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S Oshima

Publications and source records attributed to S Oshima.

337 records · Page 19Linked to original sources
PubMedDate not supplied

Stratified impairment of pulmonary ventilation in "diffuse panbronchiolitis:" PET and CT studies.

Positron emission tomography with radioactive nitrogen gas as well as CT were performed in seven patients with diffuse panbronchiolitis (DPB) to evaluate regional changes on pulmonary ventilation and lung attenuation values. Special focus of this study was on the difference between the central and peripheral parts of the lung. Mean ventilatory time constants measured in the peripheral parts of the lung were significantly greater than those in the central parts. Moreover, mean CT attenuation values in the peripheral parts were also significantly lower than those in the central parts, indicating that hyperinflation of the lung in DPB was located mainly in the peripheral parts. Such stratified distribution of ventilatory impairment is considered to be characteristic of diffuse bronchiolar narrowing because, in the peripheral parts of the lung, there are no large airways. In addition, different branching patterns of airways between the central and peripheral parts of the lung may play an important role in the mechanism of selective injury of bronchioles in the peripheral parts.

Adult↗
PubMedDate not supplied

Transient increase of plasma lipoprotein(a) in patients with unstable angina pectoris. Does lipoprotein(a) alter fibrinolysis?

It has been shown that lipoprotein(a) (Lp[a]) may interfere with the fibrinolytic system and that the Lp(a) level in an individual remains constant. To evaluate the effects of Lp(a) on the fibrinolytic system in patients with unstable angina, we measured plasma levels of Lp(a), the alpha 2-plasmin inhibitor-plasmin complex, and the thrombin-antithrombin III complex. The latter is a marker of thrombin generation, and the alpha 2-plasmin inhibitor-plasmin complex is an indicator of plasminogen activation. Venous plasma samples were taken from 18 patients with unstable angina and 18 patients with stable exertional angina who had been matched for clinical variables. On admission, plasma levels of Lp(a) were significantly higher in patients with unstable angina than in those with stable exertional angina (319 +/- 193 mg/l versus 191 +/- 141 mg/l, respectively; p less than 0.05). On admission, plasma levels of the alpha 2-plasmin inhibitor-plasmin complex and of the thrombin-antithrombin III complex were also significantly higher in patients with unstable angina than in those with stable exertional angina (0.78 +/- 0.42 micrograms/ml and 3.6 +/- 1.3 ng/ml versus 0.41 +/- 0.13 micrograms/ml and 1.9 +/- 0.5 ng/ml, respectively; p less than 0.01). In nine of the 18 patients with unstable angina, serial changes of plasma levels of Lp(a), the alpha 2-plasmin inhibitor-plasmin complex, the thrombin-antithrombin III complex, and the acute-phase proteins C-reactive protein and alpha 1-antitrypsin were examined for 3 weeks after admission.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Increased releasability of platelet products and reduced heparin-induced platelet factor 4 release from endothelial cells in bronchial asthma.

To determine whether or not platelet activation is involved in the mechanism of exacerbation of bronchial asthma, we evaluated adenosine triphosphate (ATP) release from thrombin-stimulated washed platelets, plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), and plasma beta-TG/PF4 ratios during symptomatic and asymptomatic periods in 15 patients with bronchial asthma compared with 16 normal control subjects. We also measured these parameters during allergen provocation tests and acetylcholine inhalation tests in 6 allergic asthmatics. ATP release, plasma levels of beta-TG and PF4 were significantly increased during symptomatic periods and after the allergen provocations but not after acetylcholine inhalations. However, these findings were not accompanied by the elevation of plasma beta-TG/PF4 ratios. The heparin-induced PF4 release, which is reported to reflect release of PF4 attached on endothelial cells, was significantly reduced in 12 asymptomatic asthmatic patients compared with 11 normal subjects, and it was much more reduced in 7 symptomatic asthmatic patients, suggesting the possibility of the reduced PF4 binding on endothelial cell surface. This finding may represent the prolonged half life of PF4 in asthmatics. We concluded that 1) increased releasability of platelet products and in vivo release of the platelet granular contents are involved in the mechanism of the exacerbation of bronchial asthma, 2) some functional alteration in platelet-endothelial cell interaction may be involved in bronchial asthma, and 3) plasma beta-TG/PF4 ratios are not elevated possibly because of both increased platelet releasability and prolonged half-life of PF4 in the blood in asthmatic patients.

Acetylcholine↗