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Biomedical subjects

H Kitani

Publications and source records attributed to H Kitani.

At least 37 records · Page 2Linked to original sources
PubMed1989

[Immunoallergological studies on chironomid antigen in bronchial asthma].

Immuno-allergological studies on Tokunagayusurika akamusi (TA), a chironomid, were carried out in 217 patients with bronchial asthma. 1. Skin reaction to TA was positive in 72 (33.2%) out of the 217 patients with bronchial asthma. 2. Fifteen (13.8%) of the 109 patients showed a significant amount of histamine release (more than 15%) from basophils stimulated by TA antigen. 3. There was a significant correlation between skin reaction and histamine release by TA antigen. 4. A significant amount of basophil histamine release was observed in young patients, and in those who were under 40 years old of age at the onset of the disease. The serum IgE concentration of these patients was relatively high. 5. There was a significant correlation between basophil histamine release by TA antigen and specific IgE antibody to CTT. 6. There were no significant differences in skin reaction or histamine release by TA antigen between asthmatics in Okayama and Tottori prefectures.

Adolescent↗
PubMed1989

[Clinical studies on steroid-dependent intractable asthma. Comparison between early and late onset of asthma].

The various components making for severe intractable asthma were clinically and allergo-immunologically studied in 90 patients with bronchial asthma, by comparison between early onset and late onset groups. 1. In the early onset asthma group, cases with low serum IgE levels showed a stronger tendency toward severe intractable asthma. 2. Late onset asthma cases with negative skin tests and negative specific IgE antibodies to house dust tended more often to be severe intractable cases. 3. There was no correlation between sensitization by specific antigens (house dust and Candida), especially Candida, and a tendency toward severe intractable asthma. 4. Severe intractable asthma might be caused by bronchospasm in cases under 30 years of age, by bronchospasm plus hypersecretion in cases between 31 and 40 years of age, and by bronchospasm plus bronchiolar obstruction in cases over 40 years of age.

Adolescent↗
PubMed1988

Eosinophilic leucocytes and arylsulfatase activity in bronchoalveolar lavage fluid of patients with bronchial asthma.

The arylsulfatase activity and histamine concentration of bronchoalveolar lavage fluid (BALF) were examined in patients with bronchial asthma in relation to the eosinophil count and asthma type (atopic and non-atopic). The BALF arylsulfatase activity and histamine concentration were significantly higher in atopic asthmatics than in non-atopic asthmatics. In atopic asthmatics, the activity of arylsulfatase was significantly increased in patients with a higher eosinophil count (10% or more). However, the BALF histamine concentration did not correlate with the eosinophil count. In non-atopic asthmatics, there was no significant correlation between arylsulfatase activity and the eosinophil count. The results show that arylsulfatase participates in IgE-mediated allergic reactions.

Adult↗
PubMed1987

7,12-Dimethylbenz[a]anthracene plus near-u.v. light initiates DNA damage and repair in Chinese hamster cells.

Earlier results on the photodynamic action of several carcinogenic polycyclic aromatic hydrocarbons, and particularly 7,12-dimethylbenz[a]anthracene (DMBA), have been extended to determine if DMBA + near-u.v. light produces damage to DNA. DMBA by itself (30 min, approximately 24 degrees C) introduces relatively few breaks into genomic DNA. The addition of near-u.v. light, however, inserts large numbers of single-strand breaks in a dose-dependent way. Incubation following exposure initially results in the rapid repair of these breaks. A primary role for DNA damage in photodynamic cell killing is not supported by other observations, however. First, caffeine, an inhibitor of radiation-associated DNA repair processes, has only a minor effect on the oxygen-dependent killing of cells exposed to DMBA + u.v. light. Second, along with the repair of DNA breaks, the insertion of additional breaks becomes evident leading to a massive breakdown of genomic DNA due to an endonucleolytic-like attack. And third, lethally affected cells rapidly lose their surface attachment. Because light induces damage in DNA when DMBA is present, it is likely that DMBA becomes closely associated with DNA. Thus, a starting point for mutagenic and carcinogenic action in the absence of light is suggested although activation of DMBA by a P-450 system does not appear to be a prerequisite of DMBA-DNA association. Still, DNA as such may not be the initial or the primary target for light-induced cell killing. In addition to interacting with DNA, DMBA is sequestered by membranes, suggesting that killing results from an oxygen-dependent release of catabolic enzymes. These enzymes, which may come from lysosomes, degrade DNA but concomitantly release surface-attached cells into the medium.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1986

Differentiation of lens and neural cells in chicken embryos is accompanied by simultaneous decay of DNA replication machinery.

DNA polymerase alpha was detected in cells of developing chicken embryos by an immunofluorescent method using a monoclonal antibody specific for the high molecular weight polypeptide of chicken DNA polymerase alpha, and DNA polymerase beta was detected using a rabbit anti-chicken DNA polymerase beta antibody. In lens tissue of the 3- to 4-day chicken embryo, fluorescence with anti-DNA polymerase alpha antibody was detected in nuclei of lens epithelial cells but not in nuclei of lens fiber cells which had differentiated from epithelial cells. The localization of cells containing DNA polymerase alpha coincided with the distribution of cells capable of DNA replication as detected by [3H]thymidine autoradiography. Similar results were obtained during the differentiation of neural matrix cells to neuroblasts in the developing neural tube. In contrast to DNA polymerase alpha, DNA polymerase beta was detected in nuclei of both undifferentiated and differentiated cells of these tissues. Since the disappearance of DNA polymerase alpha was very rapid after the onset of differentiation, the DNA replication machinery in which DNA polymerase alpha plays a central role is thought to decay almost simultaneously with the onset of cellular differentiation in these tissues.

Animals↗
PubMed1985

Decrease in reactivity of basophils by immunotherapy with housedust extract.

Changes of basophil reactivity to housedust extract and anti-IgE during immunotherapy was examined in thirteen patients with bronchial asthma sensitive to housedust. (i) A significant decrease in the morphological reactivity of basophils to housedust extract was observed 6 months after the beginning of immunotherapy with the antigen, and a significant decrease after 12 and 18 months' therapy, accompanied with the decrease of histamine release from the cells. The percent reactive basophils to the antigen decreased from 59.2 +/- 2.9% before the therapy to 40.0 +/- 1.8% after 18 months' immunotherapy. (ii) A decrease in the morphological reactivity of basophils to anti-IgE was also shown during immunotherapy. The basophil reactivity to anti-IgE decreased significantly at the late stage (18 months) of immunotherapy. (iii) A significant reduction of specific IgE antibody to housedust was observed 12 and 18 months after the beginning of immunotherapy. It was suggested from these results that immunotherapy causes some changes on the surface of basophils and decreased reactivity of the cells, and that a decrease of reactive basophils to anti-IgE in the process of immunotherapy might be due to a decrease in number of IgE receptors essentially or functionally.

Adolescent↗
PubMed1985

The calcium antagonist, nicardipine, inhibits antigen-stimulated and anti-IgE-induced histamine release from basophilic leucocytes of atopic asthmatics.

The inhibitory effect of nicardipine, a calcium antagonist, on the antigen- and anti-IgE-induced histamine release from basophilic leucocytes of patients with bronchial asthma was examined. The agent significantly inhibited both antigen-stimulated and anti-IgE-induced histamine release from basophils (the maximum percent inhibition was 57.8 +/- 7.2% and 56.0 +/- 8.8%, respectively). Pre-incubation of basophils with nicardipine for periods of up to 120 min did not alter the inhibitory effect. These results suggest that nicardipine modifies the histamine release from basophils which closely participate in an attack of bronchial asthma.

Antibodies, Anti-Idiotypic↗
PubMed1985

Comparison of basophil histamine release induced by the cross-linking of IgE receptors.

Basophil histamine release induced by allergens (house dust and Candida albicans) and anti-IgE was examined in 31 patients with bronchial asthma in relation to patient age, age at onset of the disease and serum IgE levels. Basophils from patients under 40 years of age generally released a significantly large amount of histamine by stimulation with house dust and anti-IgE. On the other hand, histamine release from patients over 41 years of age was generally not marked when the cells were incubated with house dust and anti-IgE, although, in some cases, the release induced by C. albicans was fairly marked. Basophils from patients under 30 years of age at onset were reactive to house dust and anti-IgE, while the cells from patients over 41 years of age at onset tended to be reactive only to C. albicans. Basophils from patients with low serum IgE levels were less reactive than the cells from patients with high levels of IgE to house dust and anti-IgE. C. albicans-induced release of histamine did not correlate with serum IgE levels.

Adult↗
PubMed1985

Candida-induced histamine release from basophils: relationship to house dust- and anti-IgE-induced secretion.

Candida albicans-induced histamine release from basophils was studied in 54 patients with bronchial asthma in comparison with the release caused by house dust and anti-IgE. The release of histamine induced by C. albicans and that induced by house dust were closely related to the serum levels of specific IgE antibodies as expressed by RAST scores. A correlation of C. albicans-induced histamine release with the release caused by anti-IgE was not generally observed. On the other hand, a close correlation was found between house dust- and anti-IgE-induced histamine release. It was suggested from these results that the differences between C. albicans- and house dust-induced histamine release might be due to the different antigenicity of the two allergens.

Adolescent↗
PubMed1984

Blood eosinophilia in bronchial asthma and its relationship to IgE-mediated reactions.

The correlation between blood eosinophilia and anti-IgE-mediated histamine release was investigated in 22 bronchial asthma patients with peripheral eosinophilia (over 8%). In the cases (Group A-1 and Group A-2) in which house dust was the specific antigen, significant histamine release from basophils was induced by anti-IgE and house dust. The result indicates a relationship between eosinophilia and the IgE-mediated mechanism of disease onset. In the cases (Group A-3) with RAST scores of 0+ and 1+ to house dust, the anti-IgE-induced histamine release varied from low to high percentages, and the participation of the IgE-mediated pathway was indicated in some cases. In the cases (Group B) with negative skin reactions, few patients had a family history of allergic disease. Their ages at onset were higher, and they demonstrated lower total IgE levels. These cases showed an extremely low percent of histamine release from basophils, which indicated the absence of a correlation between eosinophilia and IgE-mediated mechanisms.

Adolescent↗