[Interaction of Eikenella corrodens with macrophages. Mechanism of E. corrodens adherence to macrophages].
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Biomedical subjects
Publications and source records attributed to Y Miki.
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A 49-year-old man with porphyria cutanea tarda was treated with repeated small volume plasmapheresis. After the circadian change of urinary porphyrins was found to be higher between midnight and noon, approximately 250 mL of plasma was removed at 8 AM and was replaced by physiological saline. Clinical disease manifestations and abnormal laboratory findings rapidly improved following a total of 20 plasmapheresis during a 24-week period. The blood hemoglobin and plasma total protein levels were unchanged.
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Regional distributions of endogenous gamma-aminobutyric acid (GABA) and ganglion cells in Auerbach's plexus were studied in the gastrointestinal tract of cats. GABA was determined by enzymatic and fluorometric assay. There was a positive correlation between the GABA content and the number of cells in this plexus. We analyzed the precise localization of GABA and glutamic acid-decarboxylase (GAD) in individual layers, mucosa, circular and longitudinal muscles and Auerbach's plexus, from freeze-dried sections of cat colon by the enzymatic cycling method. Both GABA contents and GAD activity in Auerbach's plexus were highest in all 4 layers. Thus, the possibility that GABA is synthesized and localized within Auerbach's plexus has to be considered.
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Thirty-one patients with Bowen's disease were studied in a restricted district of Namikata and its neighborhood of Ehime, Japan. Nineteen were alive and 12 were dead; the youngest living patient was 52 years of age. Invasive skin cancers were found in 10 patients and internal malignancies in 10, including 7 patients with pulmonary cancers. Palmoplantar keratosis was present in 25 patients and raindrop-type pigment anomalies in 15. Neutron activation analysis of hair showed only slightly higher arsenic values in patients with Bowen's disease than those in normal controls, though the differences were statistically significant at p less than 0.05. A possible arsenic exposure 43 years previously was considered responsible for the occurrence of neoplasms, though the arsenic route and amount were not determined. Bowen's disease started within 10 years, invasive skin cancers after 20 years, and pulmonary cancers after 30 years following the suspected arsenic exposure.
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A 48-year-old Japanese woman with systemic lupus erythematosus-like lesions of the skin and lips was found to have hereditary angio-oedema. Complement studies revealed low CH50, C1q, C4 and C1 inhibitor levels, with normal C3 and C5 levels. Dramatic clinical improvement followed fresh normal human blood transfusion and systemic betamethasone administration, while the deficient complement component levels were unchanged.
A ruthenium red-staining capsule was observed on two pathogenic strains, but not on one nonpathogenic strain of Mycoplasma gallisepticum. The capsule appeared to mediate cytadsorption of mycoplasmas to the chicken tracheal epithelium without evidence of membrane fusion. No relationship was seen between the presence of capsule and hemagglutination titers of the strains examined.
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Involvement of stimulus-activatable serine esterase in the process of TRF-induced IgG production in a human B blastoid cell line (CESS) was demonstrated. Addition of DFP or PMSF (1 X 10(-3) M to 1 X 10(-5) M) showed a dose-dependent inhibitory effect on TRF-induced IgG induction in CESS cells. Other organophosphorous inhibitors, such as p-NPEPP and PEPP, were also effective, but a nonphosphorylating analogue of DFP, DMP, was not inhibitory. Simultaneous addition of DFP with TRF showed the inhibitory effect, and the inhibition was irreversible. However, pretreatment of the cells with DFP did not abrogate TRF-induced IgG production. In synchronized cells, signals provided by TRF could be transduced only when cells were in the G1-phase, and DFP showed an inhibitory effect only when it was added to cells in the G1-phase with TRF. One amino acid derivative (AAME) partially inhibited TRF-induced IgG production.
A clinical and pathologic analysis was made of 101 patients with surgically treated metastatic brain tumors. The most common primary site was the lung (58.4%), followed by th breast (11.9%), gastrointestinal tract (6.9%), and uterus (5.)%). In 14 patients, the disease began with cerebral symptoms. The overall average survival after craniotomy was 8.0 months, the longest survival being 8l/2 years; patients with one-year survivals composed 18.8% of the cases. The histologic features were almost the same in primary and metastatic tumors. The undifferentiated tumor metastasized most frequently to the brain, and adenocarcinoma of the papillary type also seemed to find the brain fertile ground for metastatic growth.
Generation of a cytoplasmic factor(s) that induced IgG secretion in nonstimulated cells was demonstrated in TRF-stimulated cells by using red cell-mediated microinjection. Injection of the cytoplasm from a TRF-stimulated B lymphoblastoid cell line (CESS) into nonstimulated cells induced an increase of IgG-producing cells. Injection of TRF itself did not induce an increase of IgG-producing cells. Active substance(s) in the cytoplasm were generated at 2 hr after TRF stimulation, and IgG-producing cells reached their maximum level at 40 hr after injection of the factor(s). DFP, but not actinomycin D, inhibited the generation of the cytoplasmic factor(s). The activity of the cytoplasmic factor(s) was not destroyed by RNase and not absorbed with anti-IgG. These results suggested that binding of TRF with its acceptors induced the generation of the cytoplasmic factor(s) involved in the transmission of TRF-mediated signals from membrane to nuclei.
IgG production was induced in a human B blastoid cell line, CESS, by stimulation with a human B cell-specific monoclonal antibody (IIIA4). The number of IgG-producing cells reached its maximal level within 48 hr after incubation with IIIA4. IgG-producing cells induced by an optimal concentration of the antibody was about one-half as many as those induced with TRF, but higher concentrations of the antibody were rather inhibitory. Simultaneous addition of an optimal concentration of the antibody with TRF partially inhibited TRF-induced IgG production in CESS cells, but higher concentrations of the antibody did not block TRF-induced IgG production. TRF activity was completely absorbed with IIIA4-coated CESS cells as well as nontreated CESS cells. These results suggested that the membrane antigen recognized by IIIA4 was not the acceptor molecule for TRF. IIIA4 did not show any inhibitory effect on PWM-induced proliferation of normal B cells, but completely inhibited PWM-induced Ig production of normal B cells.