[A case of psittacosis presenting as adult respiratory distress syndrome and successfully treated with steroid pulse therapy].
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Biomedical subjects
Publications and source records attributed to S Kitagawa.
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Prior exposure of granulocytes to inflammatory mediators such as chemotactic factors, colony-stimulating factors and tumor necrosis factor primes the cells for enhanced activity of the respiratory burst, which appears not only to play an essential role in the increased host-defenses against invading microorganisms but also to be responsible for tissue damage at the inflammatory sites. The molecular basis for this priming is presently under investigation. Changes in one or more of the signal transduction events may lead to more efficient stimulation of the NADPH oxidase responsible for the respiratory burst. The mechanisms of priming appear to be different according to the priming stimuli: the chemotactic peptide and the Ca2+ ionophore may prime the cells by causing an increase in cytoplasmic free Ca2+; phorbol esters by activating protein kinase C; and colony-stimulating factors and tumor necrosis factor by activating the distinct mechanism, which is independent of an increase in cytoplasmic free Ca2+ and activation of protein kinase C.
The complementary DNAs encoding interleukins (interleukins 1, 2, 3, 4, 5 and 6) and colony-stimulating factors (granulocyte-macrophage, granulocyte, and macrophage colony-stimulating factors) have been cloned. These DNA clones have allowed the large-scale production of recombinant forms of these cytokines and the extensive studies of their biological activities. These advances have led to a much better understanding of the role of these cytokines in regulation of immune responses and hematopoiesis, and have clarified that these cytokines have multiple effects on various types of cells.
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The inhibitory effects of alkyltrimethylammonium ions on ADP- and thrombin-induced aggregation of bovine platelets were investigated. The ammonium cations inhibited the two aggregation reactions to similar extents. The relationship between their inhibitory effects on ADP-induced aggregation and their alkyl chain lengths from C8 to C18 was investigated. Results showed that the inhibitory effects of ammonium cations increased with increase of their alkyl chain lengths up to C16, and that the increase was linear with chain lengths of up to C14. This linear relation and slope of the linear regression line suggested that the inhibitory effects of the ammonium cations depended on their partitioning into the membrane. However, unlike long-chain unsaturated fatty acids, they did not affect the membrane fluidity of the platelets. Fluorescence analysis of fura-2 loaded platelets revealed that, in the concentration range where the alkyltrimethylammonium ions inhibited aggregation, they inhibited agonist-induced increase in cytosolic Ca2+ both in the presence and absence of extracellular Ca2+. These results suggest that inhibition of platelet aggregation by alkyltrimethylammonium ions is mainly due to their inhibition of increase in cytoplasmic Ca2+ by inhibition of both intracellular Ca2+ mobilization and Ca2+ uptake.
The effect of nigericin on aggregation of bovine platelets was investigated in media containing the chloride salts of various alkali metal cations of quaternary ammonium cations. In medium with K+, which has the highest permeability with the ionophore among the cations tested, nigericin slightly enhanced both ADP- and thrombin-induced aggregation. In medium with Na+, nigericin scarcely affected ADP-induced aggregation, and slightly inhibited thrombin-induced aggregation. In media with Cs+, choline and tetramethylammonium, it inhibited the aggregations induced by both ADP and thrombin. Measurement of the cytoplasmic pH with the fluorescent probe 2',7'-bis(carboxyethyl)5,6-carboxyfluorescein showed that nigericin increased the intracellular pH in K+ medium and caused its stable decrease (of about 0.6) in Cs+, choline and tetramethylammonium media, but caused only a small transient decrease in medium with Na+. These results suggest that the effects of nigericin on platelet aggregation are mainly due to its effects on the cytoplasmic pH. This conclusion is supported by the findings that the effects on platelet aggregation of other types of ionophore tested were also proportional to their effects on the cytoplasmic pH.
A clinicopathologic study was done on 21 cases of early carcinoma of the gastric cardia. The disease was preponderant in men, with a male-female ratio of 17:4. Five patients had no symptoms, while the other 16 had epigastric pain, epigastric discomfort, or other symptoms. Melena or hematemesis occurred in five patients. The first detection was made by barium study in 16 and by endoscopy in five. Detailed examinations using double-contrast radiography in both the prone right anterior oblique and supine left lateral projections were useful to detect the early carcinoma of the gastric cardia. All depressed-type carcinomas were incidentally detected during endoscopic examinations of benign peptic ulcers, therefore, whenever endoscopic examinations are being done for other entities, all the stomach including the cardia should be examined, carefully and continuously. Compared with early carcinomas of the other areas of the stomach, grossly elevated and histologically well-differentiated early carcinomas were more common in the gastric cardia. In the mucosa adjacent to the carcinoma, chronic gastritis was apparent in almost all cases, although intestinal metaplasia was found less frequently than in other areas of the stomach.
Recombinant human granulocyte colony-stimulating factor (G-CSF) by itself was not an effective stimulus for inducing the release of superoxide (O-2) in human granulocytes. However, G-CSF was able to prime human granulocytes, and enhanced O-2 release stimulated by the chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP). The preincubation with G-CSF for 5-10 min at 37 degrees C was sufficient for priming the cells. The optimal enhancing effect was obtained at 25 ng/ml of G-CSF. The enhancement of O-2 release by G-CSF was observed over the complete range of effective concentrations of FMLP (10(-8)-10(-6) M). These findings indicate that G-CSF is a potent activator of mature granulocyte functions.
A cellular binding protein for 3,3',5-triiodo-L-thyronine (T3) was solubilized with 3-[(3-cholamidopropyl) dimethylammonio]-1-propanesulfonate (CHAPS) from A431 human epidermoid carcinoma cells. The binding activity is T3 specific. Analysis of the equilibrium binding data indicated that the binding protein has one class of binding sites for T3 with a Kd of (17 +/- 3) nM and Bmax of (1.8 +/- 0.6) pmol/50 micrograms of protein. The pH optimum for binding is 6.8. The T3 binding protein elutes from Sephadex G-200 in an included peak which has a Stokes radius of 40 A and sediments on glycerol gradients at 3.7 S. By affinity labeling with [3,5-125I]thyroxine a protein with a molecular weight of 58,000 was specifically labeled. Its isoelectric point was determined to be 7.1, which is different from the reported pIs of other thyroid hormone binding proteins. p58 was successively purified to apparent homogeneity by chromatography on Sephadex G-200, QAE-Sephadex, SP-Sephadex, and hydroxylapatite. Approximately 50 micrograms of purified protein was obtained from 2.5 X 10(9) cells with a yield of 1.1%. The purified protein retains its binding activity. The specific binding activity is enriched by approximately 1000-fold. With the availability of a purified protein with T3 binding activity, it becomes possible to study its cellular function.
The effects of thyroid hormones on morphology and growth were studied in rat pituitary tumor GH3 cells using medium containing serum depleted of thyroid hormones. T3 and T4 induce the cells to change from a flattened fibroblastic morphology to a rounded or spindle-shaped morphology. The induction in morphological changes is T3 and T4 specific and dose dependent. Thyronine and rT3 are ineffective in inducing morphological changes; the half-maximal effective concentrations for T3 and T4 are 0.3 and 2 nM, respectively. Concomitantly, T3 stimulates cell growth, as indicated by a 2-fold reduction in doubling time and a 2-fold increase in mitotic rate. The growth-stimulating effect has the same analog specificity and dose dependency as the morphological changes. The morphological changes could be potentially useful for evaluating the biological effects of T3 and its analogs and in studying the mechanism of thyroid hormone action.
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Although malignant fibrous histiocytoma (MFH) is the most common soft tissue sarcoma of adult, it rarely arises in the breast tissue. Only seven cases have been previously reported in Japan. One case of the MFH of the mammary gland is presented in this paper. A 39 year old woman, who had received no radiation, was referred to our hospital due to a painful right breast lump. Excisional biopsy revealed yellowish white soft tumor with an obscured margin. Histological, tumor was composed of spindle shaped cells of a storiform pattern, which was diagnosed as MFH of the breast. Radical mastectomy (Br + Mj + Ax) was added to this patient. The tumor invaded to the fat tissue without metastasis to the axillary lymph nodes. We performed the post-operative adjuvant chemotherapy of Adriamycin. She made an uneventful recovery and is now free of disease eleven months postoperatively.
We examined the in vitro effect of recombinant human granulocyte colony-stimulating factor (rhG-CSF) on neutrophil anomalies in 20 patients with myelodysplastic syndromes (MDS) and eight patients with chronic myelogenous leukemia (CML). Neutrophil alkaline phosphatase (NAP) activity was determined in nine MDS patients and eight CML patients by a scoring method. NAP scores were decreased in six of the nine patients with MDS and in all of the patients with CML. In all patients with these diseases, NAP scores increased by incubating the blood with rhG-CSF. An increase in NAP scores by rhG-CSF was observed even at a concentration of 1 U/mL in patients with MDS but was observed only at higher concentrations (1,000 to 10,000 U/mL) in patients with CML. Significant increases in NAP scores occurred at 12 hours' incubation in patients with MDS, whereas the increase was more gradual in patients with CML. This time course difference was thought to be due mainly to the difference in cell populations of circulating myeloid cells between MDS patients and CML patients. Induction of NAP activity by rhG-CSF in patients with both these diseases was suppressed by the addition of inhibitors of RNA or protein synthesis. Neutrophil superoxide anion (O2-) production induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP) was determined in the other 11 patients with MDS. This neutrophil function was decreased in seven of the 11 patients with MDS, normal in two patients, and increased in two patients. Preincubation with rhG-CSF caused a significant increase in fMLP-induced O2- production in nine of the 11 patients with MDS. rhG-CSF enhanced this neutrophil function in a time- and dose-dependent manner, and maximal stimulation was observed at 2,000 to 4,000 U/mL of rhG-CSF and at five to ten minutes' incubation. The present results show that rhG-CSF is able to repair at least in part the neutrophil anomalies in these patients, and our data, especially for patients with MDS, suggest the clinical usefulness of rhG-CSF for this preleukemic disorder.
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