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G B Wisdom

Publications and source records attributed to G B Wisdom.

At least 19 recordsLinked to original sources
PubMed2002

Autoantibodies to malondialdehyde-modified low-density lipoprotein in patients with angiographically confirmed coronary artery disease.

Oxidised low-density lipoprotein (LDL) has physicochemical properties that are pivotal in atherosclerotic plaque formation. As a consequence, antioxidant regimens may prove an important therapy in the prevention and treatment of cardiovascular disease. Since oxidised LDL is immunogenic, the aims of our study were to measure serum IgG titres to malondialdehyde-modified LDL (MDA-LDL) in patients with coronary artery disease (CAD) and control subjects and assess their potential as a clinical marker for coronary atherosclerosis and, consequently, antioxidant intervention. Serum IgG titres to MDA-LDL were measured in patients with angiographically confirmed CAD (n = 40) and aged-matched controls (n = 40) by enzyme-linked immunosorbant assay (ELISA). Titres were calculated and expressed as both the difference and the ratio of blanked absorbance units (AU) for IgG binding to MDA-LDL and native LDL. For the control population, median IgG titres were 0.26 AU (interquartile range (IQR) 0.20-0.46 AU) and 5.34 (IQR 3.40-8.58), respectively, while the patient population had median IgG titres of 0.30 AU (IQR 0.20-0.47 AU) and 5.08 (IQR 3.30-9.66), respectively. Both sets of calculated titre values were not significantly different between the two groups (P = 0.60 and 0.82, respectively). In conclusion, this study could not establish any significant association between circulating autoantibody titres to MDA-LDL and coronary atherosclerosis. Therefore, the diagnostic value of autoantibodies to oxidised LDL remains unclear.

Adult↗
PubMed2001

Measurement of asialylated LDL in the blood of patients with coronary artery disease by antibody-lectin sandwich assay.

Elevated concentrations of asialylated LDL (asialo-LDL) have been reported in patients with coronary artery disease (CAD). This may stimulate lipid accumulation in arterial intima cells and promote atherosclerosis. To investigate asialo-LDL as a potential risk-factor for coronary atherogenesis, we developed an antibody-lectin sandwich assay to measure levels in serum from CAD patients and age-matched control subjects. LDL was captured with an anti-apolipoprotein (apo) B antibody and asialylated oligosaccharides measured using the biotinylated D-galactose (D-gal) binding lectin, Ricinus communis agglutinin 120 (RCA120), and a streptavidin-alkaline phosphatase conjugate. For the control and atherosclerotic subjects, median [interquartile range (IQR)] values for total concentrations of asialo-LDL were 240 mg,L (180-310 mg/L) and 220 mg/L (186-390 mg/L), respectively (P = 0.82). When expressed as a percentage of serum apo B-100, median (IQR) values were 18% (16-23%) and 19% (15-29%), respectively (P = 0.78). These results suggest asialo-LDL has little value as a risk factor for coronary atherosclerosis.

Adolescent↗
PubMed2000

Lipopolysaccharide binding protein in acute pancreatitis.

OBJECTIVE: To assess the expression of plasma lipopolysaccharide binding protein (LBP) concentrations and its relationship to markers of the systemic inflammatory response syndrome during acute pancreatitis. DESIGN: A prospective study. SETTING: General surgical units of university teaching hospitals in the Belfast area. PATIENTS: The study included 18 patients admitted with established diagnosis of acute pancreatitis on the basis of elevated serum amylase or by contrast radiology. Patients were retrospectively stratified using the Modified Glasgow Criteria into severe (n = 7) and mild (n = 11) disease. INTERVENTIONS AND MEASUREMENTS: Blood samples were obtained at admission (day 1) and for a further 3 days for the measurement of LBP, C-reactive protein (CRP), tumor necrosis factor, and interleukin (IL)-6. Acute Physiology and Chronic Health Evaluation (APACHE) II scores were calculated on day 1 and day 2. MAIN RESULTS: LBP and CRP concentrations were significantly increased from healthy control values in acute pancreatitis patients at presentation. In the mild group LBP, CRP and IL-6 concentrations remained relatively constant throughout the study period. By comparison, severe acute pancreatitis was associated with significantly higher LBP concentrations and a marked systemic inflammatory response as evidenced by increased CRP, IL-6, and APACHE II scores. The rise in LBP occurred after the observed increase of these markers. Significant correlations were found among CRP and LBP, IL-6 and LBP, and IL-6 and APACHE II scores. There were no fatalities in the mild group, whereas four of the seven patients with severe disease died. CONCLUSIONS: LBP was significantly raised in patients with severe acute pancreatitis but would seem to be of limited use in predicting disease severity. This acute phase protein may have a role in the progression of systemic complications associated with acute pancreatitis.

APACHE↗
PubMed1999

An antibody-lectin sandwich assay for quantifying protein glycoforms.

We describe an antibody-lectin sandwich assay for quantitation of glycoforms of proteins. The assay uses deglycosylated IgG antibody immobilized on a microtiter plate to capture the protein of interest from the sample. The particular glycoform is then identified by reaction with biotin-labeled lectin, which is measured using streptavidin/alkaline phosphatase. The assay can be adapted to quantitate any protein's glycoforms by simply substituting the antibody and lectin with specific alternatives.

Antibodies↗
PubMed1997

Identification of alpha 1-acid glycoprotein (orosomucoid) in human synovial fluid by capillary electrophoresis.

Capillary electrophoresis of human synovial fluid in a phosphate borate run buffer containing sodium dodecyl sulphate separates a hydrophilic glycoprotein, hyaluronan and a number of low-molecular-mass components. The hydrophilic glycoprotein is identified as alpha 1-acid glycoprotein (AGP), orosomucoid, by co-injection methods with human AGP and by reaction with neuraminidase which released N-acetylneuraminic acid. Finally, a sample of the glycoprotein was isolated by micropreparative capillary electrophoresis, examined by sodium dodecyl sulphate-polyacrylamide gel electrophoresis methods and shown to give a positive reaction with AGP antibodies. The peak due to AGP in the capillary electrophoresis is broad and gives evidence for the presence of glycoforms.

Antibodies↗
PubMed1995

The purification and properties of phosphonoacetate hydrolase, a novel carbon-phosphorus bond-cleavage enzyme from Pseudomonas fluorescens 23F.

A novel, inducible, carbon-phosphorus bond-cleavage enzyme, phosphonoacetate hydrolase, was purified from cells of Pseudomonas fluorescens 23F grown on phosphonoacetate. The native enzyme had a molecular mass of approximately 80 kDa and, upon SDS/PAGE, yielded a homogenous protein band with an apparent molecular mass of about 38 kDa. Activity of purified phosphonoacetate hydrolase was Zn2+ dependent and showed pH and temperature optima of approximately 7.8 and 37 degrees C, respectively. The purified enzyme had an apparent Km of 1.25 mM for its sole substrate phosphonoacetate, and was inhibited by the structural analogues 3-phosphonopropionate and phosphonoformate. The NH2-terminal sequence of the first 19 amino acids displayed no significant similarity to other databank sequences.

Alkaline Phosphatase↗
PubMed1994

Inhibition of fibrin monomer polymerisation by myeloma immunoglobulin.

Myelomatosis was diagnosed in a 64 year old man on the basis of a serum paraprotein band (type IgG lambda, 42 g/l), plasma cell infiltration of bone marrow, and multiple lytic lesions evident on skull x ray picture. Blood specimens taken into plain glass tubes showed bulky gelatinous clot formation with minimal clot retraction. Coagulation tests were significantly abnormal with an increase in thrombin time, prothrombin time, and reptilase time. The possibility that the paraprotein was interfering with fibrin production was investigated. The rate of fibrin monomer polymerisation (measured turbidometrically) was reduced in patient plasma compared with control plasma. Although purified fibrin monomer prepared from the patient's fibrinogen polymerised normally, the addition of purified paraprotein caused a dose dependent reduction in the rate of polymerisation. These results suggest that the paraprotein was impairing fibrin formation by inhibiting fibrin monomer polymerisation. After chemotherapy the paraprotein concentration decreased and the coagulation results returned to normal.

Blood Coagulation Tests↗
PubMed1994

Protein blotting.

Explore the source record for details and available documents.

Blotting, Western↗
PubMed1994

Hereditary caeruloplasmin deficiency, dementia and diabetes mellitus.

We report two brothers with complete caeruloplasmin deficiency. The brothers presented with dementia and diabetes mellitus. Twelve relatives have partial caeruloplasmin deficiency. There is no copper overload. Transmission is autosomal recessive. DNA analysis showed genetic linkage between the deficiency and various polymorphic markers flanking the caeruloplasmin gene on chromosome 3q25. This is consistent with a mutation of the caeruloplasmin gene. Caeruloplasmin catalyses the oxidation of ferrous iron to ferric iron. Both brothers have low serum iron and increased liver iron. The index patient was given caeruloplasmin-containing, fresh-frozen plasma. A dose of 2.6 mg caeruloplasmin increased serum iron from 5 microM/l to 10 microM/l. A dose of approximately 72 mg increased serum iron from 5 microM/l to 19 microM/l. The abnormal serum and liver iron levels, and the caeruloplasmin-induced rise in serum iron, confirm a previous suggestion that caeruloplasmin maintains the normal rate of flow of iron from store to transferrin. Dementia and diabetes mellitus have been described in only one other homozygote. The absence of copper overload, and the linkage of the deficiency with chromosome 3q25, distinguish this condition from Wilson's disease.

Brain↗