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Biomedical subjects

M Wakashin

Publications and source records attributed to M Wakashin.

At least 37 records · Page 2Linked to original sources
PubMed1986

Experimental systemic amyloidosis induced by immunization with syngeneic organ extracts in mice.

Systemic amyloidosis was induced consistently in mice by intramuscular injection of syngeneic organ (liver and kidney) extracts mixed with CFA six times at weekly intervals. Syngeneic organ extract with CFA also induced amyloidosis of a lesser degree. All three strains of mice (C57BL/6, C3H/He, and BALB/c) injected with a syngeneic liver extract mixed with CFA developed systemic amyloidosis; the most prominent amyloid deposition occurred in C57BL/6 (B6) mice, followed by C3H/He and BALB/c. The amyloid substance deposited in these animals was identified as mouse amyloid A protein (AA). Furthermore, an organ specificity of the immunogen in inducing amyloidosis was suggested with liver and kidney extracts. Primed spleen cells of the immunized B6 mice were fractionated by a nylon-wool column and injected to normal recipient mice via the tail vein. Organs of the recipient mice developed systemic amyloidosis 8 wk after the transfer, and the most prominent histological changes occurred in the recipient mice given nylon-wool column adherent spleen cells. Using anti-Thy-1,2; Ly-1; Ly-2, antibody and complement, it was suggested that T cells, especially Ly-1,2,3+ T cell populations in the primed nylon-wool adherent cells, play an important role in the induction of systemic amyloidosis. It was shown further that the amyloidosis-inducing substance in liver extract was composed of unstable proteins or protein-bound substance.

Amyloidosis↗
PubMed1986

Experimental gold nephropathy in guinea pigs: detection of autoantibodies to renal tubular antigens.

Renal tubular dysfunction was induced in Hartley guinea pigs by injection of sodium aurothiomalate (gold) as manifested by excretion of tubular basement membrane (TBM) antigen and renal tubular epithelial (RTE) antigen in urine and tubular proteinuria. Following the tubular dysfunction, autoimmune tubulointerstitial nephritis (TIN) and/or immune complex nephropathy (ICN) developed in a large proportion of animals. TIN was associated with anti-TBM antibodies, and the histological features were characterized by tubular lesions with interstitial mononuclear cell infiltration, destruction of tubules, and interstitial fibrosis. In ICN, the glomerular lesions consisted of partial thickening of capillary walls and mesangial cellularity, and granular immune deposits were seen in the mesangial area and on capillary walls. Furthermore, electron-dense deposits were demonstrated in the mesangial area and in the glomerular basement membrane (GBM) by electron microscopy. Anti-RTE antibodies were detected in the sera and eluates from the kidney of animals with ICN. RTE antigens were also detected in the glomerular deposits by indirect immunofluorescence using anti-guinea pig RTE antibody. These results suggest that TBM and RTE antigens released from renal tubules damaged by a direct toxic action of gold may lead to antibody formation against these antigens and induce TIN and/or ICN.

Animals↗
PubMed1985

Study of cellular immunity in experimental autoimmune hepatitis in mice: transfer of spleen cells sensitized with liver proteins.

This study was based on our model of experimental autoimmune hepatitis produced by immunizing C57BL/6 (B6) mice with syngeneic liver proteins and Freund's complete adjuvant. Spleen cells obtained from these hepatitis mice were transferred to syngeneic normal recipient mice, and histological changes occurring in the liver and the role of cellular immunity in producing liver damages in recipient mice were investigated. Sensitized spleen cells from these immunized (donor) mice were fractionated by a nylon wool column and injected intravenously into normal B6 mice. Histology of the liver of the recipient mice showed mild infiltration of mononuclear cells around the periportal area 7 days after the transfer of sensitized spleen cells, and changes were most prominent in the mice injected with the fraction of nylon wool column adherent spleen cells. Induction of these liver lesions in the recipient mice was blocked by treatment of sensitized donor spleen cells with anti-Thy 1,2 monoclonal antibody and guinea pig complement before injection. Lymphocyte reactivity to liver-specific lipoprotein (LSP) in recipient mice was studied by a lymphocyte transformation system, and a high immune response was demonstrated with the fraction of nylon wool column non-adherent (T-enriched) spleen cells. These data seem to indicate T-cell interactions between donor and recipient mice in the transfer study using our experimental autoimmune hepatitis model.

Animals↗
PubMed1984

Hashimoto's thyroiditis and membranous nephropathy developed in progressive systemic sclerosis (PSS).

A case of a 36-year-old woman with progressive systemic sclerosis (PSS) was reported. The patient had two additional immune-mediated diseases: Hashimoto's thyroiditis and membranous nephropathy. It was implicated that overlapping of systemic lupus erythematosus (SLE) occurred in the course of PSS. Notably, immune complex deposition along the follicular basement lamina of the thyroid was suggested by immunofluorescence and electron microscopy. Although the glomerular lesion was in general accord with membranous nephropathy, it was complicated by occasional crescent formations and necrotic arterial changes, probably resulting from malignant hypertension that appeared during the terminal stage. It was implied that the same circulating antigen-antibody complexes might have been involved in the pathogenesis of Hashimoto's thyroiditis and membranous nephropathy in this case.

Adult↗
PubMed1984

Study of cellular immunity in experimental autoimmune hepatitis in mice.

This study was undertaken to produce experimental autoimmune hepatitis in mice, and to examine the role of liver specific lipoprotein (LSP), if any, and of cellular immunity in such a model. After immunization of three strains of mice (C57BL/6, C3H/He and BALB/c) with syngeneic crude liver proteins, most prominent liver changes histologically mimicking human hepatitis were produced in the liver of C57BL/6 (B6) mice. Antigenic and immunogenic activity of LSP in the crude liver proteins was decreased by the treatment of freezing and thawing, and the recovery of the antigenic activity seemed to correlate with the susceptibility of immunized mice to the induction of liver damage. Autoantibody against LSP was demonstrated in the serum of immunized B6 mice, but not in the sera of other strains after immunization. It was also found that EDTA contained in the buffer used for purification of LSP distinctly suppressed lymphocyte activity in vivo and in vitro. With the use of EDTA free LSP, it was shown that spleen cells of immunized B6 mice (especially of T cell enriched fraction) had a high reactivity studied by lymphocyte transformation test. Further examination showed that EDTA free LSP could induce mild liver lesions and lymphocyte reactivity against LSP, although neither histological change nor lymphocyte reactivity was found in the liver of B6 mice immunized with EDTA containing LSP.

Animals↗
PubMed1984

Renal tubular disturbances induced by tributyl-tin oxide in guinea pigs: a secondary Fanconi syndrome.

Painting of tributyl-tin oxide on the skin induced a secondary Fanconi syndrome in guinea pigs. In the urine of these animals, excretion of sodium, chloride, phosphate, glucose and many kinds of amino acids increased and reached a maximum between day 40 and 50. In sera, the concentrations of phosphate and certain amino acids were low due to excessive loss into urine. Histological examination of the kidney revealed damage to the tubular epithelium with no glomerular change. It was also found that cytochrome P-450 in the kidney and 1-25-dihydroxy vitamin D in serum were reduced in the tin-treated animals. It is most likely that tributyl-tin oxide caused a secondary Fanconi syndrome as defined by renal tubular disturbances represented by glucosuria, generalized amino aciduria, phosphaturia, and hypophosphatemia.

Administration, Topical↗
PubMed1982

Effect of hypertension on lipid metabolism and beta-oxidation in rat aorta and brain microvessels.

The effects of hypertension on various enzyme activities involved in lipid metabolism and beta-oxidation in rat brain microvessels and aorta were studied. The purity of the brain microvessel preparation was confirmed immunologically and microscopically. Activities involved in lipid synthesis, such as triacylglycerol synthesizing activity, acyl-CoA synthesizing activity, acyl-CoA: cholesterol acyltransferase and cytidine diphosphate choline:1,2-diacylglycerol cholinephosphotransferase, were significantly higher in brain microvessels than in aorta in both normotensive and hypertensive rats; lipid hydrolyzing activities, such as lipases and cholesterol esterases, were similar in the two preparations. beta-oxidation in brain microvessels was more active than in aorta in both groups. Hypertension did not alter these enzyme activities in either aorta or brain microvessels, or change beta-oxidation in the aorta. However beta-oxidation in brain microvessels was significantly lower in hypertensive rats than in normotensive rats. These results suggest that brain microvessels are metabolically more active than aorta, and that their beta-oxidation activity is more susceptible to effects of hypertension. Reduced beta-oxidation in brain microvessels might lead to angionecrosis by derangement of energy production, which in turn may cause cerebral bleeding.

Animals↗
PubMed1982

Renal tubular dysfunction as a complication of gold therapy in patients with rheumatoid arthritis.

Forty-five patients with uncomplicated rheumatoid arthritis and 45 control individuals were subjected to immunochemical investigation of the urinary excretion of renal tubular basement membrane antigen (TBM), renal tubular epithelial antigen (RTE), and beta-2-microglobulin. Tubular proteinuria occurred significantly more frequently in patients treated with gold salts than in those not treated (P less than 0.05). Large amounts of RTE and TBM were detected only in the urine of patients who received gold salt therapy. However, the amounts of these proteins in urine did no correlate with the total dose of gold. These results indicate that renal tubular damage frequently occurs in patients with rheumatoid arthritis who are treated with gold salts; the tests outlined are useful in detecting renal tubular disorders developing during gold salt therapy and have certain advantages over routine urinalysis.

Adult↗
PubMed1981

Low molecular mass IgM in urine of patients with primary and secondary renal diseases.

Urine specimens from 50 patients with various renal diseases and from 10 normal subjects were examined for the presence of low molecular mass (7S) IgM by double diffusion, using a specific anti-7S IgM serum. 7S IgM in urine was also quantitated by radial immunodiffusion in 5% polyacrylamide gel. It was found with high frequency in the urine of patients with secondary renal diseases associated with multi-system immunological disorders, especially in systemic lupus erythematosus. Two of the patients with lupus nephritis and positive results for 7S IgM in urine were initially diagnosed as nephrotic syndrome due to a primary renal disease; the symptoms and signs of systemic lupus erythematosus developed later. However, 7S IgM was not detected in the urine of patients with primary renal diseases (except for two cases of nephrotic syndrome), nor in normal subjects. Thus detection of 7S IgM in urine may be helpful in the differential diagnosis of primary and secondary renal diseases.

Acrylic Resins↗
PubMed1981

Purification and immunological characterization of human liver-specific F antigen.

Human liver specific F antigen has been purified from human liver and characterized by immunochemical and physicochemical procedures. Specific antisera were prepared by immunizing guinea pigs with the purified human F antigen. The purified F antigen had a molecular mass of approximately 80000 daltons. Using the immunodiffusion technique, it was shown that human F antigen has at least two antigenic determinants; one is species non-specific and the other human specific. This human specific determinant was also found in the liver of rhesus monkey but not in the liver of the other mammals tested. Using purified human F antigen and antibody against the human specific determinant, F antigen can be quantitated in serum and may prove to be of clinical value.

Animals↗