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Biomedical subjects

R Yoshida

Publications and source records attributed to R Yoshida.

At least 181 records · Page 10Linked to original sources
PubMed1988

Influence of suture on bronchial anastomosis in growing puppies.

A comparison study of synthetic nonabsorbable suture (nylon or Prolene) with absorbable suture (Dexon-S or Vicryl) for bronchoplasty was performed in growing puppies. The experiments (n = 15) were followed up for 185 to 381 days (average 323.8 days). Bronchoscopic and bronchographic studies were done at intervals. No stenosis was observed in the group receiving absorbable suture (n = 8), and the anastomoses grew proportionately with the proximal and distal bronchi. In the group receiving nonabsorbable suture (n = 7), variable stenoses developed; two moderate and two severe stenoses were observed during the early healing stage by bronchoscopic examination. In the sequential bronchograms, an increase of stenosis was noted in two dogs. The results suggest that absorbable suture is superior to nonabsorbable suture in pediatric bronchoplasty.

Anastomosis, Surgical↗
PubMed1987

[Bronchioloalveolar carcinoma diagnosed by bronchoalveolar lavage].

A case of bronchioloalveolar carcinoma of the lung is reported. A 63-year-old man identified during a chest mass-survey program, came to our hospital for a precise examination. He had no subjective complaints though his plain chest X-ray film showed a diffuse alveolar pattern in the bilateral hilar regions mimicking a butterfly shadow. Further, cytological examinations of both the sputa and specimens from brushings obtained on bronchoscopy failed to demonstrate malignant cells, and only a cytological examination of the fluid obtained by bronchoalveolar lavage (BAL) revealed the presence of a malignancy. Thus, BAL would seem to be a simple and reasonable method for the detection of suspected malignant cells in bronchioloalveolar carcinoma.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed1986

Tryptophan degradation in mice initiated by indoleamine 2,3-dioxygenase.

Tryptophan degradation in mice initiated by indoleamine 2,3-dioxygenase was characterized, taking advantage of its induction by bacterial lipopolysaccharide. Our results demonstrated that in various tissues, N-formylkynurenine produced by the dioxygenase from tryptophan was rapidly hydrolyzed into kynurenine by a kynurenine formamidase, but it was not further metabolized. The localization in the liver and kidney of the kynurenine-metabolizing enzymes suggested that kynurenine thus formed was transported by the bloodstream to those two organs to be metabolized. In fact, the plasma kynurenine level increased in parallel with the induction of the dioxygenase by lipopolysaccharide, and kinetic analysis indicated that at the maximal induction of the enzyme there was a 3-fold increase in the kynurenine production. The major metabolic route of kynurenine was excretion in urine as xanthurenic acid. This increase in the kynurenine production was not explained by L-tryptophan 2,3-dioxygenase in the liver, because during the induction of indoleamine 2,3-dioxygenase, the hepatic enzyme level was substantially suppressed. These findings indicated that indoleamine 2,3-dioxygenase actively oxidized tryptophan in mice and that its induction resulted in an increase in tryptophan degradation.

Animals↗
PubMed1986

Interferon: a mediator of indoleamine 2,3-dioxygenase induction by lipopolysaccharide, poly(I) X poly(C), and pokeweed mitogen in mouse lung.

When C3H/He mice were treated with lipopolysaccharide, poly(I) X poly(C), or pokeweed mitogen, the serum interferon titer increased almost instantaneously (100-2000 units/ml), and then the pulmonary indoleamine 2,3-dioxygenase was induced 50- to 140-fold. The peaks corresponding to interferon induction always preceded (approximately 24 h) those corresponding to dioxygenase induction. In C3H/HeJ (lipopolysaccharide-nonresponder) mice, however, lipopolysaccharide was totally inert in induction of both interferon and dioxygenase, although treatment with poly(I) X poly(C) and pokeweed mitogen led to a remarkable increase in the serum interferon titer and the enzyme activity. When lymphocytes of C3H/HeJ mice were inactivated by X irradiation and then reconstituted by the transfer of spleen cells from C3H/He mice, both enzyme and interferon from C3H/HeJ mice thus treated were induced almost normally after the lipopolysaccharide treatment. In addition, murine interferon alpha/beta, which was injected intravenously in C3H/He or C3H/HeJ mice, almost instantaneously and dose-dependently induced the pulmonary enzyme, and at a dose of 10(5) units per mouse the enzyme activity was enhanced 20- to 26-fold in these two strains of mice. These results suggest that interferon, which is generated by the interaction of lymphocytes with lipopolysaccharide, poly(I) X poly(C), or pokeweed mitogen, is a mediator of indoleamine 2,3-dioxygenase induction in the mouse lung by these agents.

Animals↗
PubMed1986

Exercise P-vector magnitude changes in angina pectoris: Frank-Vectorcardiographic and hemodynamic correlations.

Multistage bicycle ergometer exercise testings with Frank vectorcardiogram and M-mode echocardiogram were performed on 12 patients with effort angina pectoris. The left atrial and left ventricular end-diastolic volume (LAV and LVEDV) were calculated as a cube of the left atrial and left ventricular end-diastolic dimension. The mean pulmonary artery wedge pressure (mPAWP) was measured with a Swan-Ganz catheter during the testing. At peak exercise a statistically significant increase was observed in mPAWP (p less than 0.001), LAV (p less than 0.005), the maximal horizontal P-vector magnitude (Hmax) (p less than 0.05) and the percent change in Hmax (%Hmax). %Hmax showed a significant correlation with the increment of mPAWP (delta mPAWP) (r = 0.66, p less than 0.05), the increment of LVEDV (delta LVEDV) (r = 0.83, p less than 0.01) and the increment of LAV (delta LAV) (r = 0.81, p less than 0.001). Multiple regression analysis was performed on %Hmax as a dependent variable with delta LAV, delta mPAWP, and the increment of heart rate (delta HR) as independent variables (r = 0.84, p less than 0.05), but the partial correlation coefficients of delta mPAWP and delta HR were not significant. The present study demonstrated that the increase in Hmax had a close relationship with the increase in mPAWP and LVEDV and that the preload of the left ventricle during exercise-induced anginal attack could be predicted noninvasively by %Hmax. The increase in Hmax was thought to be due to the increase in LAV during anginal attack.

Adult↗
PubMed1986

Interferon enhances tryptophan metabolism by inducing pulmonary indoleamine 2,3-dioxygenase: its possible occurrence in cancer patients.

Human lungs bearing cancer (n = 27) exhibited up to an approximately 20-fold [on average approximately 5-fold (P less than 0.005)] increase in the enzyme activity that degrades tryptophan to form formylkynurenine, in comparison with lungs with benign lesions (blebs) (n = 7) taken as controls. On the basis of molecular and kinetic properties, this activity was ascribed to indoleamine 2,3-dioxygenase (IDO) [indoleamine:oxygen 2,3-oxidoreductase (decyclizing)]. In vitro studies with human lung slices revealed that human interferon gamma (IFN-gamma) induced the de novo synthesis of IDO dose dependently (10-10(4) units/ml), and at maximum the activity reached nearly 100 times that in the control lungs described above. Human IFN-alpha also served as an inducer, but it was two to three orders of magnitude less potent than IFN-gamma relative to the antiviral titers, suggesting that IFN-gamma is the main mediator of the IDO induction. IDO thus induced in slices avidly metabolized tryptophan in situ: Upon a 24-hr incubation of lung slices pretreated with varied doses of IFN-gamma (10-10(3) units/ml), up to 96% of the tryptophan in the slices was depleted and up to 70% of the tryptophan in the medium was converted, mainly to formylkynurenine, kynurenine, or both. The foregoing results suggest that an IFN-mediated induction of IDO also takes place in vivo in human lungs as a response to cancer, leading to metabolic consequences such as depletion of tryptophan and accumulation of (formyl)kynurenine, which may provide a unique host defense mechanism.

Cycloheximide↗
PubMed1986

Analysis of the exercise-induced orthogonal P wave changes in normal subjects and patients with coronary artery disease.

Near-maximal treadmill exercise testing was performed on 26 normal individuals (NL) and 78 patients with coronary artery disease (CAD) using a modified Bruce's protocol. Exercise-induced changes in orthogonal P wave measurements were made automatically, using an averaging technique, immediately before and 30 sec after treadmill exercise to assess their diagnostic significance in evaluation of left ventricular (LV) function in CAD patients. The maximal inferior and posterior components of the P wave and the maximal P-vector magnitude in the frontal and left sagittal planes showed a statistically significant increase after treadmill exercise both in NL and CAD patients. These changes were considered to be physiological responses of the P wave to dynamic exercise. The percent changes of the maximal horizontal P-vector magnitude (%Hmax) were significantly higher after treadmill exercise in CAD patients than in NL. In patients with effort angina pectoris and without a previous myocardial infarction, the %Hmax showed a highly significant negative correlation with the percent changes of the LV ejection fraction (r = 0.66, p less than 0.01), measured by exercise RI angiography. These results suggest that the exercise-induced increase in %Hmax reflects transient impairment of LV function during exercise. It was concluded that a %Hmax of more than 120% provided a useful, noninvasive index for assessing LV function in treadmill exercise testing.

Adult↗