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Biomedical subjects

T Onodera

Publications and source records attributed to T Onodera.

At least 163 records · Page 9Linked to original sources
PubMed1989

Studies on experimental conditions for detecting phototoxic potentials of drugs in Balb/c mice.

This study was designed to establish a procedure for detecting the phototoxicity of drugs in an animal model. Experimental conditions in relation to intensity distribution of ultraviolet-A (UVA), duration of irradiation, and suitable region for irradiation were investigated. One black light gave a wide constant-energy region when the distance from the light source to the irradiation area was 15 cm. The intensity distribution of a bank of 10 black lights formed a pattern like the contour map of a truncated cone in the irradiation area. In phototoxic studies, Balb/c strain mice were orally administered chlorpromazine and nalidixic acid, clinically known as photosensitizers, and were immediately exposed to UVA irradiation. The optimal irradiation time was 4 hours at an energy of 20 Joules/cm2, which with a high frequency caused erythema on the surface of the ears in the central area, which received about 1.5 mW/sec.cm2, but no reaction occurred in the surrounding area (0.5-0.8 mW/sec.cm2). These results indicate that it is important to select a suitable irradiation area and sufficient intensity of irradiation in order to determine whether a drug has phototoxic potential.

Animals↗
PubMed1989

[Studies related to the discoloration in the surrounding gingiva of fixed prosthesis. 2. Detection period of silver-sulfate and the effects of metal alloys].

The purpose of this study is to investigate the relationship between gingival discoloration and Ag2S. Minute granules of dental alloys were embedded in the gingiva during a 5-11 months span, and their histological and colorimetric analyses were undertaken. Results showed the following; 1. Cases of low melting silver alloy, 12% Au-Ag-Pd alloy, and Ni-Cr alloy all resulted in gingival discoloration, but it did not occur during the specified experimental period. 2. Regardless of the size of the granules or time, the electron microanalyser showed no signs of sulfer detection in cases of low melting silver alloy. However, in the case of 12% Au-Ag-Pd alloy, sulfer was detected 5 months later for only those granules having the size of 0.2-0.3 microns. No sulfer was detected in cases of Ni-Cr alloy. 3. Although no proliferation of inflammatory cells were observed around those areas surrounding the 12% Au-Ag-Pd alloy granules, they appeared in cases of the low melting silver alloy and Ni-Cr alloy.

Dental Alloys↗
PubMed1989

[Correlations between results of selective intracoronary thrombolysis and histologic findings of the infarct-related coronary arteries].

To define the histopathogenesis of successful and unsuccessful recanalization following selective intracoronary thrombolysis, coronary angiography (CAG) in thrombolysis and histologic findings were compared in 13 patients who died within four days (mean 1.5 days) after the procedure. Thirteen infarct-related arteries were evaluated in respect to recanalization; presence of an intraluminal thrombus, and rupture and hemorrhage of atheromatous plaques were histologically evaluated in serial sections. Intraluminal thrombi of the infarct-related coronary artery were found in all of the five cases with unsuccessful recanalization and in none of the eight cases with successful recanalization. Rupture and hemorrhage of atheromatous plaques in infarct-related arteries were observed in all of the five cases with unsuccessful recanalization and in seven of the eight cases with successful recanalization. It was concluded that 1) in recanalized cases, thrombi are considered to be lysed; 2) unsuccessful recanalization does not necessarily indicate the absence of thrombi; and 3) rupture and hemorrhage of atheromatous plaques do not affect recanalization.

Aged↗
PubMed1989

Rapid development of renal lesions in diabetic DBA mice infected with the D-variant of encephalomyocarditis virus (EMC-D).

Marked hyperglycaemia and renal lesions developed rapidly in DBA mice infected with 10 plaque-forming units of the D-variant of encephalomyocarditis virus (EMC-D). Renal alterations were demonstrated in the glomeruli, tubular epithelium and small vessels 2 months after infection. Glomerular changes were characterized by mesangial thickening due to an increase of basement membrane-like material in the mesangial matrix. Nodular glomerular lesions were commonly observed 3 months after infection, whereas distinct thickening of the glomerular basement membrane was rarely seen. Besides these glomerular changes, glycogen inclusions in the distal tubular epithelium and medial degeneration in the arterioles were also noticed. The EMC-D-infected DBA mouse appears to be a useful experimental model for the study of human diabetic nephropathy.

Animals↗
PubMed1988

Morphological investigation of cavity formation in articular cartilage induced by ofloxacin in rats.

Ofloxacin, a quinolone antibacterial agent, induced blisters and/or erosions in the articular cartilage of the humeral trochlea, femoral condyle, and femoral head of immature rats. Histologically, cavity formation was seen in the middle zone of the articular cartilage. Changes were detected as early as 5 hr after a single oral administration of 1000 or 3000 mg/kg. These changes were characterized by condensation, atrophy, and deformation of the nuclei of chondrocytes distributed in the middle zone. In such nuclei, aggregation of heterochromatin was observed. Degenerated cells with vacuolated and partially disintegrated cytoplasms were also seen in this zone. These lesions were followed by edema of the matrix accompanied with markedly decreased stainability with safranin-O, and a cavity was formed later by liquefaction of the cartilage. The changes were reversible, with rebounding occurring even with continued treatment with ofloxacin. The proliferation of chondrocytes around the lesion chiefly contributed to the repair. Ofloxacin had no adverse effects on the articular cartilage in rats when treatment was initiated at 8 weeks of age or later.

Animals↗
PubMed1988

Morphological investigation of osteochondrosis induced by ofloxacin in rats.

Oral doses of 300 or 900 mg/kg/day of ofloxacin, a quinolone antibacterial agent, for 8 weeks induced a high incidence osteochondrotic lesions in rats. The predilection site of the lesions was the caudal area of the medial femoral condyle. Early changes included thickening of the middle zone of the articular cartilage with a markedly thinned deep zone. As the course of administration progressed, the columns of chondrocytes in the thickened middle zone became more and more numerous, many degenerated cells were seen, and the staining intensity of the matrix of the cartilage with with safranin-O decreased slightly. After the completion of dosing, the articular cartilage was markedly thickened and was made up mainly of middle zone cartilage. In advanced cases, a cleft was formed along the tidemark which occasionally extended to the articular surface. This resulted in erosion of the articular cartilage. Beneath the cleft there were focal necrosis of the subchondral bone and fibrotic lesions in the marrow space. Nalidixic acid also produced similar lesions in rats. The two drugs induced osteochondrosis in rats when treatment began at 4 weeks of age, but not at 8 weeks of age. This lesion was different in developmental process from the spontaneous osteochondrosis of rats, which is characterized by retention of the inherently thick deep zone.

Animals↗
PubMed1988

Effect of ofloxacin on the uptake of [3H]thymidine by articular cartilage cells in the rat.

Ofloxacin (900 mg/kg) was orally administered to Sprague-Dawley rats aged 4 weeks. A single dosage induced chondrocyte degeneration in the middle zone of the articular cartilage 5 h later and cavity formation 12 and 24 h later. The number of cells labeled with [3H]thymidine was decreased in histologically normal and abnormal cartilage at 5 h. Incorporation rate of [3H]thymidine into the articular cartilage was gradually decreased until 12 h later, but increased above the control level at 24 h. Another experiment showed that labeled cells were retained for a longer period than in control rats in the middle zone at the predilection site of osteochondrosis.

Administration, Oral↗
PubMed1988

Role of the left atrium in adaptation of the heart to chronic mitral regurgitation in conscious dogs.

The manner in which the left atrium adapts to chronic mitral regurgitation and the role of the adapted left atrium as a modulator of excessive central blood volume were analyzed in seven conscious dogs, instrumented with high-fidelity pressure transducers and ultrasonic dimension gauges for measurement of left atrial and left ventricular pressure and cavity size. After obtaining data in a control situation, mitral regurgitation was produced by transventricular chordal sectioning. Heart rate was matched by right atrial pacing. In the "early" stage (7-14 days), left ventricular end-diastolic and mean left atrial pressures increased from 6 to 16 mm Hg and from 4 to 12 mm Hg, respectively. Both left ventricular end-diastolic segment length and left atrial diameter prior to atrial contraction increased by 7%. In the "late" stage (20-35 days), despite significant decreases in left ventricular filling pressure (11 mm Hg) and left atrial pressure (8 mm Hg), there was a continuous increase in left ventricular end-diastolic dimension (10%) and atrial end-diastolic diameter (10%). After the onset of mitral regurgitation, the left atrium performed greater work with a more enlarged cavity. Left atrial chamber stiffness was progressively decreased. These changes were associated with progressive increase in the left atrial diameter at zero stress, and there was a significant increase in the diameter of the left atrial myocyte. These results indicate that during chronic mitral regurgitation, the left atrium enlarges in size and mass, with a more potent booster action. The left atrial chamber becomes more compliant. Thus, the enlarged left atrium appears to exert an important compensatory mechanism in the case of excessive central blood volume by buffering pressure rise in the atrium and by providing an adequate ventricular filling volume.

Adaptation, Physiological↗
PubMed1988

Virus-induced thyroiditis.

Mice infected with reovirus type 1 developed a mild thyroiditis characterized by focal destruction of acinar tissue, infiltration of inflammatory cells, and autoantibodies to thyroglobulin and microsomal antigens. Thyroid involvement appears to be part of a more generalized virus-induced polyendocrine disease.

Animals↗
PubMed1988

Distribution and progression of coronary arterial and aortic lesions in the conventional Watanabe heritable hyperlipidemic rabbit--quantitative analysis.

The distribution and progression of coronary arterial and aortic lesions were examined in 40 conventional Watanabe heritable hyperlipidemic (WHHL) rabbits. They were classified according to age into stage I (3-5 months old, 14 rabbits), stage II (6-12 months old; 12 rabbits) and stage III (14-28 months old; 14 rabbits). Fifteen normal Japanese rabbits served as controls. The findings obtained from serial and transverse sections of each of the extramural coronary arteries (ECA) and transverse sections of 4 to 5 equal pieces of whole ventricle for intramural coronary arteries (ICA) were quantified by an image analyzer. Atherosclerosis with positive Sudan III stain was seen in aorta, ECA and ICA over 200 mu in diameter. Atherosclerotic lesions were noted in the aortic arch in stage I rabbits and in the whole aorta in stages II and III rabbits. In ECA, stenosis due to atherosclerosis was noted in 14, 33 and 93% of stages I, II and III rabbits, respectively. Stenosis of over 75% in the orifices of the left and right coronary arteries was noted frequently (71%), while mural thrombi, hemorrhage, intimal rupture and recanalization were seen rarely. Striking features were non-atherosclerotic stenosis with negative Sudan III, seen in the ICA less than 200 mu in diameter of almost all the hearts of stages II and III rabbits. Acute and old myocardial infarction appeared in 5 of the 14 hearts of the stage III rabbits and the infarct-related ECA showed severe stenosis of over 90%. In conclusion, to detect coronary atherosclerosis, serial and transverse sections of ECA are needed. In conventional WHHL rabbits, the incidence of stenosis in ECA is very high, compared with that of the previous reports, and myocardial infarction is due to severe stenosis in ECA. Non-atherosclerotic lesions in ICA occur before the appearance of the atherosclerotic lesions in ECA.

Animals↗
PubMed1988

Effect of intraoperative radiotherapy on pancreatic carcinoma: histopathological findings from autopsy cases.

Histopathological examinations of 18 necropsy patients with pancreatic carcinoma who died after receiving intraoperative radiotherapy (IOR) revealed the following: 1) Cancer cells were suspected of remaining in the periphery of the irradiated areas. 2) Thickening of intima of small arteries, some of which were obstructed, was found in the tumor tissues. 3) Highly degenerated nerve fibers were observed within the necrotic or viable tumor tissues. These findings provide evidence of the effects of IOR, while they also demonstrate the problems encountered in improving this treatment and the necessity of a complementary therapy for complete local control of pancreatic cancer by IOR.

Adult↗
PubMed1988

Histopathology of BALB/c mice infected with the D variant of encephalomyocarditis virus.

BALB/c mice infected with 10(5) pfu of the D variant of encephalomyocarditis virus were examined histopathologically during the subacute stage of infection. Main pathologic changes were observed in the brain, heart (massive myocardial necrosis with subsequent organization (i.e., replacement of necrotic myocardium by connective tissue) and congestion and dilatation of the right ventricle) and pancreas (moderate degranulation of beta-cells resulting in elevation of blood glucose level). The brain lesions were found most frequently in the pyramidal layer of the hippocampus and the granular layer of the cerebellum and were characterized by degeneration of neurons containing virus antigens. Perivascular mononuclear cell infiltration, spreading to the adjacent brain tissue, and thrombosis in small vessels were also frequently seen. Focal loss of neurons and gliosis developed later in these lesions.

Animals↗
PubMed1988

Acute toxicity of muroctasin in mice, rats and dogs.

Acute toxicity of N2-[(N-acetylmuramoyl)-L-alanyl-D-isoglutaminyl]-N6-stearoyl-L-lysine (MDP-Lys(L18), muroctasin), a synthetic muramyl dipeptide derivative, was studied in Std-ddy mice, Std-Wistar rats and beagle dogs by subcutaneous and intravenous administration. Subcutaneous LD50 values were 436 mg/kg for male, 625 mg/kg for female in mice, 761 mg/kg for male, 801 mg/kg for female in rats and more than 200 mg/kg for dogs. Toxic signs included screaming, decrease of locomotor activity, weakness, emaciation and loss of hair, crust formation, necrosis and ulceration around the injection site in all species. Death occurred within 7 days after treatment. Pathological examination revealed inflammation around the injection site. In dogs a subcutaneous cavity with puruloid fluid and enlargement of the axillary lymphnodes were seen in addition. No marked toxic signs and pathological findings were observed in mice and rats after intravenous administration of 90 mg/kg, a critical dose of treatment.

Acetylmuramyl-Alanyl-Isoglutamine↗