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Biomedical subjects

M K Jasani

Publications and source records attributed to M K Jasani.

At least 37 records · Page 2Linked to original sources
PubMed1981

Effect of inflammatory arthritis on dexamethasone receptors in phagocytes--a possible role for plasma factors.

Synovial tissue cells from patients with seropositive rheumatoid arthritis bind dexamethasone in a similar fashion to the classical steroid receptors on other cells. In contrast, synovial fluid cells and blood PMNLs from these patients bind dexamethasone with much reduced affinity. Some component of plasma may interfere with the binding of dexamethasone to its receptor.

Arthritis, Rheumatoid↗
PubMed1980

Models of immune complex disease.

An inflammatory lesion commonly develops in certain organs (e.g. skin, brain, kidneys and joints) either when antigen in the tissue spaces reacts with precipitating antibody forming microprecipitates in and around small blood vessels or when antigen in excess in the blood stream reacting with potentially precipitating antibody forms immune complexes (ICs) that lodge in the blood vessels. Other factors known to be essential for the pathogenesis of such lesions include (a) the activation of complement components, (b) chemotaxis towards ICs of PMN leucocytes and macrophages, (c) phagocytosis of ICs and (d) the formation and release by the phagocytes of prostaglandins, lysosomal enzymes, toxic metabolites of oxygen and other mediators of inflammation and tissue damage. Knowledge of these pathogenetic mechanisms opens up possibilities for chemotherapeutic attenuation or abolition of the development of antibody-dependent inflammatory lesions. The extent to which this goal has been achieved in the clinic with the aid of substances selected through the use of models of immune complex disease will be reviewed in this presentation.

Adrenocorticotropic Hormone↗
PubMed1979

Prostaglandins, rheumatoid arthritis, fibrin and lymphoedema.

Rheumatoid joint swelling is in part due to lymphoedema accompanying extravascular (E-V) deposition of fibrin. Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin (ASA), phenylbutazone (PBZ) and indomethacin (INDO) which share the ability to inhibit prostaglandin synthetase fail to prevent fibrinous lymphoedema occurring in rabbit skin homografts in association with the presence of sensitised lymphocytes. The data highlight the need to define whether or not prostaglandins promote lymphocytic fibrinous lymphoedema.

Animals↗
PubMed1978

Characterization of two acid proteinases found in rabbit skin homografts.

Two types of acid proteinase activity found in rabbit skin homografts were characterized by studying the effect of temperature, pH and polyacrylamide-gel electrophoresis. Their chromatographic behaviour was characterized on DEAE-cellulose, Sephadex G-75, G-100 and G-200, and their molecular weights were estimated by gel filtration. One of the acid proteinases in the homograft resembled cathepsin D (EC 3.4.23.5) of normal skin. The other acid proteinase differed from cathepsin D with respect to heat inactivation, pH optimum and molecular weight; it was not inactivated on heating at 60 degrees C for 60 min, its pH optimum was 2.5 and its molecular weight measured by Sephadex G-100 chromatography was 100 000. In all these respects, the heat-stable proteinase resembles cathepsin E (EC 3.4.23.5) of rabbit polymorphonuclear leucocytes.

Animals↗
PubMed1977

'Morphology of immune lymphocytes in homograft lymph'.

Uropod-bearing lymphocytes (UBLs) resembling cytotoxic cells found in vitro were identified in lymph collected from rabbit hind-limbs bearing homografts. UBLs were found in lymph leaving the regional lymph node (efferent), both before and after rejection, but not in that draining the homograft (afferent) even though they were present in the graft tissue itself. UBLs may represent the sub-class of immune lymphocytes which induce necrosis of the grafted cells. Mitotic lymphocytes and cells resembling lymphocytes transformed by phytohaemagglutinin were also found in efferent homograft lymph.

Animals↗
PubMed1975

Bone loss in patients with rheumatoid arthritis.

Both male and female patients with rheumatoid arthritis show a significant bone loss in the femur, compared with the loss of bone seen in normal subjects with increasing age. A very similar pattern is seen in corticosteroid treated patients with rheumatoid arthritis. There is no evidence to suggest that the corticosteroid therapy has caused a greater loss of bone from the femur than would have occurred as a result of the rheumatoid arthritis alone. There was a statistically significant relation between the duration of the rheumatoid arthritis and femoral bone lo-s in women over the age of 45 years, whether or not they had been given steroid therapy in both male and female patients over 45 years of age, but again it appears unlikely that corticosteroid therapy had contributed significantly to the femoral bone loss. The Metacarpal and Femoral Indices of the patients were significantly related in both male and female groups.

Adrenal Cortex Hormones↗