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Biomedical subjects

J F Knight

Publications and source records attributed to J F Knight.

At least 19 recordsLinked to original sources
PubMed1990

End-stage renal failure in children: 16 years' experience at one Australian centre.

Sixty-five children over one year and under 15 years of age began treatment for end-stage renal failure between 1973 and 1988. Sixty-one renal transplants were performed in 53 children, 39 of these were from living donors (38 were first-degree relatives and one was an emotionally related volunteer). Thirteen children, of whom seven had received transplants and six had not, died, including three children with functioning transplants; nine deaths occurred in the first eight years of the programme. Cumulative five-year and 10-year patient survival rates were 78% and 75%, respectively. Eighteen transplants failed, 12 as a result of rejection, five as a result of disease recurrence and one due to primary non-function. Cumulative five-year and 10-year transplant survival rates for first grafts were 66% and 53%, respectively. For living donor transplants these rates were 85% and 68%, respectively. Growth rates fell by 0.4 +/- 0.05 standard deviation score (SDS) per year in children undergoing dialysis, were normal in children with renal transplants receiving prednisone (change in SDS per year, -0.02 +/- 0.08) and increased by 0.36 +/- 0.07 SDS per year in children with transplants receiving cyclosporin A alone. Currently, 32 (82%) of 39 transplant recipients and 7 (58%) of 12 patients undergoing dialysis attend school or work full time. Although both dialysis and transplantation are acceptable therapies for children with end-stage renal failure, successful transplantation provides the best opportunity for satisfactory growth and development.

Actuarial Analysis↗
PubMed1990

The rheumatic poison: a survey of some published investigations of the immunopathogenesis of Henoch-Schönlein purpura.

Laboratory studies of the pathophysiology of Henoch-Schönlein purpura (HSP) have become more numerous in recent years with the recognition of the disease's links with the mucosal immune system in general and IgA nephropathy in particular. There are weak genetic associations with C4 null phenotypes and with HLA B35 and DR4. Studies of plasma proteins in HSP patients show an increased IgA concentration, activation of the alternative pathway of complement and consumption of factor XIII. High molecular weight (polymeric) IgA has been detected in affected individuals, which some investigators have called "immune complexes". Many patients synthesise an IgA rheumatoid factor in the acute phase, but other autoantibodies are largely absent. In vitro studies of lymphocytes from HSP patients have demonstrated an increased number of IgA-bearing and secreting B-cells, with altered T-cell regulation of antibody synthesis. While these observations point to immune dysregulation--primarily of IgA production--as a consistent feature of acute HSP, there is as yet insufficient information available to allow a consistent theory of pathogenesis to be formulated.

Blood Proteins↗
PubMed1990

Hyperglycaemia complicating haemolytic uraemic syndrome.

The occurrence of hyperglycaemia and insulin deficiency in a young child receiving peritoneal dialysis during the course of haemolytic uraemic syndrome (HUS) is described. This unusual complication may have been due to microvascular disease involving the pancreas. Plasma glucose should be monitored during HUS, particularly if dialysis with fluids containing high dextrose concentrations is required.

Blood Glucose↗
PubMed1989

Charge distribution of plasma IgA in IgA nephropathy.

The spectrotype of plasma IgA in patients with IgA nephropathy was studied by isoelectric focussing. Densitometry of the gels showed a significant increase in the anionic region at isoelectric points (pI) 4.7-5.1 (P = 0.02) and a reduction in the cationic region pI 5.8-6.0 (P = 0.03) in patients (n = 15) compared with controls (n = 8). Measurement of the IgA concentration in eluates of sequential slices of the gels showed that the ratio of anionic-to-cationic IgA, using pI 5.6 as the dividing point, was significantly greater in patients (n = 10) than in controls (n = 10) (P = 0.03). Two different methods of analysis have therefore demonstrated an increased proportion of anionic and decreased proportion of cationic IgA in the plasma of patients with IgA nephropathy.

Adolescent↗
PubMed1988

Relation of mesangial IgA glomerulonephritis to polymorphism of immunoglobulin heavy chain switch region.

We have investigated the switch regions of Ig heavy chain genes of patients with IgA glomerulonephritis (IgA-GN) using restriction fragment length polymorphism (RFLP) analysis. Genomic DNA from patients and controls was digested with the restriction endonuclease Sst I and transferred to nylon membranes using the Southern blot procedure and hybridized with a probe homologous to the switch region of the Ig C mu gene (S mu) which detects RFLPs in both S mu and the switch region of the Ig C alpha 1 gene (S alpha 1). A significant decrease in the frequency of the 2.6;2.1 kb heterozygous S mu phenotype was found in patients with IgA-GN (P = 0.003). With respect to the S alpha 1 region, there was a significant increase in the frequency of the 7.4 kb S alpha 1 phenotype (P = 0.002). In addition, a significant increase in the frequency of the 7.4 kb S alpha 1 allele was found (P = 0.0002). These results suggest that gene(s) within the Ig heavy chain loci may be important in the pathogenesis of IgA-GN.

Genes, Regulator↗
PubMed1982

Chronic exposure of rats to enflurane 200 p.p.m.: no evidence of toxicity or teratogenicity.

Adult male or female rats were exposed either to enflurane 200 p.p.m. or to air for up to 63 days before mating and subsequently throughout the pregnancy of the females. The treated animals were exposed for 8 h per day, 5 days per week for a maximum total of 100 days. The parents and progeny-were studied. Additional positive controls with vitamin A palmitate demonstrated that the strain of animals was susceptible to a known teratogen. No abortifacient effect was observed with these conditions of exposure to enflurane. Skeletal examination of the fetuses failed to reveal any major teratogenic effect. The parents remained healthy clinically, whilst autopsy and histopathological examination failed to reveal any consistent organ injuries which could be blamed on exposure to enflurane. In rats at least, environmental pollution with enflurane appears not to be associated with significant toxicity or teratogenicity.

Abnormalities, Drug-Induced↗
PubMed1975

Letter: Rauwolfia.

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Breast Neoplasms↗