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Biomedical subjects

K Chida

Publications and source records attributed to K Chida.

At least 235 records · Page 13Linked to original sources
PubMed1989

[Clinical aspects of sarcoidosis with autoantibodies].

Among 64 sarcoidosis cases, 6 cases with autoantibodies or autoimmune disorders are described. All 6 cases were females over 40 years old, and made up 24% of the original 25 patients over 40 years old. Rheumatoid factor was observed in 2 cases, anti-DNA antibody in 4 cases and anti-microsomal antibody in 2 cases. Four cases of sarcoidosis were associated with ITP or Hashimoto's disease or rheumatoid arthritis. The presence of these autoantibodies or autoimmune diseases seemed to correlate with continued disease activity of sarcoidosis. The analysis of the clinical features of sarcoidosis with coexistent autoimmune diseases may clarify immunologic processes involved in the pathogenesis of both disorders and also provide clues to understanding the relatively poor clinical outcome of longstanding sarcoidosis.

Aged↗
PubMed1989

[Role of bronchoalveolar lavage in analysis of diffuse pulmonary diseases].

Bronchoalveolar lavage (BAL) is often referred to as "Liquid biopsy of the lung". We reviewed the usefulness of BAL in the analysis of diffuse pulmonary diseases, focussing on the influences of smoking on cellular and soluble components in BAL, what causes the discrepancy between findings in BAL fluids and those in biopsy specimens and how cardiovascular system is influenced during this procedure. BAL offers a practical approach to not only academic, but clinical analysis such as therapeutic guide and prognosis.

Bronchoalveolar Lavage Fluid↗
PubMed1989

[Activation and metabolic changes of macrophages in immunology of tuberculosis].

The effects of aging and malnutrition on BAL cells, such as metabolic disorders and various immune responses, have been examined. In malnourished animals, the composition of phospholipids in BAL cells were changed, and the decrease in the number of specific prednisolone binding sites was recognized. Furthermore, the decrease of total cell counts and the population of lymphocytes, neutrophils and Ia-positive macrophages were observed in BAL cells. However, BAL cells obtained from heat-killed BCG sensitized animals in malnutrition preserved a good responsiveness. These impaired cellular development following starvation could be partly reversed by some antigenic factors, resulting in heavier cell infiltration and granuloma formation in the lung tissues. These observations suggest that alterations in immune responses accompanying malnutrition may be closely related to the mechanism of reactivation and the clinical course and profile of tuberculosis.

Aging↗
PubMed1988

Enhancement of inositol phospholipid metabolism and activation of protein kinase C in ras-transformed rat fibroblasts.

The inositol phospholipid metabolism is one of the main pathways of signal transduction in cells. We measured the activities of its key enzymes in v-Ha-ras-transformed 208F rat fibroblasts. In the ras-transformed clones, incorporation of [32P]Pi into intermediates of the inositol phospholipid metabolism was stimulated. The activities of phosphatidylinositol and phosphatidylinositol-4-phosphate kinases in the transformed clones were about 35-50% more than in untransformed cells, indicating increased inositol phospholipid metabolism. However, the activity of diacylglycerol kinase in their membrane fraction was 25-35% less than that of untransformed cells, although the total diacylglycerol kinase activity did not change. The imbalance of these kinases could constitute one of the main reasons leading to the increased level of inositol phosphates and the accumulation of diacylglycerol to 2-2.2 times that in control 208F cells. Phosphatidylinositol-4,5-bisphosphate-phospholipase C activity did not change on the transformation when assayed under various conditions. The increased level of diacylglycerol caused intracellular translocation, activation, and down-regulation of protein kinase C changes which may be one of the essential events in transformation by the v-Ha-ras gene.

Animals↗
PubMed1988

Protein kinase C activities and bindings of a phorbol ester tumor promoter in 41 cell lines.

The activities of protein kinase C (PKC) and the bindings to phorbol-12,13-dibutyrate (PDBu) of 41 cell lines were measured. The activities of PKC varied from 0.2 to 37 mU/10(6) cells in different cell lines, and in general were high in normal or untransformed cells and low in malignant, or transformed cells. The PDBu binding also varied considerably in different cell lines, and was again higher in normal or untransformed cells. In some cell lines, the binding was much higher at 4 degrees C than at 37 degrees C, suggesting rapid down-regulation of the binding. A correlation between PKC activity and PDBu binding was found only within certain cell types, i.e., epithelial cell lines derived from human tumors.

Animals↗
PubMed1988

Inhibition of phorbol ester-caused induction of ornithine decarboxylase and tumor promotion in mouse skin by staurosporine, a potent inhibitor of protein kinase C.

We found that staurosporine, a potent inhibitor of protein kinase C, inhibits induction of ornithine decarboxylase (ODC) and tumor promotion caused by 12-O-tetradecanoylphorbol-13-acetate (TPA) in CD-1 mouse skin. When applied 5 min either before or after treatment with TPA, 1 microgram of staurosporine cause about 56% inhibition of ODC-induction by 5 micrograms of TPA. However, staurosporine did not inhibit TPA-induced epidermal hyperplasia. In two-stage carcinogenesis, staurosporine at 1 microgram was applied 5 min before application of 5 micrograms of TPA to the initiated skin: number of tumors was suppressed by about 40% although the incidence was not affected. No tumors developed when staurosporine alone was applied to the initiated skin.

Alkaloids↗
PubMed1988

Phosphorylations of Mr 34,000 and 40,000 proteins by protein kinase C in mouse epidermis in vivo.

Activation of protein kinase C (PKC) and the resulting phosphorylations of proteins in vivo were examined in mouse epidermis, a target tissue of tumor-promoting phorbol diesters, such as 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Treatment of mouse skin with TPA caused rapid translocation of PKC from the cytosol to the membrane fraction of skin tissue, followed by its down regulation. Epidermal proteins were labeled locally with 32P using the ring-shaped forceps technique that economizes on the amount of 32Pi required. Treatment with TPA in vivo resulted in about 2-fold increases in the phosphorylations of epidermal proteins with molecular weights of 34,000 and 40,000 and isoelectric points of 4.7-5.1 and 5.2-6.2 (p34 and p40, respectively). The phosphorylations of these proteins were also stimulated by teleocidin B. Inhibitors of PKC, such as chlorpromazine, quercetin, and staurosporine inhibited these increases in phosphorylations of p34 and p40 on TPA treatment. Furthermore, p34 and p40 were phosphorylated by purified PKC in a cell-free system. These results indicate that p34 and p40 are phosphorylated by PKC in mouse epidermis in vivo and may be involved in tumor promotion.

Animals↗
PubMed1988

Four monoclonal antibodies, AMH-1, -2, -3, and -4, give varied reactivities with monocytes, alveolar macrophages, and epithelioid-cell granulomas.

Four monoclonal antibodies, termed AMH-1, AMH-2, AMH-3, and AMH-4, raised against human lung macrophages in bronchoalveolar lavaged fluid, alveolar spaces, and interstitia of lung tissue are described. The antibodies were produced according to hybridoma technique by immunizing mice with bronchoalveolar lavaged cells. All four monoclonal antibodies reacted with macrophages in bronchoalveolar lavaged fluid and alveolar spaces by immunohistochemical staining and flow cytometric analysis, but they gave different reactivity patterns with the monocyte-macrophage lineage. AMH-1 did not react with peripheral blood monocytes, peritoneal macrophages, or pulmonary interstitial macrophages. Although AMH-2 reacted weakly with blood monocytes and with some of the pulmonary interstitial macrophages, it did not react with peritoneal macrophages. AMH-3 did not show reactivities with either blood monocytes or peritoneal macrophages but was positive for most of the pulmonary interstitial macrophages. AMH-4 was reactive with cells from the monocyte-macrophage lineage. There was a correlation between the reactivity patterns of all four antibodies to macrophages in bronchoalveolar lavaged fluid and the patients' smoking habits. Most significantly, epithelioid cells of lung granulomas obtained from patients with sarcoidosis and hypersensitivity pneumonitis were negative for AMH-1 but were strongly stained by AMH-2, AMH-3, and AMH-4. Differences among the four antibodies in their reactivities with macrophages and granulomas in lungs indicate that lung macrophages contain heterogeneous populations which are in various states of differentiation and maturation and that the epithelioid cells and lung macrophages share the same membrane antigens. Therefore, these antibodies would be useful reagents for investigating the subpopulations and functions of macrophages in lungs and for clarifying the pathogenesis of granulomatous lung diseases.

Animals↗
PubMed1988

The Marfan syndrome with an XYY chromosome pattern.

A 36-year-old man who was diagnosed to have the Marfan syndrome with an XYY chromosome pattern is reported. He was tall with long limbs and arachnodactylia, and had severe aortic regurgitation (AR). The chromosome pattern studied in specimens of blood and bone marrow revealed an XYY chromosome pattern. The relationship between the Marfan syndrome and an XYY chromosome pattern is discussed.

Adult↗
PubMed1987

Systemic inhibition of tumor promoter-induced ornithine decarboxylase in 1 alpha-hydroxyvitamin D3-treated animals.

Topical application of 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3], an active form of vitamin D3, was previously shown to inhibit the induction of ornithine decarboxylase (ODC) and tumor promotion by tumor promoters in mouse skin. In the present study, this observation in skin was extended to other tissues, such as the stomach, colon, and liver, using 1 alpha-hydroxyvitamin D3 [1 alpha (OH)D3], which is converted to 1 alpha,25(OH)2D3 in the liver without hormonal control and thus evokes the systemic effects, if any, of 1 alpha,25(OH)2D3. When mice were given 1 alpha (OH)D3 at a dose of 5 micrograms by gastric tube, their plasma level of 1 alpha,25(OH)2D3 increased to a peak of about 18-fold the normal level after 12 h, followed by hypercalcemia (about 14 mg/dl), which reached a peak on Days 2 to 3. In 1 alpha (OH)D3-treated mice, induction of epidermal ODC by 12-O-tetradecanoylphorbol-13-acetate was markedly inhibited, the inhibition being maximal 2 to 4 days after 1 alpha (OH)D3 administration. ODC induction in the glandular stomach mucosa of rats by NaCl, a tumor promoter in stomach carcinogenesis, was also inhibited dose and time dependently by 1 alpha (OH)D3. Similarly, 1 alpha (OH)D3 treatment of rats markedly inhibited the induction of ODC in the colon mucosa by deoxycholate, a tumor promoter of colon carcinogenesis, and of ODC in the liver by phenobarbital, a promoter of liver carcinogenesis. These results suggest that an active form of vitamin D3 has a systemic inhibitory effect on induction of ODC activity by tumor promoters.

Animals↗
PubMed1987

Cardiovascular responses elicited by stimulation of neurons in the central amygdaloid nucleus in awake but not anesthetized rats resemble conditioned emotional responses.

Cardiovascular responses elicited by electrical stimulation of the central amygdaloid nucleus were examined in awake and anesthetized rats. Stimulation through chronically implanted electrodes evoked increases in arterial pressure and heart rate in awake, freely behaving rats. The responses, which were dependent upon the frequency and the intensity of the stimulus, were not consistently related to the presence of evoked amygdaloid afterdischarges or to evoked behavioral reactions. Following induction of anesthesia, stimuli delivered to the same rats through the same fixed electrodes produced decreases in blood pressure and heart rate. Microinjection of L-glutamate into the amygdala of freely behaving rats also elicited increases in arterial pressure and heart rate, indicating that the cardiovascular changes evoked by electrical stimuli are due to excitation of local neurons rather than fibers of passage. The timing and pattern of the response elicited by electrical stimulation of the amygdala in the awake but not the anesthetized rat closely corresponds with that evoked by an acoustic conditioned emotional stimulus.

Action Potentials↗