[Usefulness of the CT and US for the diagnosis of the hepatic abscess (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Sumiya.
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A 29 year old female with systemic lupus erythematosus had a splenic infarct. The echogram showed a 4 x 4 x 5 cm cluster of echoes. After splenectomy the preoperative echograms were matched to the gross pathological findings and a post mortem water bath scan. In this single patient, the echosplenograms were of considerable aid in confirming the accuracy of the diagnosis of splenic infarct.
Initiation and localization of the capacity of self-differentiation in the 1-2 day old chick embryo were studied by means of culturing endoderm fragments, wrapped in a piece of viteline membrane and completely deprived of mesenchyme.
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OBJECTIVE: To clarify the pathogenetic role of autoantibodies against U1-RNP (ribonucleoprotein) (anti-U1-RNP) in mixed connective tissue disease (MCTD), we examined whether supernatants of monocytes which were stimulated with anti-U1-RNP could induce the production of proinflammatory cytokines by human pulmonary artery endothelial cells (HPAECs). METHODS: Monocytes from MCTD patients (n = 11) and normal volunteers (n = 11) were stimulated with purified antibodies against U1-RNP or double-stranded DNA and their supernatants were added to cultures of HPAECs. Cell-associated cytokines were assayed by an enzyme-linked immunosorbent assay. RESULTS: The supernatants of anti-U1-RNP-stimulated MCTD monocytes significantly up-regulated the cell-associated production of IL-1 alpha (p < 0.01) and IL-6 (p < 0.01) by HPAECs compared with their production by normal IgG-stimulated MCTD monocytes, whereas the cell-associated production of IL-1 beta and TNF-alpha by HPAECs was not up-regulated. The supernatants of anti-U1-RNP-stimulated monocytes from normal volunteers similarly up-regulated the cell-associated production by HPAECs of IL-1 alpha (p < 0.01) and IL-6 (p < 0.01), but not of IL-1 beta and TNF-alpha. Supernatants of monocytes stimulated with the F(ab')2 preparation of anti-U1-RNP antibodies enhanced the amounts of both Il-1 alpha and IL-6 associated with HPAECs almost as effectively as those stimulated with intact autoantibody molecules. Inhibition experiments employing specific anti-cytokine antibodies of anti-U1-RNP-stimulated monocyte supernatants suggested that soluble factors, including cytokines, in monocyte supernatants could enhance the cytokine association with HPAECs. CONCLUSION: Up-regulation by anti-U1-RNP autoantibodies of proinflammatory cytokines associated with vascular endothelial cells may play a role in the immunopathological processes leading to proliferative vasculopathy, a characteristic of MCTD.
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The lymphocytes from the patients with primary immunodeficiency diseases and those under immunosuppressive conditions such as viral infection or administration of antimetabolites were studied by various parameters of T- and B-lymphocytes. T-lymphocyte specific antigen, spontaneous rosette formation with sheep erythrocytes, phytohaemagglutinin response of the lymphocytes and delayed hypersensivity skin reaction were used to assess T-lymphocytes, while complement receptor, surface immunoglobulin, serum immunoglobulin levels and antibody response to antigens were estimated as parameters of B-lymphocytes. 9 of infantile agammaglobulinemia, 8 severe combined immunodeficiency, 5 ataxia telangiectasia, d Di-George syndrome, 11 common variable immunodeficiency, 3 isolated IgA deficiency and 4 cases thymectomized more than 10 years previously were studied and discussed for the results. The peripheral blood lymphocytes, especially T-lymphocytes were reduced in the acute stage of measles infection, while they were increased in infectious mononucleosis caused by EB (Epstein-Barr) virus. Atypical lymphocytes observed in the later disease seemed to originate from mainly T-lymphocytes. Cyclophosphamide had suppressive effect selectively on B-lymphocytes.
OBJECTIVE: To determine the clinical significance of serum lipoprotein(a) [Lp(a)] levels in patients with systemic lupus erythematosus (SLE). METHODS: Serum Lp(a) levels in 77 patients with SLE were measured by turbidimetric immunoassay. RESULTS: The median serum Lp(a) levels in all the SLE patients (14.4 mg/dl) and in those with active disease (Group A; 19.6 mg/dl, n = 39) at admission were significantly higher than those in healthy subjects (11.9 mg/dl, p < 0.05 and p < 0.001, respectively). The serum Lp(a) levels in SLE patients correlated directly with the serum cholesterol (p < 0.001) and urinary protein (p < 0.001) levels and inversely with the serum albumin levels (p < 0.02). Analysis limited to Group A patients with renal disease (Group A + RD, n = 28) revealed that the median serum Lp(a) level at the time of admission (OM) was significantly higher than those at 6 months before (-6M, p < 0.01) and at 6 months after admission (+6M, p < 0.01). Moreover, the serum Lp(a) level decrease from 0M to +6M in Group A+RD correlated significantly with the serum albumin level increase (p < 0.05). Multiple regression analysis demonstrated that the serum albumin level increment, the SLEDAI score decrement, the cholesterol level at 0M and the total dose of oral corticosteroids administered during the 0M to +6M period contributed independently and significantly to the serum Lp(a) level decrement from 0M to +6M in Group A + RD. CONCLUSION: Our study is the first to reveal that hypoalbuminemia appearing during disease flare plays an important role in increasing the serum Lp(a) levels in lupus patients with renal disease and shows that corticosteroid treatment reduced the elevated serum Lp(a) levels almost to original levels.
A 21-year-old woman with a 6-year history of SLE presented with a speech disturbance and right hand clumsiness along with manifestations of active disease suggesting central nervous system SLE. Despite aggressive treatment for SLE, her neurological condition worsened. MRI demonstrated low intensity in T1-weighted images and high intensity in T2-weighted images in the white matter of the bilateral cerebrum and cerebellum, compatible with progressive multifocal leukoencephalopathy (PML). Intraspinal administration of interferon-beta seemed to slow the deterioration of her MRI and neurological findings. However, she eventually developed decerebrate rigidity and died due to candidemia. DNA of the JC virus was detected in the autopsied brain by the polymerase chain reaction technique. PML should always be borne in mind when examining patients with SLE showing neurological abnormalities.
OBJECTIVE: To determine the matrix metalloproteinase-3 (MMP-3) levels in sera from patients with systemic lupus erythematosus (SLE) and to analyse the relationships between MMP-3 and clinical and laboratory features. METHODS: Serum MMP-3 levels were measured by an enzyme immunoassay in 124 patients with SLE and 237 patients with other systemic rheumatic diseases. RESULTS: The frequencies of patients with high MMP-3 levels were 76% in SLE and 82% in rheumatoid arthritis (RA). The level of MMP-3 in the SLE patients was 193.0 +/- 171.5 ng/ml (mean +/- SD) and was almost equal to the level in the RA patients (259.5 +/- 255.6 ng/ml). The MMP-3 levels were significantly higher in SLE patients who had a history of the following abnormalities: persistent proteinuria, cellular casts, anti-double stranded DNA antibodies, decreased C3, decreased creatinine clearance (p < 0.001), circulating immune complex (p < 0.01), malar rash, hypoalbuminemia, or decreased C4 (p < 0.05). The serum MMP-3 level in patients with SLE at admission showed direct correlations with serum uric acid, total cholesterol (p < 0.001), triglyceride, the white blood cell count, and the neutrophil count (p < 0.05), as well as inverse correlations with the total protein (p < 0.01), and IgG (p < 0.05). In SLE patients with active renal disease, the median MMP-3 level at admission and that at 6 months after admission were significantly higher than that at 6 months before admission. CONCLUSIONS: The increased level of serum MMP-3 in SLE is closely associated with clinical features relevant to lupus nephritis, suggesting that it plays a role in the pathogenesis of this condition.