.64 versus 10.60 +/- 2.13 in the body) compared with those less than 65 years old. In the antral mucosa of the older group the adenosine diphosphate (ADP) level was also significantly lower than that in the group less than 65. In conclusion, in the elderly, the energy metabolism in human gastric mucosa is impaired, and this may weaken their defensive mechanism.

Adenine Nucleotides↗

[Antitumor effects of a new antitumor agent, zinostatin stimalamer (YM881)--effects on experimental tumors in vitro and in vivo].

Zinostatin stimalamer (YM881) is an antitumor agent, chemically synthesized by coupling one molecule of neocarzinostatin (NCS), with 2 molecules of styrene maleic acid half-butylester copolymer. YM881 showed strong cytotoxicity to human (KB, ST4 and others) and mouse (P388, L1210) tumor cell lines and also drug-resistant tumor cell lines. The antitumor effects were observed in murine MM46, colon 26 and other tumor models. The antitumor activity was as effective as NCS or better than NCS at the effective dose ranges.

Animals↗

Role of blood ethanol on gastric mucosal injury and gastric hemodynamics.

The present series of studies were performed to test the hypothesis that ethanol in the blood may play a role in the pathogenesis of gastric mucosal injury. Another hypothesis to be examined was that endothelin may be involved in ethanol-induced gastric mucosal injury. Elevated levels of blood ethanol induced by intraperitoneal infusion of ethanol increased vulnerability of the stomach to hydrochloric acid in a dose-dependent manner in rats. This may be due to impaired gastric mucosal hemodynamics and oxygenation as demonstrated by the results obtained by organ reflectance spectrophotometry (decreases in indices of mucosal hemoglobin contents and hemoglobin oxygen saturation). Ethanol infusion caused a dose-dependent increase in gastric vascular resistance in perfused rabbit stomach, which was accompanied by an increased production of endothelin-1. The results suggest that endothelin may be involved in the pathogenesis of ethanol-induced gastric mucosal injury.

Animals↗

[Intracellular calcium level, lipid peroxidation, and development of gastric mucosal injury in rat hemorrhagic shock].

Although acute gastric mucosal lesions (AGMLs) develop after the mucosal ischemia and reperfusion, precise intracellular mechanism for the development of AGMLs remains unclear. In the present paper, we investigated intracellular calcium level, lipid peroxidation, and gastric mucosal lesion in rat hemorrhagic shock model. We estimated intracellular calcium by measuring phosphorylase a activity in the gastric mucosa. The mucosal phosphorylase a increased during hemorrhagic shock, while it returned to be normal after the reinfusion of shed blood. Although mucosal lipid peroxide and area of AGMLs did not increase significantly during hemorrhagic shock, they increased significantly after the reinfusion. Diltiazem, a calcium antagonist, prohibited both of the increase in mucosal phosphorylase a activity during hemorrhagic shock and the increase in lipid peroxide content and area of AGMLs after the reinfusion of the shed blood. Organ reflectance spectrophotometry revealed that the gastric corpus suffered mucosal ischemia and hypoxia during the hemorrhagic shock. The are of AGMLs had a good correlation with a level of lipid peroxidation in the gastric mucosa. These results suggest 1) that intracellular free calcium in gastric mucosa increases during the mucosal ischemia; 2) that a calcium antagonist prohibits the increased intracellular free calcium during mucosal ischemia; and 3) that a calcium antagonist prohibits the increased mucosal lipid peroxide and the development of AGMLs after the mucosal reperfusion. Thus it is concluded that the increased intracellular free calcium during ischemia plays a key role in the mucosal tissue injury in the ischemia-reperfusion state.

Animals↗

Establishment and characterization of human myelomonocytic (TYS) and histiocytic (TYH) cell lines.

Two human hematopoietic cell lines (TYS and TYH) with monocytic characteristics were derived from the peripheral blood of a patient with acute myelomonocytic leukemia and of another with a follicular large-cell type of malignant lymphoma. The TYS cells, derived from the leukemia patient, revealed a monocytic appearance with microvilli at one side and had many granules and vacuoles. They showed strongly positive reactions with alpha-NBE, NASDAE, and AcP, and were reactive with monoclonal antibodies such as OKlal, 12 and Bl. The TYS cells, which phagocytized carbon particles and antibody-coated SRBC but not latex particles, released lysosomal enzymes and tumoricidal factor into the supernatant. The TYH cells, derived from the malignant lymphoma patient, had abundant cytoplasm and pseudopods detectable by electron microscopy with a monocytoid appearance and virus-like particles in the cytoplasm. They showed strongly positive reactions with alpha-NBE, NASDAE and beta-Gase, but no reactivity with monoclonal antibodies or with surface markers except Fc gamma-R. TYH cells phagocytized latex particles very well. Two different human monocyte-histiocyte lineages were thus established. During culture, the TYS and TYH cells maintained their characteristics over 28 and 16 months of passage, respectively.

Animals↗

Effect of trypsin modification of the Escherichia coli elongation factor Tu on the ternary complex with aminoacyl-tRNA.

The ribonuclease resistance assay has been used to probe the effect of trypsin modification of the Escherichia coli elongation factor Tu X GTP on the interaction with E. coli aminoacyl-tRNAs. First, the equilibrium dissociation constant of the trypsin-modified Tu X GTP X Thr-tRNA complex was determined to be 2.3 (0.1) X 10(-5)M at 4 degrees C, pH 7.4. Second, binding of 17 of 20 noninitiator aminoacyl-tRNAs and four sets of purified isoacceptor tRNAs to the modified protein was measured. At 4 degrees C, the complex stabilities vary 500-fold over the range of aminoacyl-tRNAs, with Gln-tRNA forming the strongest ternary complex and Val-tRNA, the weakest. The results are compared to a similar study of ternary complex formation using intact elongation factor Tu X GTP, and the major differences are discussed. An analysis of both data sets, particularly that for the leucine isoacceptor tRNAs, suggests that the trypsin modification of elongation factor Tu X GTP disrupts a region of protein that is involved with the aminoacyl side chain rather than that of the acceptor stem helix region of the aminoacyl-tRNA.

Amino Acid Sequence↗

Affinity purification of aminoacyl-tRNA.

A procedure for separating Escherichia coli aminoacyl-tRNA from unacylated tRNA or components of the aminoacylation reaction, thereby achieving an aminoacyl-tRNA product with a very high specific activity, is described. The method utilizes the specific recognition of aminoacyl-tRNA for E. coli protein synthesis elongation factor Tu which has been immobilized on an affinity matrix. The application of the affinity procedure as a means of purifying a single aminoacyl-tRNA from an unfractionated mixture of tRNAs is also discussed.

Chemical Phenomena↗

Regulation of allergic reaction by aerobic Corynebacterium equi extract, CEF. III. Inhibition of histamine release from rat peritoneal mast cells.

Effects of a water soluble fraction of Corynebacterium equi (CEF) on the histamine release from rat peritoneal mast cells (RPMC) were investigated. The treatment of RPMC with CEF resulted in a significant inhibition of the histamine release from RPMC which was induced by IgE antibody-antigen interaction as well as nonimmunological histamine liberators. CEF was much more effective in inhibition of IgE-mediated histamine release and compound 48/80 or polymyxin B-induced histamine release when the mast cells were treated with CEF prior to the incubation with the antigen or the liberators. In contrast, CEF was equally effective in inhibition of the histamine release by concanavalin A with phosphatidyl serine when the mast cells were treated with CEF prior to or simultaneously with the liberator. Evidence was also presented that CEF inhibits degranulation of mesenteric mast cells induced by immunological as well as nonimmunological mechanisms.

Animals↗

Induction of suppressor macrophages in mice by Fusarenon-X.

Intraperitoneal injection of Fusarenon-X into BALB/c mice, a mycotoxin produced by Fusarium nivale Fn 2B, depressed polyclonal antibody formation of splenic lymphocytes in response to pokeweed mitogen (PWM). This inhibitory activity was found to reside in the surface immunoglobulin-negative spleen cell fraction of Fusarenon-X-treated mice, sIg-(FX), which comprised mainly T lymphocytes and smaller number of non-lymphocytic cellular elements. However, reconstitution experiments for in vitro antibody formation provided evidence that T lymphocytes from Fusarenon-X-treated mice, T(FX), which were separated from non-lymphocytic cells by use of carbonyl iron/magnet, were as effective as T lymphocytes from normal mice, T(N), in supporting antibody formation. Furthermore, addition of non-lymphocytic cells, NL(FX), or adherent cells, AD(FX), prepared from spleen cells of Fusarenon-X-treated mice to normal spleen cells strongly inhibited in vitro antibody formation against PWM or a bacterial lipopolysaccharide (LPS). These results strongly indicated that Fusarenon-X induced non-lymphocytic suppressor cells in the spleen of the treated mice which had features in common with activated macrophages.

Animals↗

Immunosuppressive effect of a trichothecene mycotoxin, Fusarenon-X in mice.

The in vitro treatment with Fusarenon-X, a mycotoxin produced by Fusarium nivale Fn 2B, depressed the mitogenic responses of mouse lymphocytes to the T-cell mitogens, phytohaemagglutinin (PHA) and concanavalin A (Con A), but to a lesser extent to B-cell mitogen, a bacterial lypopolysaccharide (LPS). The in vitro treatment of mice with Fusarenon-X also decreased the responsiveness of splenic lymphocytes to the T-cell mitogen, Con A. Administration of Fusarenon-X to BALB/c mice before immunization significantly reduced anti-DNP IgE and IgG1 responses, while the treatment of mice after immunization was less effective. The number of spleen cells of the treated mice was increased with a reduction of T lymphocytes and an increase of granulocytic elements. In vitro antibody responses of spleen cells from Fusarenon-X treated mice by pokeweed mitogen (PWM) or LPS were also suppressed. Reconstruction experiments using sIg positive and negative spleen cells from normal and Fusarenon-X treated mice showed that this inhibitory effect resided in the sIg negative cell population.

Animals↗