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M Kido

Publications and source records attributed to M Kido.

198 records · Page 11Linked to original sources

[Oxygen transport].

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Biological Transport↗

[Respiratory organs].

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Adrenocorticotropic Hormone↗

High-resolution computed tomography of Japanese summer-type hypersensitivity pneumonitis.

The high-resolution computed tomographic (CT) manifestations of Japanese summer-type hypersensitivity pneumonitis in eight patients were correlated with those of their chest radiography and with their histological findings. Histologically proven small granulomas were clearly demonstrated on CT as miliary opacities in five patients whose chest radiographic findings were normal. In two patients, these abnormalities were observed both by CT and chest radiography. High-resolution CT provides detailed morphological information about the lung parenchyma; it is an excellent means of following the clinical courses of hypersensitivity pneumonitis. CT is particularly useful for detecting persistent granulomas when symptoms subside and chest radiography becomes normal or nearly so.

Adult↗

The distribution of fibronectin and laminin in the murine periodontal membrane, indicating possible functional roles in the apical migration of the junctional epithelium.

Periodontal tissue shows various morphological changes with ageing. A typical example of these changes is the apical migration of the junctional epithelium. The distribution of fibronectin and laminin was investigated by immunofluorescent and immunoelectron-microscope methods in mice to clarify any possible functional roles of these proteins in the apical migration of junctional epithelium. Apical migration begins in 20-week-old mice, and then progresses with increasing age until the mice reach 80 weeks. In the apical tip of the junctional epithelium, fibronectin was demonstrated in the sub-epithelial fibrillar matrix, preceding the progression of apical migration. Fibronectin was also demonstrated in association with the stromal side of focal contacts between epithelial cells and basement membrane. Therefore, these focal contacts are assumed to be fibronectin receptors. There was no apparent relation between the localization of laminin and the migration of the junctional epithelium. These results suggest that the fibronectin provides a provisional matrix for the apical migration of junctional epithelium, but laminin does not appear to play a major part in that migration.

Aging↗

Effects of the Na+/H+ exchange inhibitor cariporide (HOE 642) on cardiac function and cardiomyocyte cell death in rat ischaemic-reperfused heart.

1. Na+/H+ exchange has been implicated in the mechanism of reperfusion injury. We examined the effects of the cardiac-specific Na+/H+ exchange inhibitor cariporide (HOE 642) on postischaemic recovery of cardiac function and cardiomyocyte cell death (i.e. necrosis and apoptosis). 2. Rat isolated and buffer-perfused hearts were subjected to 25 min normothermic global ischaemia followed by 120 min reperfusion. Cariporide (10 micromol/L) or its vehicle (0.01% dimethylsulphoxide) was administered for 15 min before ischaemia and for the first 30 min after reperfusion. 3. Cariporide significantly improved the recovery of isovolumic left ventricular function (heart rate, left ventricular developed pressure and left ventricular end-diastolic pressure) and coronary flow throughout reperfusion. Creatine kinase release during reperfusion was significantly less in the cariporide-treated heart. In situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL)-positive cardiomyocytes were also significantly less in the cariporide-treated heart after 120 min reperfusion. Electron microscopy showed necrotic changes without typical apoptotic features in cardiomyocytes after reperfusion. Such necrotic changes were mitigated by cariporide. Simultaneous detection of necrotic and apoptotic cardiomyocytes using propidium iodide (PI) and Annexin V revealed that cardiomyocytes in the infarct area were stained with only PI or both PI and Annexin V. Cariporide did not alter the pattern of cardiomyocyte staining with PI and Annexin V, although the number of cardiomyocytes stained with PI or PI plus Annexin V was less than that in vehicle-treated hearts. 4. These results suggest that apoptosis is not a major manifestation of cardiomyocyte cell death in the ischaemic-reperfused myocardium and a cariporide-sensitive mechanism of reperfusion injury promotes both necrotic and apoptotic processes of cell death.

Animals↗

Lung burden of a glass fiber by inhalation.

Pulmonary deposition and clearance of deposited particles from lungs are very important factors in order to induce pneumoconioses. In this paper, five Wistar male rats were exposed to glass fiber particles (mass median aerodynamic diameter (MMAD), 2.8 microns) for 6 hrs/day, 5 days/week for 4 weeks. The average exposure concentration was controlled by a continuous fluidized bed with a screw feeder and an overflow pipe at 0.79 mg/m3 during the exposure period. The fibrous particles concentrations in the exposure chamber were monitored by a light scattering method and showed to be constant during the exposure. The rats were sacrificed at 24 hours after the termination of the exposure and then the wet lung weight and the silica concentration in the lungs were measured. The lungs were treated for low temperature ashing (ca. 150 degrees C) by a plasma asher. After ashing, these samples were melted with sodium carbonate in platinum pot for the measurement of the silica content by the absorption spectrophotometry. The maximum content of SiO2 was 45 micrograms in the exposed rats and 20 micrograms in the control. The deposited amount of SiO2 by the exposure to glass fiber was 25 micrograms. The apparent deposition fraction defined as the deposited amount in the lungs to the amount of the inhaled glass fiber during the exposure was 6.8%. There was no significant difference of the apparent deposition fraction at same MMAD between glass fiber in this study and non-fibrous particles.

Administration, Inhalation↗