Search PubMed⌕ Search

Biomedical subjects

C Bowman

Publications and source records attributed to C Bowman.

At least 55 records · Page 3Linked to original sources
PubMed1985

The reduction in the peritonitis rate among high-risk CAPD patients with the use of the Oreopoulos-Zellerman connector.

We have described a prospective controlled study of the Oreopoulos-Zellerman peritoneal dialysis connection system which is based on the principle of chemical sterilization of the connector between each dialysis exchange. This system, in a short-term study of 27 high-risk patients, has resulted in a fourfold difference in the peritonitis rate between the concurrent control group (1/8.8 patient months) and the O-Z group (1/35.7 patient months). The probability of developing peritonitis by 6 mos was 0.15 using the O-Z connector and 0.46 in the control group.

Adult↗
PubMed1985

Clinical application of a radio-immunoassay for auto-antibodies to glomerular basement membrane.

We describe a sensitive radio-immunoassay for auto-antibodies to glomerular basement membrane (GBM). The assay discriminates patients with glomerulonephritis associated with circulating auto-antibodies to glomerular basement membrane from those with other forms of nephritis. Monitoring of antibody levels in sequential serial serum samples enables drug therapy to be tailored precisely to control the aberrant immune response, a situation unique in the management of glomerulonephritis.

Autoantibodies↗
PubMed1984

Autoregulation of autoantibody synthesis in mercuric chloride nephritis in the Brown Norway rat. I. A role for T suppressor cells.

Mercuric chloride injections in the Brown Norway rat induce the transient formation of anti-glomerular basement membrane (GBM) autoantibodies. Transfer of spleen cells from convalescent animals, after circulating anti-GBM autoantibodies are no longer detectable, inhibits reinduction of the disease by HgCl2 in naive recipients. This inhibition is significantly less when the T suppressor cell population is depleted by the monoclonal antibody, MRC OX8 , before transfer. Our studies suggest a role for T suppressor cells in autoregulation in this animal model of autoimmune nephritis and may form a basis for the design of specific therapy for anti-GBM disease in man.

Animals↗
PubMed1984

Recurrence of circulating anti-glomerular basement membrane antibody three years after immunosuppressive treatment and plasma exchange.

A patient with auto-antibody mediated Goodpasture's syndrome was successfully treated with cytotoxic drugs, steroids and plasma exchange. After an absence of three years, circulating anti-glomerular basement membrane antibodies reappeared, and linear IgG staining of the glomeruli was shown by immunofluorescent studies. Renal function did not change and there was no evidence of pulmonary hemorrhage. Antibody levels then fell spontaneously over the succeeding 18 months.

Adult↗
PubMed1983

Anti-glomerular basement membrane autoantibodies in the Brown Norway rat: detection by a solid-phase radioimmunoassay.

A solid-phase radioimmunoassay (RIA) is described for the detection of IgG autoantibodies to glomerular basement membrane (GBM) induced in the Brown Norway rat by mercuric chloride. The assay involves the adsorption of a collagenase digest of GBM to plastic microtitre plates and detection of bound antibody with affinity purified radiolabelled rabbit anti-rat IgG. Comparison with existing immunofluorescence methods for detection of anti-GBM antibody showed that the solid-phase RIA is highly sensitive, allowing detection of antibody in solutions with as low as 0.5 ng protein/ml. The assay is suitable for detection of anti-GBM antibody both in serum and in eluates from nephritic kidneys. The assay proved to be specific in competitive studies of inhibition brought by GBM, keyhole limpet antigen and ovalbumin. This solid-phase RIA is reproducible, robust and easy to perform.

Animals↗
PubMed1983

Effects of cyclophosphamide on autoantibody synthesis in the Brown Norway rat.

The effects of cyclophosphamide on autoantibody synthesis were studied in an experimental model of glomerulonephritis due to autoantibodies to the glomerular basement membrane (GBM). Brown Norway rats develop anti-GBM antibodies, as part of a polyclonal response, when repeatedly injected with mercuric chloride (HgCl2). Anti-GBM antibody levels peak between days 11 and 14 and thereafter rapidly fall; convalescent animals show a time-dependent resistance to rechallenge with HgCl2 which remains significant for up to 3 months. The administration of cyclophosphamide, as a single intramuscular injection at day 0, has three distinct dose-dependent effects on anti-GBM antibody production. Firstly, lower doses (2.5 mg/kg) increase antibody levels at the time of peak response; secondly, higher doses (greater than or equal to 20 mg/kg) prevent antibody synthesis following HgCl2; and thirdly, the higher doses also reduce the response to rechallenge with HgCl2 3-4 months later. These effects of cyclophosphamide also apply to the polyclonal response to HgCl2, as judged by measurement of total IgG concentrations. Further investigation of the mechanisms of action of cyclophosphamide in this model should provide information relevant to the treatment of human autoimmune disease.

Animals↗
PubMed1981

Lymphocytotoxic activity in primary glomerulonephritis: evidence for immune complex-mediated cytotoxicity.

Sera from 84 patients with primary glomerulonephritis (GN) were tested for lymphocytotoxic activity (LCA) against panels of (a) normal peripheral lymphocytes and (b) B-lymphocytes obtained from patients with chronic lymphatic leukaemia (CLL). Significant LCA was found particularly in minimal change GN, acute post-streptococcal GN (AGN-PS) and mesangiocapillary GN (MCGN) where 62%, 75% and 45% respectively of samples were positive. No correlation was observed between LCA and levels of C3 or immune complexes. All but three positive sera showed reactivity against T and B cells; these three showed only T cell cytotoxicity. Fractionation of 6 sera (2 minimal change GN; 2 AGN-PS; 2 MCGN) on Sephadex G200 showed cell killing to reside in the exclusion peak. When samples were separated under dissociating conditions at pH 3.0, there was significant reduction in LCA (P less than 0.001) compared to that of fractions collected at pH 7.2. The same protocol did not affect the lymphocytotoxicity of anti-human lymphocyte globulin. The data suggest that lymphocyte killing in GN is mediated at least in part by antigen/antibody complex activity. The reaction is immunochemically similar to that seen in systemic lupus erythematosus and may have comparable implications for antibody regulation in GN.

Antigen-Antibody Complex↗
PubMed1980

Electrophoretic injection of a fluorescent dye into giant mitochondria and mitoplasts.

Studies of the electrical properties of giant mitochondria and mitoplasts with microelectrodes have indicated that there are no significant metabolically dependent membrane potentials. The internal location of the microelectrode has been confirmed by electrophoretically microinjecting the water-soluble dye Lucifer yellow CH into giant mitochondria or mitoplasts.

Animals↗
PubMed1980

Studies of lymphocytotoxins in infectious mononucleosis and systemic lupus erythematosus: evidence for immune complex-mediated cytotoxicity.

The hypothesis that serum lymphocytotoxins are antigen-antibody complexes was examined. High molecular weight fractions from the sera of eighteen patients with infectious mononucleosis (IM), thirteen patients with systemic lupus erythematosus (SLE) and six healthy controls, were prepared by precipitation with polyethylene glycol 6000 (PEG). The lymphocytotoxic activity (LCA) of these PEG precipitates was significantly greater (P less than 0.01) than that of the corresponding sera and a significant correlation (r = 0.66, P less than 0.01) was observed between the LCA of sera and the PEG precipitates. In contrast to the concentration of LCA in the PEG precipitates, the heterophil antibody titres of the precipitates from IM sera were significantly less (P less than 0 05) than serum titres. Antisera raised against PEG precipitates from sera from nine patients with IM contained significant LCA. The nature of this LCA differed from that of the LCA in the original sera in temperature dependence and the molecular size. Antigen-antibody complexes in seven sera (four IM, three SLE) were dissociated at low pH (3.0) and fractionated by gel filtration at pH 3.9. The LCA of these fractions was compared with the LCA of equivalent fractions obtained by gel filtration at pH 7.2. The heterophil antibody present in sera from patients with IM and the cytotoxicity of anti-lymphocyte globulin (ALG) were used as 'antibody controls'. In this way it was shown that the LCA in patient sera, but not heterophil antibody or ALG cytotoxicity was significantly reduced (P less than 0.001) by low pH gel filtration.

Antigen-Antibody Complex↗
PubMed1979

Cation transport and membrane potential properties of primary astroglial cultures from neonatal rat brains.

This paper describes K+ and Na+ content and transport in primary monolayer cultures from dissociated newborn rat brains, considered to consist predominantly of astroglial cells. Net changes in cation content after addition of ouabain, and steady state fluxes using 86Rb+ as a marker for K+ and 22Na+ as a marker for Na+, were measured. The results found indicate that the cells maintained a conventional pattern of cation homeostasis with net efflux of K+ being balanced by its active uptake and net uptake of Na+ balanced by active extrusion mediated by a ouabain sensitive (Na+K) pump. These processes maintained internal measured K+:Na+ ratios of 12--25:1. The cells were normally flat but addition of DBcAMP caused them to round up and form numerous processes, an appearance resembling that of astroglial cells in vivo. DBcAMP treatment also reduced the steady state levels of K+ measured with 86Rb+ by 15--30%, and had no effect on initial rates of 86Rb+ and 22Na+ uptake. The membrane potentials of cells treated with DBcAMP were studied, since only these were easily impaled. The membrane potentials of separate groups of cells gave means ranging from --65 to --75 mV at 35 degrees C, at an external K+ concentration ([K+]o) of 4.5 mM. The dependence of the membrane potentials of individual cells and groups of cells on [K+]o was studied. The slope of the potential per 10-fold change in [K+]o was 55--57 mV, at concentrations of K+ greater than 10--20 mM K+, and diverged from this slope at concentrations below this. This shows that these cells had some permeability to ions other than K+. Assuming that Na+ was the only other ion affecting the membrane potential, it was calculated that the permeability to Na+ was about 30 times less than K+. A similar result was obtained based on estimates of Na+ and K+ permeability from transport experiments on cells also treated with DBcAMP. The results obtained from these cells are compared to those found for other cultured glial cells and glial cells in vivo. We conclude that the membrane potentials of the cultured cells used in the present study show the closest resemblance so far to glia in vivo, since they are large and negative and are determined mainly by K+. However, the cultured cells have different properties from those reported in some studies for glial cells in vivo by showing free permeability to ions other than K+.

Animals↗
PubMedDate not supplied

Parotid salivary secretion in diabetic autonomic neuropathy.

Parotid salivary flow rates and amylase concentrations were measured in three groups of eight subjects each (normal control, non-neuropathic diabetic, and neuropathic diabetic). Flow rates were significantly reduced in neuropathic diabetic patients as compared with normal controls (p less than 0.001) and non-neuropathic diabetic patients (p less than 0.02). Amylase concentrations were similar. These data are consistent with parasympathetic denervation of the parotid gland in diabetic neuropathy and provide evidence for a widespread distribution of autonomic denervation in diabetes.

Adult↗