Anti-annexin antibody in the sera of patients with habitual fetal loss or preeclampsia.
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Biomedical subjects
Publications and source records attributed to N Saitoh.
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Several episodes of "smelter disease", previously assumed to be caused by sulphur dioxide (SO2) poisoning, have been reported in workers replacing pipes in sulphuric acid manufacturing plants. One such incident, affecting 20 men, was recorded in Akita, Japan, in July, 1993, but the protection these workers used suggested that some cause other than SO2 needed to be looked for. 10 workers were affected despite wearing respirators with SO2 cartridges, the symptoms including dyspnoea, diarrhoea, colicky pain, muscle pain and eczema with erythema. Subsequently 10 other workers using face masks with supplied air were affected, though without respiratory symptoms. Sludge in the piping contained mercuric sulphate, and mercury fumes resulted when pipes were cut with gas burners. Blood and urine measurements confirmed heavy exposure to the metal, and simulation experiments in rats showed that skin absorption was likely too. The masks with supplied air ought to have excluded both SO2 and mercury fumes. The only way to avoid smelter disease reliably is to wear an encapsulated suit that prevents inhalation and skin absorption of industrial toxins.
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We investigated anti-annexin V antibody (aANX) in patients with systemic lupus erythematosus (SLE), and correlated to positivity with lupus anticoagulant (LA)/anticardiolipin antibody (aCL). aANX was positive in 12/47 SLE patients (26%), including 7 with beta 2-glycoprotein 1 (GPI)-dependent aANX. The positivity of aANX was higher in patients with aCL (19%) and LA/aCL (50%) than in those without LA/aCL (10%). From these results, it is concluded that aANX is an autoantibody closely related to LA/aCL, and can be a possible new risk marker for thrombosis.
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We conducted an investigation to clarify whether or not the levels of total, free, and functional protein S and C4-binding protein (C4bp) in plasma are decreased in systemic lupus erythematosus (SLE) patients, especially those with antiphospholipid antibody (aPL), which is known to be a causative factor of such complications as habitual abortion and arteriovenous thrombosis. Fifty patients with SLE were recruited as subjects of the study. Serum aPL (anticardiolipin, antiphosphatidyl serine, antiphosphatidyl inositol, and antiphosphatidic acid antibodies) were measured by ELISA. Lupus anticoagulant was determined by a PTT, KCT, and diluted RVVT. Furthermore, plasma concentrations of total, free, and functional protein S and C4bp were measured. There were no significant differences in the mean levels of total, free, or functional protein S and C4bp between aPL-positive, aPL-negative SLE patients, and the healthy controls. From these results, we concluded that the protein S level is not the sole factor causing complications, and that other factor(s) may be involved in the induction of such complications in this clinical setting.
Here, we describe the cloning and characterization of ScII, the second most abundant protein after topoisomerase II, of the chromosome scaffold fraction to be identified. ScII is structurally related to a protein, Smc1p, previously found to be required for accurate chromosome segregation in Saccharomyces cerevisiae. ScII and the other members of the emerging family of SMC1-like proteins are likely to be novel ATPases, with NTP-binding A and B sites separated by two lengthy regions predicted to form an alpha-helical coiled-coil. Analysis of the ScII B site predicted that ScII might use ATP by a mechanism similar to the bacterial recN DNA repair and recombination enzyme. ScII is a mitosis-specific scaffold protein that colocalizes with topoisomerase II in mitotic chromosomes. However, ScII appears not to be associated with the interphase nuclear matrix. ScII might thus play a role in mitotic processes such as chromosome condensation or sister chromatid disjunction, both of which have been previously shown to involve topoisomerase II.
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We developed and evaluated an automated screening test for antibody to human immunodeficiency virus type 1 (HIV-1) using EDTA-2Na-treated whole blood and an extract of paper disk-absorbed dried whole blood from 60 hemophiliacs infected with HIV-1 and 210 diseased and healthy controls. The specificity and the sensitivity of this system were judged to be 100% with both the whole blood and the extract. This test allows measurement of HIV-1 antibody in whole blood and dried whole blood on a small paper disk and gives a result within 13 minutes; the system can process 150 samples per hour. Therefore, it may be useful at many testing sites, such as emergency departments, intensive care units, blood banks, and commercial laboratories, as well as for mail-order testing from remote areas and developing countries.
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We measured serum 2,5-oligoadenylate synthetase (2,5-AS) levels and soluble interleukin-2 receptor (sIL-2R) levels in human immune deficiency virus type 1 (HIV-1)-positive and HIV-1-negative hemophiliacs in order to clarify the clinical significance of these parameters in hemophiliacs. Serum 2,5-AS levels were measured by a radioimmunosorbent assay, and sIL-2R levels were measured by an enzyme-linked immunosorbent assay. The mean serum 2,5-AS levels were higher in AIDS-related-complex and AIDS patients, asymptomatic carriers, and HIV-1-negative hemophiliacs than in hepatitis C virus-positive patients and healthy controls. Serial determinations showed that the 2,5-AS levels tended to increase in HIV-1-positive patients, especially those with AIDS-related complex or AIDS, although it showed a substantial decrease in the terminal stage. The serum sIL-2R levels were higher in HIV-1-positive patients, HIV-1-negative patients, and hepatitis C virus-positive patients than in controls. Serial studies showed little change in the HIV-1-positive and HIV-1-negative groups, although sIL-2R levels showed a tendency to decrease with zidovudine treatment. On the basis of the present results, we may well conclude that 2,5-AS and sIL-2R are not specific markers for hemophiliacs with HIV-1 infection. However, serial measurement of these markers can still be useful for assessing the progression of AIDS and the prognosis for patients with AIDS, as well as for monitoring the response to zidovudine.
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We investigated whether or not antiphospholipid antibodies (aPLs; antiphosphadidylserine antibody, aPS; antiphosphatididylinositol antibody, aPI; antiphosphatidic acid antibody, aPA, and antiphosphadidylethanolamine antibody, aPE) were beta 2-glycoprotein-I (GPI)-dependent antibodies like anticardiolipin antibody (aCL) in patients with systemic lupus erythematosus (SLE). None of the patients with syphilis or healthy controls was positive for any GPI-dependent aPL. By contrast, GPI-dependent aCL (40%), aPS (20%), aPI (18%), aPA (12%) and aPE (8%) were detected in patients with SLE. Among these, 4 patients were negative for aCL, but positive for aPS. Those who were positive for more than 2 types of aPL, along with lupus anticoagulant, had a high incidence of arteriovenous thrombosis, fetal loss, thrombocytopenia and biological false-positive reaction to syphilis. From these findings we conclude that GPI-dependent aPLs, other than aCL, are present in patients with SLE, and we should examine more than 2 types of aPL, such as a combination of aCL and aPS, to avoid overlooking aPL. Furthermore, we confirmed that GPI-independent aPL was not rare in SLE patients, but the clinical significance of this type of aPL in this clinical setting is unclear.
We investigated whether anticardiolipin antibody (aCL), which is common in patients with end-stage renal disease (ESRD), was dependent on beta 2-glycoprotein I (GPI), a cofactor of aCL. Lupus anticoagulant (LA) was identified in 13/39 hemodialysis (HD) patients. GPI-independent aCL was positive in 12/39 of this group, five of whom had both GPI-independent aCL and LA. Three of the 20 patients on symptomatic and supportive treatment other than HD had LA, but none of them were aCL positive. When GPI was added to the assay system to allow for GPI-dependent aCL measurement, the optical density (OD) readings of 10/12 HD patients decreased, thus proving that they were negative for aCL. In contrast, the OD readings of 6 control patients with systemic lupus erythematosus (SLE) increased markedly (3/6) or decreased slightly to moderately (3/6), however, within the limits of positive range, indicating GPI-dependent cCL positivity. These results suggested that LA and GPI-independent aCL were produced in ESRD patients, especially those on HD, possibly through mechanisms related to the hemodialysis membrane. However, the significance of GPI-independent aCL in this clinical setting, which may differ from the GPI-dependent aCL detected in SLE patients, as well as the possible participation of serum GPI in the production of aCL remain to be clarified.