Search PubMed⌕ Search

Biomedical subjects

J Chihara

Publications and source records attributed to J Chihara.

138 records · Page 8Linked to original sources
PubMed1985

The strong association of HLA-DR4 with spherical mesangial dense deposits in IgA nephropathy.

41 Japanese patients with primary IgA nephropathy (IgA GN) were determined for HLA-A, -B, -C and -DR antigens. The frequency of HLA-DR4 increased slightly in total patients compared with 63 normal control persons, but this increase was not statistically significant. However, 24 patients with spherical mesangial dense deposits (SMDD) in electron micrograph out of 41 patients with IgA GN were found to have markedly increased incidence of HLA-DR4 (chi 2 = 11.52, Relative risk = 6.45, Corrected p less than 0.03). In contrast to this finding, 17 patients without SMDD had no association with any particular HLA antigens. These results suggest that IgA GN might be subdivided by the association of HLA and electron microscopic findings into at least 2 types.

Adolescent↗
PubMed1977

Catecholamine-storing cells in the cyclostome heart.

The lamprey heart contains characteristic catecholamine-storing cells in both the atrium and the ventricle. Sufficient circumstantial evidence is available indicating that catecholamines together with protein carbohydrate complexes are contained in these cells within the membrane bound cytoplasmic granules. If the "recepto-secretory function" and "neuroectodermal origin" of these cells are proved, then they may be classified as typical paraneurons.

Animals↗
PubMedDate not supplied

Induction of hypodense eosinophils and nuclear hypersegmentation of eosinophils by various chemotactic factors and lymphokines in vitro.

We have previously reported pulmonary eosinophils in eosinophilic pneumonia (PIE syndrome) showed two characteristics: hypodensity and nuclear hypersegmentation. Our present working hypothesis is that the eosinophil chemotactic factor and certain lymphokines may be involved in the induction of these characteristic features. Therefore, we examined whether these stimuli can induce two characteristics in vitro. Results were as follows. 1) Chemoattracts (ECF-A, histamine and PAF) can induce both nuclear hypersegmentation and hypodense eosinophils. 2) Hypodense eosinophils can be induced earlier than induction of hypersegmented nuclei (hypodense eosinophils within three hours, hypersegmented nuclei: 12 hrs). 3) Furthermore, lymphokines can not induce hypodense eosinophil. 4) However, PHA-lymphocyte culture medium (PHALCM), gamma-IFN and IL-3 + GM-CSF can induce hypersegmented nuclei but IL-2 has no effect on nuclear segmentation of eosinophils.

Biological Factors↗
PubMedDate not supplied

Induction of CD23, CD25 and CD4 expression on an eosinophilic cell line (EoL-3) by interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-5 (IL-5).

The effects of IL-3, GM-CSF and IL-5 on the expression of CD23 (Fc epsilon RII), CD25 (IL-2R/p55) and CD4 on an eosinophilic cell line (EoL-3) were investigated by flow cytometry. A separate incubation with IL-3, GM-CSF or IL-5 alone, did not induce the expression of CD23, CD25, or CD4. However, a sequential incubation with IL-3 for 6 days, then with IL-3 and GM-CSF for the following 6 days, induced a significant expression of CD23 and CD25. After a further incubation for 6 days with IL-3, GM-CSF and IL-5, CD4 was then expressed, while CD23 and CD25 expression still increased. The kinetics of expression of CR3/CD11b were parallel to that of CD23, but the expression of the transferrin receptor (CD71) remained negative. Northern blot analysis revealed the presence of mRNA encoding CD23, CD25 and CD4 in EoL-3 stimulated by IL-3, GM-CSF and IL-5. Culture with GM-CSF induced the binding of radiolabeled IL-5 to EoL-3 cells, with an increased affinity after incubation with IL-3, GM-CSF and IL-5. These data indicate that IL-3, GM-CSF and IL-5, might be involved in the expression of functional markers on eosinophil membrane.

Adult↗
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↗