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Biomedical subjects

T Onodera

Publications and source records attributed to T Onodera.

At least 253 records · Page 14Linked to original sources
PubMed1980

Induction of diabetes by cumulative environmental insults from viruses and chemicals.

Encephalomyocarditis virus (EMC) induces diabetes in certain inbred strains of mice by infecting and destroying pancreatic beta cells, the severity of the diabetes depending on the number of beta cells destroyed. In strains of mice resistant to EMC-induced diabetes, insufficient beta cells are damaged to alter glucose homeostasis. However, diabetes can be produced in many species by streptozotocin, a highly specific beta-cell toxin. Here, we used concentrations of streptozotocin that did not produce diabetes, but reduced the beta-cell reserve. When strains of mice normally resistant to EMC-induced diabetes were first treated with sub-diabetogenic doses of streptozotocin, then infected with EMC virus, diabetes developed. Furthermore, when mice were infected with viruses such as Coxsackie B3 and B5, which ordinarily produce little if any beta-cell damage, diabetes developed if the mice were first treated with sub-diabetogenic doses of streptozotocin. These findings suggest that diabetes may result from cumulative beta-cell damage induced by sequential environmental insults.

Animals↗
PubMed1980

Virus-induced diabetes mellitus. XVIII. Inhibition by a nondiabetogenic variant of encephalomyocarditis virus.

Plaque purification of the M variant of encephalomyocarditis (EMC) virus resulted in the isolation of two stable variants: one diabetogenic and designated D and the other nondiabetogenic and designated B. When the D variant was inoculated into SJL/J male mice, hypoinsulinemia and hyperglycemia developed in > 90% of the animals. In contrast, none of the mice inoculated with the B variant developed diabetes. Histologic examination of pancreata from mice infected with the D variant revealed insulitis and necrosis of beta cells, whereas islets from mice infected with the B variant showed little, if any, change. When islets were assayed for infectious virus, approximately 10 times more virus was recovered from animals inoculated with the D as compared with the B variant. Moreover, approximately 60% of islet cells from mice infected with the D variant contained viral antigens when stained with fluorescein-labeled anti-EMC virus antibody, whereas < 5% of islet cells from animals infected with the B variant contained viral antigens. Co-infection experiments showed that the induction of diabetes by the D variant was inhibited by the B variant. When the B and D variants were mixed together at B:D ratios of 1, 9, and 99, diabetes developed in 60, 11, and 0% of the mice, respectively. Tissue-culture experiments revealed that the B variant induced considerably more interferon than the D variant, and studies in animals showed that interferon appeared earlier and in greater amounts in the circulation of mice infected with the B as compared with the D variant. These studies suggest that the induction of interferon by the B variant is, at least in part, responsible for the inhibition of diabetes by the D variant.

Animals↗
PubMed1980

Combined treatment by chemotherapy and intravenous hyperalimentation in Japanese patients with advanced breast cancer.

To treat advanced breast cancer that proved refractory to endocrine therapy or other forms of chemotherapy, we administered intravenous administration of adriamycin every 3--4 weeks, in principle, at a dose of 100 mg per 50 kg body weight (total dose, 300--400 mg). At the same time, 50 mg of cyclophosphamide was administered orally every day. In all cases, concomitant hyperalimentation treatment, which is considered an effective method for ameliorating the toxicity of the chemotherapeutic treatment, became necessary. Of 13 cases so treated, 10 showed significant improvement. It was almost impossible in general to administer such a dosage of adriamycin with cyclophosphamide to Japanese patients with advanced breast cancer, since the treatment brought on severe side effects such as depletion of oral intake and suppression of bone marrow function.

Administration, Oral↗
PubMed1980

Characteristics of phospholipids in human lung carcinoma.

Human lung carcinoma tissues with histological types of adenocarcinoma, squamous cell and small cell carcinoma were investigated for phospholipids. There were marked differences in the phospholipids between these lung carcinoma and normal lung tissue. A marked decrease in saturated phosphatidylcholine (PC), predominantly the dipalmitoyl species, was noted in the carcinoma, although they still contained 17-20% of the saturated classes. The lung carcinoma contained less phosphatidylglycerol (PG) and lyso-bis-phosphatidic acid and more cardiolipin and phosphatidylinositol (PI) than the normal lung tissue. These alterations observed in the lung carcinoma appeared to show that they lose the characteristic feature of phospholipids in the lung tissue. The differences in the lipid composition among different cell types of lung carcinoma were also noted. The squamous cell and small cell carcinoma contained more triacylglycerol and relatively higher dienes I (monoenoic-monoenoic) and lower dienes II (saturated-dienoic) of PG, respectively, as compared to adenocarcinoma.

Adenocarcinoma↗
PubMed1979

Isolation of a virus from the pancreas of a child with diabetic ketoacidosis.

A healthy 10-year-old boy was admitted to the hospital in diabetic ketoacidosis within three days of onset of symptoms of a flu-like illness. He died seven days later and post-mortem examination showed lymphocytic infiltration of the islets of Langerhans and necrosis of beta cells. Inoculation of mouse, monkey and human cell cultures with homogenates from the patient's pancreas led to isolation of a virus. Serologic studies revealed a rise in the titer of neutralizing antibody to this virus from less than 4 on the second hospital day to 32 on the day of death. Neutralization data showed that the virus was related to a diabetogenic variant derived from Coxsackievirus B4. Inoculation of mice with the human isolate produced hyperglycemia, inflammatory cells in the islets of Langerhans and beta-cell necrosis. Staining of mouse pancreatic sections with fluorescein-labeled antiviral antibody revealed viral antigens in beta cells. Both the clinical picture and animal studies suggested that the patient's diabetes was virus induced.

Animals↗
PubMed1978

Virus-induced diabetes mellitus. XV. Beta cell damage and insulin-dependent hyperglycemia in mice infected with coxsackie virus B4.

Coxsackie virus B4 that had been passaged in cultures enriched for pancreatic beta cells produced a diabetes-like syndrome when inoculated into SJL/J mice. The infection resulted in insulitis and destruction of beta cells. Viral antigens were found in beta cells by staining with fluorescein-labeled antibody to Coxsackie virus B4. The destruction of beta cells led to a decrease in the immunoreactive insulin content of the pancreas and hypoinsulinemia. The reduction in immunoreactive insulin correlated inversely with the elevation of glucose in the blood and over 80% of the animals were found to be hyperglycemic within 14 days after infection. The percentage of animals with hyperglycemia decreased with time and at the end of 60 days, less than 5% of the animals were still hyperglycemic. However, many of the normoglycemic mice were found to be metabolically abnormal when evaluated by glucose tolerance tests. Studies on the susceptibility of the host showed that only certain inbred strains of mice became diabetic when infected with Coxsackie virus B4. It is concluded that both the passage history of the virus and the strain of the host influence the development of diabetes.

Animals↗
PubMed1978

Virus-induced diabetes mellitus: reovirus infection of pancreatic beta cells in mice.

Reovirus type 3, passaged in pancreatic beta-cell cultures, produced an insulitis when inoculated into 1- to 2-week-old mice. By means of a double-label antibody technique, in which we used fluorescein-labeled antibody to reovirus and rhodamine-labeled antibody to insulin, reovirus antigens were found in beta cells. By electron microscopy, viral particles in different stages of morphogenesis were observed in insulin-containing beta cells but not glucagon-containing alpha cells. The infection resulted in destruction of beta cells, reduction in the insulin content of the pancreas, and alteration in the host's capacity to respond normally to a glucose tolerance test.

Animals↗