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Biomedical subjects

C L Hall

Publications and source records attributed to C L Hall.

At least 19 recordsLinked to original sources
PubMed1991

A nuclear magnetic resonance study of the glucose metabolism of Hymenolepis diminuta exposed to histamine and serotonin in vitro.

The direct effects of the inflammatory mediators, histamine (HI) and serotonin (SE), on the glucose metabolism of Hymenolepis diminuta in vitro were studied by analyzing the excretory products from culture media, containing D-1-13C-glucose and various concentrations of HI and/or SE, by 1H-nuclear magnetic resonance (n.m.r.) spectroscopy. The results revealed that HI markedly accelerated the glycolysis process by increasing the amount of lactate production. The increased glycolytic activity was reflected in a concentration-dependent increase in glucose uptake. Excretion of acetate was also stimulated by HI. A low concentration of SE significantly increased succinate, acetate and lactate excretions, whereas a high concentration had little effect on lactate production and significantly decreased succinate and acetate excretions. A combination of HI and SE treatment at a low concentration had no significant effect, but at a high concentration showed an additive effect, with an increase in lactate production, a decrease in succinate production and an increase in glucose uptake. Thus this work confirms that HI and SE directly influence, albeit differently, energy metabolism of the tapeworm H. diminuta.

Animals↗
PubMed1990

Atypical antiglomerular basement membrane disease associated with thin membrane nephropathy.

Antiglomerular basement membrane (anti-GBM) disease is characteristically described with linear deposition of IgG along the GBM. We report two unusual cases of IgA and IgM anti-GBM disease associated with diffuse thinning of the GMB, and review the literature on atypical immunoglobulin species in this disorder. Both patients were male, aged 55 and 49 years, and presented with isolated microscopic haematuria, neither having shown evidence of impaired renal or pulmonary function on follow-up for 4 and 6 years respectively. Renal histology revealed minor focal mesangial changes only, but immunoperoxidase preparations demonstrated intense linear staining of the GBM with IgA in one case, and IgM with C3 in the other. On electron-microscopy there was diffuse thinning of the GBM in both cases, mean thickness 220 and 295 nm respectively (normal range 350-450 nm). Antinuclear antibodies were not detected and their glucose tolerance tests were normal. Assays for circulating IgG anti-GBM antibodies using indirect immunofluorescence (IF) and radioimmunoassay (RIA) were negative in both patients, although IgA anti-GBM antibodies with specificity confirmed by inhibition studies were identified in the first case. Thin GBMs in these patients may expose the Goodpasture antigen to toxic or infectious insults, thus altering its antigenic profile and promoting this unusual immune response.

Autoimmune Diseases↗
PubMed1979

Radioimmunoassay for Gram-negative bacterial lipopolysaccharide O antigens: influence of antigen solubility.

We have developed a solid-phase radioimmunoassay technique for specific gram-negative bacterial lipopolysaccharide (LPS) O antigens. The method exploits the high-titer, specific immunoglobulin M response of the rabbit to LPS immunization to measure as little as 5 ng of homologous LPS per ml with less than 0.5% cross-reactivity toward heterologous LPS or culture supernatants. We found that O antigen in complete LPS was less available for antibody binding than O antigen in the soluble polysaccharide derived by mild acid hydrolysis of LPS and that triethylamine-induced disaggregation of complete LPS increased its activity in the assay. Quantitation of O antigen with the assay was thus influenced by the physical state of LPS or "free" O antigen.

Escherichia coli↗
PubMed1979

Origin of urinary fibrin-fibrinogen degradation products in renal glomerular disease.

The origin and mechanism of renal clearance of urinary 'fibrin-fibrinogen degradation products' (FDP) were studied in patients with renal glomerular diseases associated with heavy, non-selective proteinuria and high levels of urinary FDP. The results indicated that the urinary FDP arose primarily by the filtration of unaltered plasma fibrinogen through a damaged and abnormally permeable glomerular basement membrane and that a variable degree of lysis of the filtered fibrinogen occurred in the urine. The lysis of cross-linked fibrin in intraglomerular deposits, as evidenced by the presence of dimeric fragment D in the urine, appeared to contribute only a small amount to the total urinary FDP excretion.

Electrophoresis, Polyacrylamide Gel↗
PubMed1978

Circulating immune complexes in Hodgkin's disease.

Levels of circulating immune complexes (CIC) in the serum of patients with Hodgkin's disease were measured by the Raji cell radioimmunoassay. Elevated levels of immune complexes (mean value of 49 microgram/ml +/- 21 SE) were detected in 20 of 40 (50 per cent) untreated patients. After treatment, the level of CIC was normal (less than 15 microgram/ml) in 39 of 41 patients. Recurrent disease developed in two of the 39 patients with normal post-treatment levels of CIC and in one of the two patients with elevated post-treatment levels during the follow-up period of six months to six years. Elevated levels of CIC were detected in patients with Hodgkin's disease in stages I, II and III but not in stage IV. No significant correlations were found in the frequency of elevated levels of CIC or the values observed, and the presence or absence of symptoms (fever, sweats, weight loss) or the histologic subtype of the tumor. Our data indicate that the measurement of CIC by the sensitive and specific raji cell assay may prove useful in the management of patients with Hodgkin's disease. In particular, serial measurement of the level of CIC could be employed to monitor the response to treatment and to detect recurrent diseases.

Antigen-Antibody Complex↗
PubMed1978

Immune complex mediated diseases.

Immune complexes formed in the circulation are believed to be the principal pathogenetic agents in certain human diseases, notably in various forms of glomerulonephritis and arteritis. Criteria for the recognition of immune complex deposits in tissue are discussed and recently developed sensitive methods that detect circulating immune complexes are reviewed. In addition, the evidence implicating certain antigens and causative agents in human immune complex mediated glomerulonephritis and arteritis is evaluated.

Animals↗
PubMed1978

Cultured Plasmodium falciparum used as antigen in a malaria indirect fluorescent antibody test.

Human sera obtained from persons infected with Plasmodium falciparum were tested by a standard indirect fluorescent antibody (IFA) technique using antigen obtained from long term in vitro cultures of two strains of P. falciparum, and antibody in high titer was reproducibly detected. Sera from uninfected persons had undetectable or very low titers of antibody. The use of cultured parasites offers a convenient, stable source of antigens from different P. falciparum strains without requiring their adaptation to primates. Differences observed in IFA titers obtained by reacting immune serum with two different P. falciparum strains suggests the need for further evaluation of strain specificity.

Animals↗
PubMed1978

The significance of vascular anomalies in human renal transplantation.

In a review of 250 consecutive human cadaveric kidney transplants the primary failure rate of donor kidneys with an anatomically abnormal blood supply was 36.7% as compared with 16.2% for kidneys with a single artery and vein (P less than 0.001). The incidence of primary failure due to renal vascular thrombosis in the abnormal group was 24.2%, compared with 4.1% in the normal group (P greater than 0.001). A significantly greater incidence of anastomotic haemorrhage and urinary leak was also associated with an abnormal blood supply in the donor kidney.

Cadaver↗
PubMed1977

Passive transfer of autoimmune disease with isologous IgG1 and IgG2 antibodies to the tubular basement membrane in strain XIII guinea pigs: loss of self-tolerance induced by autoantibodies.

Initiation of an autoimmune tubulointerstitial disease was achieved in strain XIII guinea pigs by passive transfer of functionally pure IgG1 or IgG2 fractions of isologous anti-tubular basement membrane (TBM) serum. IgG2 appeared to be somewhat more effective than IgG1. The immunopathologic features in the IgG1 and IgG2 recipients were similar at the time of sacrifice, 14 days after transfer. The recipients that developed disease had higher than expected anti-TBM titers at 14 days. Furthermore, anti-TBM antibodies were of both IgG isotypes. In contrast, simultaneously administered IgG1 or IgG2 anti-BGG antibodies declined in titer in the recipients and were never found in the isotype fraction that had not been transferred. These findings indicate that the recipients of anti-TBM antibodies of either IgG1 or IgG2 isotype were stimulated to produce anti-TBM autoantibodies, which participated in the pathogenesis of the renal disease. The model demonstrates that autoantibodies may provide a mechanism (autoimmune amplification) for the intensification and perpetuation of antibody-mediated autoimmune diseases.

Animals↗
PubMed1977

Binding of soluble immune complexes in serum of patients with Hodgkin's disease to tissue cultures derived from the tumor.

We examined 90 serums from patients with Hodgkin's disease for immune complexes and for reactivity with established monolayer tissue cultures prepared from the tumor. All 23 serums with immune complex levels greater than 20 microgram per milliliter were found to react with cultured cells of patients with Hodgkin's disease when tested with antiserums against immunoglobulin heavy and light chains and the C3 component of complement. Five of 11 serums with borderline elevations of immune complexes (10 to 20 microgram per milliliter) and only four of 56 with levels less than 10 microgram per milliliter reacted. Absorption of patients' serums with cultured cells removed immune complexes and eliminated binding to monolayers. Immune-complex-containing serums from 19 control patients did react with cultured cells of patients with Hodgkin's disease; none of serums reacted with normal cultured spleen. Antibodies within complement-containing immune complexes in serums of patients with Hodgkin's disease react with an antigen on the surface of cultured cells of such patients.

Animals↗