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Biomedical subjects

C M Taylor

Publications and source records attributed to C M Taylor.

At least 91 records · Page 5Linked to original sources

Circulating soluble adhesion molecules in systemic vasculitis.

The plasma levels of soluble intercellular adhesion molecule-1 (sICAM-1), E-selectin (sE-selectin), and vascular cell adhesion molecule-1 (sVCAM-1), might reflect endothelial activation and injury and would therefore be useful markers of disease activity in vasculitis. To investigate this we measured the levels of sICAM-1, sE-selectin, and sVCAM-1 by two-site ELISAs in the plasma of patients with (a) active vasculitis (n = 16), (b) vasculitis in remission (n = 15), (c) chronic renal failure (CRF) (n = 10), and (d) normal healthy controls (n = 10). Plasma sICAM-1 levels were significantly higher in patients with active vasculitis, 323 ng/ml (193-607) compared with patients with inactive vasculitis, 199 ng/ml (131-297); P = 0.0006 and healthy controls, 188 ng/ml (138-259); P = 0.0002. Plasma sE-selectin levels were also significantly higher in the patients with active vasculitis, 45 ng/ml (15-65) compared with patients with inactive vasculitis, 25 ng/ml (15-55); P = 0.027 but not when compared with healthy controls, 35 ng/ml (20-55); P = 0.16. There was no difference in plasma sVCAM-1 levels between patients with active vasculitis, OD 0.56 (0.45-0.85) and inactive disease, OD 0.58 (0.47-0.79) (P = 0.12) or with healthy controls OD 0.49 (0.42-0.68) (P = 0.48). There were no significant differences between the plasma levels of any of the soluble adhesion molecules between patients with active vasculitis and patients with chronic failure.(ABSTRACT TRUNCATED AT 250 WORDS)

C-Reactive Protein↗

Pooled human IGG (PHIG) inhibits the binding of anti-myeloperoxidase antibodies to myeloperoxidase.

This study demonstrates that pooled human immunoglobulin (PHIG) contains anti-idiotypes to anti-myeloperoxidase (MPO) antibodies and can inhibit the binding of anti-MPO to MPO. The variability seen in the inhibitory effect of different PHIG preparations in the same and also in different patient sera suggests heterogeneity in the idiotypic repertoire of anti-MPO antibodies.

Antibodies, Anti-Idiotypic↗

Little evidence for anti-endothelial-cell antibodies in microscopic polyarteritis and Wegener's granulomatosis.

Sera from patients with a vasculitis and controls were investigated for the presence of anti-endothelial cell antibodies(AECA), anti- neutrophil cytoplasmic antibodies(ANCA) and anti-myeloperoxidase (MPO) antibodies. Only 19% of patients with Wegener's granulomatosis and 2% of patients with microscopic polyarteritis had AECA. Our data suggests that AECA are a minor antibody system in vasculitis.

Antibodies, Antineutrophil Cytoplasmic↗

Prostacyclin in diarrhoea-associated haemolytic uraemic syndrome.

The role of prostacyclin (PGI2) in the pathogenesis of haemolytic uraemic syndrome (HUS) is controversial. In part, confusion has been caused by failure to distinguish between two main sub-types of the syndrome: extrinsic, diarrhoea-associated HUS (D+ HUS), usually caused by infection with verocytotoxin-producing Escherichia coli or Shigella dysenteriae, and the heterogeneous group of non-prodromal forms where intrinsic factors predominate (D- HUS). This paper critically reviews data confined to D+ HUS. Two methods have been used to assess PGI2 synthesis; the generation of PGI2 from endothelium in the presence of HUS plasma in vitro and the measurement of stable metabolites in body fluids. No concensus could be reached with regard to the former. The reported increase of PGI2 stable metabolites in plasma may represent reduced clearance or increased carriage by plasma lipids. Apparent differences between studies of urinary excretion of PGI2 metabolites may reflect the way excretion was expressed. If the metabolite concentration is factored for urinary creatinine, it appears that renal excretion and thus renal synthesis of PGI2 is reduced. However, these are insufficient data on which to attribute the pathogenesis of D+ HUS to disordered PGI2 metabolism.

6-Ketoprostaglandin F1 alpha↗

Little evidence for anti-endothelial cell antibodies in microscopic polyarteritis and Wegener's granulomatosis.

We studied sera from patients with vasculitis and controls for the presence of anti-endothelial cell antibodies (AECA) and correlated these with disease type, anti-neutrophil cytoplasmic antibodies (ANCA) and anti-myeloperoxidase (MPO) antibodies. AECA were detected by a cellular ELISA on cultured human umbilical vein endothelium. AECA were found in the sera of one of 43 patients with microscopic polyarteritis (2%), five of 27 patients with Wegener's granulomatosis (19%), three of 23 patients with an idiopathic glomerulonephritis (13%), none of eight patients with rheumatoid arthritis and three of 12 patients with rheumatoid vasculitis (25%). In patients with a vasculitis AECA titres were higher in sera with a positive ANCA as compared with ANCA negative sera although the difference was not significant (P = 0.0702) and there was no correlation between AECA and anti-MPO titres (r = 0.1171 P = 0.114). AECA binding was not enhanced following upregulation of endothelial ICAM-1 and ELAM-1 by TNF alpha. This study shows that AECA occur infrequently in microscopic polyarteritis and Wegener's granulomatosis, and are not a major antibody system in these vasculitides.

Antibodies, Antineutrophil Cytoplasmic↗

Recovery of protein from urine specimens collected in cotton wool.

Cotton wool balls have been used to aid the collection of urine from infants. Concentrations of two urinary proteins, albumin and retinol binding protein, decreased by 40 and 80% respectively within 15 minutes of contact with the cotton wool. Cotton wool balls should not be used when investigating proteinuria.

Female↗

Symptomatic zinc deficiency in experimental zinc deprivation.

An evaluation of indices of poor zinc status was undertaken in five male subjects in whom dietary zinc intake was reduced from 85 mumol d-1 in an initial phase of the study to 14 mumol d-1. One of the subjects developed features consistent with zinc deficiency after receiving the low zinc diet for 12 days. These features included retroauricular acneform macullo-papular lesions on the face, neck, and shoulders and reductions in plasma zinc, red blood cell zinc, neutrophil zinc and plasma alkaline phosphatase activity. Alcohol induced hepatitis, which was suspected in this subject, may have caused a predisposition to altered zinc metabolism and possible zinc deficiency which was exacerbated by subsequent zinc deprivation. The report supports the value of neutrophil zinc concentration as an indicator of poor zinc status.

Adult↗

Concentrations of endothelial-cell-stimulating angiogenesis factor, a major component of human uterine angiogenesis factor, in human and bovine embryonic tissues and decidua.

Embryonic development involves the establishment of new patterns of vascular growth in the fetus and within the lining of the womb. A factor, human uterine angiogenesis factor, has been purified from the decidua and stimulates the growth of blood vessels in collagen sponge implants and in the chick chorioallantoic membrane. Evidence is presented that suggests that a major active component of human uterine angiogenesis factor is an activator of latent matrix metalloproteinases, of low M(r), called endothelial-cell-stimulating angiogenesis factor and that this factor is present in substantial quantities in a number of embryonic tissues.

Angiogenesis Inducing Agents↗

Endothelium myeloperoxidase-antimyeloperoxidase interaction in vasculitis.

Antibodies to myeloperoxidase (MPO) are found in the sera of patients with microscopic polyarteritis and idiopathic crescentic glomerulonephritis. Their pathogenicity is unknown. Studies were carried out on the binding of MPO to cultured human umbilical vein endothelial cells and the recognition of endothelium-bound MPO by antibody to MPO. Endothelial cells were cultured from human umbilical veins. The binding of MPO to endothelial cells and its inhibition by poly-D-lysine was detected using a monoclonal antibody to MPO and direct staining with APAAP and also by an enzyme-linked immunoassay (ELISA). The binding of anti-MPO antibody in the sera of patients with microscopic polyarteritis to endothelium-coated MPO was detected by ELISA. MPO bound to endothelial cells both on direct staining and ELISA and this binding was inhibited by the polycation poly-D-lysine, suggesting that it was charge mediated. Binding of anti-MPO antibody in the sera of patients with microscopic polyarteritis to endothelium-coated MPO was significantly higher than the binding of sera from normal subjects (P = 0.04), patients with idiopathic glomerulonephritis (P = 0.0005), and patients with lupus nephritis (P = 0.009). MPO binds to cultured human umbilical vein endothelium probably by a charge mechanism, and can react with anti-MPO antibodies in the sera of patients with microscopic polyarteritis as well as with a mouse monoclonal anti-MPO antibody. This binding of anti-MPO antibody to MPO fixed to the endothelial cell surface provides a mechanism by which endothelial injury and inflammation might occur in microscopic polyarteritis.

Endothelium, Vascular↗

Serological identification of Escherichia coli O157:H7 infection in haemolytic uraemic syndrome.

To test the value of serological tests as an adjunct to bacteriological methods and toxin testing in haemolytic uraemic syndrome (HUS), 60 patients with the disorder were examined for evidence of faecal Escherichia coli producing verocytotoxin (VTEC), particularly of serogroup O157. They were also tested for serum antibodies reacting with the lipopolysaccharide of E coli O157 by means of an enzyme-linked immunosorbent assay (ELISA) and immunoblotting; for faecal VTEC by means of DNA probes hybridising with the genes encoding verocytotoxins VT1 and VT2; and for "free" faecal VT. Strains of E coli serotype O157:H7 were isolated from 9 patients, and faecal VT2 was detected in 3 of them. Strains of E coli of serotypes 05:H-, O55:H10, O105ac:H18, and O163:H19 were isolated from 4 patients, but faecal VT was not detected. Faecal VT2 was present in 1 patient from whom VTEC were not isolated. Antibodies to the lipopolysaccharide of E coli O157 were detected in serum samples from 44 patients. The 9 patients with faecal O157:H7 all had high titres of these antibodies, but serum samples from 16 healthy control children were negative. Serological testing of patients with HUS for antibodies to the lipopolysaccharide of E coli O157 provides evidence of infection with E coli O157 when faecal bacteria or VT cannot be detected.

Antibodies, Bacterial↗