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Biomedical subjects

T Onodera

Publications and source records attributed to T Onodera.

At least 145 records · Page 8Linked to original sources
PubMed1990

Characterization of lymphocyte subpopulations in the blood of the cynomolgus monkey using flow cytometry.

This study was performed to assess the usefulness of flow cytometry in comparison with acid alpha-naphthyl acetate esterase (ANAE) staining for the enumeration of lymphocyte subpopulations in cynomolgus monkeys. For flow cytometry, use was made of mouse antihuman leukocyte monoclonal antibody (T11), recognized to undergo cross-reaction with monkey T lymphocytes or antimonkey IgG serum labelled with fluoroscein isothiocyanate. The percentages of lymphocyte subpopulations in mononuclear cells of thirty healthy female cynomolgus monkeys were 72.1 +/- 2.4% for T cells and 24.6 +/- 2.4% for B cells as assayed by flow cytometry evaluation, and 63.8 +/- 2.5% for T cells and 15.8 +/- 2.2% for B cells as determined by ANAE staining. Although the percentage of T cells shown by ANAE staining was significantly lower than that seen with flow cytometry, the coefficient of correlation indicated a close correlation in both T and B cell subsets between these two methods. In monkeys receiving 20 mg kg-1 cyclophosphamide daily for 14 days, counts of all leukocytes and T and B cells were decreased, whereas animals treated with 1.0 mg kg-1 muroctasin daily for 14 days showed higher monocyte and neutrophil counts without changes in T or B cells. These results suggest that flow cytometry evaluation has several advantages over ANAE staining with respect to rapidity and precision in toxicological studies using large numbers of monkeys.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1990

Reovirus type 2-induced diabetes in mice prevented by immunosuppression and thymic hormone.

Reovirus type 2 that had been isolated from a cow with diarrhoea and passaged in bovine kidney cell culture produced a Type 1 (insulin-dependent) diabetes-like syndrome when inoculated into NC mice. The infection resulted in insulitis and destruction of islet cells. Viral antigens were found in islet cells by staining with fluorescein-labelled antibody to reovirus type 2. The destruction of islet cells resulted in abnormalities shown on glucose tolerance testing. Studies on the susceptibility of the host showed that only certain strains of mice had overtly abnormal glucose tolerance tests when infected with reovirus type 2. To assess the immunological role in the pathogenesis of reovirus type 2-induced diabetes, infected mice were subjected to immunosuppressive or thymic hormone treatment. The administration of either anti-thymocyte serum or serum thymic factor reduced or prevented the development of the diabetes-like syndrome, while Arg-Lys-Asp-Val-Try did not show any therapeutic effects.

Animals↗
PubMed1990

A single gene controls resistance to Japanese encephalitis virus in mice.

The inheritance of resistance to Japanese encephalitis virus (JEV) was investigated using inbred strains of mice to study genetic resistance against JEV infection. C57BL/6 mice immunized intraperitoneally (i.p.) with an infective dose of JEV were resistant to intracerebral (i.c.) challenge with JEV, whereas most C3H/He mice treated in the same manner died. C57BL/6 mice developed this resistance 2 weeks earlier than C3H/He after intraperitoneal (i.p.) immunization. Passive transfer of spleen cells from immunized C57BL/6 protected the recipient mice from i.c. challenge, while transfer from immunized C3H/He was less effective. Since immunized athymic nude mice were not resistant to i.c. challenge with JEV, T lymphocytes were considered to be necessary for protection. When F1, F2 and backcross mice derived from C57BL/6 and C3H/He were challenged i.c. with JEV after i.p. immunizations, the number of resistant and susceptible mice were consistent with Mendelian ratios. Thus it can be concluded that resistance to JEV in mice was controlled by a single, dominant autosomal gene which was not linked to a (non agouti)-locus (chromosome 2).

Animals↗
PubMed1990

Influences of cephem antibiotics on the immune response in mice.

The effects of six cephem antibiotics, including ceftezole, cefmetazole, cefoxitin, cefotiam, cefoperazone, and cefotaxime, on murine humoral immunity were examined. In female BDF1 mice each cephem antibiotic was administered at a dose of 800 mg/kg/day i.v. for 7 consecutive days. Among the antibiotics tested, only ceftezole and cefoperazone induced a significant increase in serum total IgM, but not in serum total IgG. Especially in case of ceftezole, the mice developed splenomegaly due to the proliferation of IgM-producing cells in the germinal centers. The proliferation of splenic IgM-producing cells was also observed in female thymus-deficient Balb/c-nu/nu mice receiving intravenous ceftezole. Thus, the drug was indicated to enhance the polyclonal IgM production in mice by acting as a B cell mitogen. This is consistent with the in vitro finding that ceftezole exhibited a mitogenic effect on whole spleen cells from BDF1 mice, but not on B cell depleted spleen cells.

Animals↗
PubMed1990

Anti-thyroglobulin antibodies induced with recombinant reovirus infection in BALB/c mice.

BALB/c mice that are infected with reovirus Type 1 develop thyroiditis. Viral antigens were seen in the cytoplasm of epithelial cells but not in the surrounding colloidal space of the thyroid. Examination of sera from the infected mice revealed autoantibodies that, by immunofluorescence, reacted with second antigens in the colloid (ground-glass staining pattern) and thyroglobulin (puffy staining pattern). An enzyme-linked immunosorbent assay designed to identify the reactive antigens showed the autoantibodies to direct against thyroglobulin. Synthetic serum thymic factor (FTS) suppressed autoantibody production to the thyroid after reovirus Type 1 infection. Reovirus Type 3, in contrast to reovirus Type 1, did not induce autoantibodies to react against thyroglobulin. By the use of recombinants between reovirus Type 1 and Type 3, the segment of the reovirus genome responsible for the induction of autoantibodies to thyroglobulin was identified. Virus containing the S1 genome segment from reovirus Type 1, which codes the sigma 1 polypeptide (i.e. haemagglutinin), infected epithelial cells in the thyroid and induced autoantibodies against the thyroglobulin. However, virus containing the S1 gene segment from reovirus Type 3 failed to infect cells in the thyroid and did not induce autoantibodies against thyroglobulin. In this study, reovirus Type 1 induces thyroiditis and autoimmunity, and the S1 gene segment is required for the induction of autoantibodies against thyroglobulin.

Animals↗
PubMed1989

Acceleration of cell necrosis following reperfusion after ischemia in the pig heart without collateral circulation.

A study of whether reperfusion accelerates cell death was performed in 35 pig hearts without collateral circulation. In 15 animals, the distal one-third of the left anterior descending coronary artery was occluded for 1 hour followed by 1-, 3-, or 7-hour reperfusion in 5 animals each. As controls, 5 hearts each were examined after 1, 2, 4 and 8 hours of occlusion of the artery without reperfusion. Heart rate and aortic pressure before and during occlusion and reperfusion did not change in any group. The subepicardial and subendocardial regional blood flow decreased to almost zero in all hearts after occlusion (85 +/- 1 to 2 +/- 2) but recovered during reperfusion (65 +/- 15 ml/100 g/min). Specimens were histologically examined by an enzyme method using nitrotetrazolium blue, an immunohistochemical method using myoglobin antibody, by staining with hematoxylin-eosin and Masson's trichrome. In the control hearts, clear demarcation of the infarct area was observed 4 hours after occlusion. However, in the reperfusion group, clear demarcation of the infarct was seen after 1-hour reperfusion, namely, 2 hours after the onset of infarct. Demarcation was seen not only in the tissue with contraction band necrosis, but also in the tissue with coagulation necrosis. Therefore, it is concluded that reperfusion accelerates cell death due to both contraction band necrosis and coagulation necrosis.

Animals↗
PubMed1989

Response of large and small coronary arteries of pigs to intracoronary injection of acetylcholine: angiographic and histologic analysis.

With coronary arteriography we examined the effect of acetylcholine (ACh) on large and small coronary arteries. ACh (12.5 to 200 micrograms) was injected into the right coronary arteries of 10 pigs during left ventricular pacing. The percentage of narrowing of the epicardial major coronary artery was used as an indicator of the constriction of the large coronary arteries, and the time required for the contrast medium to reach the posterior descending coronary artery from the ostium of the right coronary artery (blood-flow delay) was used as an indicator of the constriction of the same coronary arteries. A small dose of ACh (12.5 to 100 micrograms) induced mild narrowing (14 to 41%) of the epicardial major coronary artery and a marked blood-flow delay of over 7.0 sec (control: less than or equal to 1.8 sec) in all 10 pigs. A large dose of ACh (100 to 200 micrograms) caused over 75% narrowing of the epicardial major coronary artery and a marked blood-flow delay in 4 of the 10 pigs. When the marked blood-flow delay appeared, the perfused right ventricular myocardium became macroscopically anemic (ischemic). The constriction of large and small coronary arteries was not prevented by diphenhydramine (H1 blocker: 100 mg i.v.), but was prevented by pretreatment with atropine (1.0 mg i.v.). The intracoronary injection of histamine (1.5 mg) in 5 pigs constricted the epicardial major coronary artery over 75% in 2 pigs, 50 to 75% in 1 pig, and 25 to 50% in 2 pigs, but there was no evidence of blood-flow delay. Neither methoxamine nor norepinephrine caused any significant coronary artery narrowing. The histology of the large and small coronary arteries was examined quantitatively with an image analyzer. The coronary artery showed no intimal thickening, and the endothelium was intact on light microscopic examination. The % area of the smooth muscle layer (media) to the calculated total vascular area, and the ratio of the calculated medial thickness to the calculated inner radius (h/Ri) were 64 +/- 7% (mean +/- SD) and 0.69 +/- 0.16, respectively, in the small coronary arteries less than 100 microns in external diameter, 47 +/- 9% and 0.39 +/- 0.12 in the small coronary arteries 100 to 2000 microns in external diameter, and 34 +/- 4% and 0.24 +/- 0.03 in the large right coronary arteries over 2000 microns in external diameter; the % area of the media and the h/Ri showed a negative correlation with the size of the coronary arteries.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1989

Influence of propranolol on high energy phosphate and tissue acidosis in regional ischemic myocardium of pigs: assessment with arterial pressure and respiration gated in vivo 31-phosphorus magnetic resonance spectroscopy.

In an attempt to define the metabolic abnormalities of the ischemic myocardium, the changes in high energy phosphates, inorganic phosphate and intracellular pH were serially and quantitatively evaluated in ischemic porcine hearts having no collateral circulation, using arterial pressure and respiration gated in vivo 31P magnetic resonance spectroscopy. The protocol was also modified for propranolol pretreatment (0.6 mg/kg intravenously) to define its effect on the metabolism of ischemic myocardium. In the non-treated group, creatine phosphate was rapidly depleted by 10 minutes after ischemia; by 40 minutes, ATP and intracellular pH gradually decreased to 10 +/- 11% of control and to 5.90 +/- 0.26, respectively, and inorganic phosphate rose to 303 +/- 43% of control. In the propranolol treated group, the concentrations of creatine phosphate and ATP were higher, and those of inorganic phosphate and tissue pH were similar compared with controls during 40 minutes of ischemia. This suggests that the beneficial effect of propranolol on the ischemic myocardium is due to the preservation of ATP, an essential energy resource for numerous enzymatic reactions in viable myocardium.

Acid-Base Equilibrium↗
PubMed1989

Endotoxic properties of chemically synthesized lipid A analogs. Studies on six inflammatory reactions in vivo, and one reaction in vitro.

Biological activities of two groups of synthesized lipid A analogs, the counterpart of biosynthetic precursor, Lehmann's Ia type, 406, and E. coli lipid A type, 506, as well as their non-phosphorylated, and mono-phosphorylated analogs were investigated. The activities employed included four bone marrow cell reactions in mice, mice skin reaction, leukocytes migration in rabbits' cornea, and hemagglutination. Compound 406 and 506 elicited bone marrow reactions in mice and hemagglutination of mouse RBC, although 406 failed to elicit hemorrhage and necrosis also in mice skin. Compound 406 did not elicit corneal reaction in rabbits. The results suggest that for elicitation of this reaction and mice skin reaction, acyloxyacyl structure is required. Cytotoxicity and thromboplastin production of four bone marrow reactions had been reported by us to be endotoxic reactions, since these had not been elicited by peptidoglycan of Lactobacillus and Staphylococcus (1981) and 300 series synthesized analogs (1984) which did not have endotoxic structures. From these results, it seems that these two marrow reactions and hemagglutination require, as does the limulus test, the lipid A part structure as is present in 406.

Animals↗
PubMed1989

Cineangiographic and pathological features of the infarct related vessel in successful and unsuccessful thrombolysis.

The postmortem histology and the results of cineangiography after selective intracoronary thrombolysis in vessels that were recanalized and in those that were not were compared in 21 patients who died within seven days (mean 2 days) of selective intracoronary thrombolysis. There was a persistent intraluminal thrombus in the infarct related coronary artery in five of six segments in which recanalisation was unsuccessful and in one of 15 segments in which recanalisation was successful. Rupture and haemorrhage of the atheromatous plaque were seen in most of the infarct related segments, both in those in which recanalisation was achieved and in those in which it was not. Irregular narrowing and filling defects on the coronary cineangiograms were associated with rupture and haemorrhage of the atheromatous plaque. These results suggest that failure of coronary thrombolysis to recanalize the infarct related artery does not indicate that the occlusion was not caused by thrombus.

Aged↗
PubMed1989

Experimental encephalomyocarditis virus infection in Mongolian gerbils (Meriones unguiculatus).

Two strains of Mongolian gerbils (Meriones unguiculatus), Tumble Brook (TUM) and Japan Medical Science (JMS), were intraperitoneally inoculated with the D variant of encephalomyocarditis virus (EMC-D) and killed 3 days later. Mortality was significantly higher in females than in males. Evidence of viral replication was detected in the heart of both strains and in the pancreas of the TUM strain. Histopathological alterations were found in the heart and pancreas. Heart lesions involved foci of necrosis with inflammatory cell infiltration and calcification in both strains. Pancreatic lesions were restricted to the exocrine glands; islets of Langerhans were rarely and secondarily involved in the extensive destruction of exocrine glands. Severe acinar cell necrosis with marked inflammatory edema was conspicuous in TUM, whereas only slight acinar cell involvement was detected in JMS gerbils. Immunoperoxidase staining showed viral antigens in intracytoplasmic vacuoles in damaged acinar cells.

Animals↗
PubMed1989

Susceptibility of four species of small rodents to encephalomyocarditis (EMC) virus infection.

The D variant of encephalomyocarditis virus (10(1)-10(5) PFU/head) was intraperitoneally inoculated into 4 species of small rodents, rats, mice, Syrian hamsters, and Mongolian gerbils, and the susceptibility of these animals to EMC virus was examined virologically and histopathologically 3 days after infection. Viral replication was detected in the brain (mice), in the heart (mice and gerbils), and in the pancreas (mice, hamsters, and gerbils). No viral replication was detected in rats. Histopathological changes were seen in the brain (mice and hamsters), in the heart (mice and gerbils), and in the pancreas (mice, hamsters, and gerbils). No histopathological changes were seen in rats. The present results suggest that it may be quite possible to produce EMC virus-induced diabetes mellitus not only in mice but also in hamsters and gerbils.

Animals↗
PubMed1989

Influence of L-methionine-deprived total parenteral nutrition on the tumor tissue and plasma amino acids fraction and the host metabolism: experimental study with Sato lung carcinoma-bearing rats.

Creation of an amino acid imbalance, particularly curtailment of L-methionine, at the tumor cell level is thought to have a favorable effect on the inhibition of tumor growth. In the present study, we examined the influence of a specially-formulated amino acid mixture, avoid of sulfur-containing amino acids (L-methionine and L-cysteine), on the growth and amino acid fraction of Sato lung carcinoma (SLC) and the host metabolism in SLC-bearing rats. The rats were treated by total parenteral nutrition containing the above amino acid mixture, plus other nutrients (methionine-deprived TPN) for 10 days. Tumor growth began to decrease 4 days after the start of this treatment and the size was significantly less at the end of the treatment than in rats receiving conventional TPN with general purpose Vuj-N type amino acid solution as a protein source. The tumor-to-carcass weight ratio also showed a similar trend. In biochemistry, the albumin level and albumin-to-globulin ratio were significantly lower than in the rats receiving conventional TPN but other parameters such as total protein, glucose, GOT and GPT were not affected by the treatment. In the amino acid fraction of the tumor tissue extraction, both L-methionine and L-tyrosine were decreased and L-serine was increased significantly compared with the control group.

Amino Acids↗