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T Onodera

Publications and source records attributed to T Onodera.

At least 217 records · Page 12Linked to original sources

Monoclonal autoantibodies that react with hormones also react with cells not containing those hormones.

Two immunoglobulin M monoclonal autoantibodies, PI-6 and AP-2, were found by immunofluorescence, hormone absorption, and enzyme-linked immunosorbent assay to react with insulin and GH, respectively. The same antibodies were also found to react with a variety of organs that do not contain those hormones. Absorption of PI-6 with insulin, but not with GH, and absorption of AP-2 with GH, but not with insulin, eliminated the capacity of these antibodies to react with all organs tested. It is concluded that these monoclonal antibodies are broadly reactive and recognize epitopes on more than one protein.

Animals↗

Macroscopic hemorrhagic infarction following selective coronary thrombolysis in acute myocardial infarction.

Macroscopic hemorrhagic infarction was studied in 14 autopsied hearts with selective coronary thrombolysis (SCT) after acute myocardial infarction (AMI). In all patients urokinase, 240,000 - 720,000 units, had been selectively injected into ischemia-related coronary artery at 2 - 7 hours after the onset of AMI. The degree of stenosis after SCT was 90 - 99% in 13 patients and 100% in one patient. According to the duration of illness at death, the 14 patients were classified into 3 stages; stage I: 4 - 9 hours; stage II: 15 hours to 11 days; stage III: 19 days to 12 months. Three hearts in stage I had no macroscopic hemorrhage. In stage II, marked and diffuse hemorrhage in the infarct area was macroscopically evident in 6 of 7 hearts. In a stage II patient, extravasation of contrast medium into the myocardium was found at 3 hours after the onset of AMI. In stage III, 4 hearts had massive fibrosis or granulation in the left ventricular wall without macroscopic hemorrhage. Cardiac rupture was seen in 4 of 10 patients from stages I and II. It is concluded that macroscopic bleeding appears in most patients with AMI treated with coronary thrombolysis. In the majority of cases, the hemorrhage increases gradually after SCT and becomes macroscopically definite approximately 15 hours after the onset of AMI. Rarely, massive bleeding appears earlier. Hemorrhagic infarction is replaced by massive fibrosis after approximately 2 weeks.

Aged↗

[Orem's theory].

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Humans↗

Progression from hypertrophic obstructive cardiomyopathy to typical dilated cardiomyopathy-like features in the end stage.

An autopsied patient who had shown typical dilated cardiomyopathy (DCM)-like feature in the end stage of familial obstructive hypertrophic cardiomyopathy (HCM) is presented. The patient, a 38-year-old male, had 2 sisters with HCM. Six years before death, the echocardiogram revealed marked asymmetric septal hypertrophy (ASH) with systolic anterior motion (SAM). The ventricular septum (VS) to left ventricular posterior wall (LVPW) ratio was 19 mm/10 mm and LVEDd was 47 mm. Subsequently, the signs and symptoms of congestive heart failure became progressively worse and DCM-like findings appeared insidiously. Two months before death, the echocardiogram revealed LV dilatation (LVEDd = 55 mm) with diffuse poor contraction, no ASH (VS/LVPW = 7 mm/9 mm) and no SAM. At autopsy, the heart weighed 480g and showed dilated LV hypertrophy with normal wall thickness (VS/LVPW = 9 mm/13 mm). Massive fibrosis (30% in the VS), diffuse disarray (18% in the VS) and severe narrowing of the intramural small arteries and arterioles were found in the middle and outer thirds of the VS and the anterior LV wall. The extramural coronary arteries were not stenosed. The insidious progression from HCM to typical DCM-like feature related to the chronic progression of necrosis and massive fibrosis, due to severe stenosis of the intramural coronary artery. The data indicate that patients diagnosed clinically as DCM may be HCM, especially in those with family history of HCM.

Adult↗

Pulmonary embolism as a complication of transfemoral arteriography--incidence, symptoms, and prevention.

In order to evaluate the pulmonary embolism as a complication of transfemoral arteriography, we performed lung perfusion scintigrams before and after arteriography in consecutive 120 patients. Of the initial 60 patients who did not receive subcutaneous low-dose heparin, 19 (32%) demonstrated new pulmonary perfusion defects. There was no significant difference in regard to the incidence of new defects with or without right heart catheterization. On the other hand, in the latter 60 patients who received prophylactic heparin, the incidence of new defects decreased to 10%, without increasing clinically important bleeding. We believe that the source of emboli is from the leg vein thrombosis due to compression of the groin and subsequent bed rest. These data suggest that pulmonary embolism is a more common complication of transfemoral arteriography than previously appreciated and low-dose heparin is useful in reducing this complication.

Adult↗

Inheritance of hydronephrosis in the inbred mouse strain DDD.

The mode of inheritance of hydronephrosis was investigated by crossing inbred DDD mice having a high incidence of hydronephrosis and C57BL/6 mice having normal kidneys. In the males, incidences of hydronephrosis in F1 animals were intermediate between the two parental strains at a rate of 32.6% in (DDD x C57BL/6)F1 and 23.4% in reciprocal F1. The same tendency was observed in F2 male animals. In BCF1 males, the number of affected mice was higher in (C57BL/6 x DDD) F1 x DDD (72.4%) than in (DDD x C57BL/6)F1 x C57BL/6 (11.1%). A few affected mice were found among the females of hybrids F1, F2 and BCF1. These results suggested that hydronephrosis in the DDD strain of mice was controlled by polygenes, and that male hormones may have some effect on the occurrence of hydronephrosis.

Animals↗

Spontaneous osteochondrosis in rats.

143 Sprague Dawley rats, ranging from 19-63 weeks of age, were examined pathologically for the occurrence of spontaneous joint lesions. Macroscopically, a white round plaque was observed in the caudocentral portion of the medial femoral condyle or humeral head and sometimes it had a partially detached margin. Microscopic examination revealed a local thickening of the articular cartilage protruding into the subchondral bone, which suggested cessation of endochondral ossification and retention of cartilage. As the lesion advanced there was fissure formation in the thickened cartilage and proliferation of fibrous tissue beneath the fissure. Formation of a cartilage flap and extensive fibrosis with large cysts were also observed in the most advanced cases. Total incidence of the lesion in the distal femur was 22.2% in male and 2.8% in female rats. The change detected in the rats was identical with pathologic descriptions of osteochondrosis in domestic animals.

Animals↗

[Prognostic nutritional index in gastrointestinal surgery of malnourished cancer patients].

Based on assessment of 200 malnourished cancer patients of digestive organs, a multiparameter index of nutritional status was defined to relating the risk of postoperative complications to base line nutritional status. The linear predictive model relating the risk of operative complication, mortality or both to nutritional status is given by the relation: prognostic nutritional index (PNI) = 10 Alb. + 0.005 Lymph. C., where Alb. is serum albumin level (g/100 ml) and Lymph. C. is total lymphocytes count/mm3 peripheral blood. When applied prospectively to 189 gastrointestinal surgical patients those who were malnourished and treated by TPN preoperatively, this index provided an accurate, quantitative estimate of operative risk. In general, resection and anastomosis of gastrointestinal tract can be safely practiced when the index is over 45. The same procedure may be dangerous between 45 and 40. In below 40, this kind of operation may be contraindicated. The prognostic nutritional index is useful also to know the prognosis of patients with terminal cancer. Despite practicing TPN to cancer patients with near terminal stages, if the PNI remains below 40 and total lymphocytes count remains below 1,000/mm3, the patients has high possibility to die within the next two months.

Digestive System Neoplasms↗

Virus-induced autoimmunity: monoclonal antibodies that react with endocrine tissues.

Mice infected with reovirus type 1 develop an autoimmune polyendocrine disease. Spleen cells from these mice were fused with myeloma cells and the culture fluids were screened by indirect immunofluorescence for autoantibodies reactive with normal mouse tissues. A large panel of cloned, stable antibody-producing hybridomas has been obtained. Fourteen of the hybridomas make autoantibodies that react with cells in the islets of Langerhans, 24 with cells in the anterior pituitary, 11 with cells in gastric mucosa, and 5 with nuclei. Except for the antibodies to nuclei, the monoclonal autoantibodies are organ-specific. Some, however, show broad cross-species reactivity, recognizing similar antigenic determinants in mouse, rat, pig, and human organs, whereas other recognize determinants only in rodent tissues. Several of the antigens recognized by these monoclonal autoantibodies have been identified as hormones (for example, glucagon, growth hormone, and insulin).

Animals↗

Hydronephrosis in the inbred mouse strain DDD.

The inbred mouse strain DDD was found to have an extremely high incidence of hydronephrosis (37/37 in adult males and 12/32 in adult females). The hydronephrosis was classified as open with no definite cause for obstruction. The condition was either unilateral in the right kidney or bilateral. Another feature of the hydronephrotic kidney was circulatory failure. Hydronephrosis in strain DDD mice is considered to be a useful experimental animal model with additional possible use, in investigating disturbances of renal haemodynamics and function.

Age Factors↗

Biochemical characterization of pulmonary washings of patients with alveolar proteinosis, interstitial pneumonitis and alveolar cell carcinoma.

We have studied the biochemical compositions of fifteen pulmonary washings from seven patients with alveolar proteinosis, and two washings from two patients with interstitial pneumonitis and two from two patients with alveolar cell carcinoma. The pulmonary washing was separated into the supernatant and precipitate fractions by a brief centrifugation. Analytical results revealed that the pulmonary washings from patients with alveolar proteinosis contained much more protein and lipids as well as a higher percentage of phospholipid than did the pulmonary washings from other patients. With regards to alveolar proteinosis, the precipitate fraction, i.e., water-insoluble material, contained lipids as the major component, the majority of which was dipalmitoyl phosphatidylcholine. Protein in the sedimental material was small in amount, but was composed of proteins mainly of molecular weights of 62,000, 36,000, 28,000 and 15,000 as measured by SDS-gel electrophoresis. On the other hand, the supernatant fraction, i.e., water-soluble material, was composed predominantly of serum proteins, with the lipid content being lower than those in the precipitate fraction. These analytical findings support the idea that materials normally existing in the alveoli are excessively accumulated as alveolar-filling materials in alveolar proteinosis. It was also noted that there were marked differences in the lipid profiles between pulmonary washings from patients with alveolar proteinosis, and those from patients with other diseases, indicating that the biochemical composition of pulmonary washings tends to reflect the nature of an underlying disease. From these findings, the cause of the alveolar-filling materials found in alveolar proteinosis was discussed.

Adenocarcinoma, Bronchiolo-Alveolar↗