[Chemical activities and oxidation-reduction potentials of mycobacteria].
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Biomedical subjects
Publications and source records attributed to M Takei.
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Cardiac myxomas are benign tumors which sometimes secrete interleukin-6 (IL-6), however, the pathogenesis and the IL-6 secreting cells are not clear. There are vascular myosin heavy chain isoforms; SM2 expression is specific to mature smooth muscle cells, while SMemb is a nonmuscle-type isoform which is expressed in immature mesenchyme cells. We hypothesized that immature mesenchyme cells play pivotal roles in the secretion of IL-6; we studied these expression in resected samples of myxoma. SMemb expression was increased but SM2 expression was not in the channels of myxoma. Increased IL-6 transcription was observed in the SMemb expressing cells in the channel. Therefore, mesenchyme cells with immature phenotype in the channel play pivotal roles of inflammation and pathogenesis of cardiac myxoma.
Although nitrated polycyclic aromatic hydrocarbons (nitrated PAHs), specifically, dinitrated PAHs, have been indicated as potent mutagenic and carcinogenic environmental pollutants, only a few di- and trinitrophenanthrenes (DNPHs and TNPHs) have been reported up to the present time. Methods for the preparation of DNPHs and TNPHs by direct nitration of phenanthrene were established in this study. The reaction of phenanthrene with fuming nitric acid in acetic anhydride gave a complex mixture of DNPHs. Eleven DNPHs were isolated by using preparative HPLC with a total of 62.6% yield. Their chemical structures were determined using 1H NMR and electron impact mass spectrometry (EI-MS). The isolated DNPHs and their yields were 2,10-DNPH (14.2%), 1,10-DNPH (8.0%), 3,10-DNPH (6.9%), 3,6-DNPH (6.6%), 2,9-DNPH (5.3%), 1,6-DNPH (5.1%), 3,5-DNPH (4.6%), 4,9-DNPH (3.2%), 4,10-DNPH (3.1%), 1,5-DNPH (2.8%), and 2,6-DNPH (2.8%). Similarly, nine TNPHs were obtained from the nitrated reaction mixture of phenanthrene with fuming nitric acid without solvent: 3,6,9-TNPH (9.2%), 2,6,9-TNPH (9.0%), 1,6,9-TNPH (8.2%), 1,5,10-TNPH (9.0%), 2,6,9-TNPH (9.0%), 1,6,9-TNPH (4.0%), 1,7,9-TNPH (3.4%), 2,5,10-TNPH (2.5%), 2,6,10-TNPH (2.4%), 3,5,10-TNPH (1.8%), and 2,7,9-TNPH (0.2%) in 46.5% of the total yield. The reduction properties of the DNPHs and TNPHs were examined using cyclic voltammetry. The LUMO energy levels of the DNPHs and TNPHs calculated by the AM1 method were correlated to the first reduction potentials (E1/2). The coplanar or noncoplanar conformations of the nitro substituents to the phenanthrene ring system were also discussed.
The clinical use of antithymocyte globulin is rarely reported in patients with rheumatic diseases. We describe the use of this agent in a patient with systemic lupus erythematosus who concomitantly developed severe pancytopenia. High-dose methylprednisolone therapy had been unsuccessful in controlling either the disease exacerbation or the pancytopenia. Antithymocyte globulin and cyclosporin A were therefore administered to achieve immunosuppression. The exacerbation of disease activity was gradually lessened, except for persistent thrombocytopenia and anaemia. Severe and persistent immunosuppression, however, led to a fatal brain abscess. The combined use of both antithymocyte globulin and cyclosporin A induced potent immunosuppression, and should be confined to selected patients with systemic lupus erythematosus, and administered under detailed monitoring.
We investigated the concentration of soluble CD4 molecules (sCD4) in serum, and the mechanism of sCD4 production from T lymphocytes, in patients with rheumatoid arthritis (RA). The concentration of sCD4 molecules was determined using a solid-phase enzyme-linked immunosorbent assay method. Using reverse transcription polymerase chain reaction (RT-PCR) techniques, we studied the presence of alternatively spliced mRNA encoding the transmembrane site of CD4, and the mRNA encoding a conservative region of the CD4 binding site of the human immunodeficiency virus (HIV), in the serum of RA patients. Levels of sCD4 found in RA patients were higher than in normal controls (199 U/ml compared with 8.4 U/ml, respectively), and correlated with additional medical parameters. The results of RT-PCR suggested that the higher sCD4 levels may be due to shedding from the cell membrane after protease digestion, not to alternative splicing or a reaction to viral binding to sCD4.
We used a new tactile sensor to measure the elastic properties of skin in patients with systemic sclerosis or Raynaud's phenomenon. The sensor consists of a piezoelectric vibrator with vibration pickup to measure frequency changes when the sensor is placed on the skin. The mean frequency change at the skin surface of the proximol third phalanx in patients with systemic sclerosis was significantly lower than in age- and sex-matched controls. The results in systemic sclerosis patients were statistically correlated to the Modified Rodnan Skin Thickness Score. This technique was also used to measure the therapeutic efficacy of salpogrelate, a new specific serotonin receptor antagonist. A greater mean frequency change was seen after treatment. We conclude that this new tactile sensor is useful for quantitatively measuring skin sclerosis and may help determine the efficacy of therapeutic treatments.
The pathogenesis of Sjögren's syndrome (SS) is poorly understood. In this study we used an in-house mouse spleen cDNA microarray to analyse genes in spleens from MRL/lpr (an SS mouse model) mice. We have previously demonstrated that GRAP genes were up-regulated in salivary glands of the same mice. The microarray analysis showed that seven out of 2304 genes were highly expressed in spleens from the MRL/lpr mice, one of which was the GRAP gene. In other words, the GRAP gene is highly expressed in the salivary glands and spleen of MRL/lpr mice. We also carried out immunohistochemical studies. Mouse and human Grb-2-related adaptor protein (GRAP) antigens were expressed on ductal cells and infiltrating lymphocytes in salivary glands of MRL/lpr mice and SS patients, but only weakly in controls (MRL/+ mice and individuals with salivary cysts). These results suggest that the GRAP gene might have a role in the pathogenesis of SS.
A 57-year-old woman was diagnosed in January 1982 with SLE based on ANA 1:640, positive LE cell preparation, proteinuria (3+), and pericarditis. In 1984, 1994, and 1997, the pericardial effusion was noted to have increased without signs of disease exacerbation or cardiac tamponade, and pericardial drainage was repeated to control the effusion. A massive pericardial effusion developed in August 1997. After tuberculosis, hypothyroidism, neoplasm, and progression of SLE were ruled out, we decided to perform pericardial fenestration. A safe and minimally invasive pericardial fenestration was successfully completed endoscopically. Pathologic study of the specimen revealed chronic pericarditis. We consider endoscopic pericardial fenestration to be useful for at risk patients with pericarditis to control the effusion and establish a differential diagnosis.
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OBJECTIVE: We examined the soluble CD23 (sCD23) molecules in sera and saliva from patients with Sjögren's syndrome. METHODS: The determination of sCD23 and other soluble molecules were made by the enzyme-linked immunosorbent assay. RESULTS: The amounts of sCD23 in the sera/saliva were significantly increased in the patients compared to the controls and the levels were significantly correlated with sialoectasis. CONCLUSION: The findings suggest that increased sCD23 molecules in saliva from patients with Sjögren's syndrome may reflect active sialoectasis.