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Biomedical subjects

I Ríha

Publications and source records attributed to I Ríha.

6 recordsLinked to original sources

Thy 1 expression in the brain of nude mice.

The expression and cell distribution of Thy 1 antigen was studied in the brain of both normal and athymic (nude) young adult mice of the BALB/c strain by immunochemistry. In nude animals Thy 1 fluorescence was less intense and less regularly distributed in the molecular layer of the cerebellum and hippocampus. Thy 1 content determined by ELISA was lower by 10-16% in the cerebellum and 20-25% in the olfactory bulbs of nude mice. The total wet weight of the brain was lower by 16% than in control animals; the deficit in body weight ranged from 34-45%. It is supposed that the changes in Thy 1 expression in nude animals are caused mainly by the underdevelopment of late developing brain regions due to thermoregulatory problems and other postnatal strains occurring in the mutants.

Animals

Experimental ablation nephropathy. Fine structure, morphometry, cell membrane epitopes, glomerular polyanion and effect of subsequent transplantation.

The subtotal (5/6) nephrectomy performed in 23 adult female rats induced severe hypertrophy of residual parenchyma with interstitial fibrosis, tubular dilatation, and focal and segmental glomerulosclerosis (FSG). This ablation nephropathy (AbN) caused proteinuria, progressive renal failure, and hypertension. The extent of FSG was assessed by semiquantitative scoring. The ultrastructure revealed widespread foot process fusion, many dense cytoplasmic inclusions in podocytes, and degenerative changes or disruption of mesangium with glomerular "microcysts". Numerous granular deposits of rat Ig were seen in the glomeruli but a short praeterminal i.v. load by heat-aggregated human Ig did not alter the morphology of AbN and produced discrete and inconstant glomerular deposits. Similarly an i.v. injection of protamine and heparin generated protamine-heparin complexes seen in various layers of glomerular capillary wall, similar to those found previously in normal rats. AbN displayed a partial irregular depletion of polyanion sites reactive with polyethylenimine in lamina rara externa. A significant increase in both glomerular and interstitial Ia+ cells and a marked predominance of W3/25+ cells in the interstitial infiltrates were documented by immunohistochemistry in the remnant kidneys. Both AbN and FSG could be largely corrected (or prevented?) by subsequent syngeneic renal transplantation (TPL; 6 animals). On the other hand a severe AbN was found in two post-ablation residues after unsuccessful TPL with graft necrosis or sclerosis.--AbN has some analogies to various chronic human nephropathies (e.g. FSG) and may explain their progression to the terminal failure. Degenerative and finally destructive mesangial lesion seems to be of prime importance in AbN.

Animals

Omental dendritic cells: Ia expression and relation to macrophages.

Rat omental dendritic cells (ODC) occur in two forms, mainly spindle-shaped, Ia-, on the surface, and stellar, Ia+ within the omentum. Like macrophages, most ODC label with W3/25 mAb and have a demonstrable activity of non-specific esterase, acid phosphatase and ATPase. Up to 30% of ODC are actively phagocytic. The proportion of Ia+ ODC rises 7 days after ip antigenic stimulation and there seems to be a reciprocal development of Ia positivity and phagocytic capacity between ODC and macrophages 3 and 5 days after ip immunization. ODC contribute to the overall fluctuation of Ia expression in the entire omentum after immunization. Ia+ ODC display a linear arrangement along preilymphatic spaces and may be related to the formation of new lymph vessels. They also constitute the stroma of pseudofollicles containing clusters of what are presumably T-helper lymphocytes closely attached to ODC, scattered suppressor T lymphocytes and B cells accumulating in later stages at the immune response.

Acid Phosphatase

Simple method of circulating immune complex detection in human sera by polyethylene glycol precipitation.

A rapid test for detection of circulating immune complexes in a small serum sample was developed to facilitate clinical diagnosis of immune complex disorders. The test is based on a selective precipitation of soluble circulating complexes of antigen-antibody in 3.75% concentration of high-molecular polyethylene glycol. Precipitation is followed photometrically at 450 nm, 1 cm cuv. after 1 h incubation at room temperature. Comparison of E450 values in groups of patients with immune complex disorders, such as rheumatoid arthritis, systemic lupus erythematosus and glomerulonephritis, with healthy controls or patients with non-immunological disorders revealed highly significant differences. Sera of all patients with high clinical activity of disease exhibited positive reaction. In 121 human sera the results of this examination were compared with the results of C 1 q binding test. There was 73.5% agreement between the results of both methods. Our test is more rapid, suited for routine clinical use.

Antigen-Antibody Complex

Experimental immune complex glomerulopathy: immunomorphological aspects and correlations with human disease.

Thirteen rabbits received parenteral injections of human serum albumin (HSA) in regular doses and intervals during 6-32 seeks. The antigen load elicited immune responses of variable degree, giving a good correlation with the extent and quality of immune complex (IMC) deposition, as shown by immunological methods, electron and fluorescence microscopy and by histoautoradiography. Morphology of immune deposits (IMD) depended on the composition of the IMC and produced a continuous scale of glomerular involvement, ranging from minimal and focal to massive and diffuse deposition. Probable rudimentary traces of IMD were apparent in the ultrastructure even in animals with negative results of both immunological and immunfluorescence examinations. The relationships are discussed between experimental IMC-induced glomerulopathy on the one hand, and some problems of development and bioptic evaluation of human glomerulonephritis.

Animals