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Biomedical subjects

A C Turner

Publications and source records attributed to A C Turner.

At least 19 recordsLinked to original sources
PubMed1991

Three aspecific ATPases in Trichomonas vaginalis.

1. Three aspecific ATPases were found in the sedimentible fractions of Trichomonas vaginalis. 2. One, with a pH optimum of 5.5, was equally activated by Ca2+ or Mg2+, moderately stable, preferred nucleotide diphosphates as substrates, and was inhibited by vanadate, oligomycin, nitrate and Na+. 3. A second, with a pH optimum of 7.5, was activated by Mg2+, preferred guanosine diphosphate as substrate, and was the least stable and most subject to inhibitors (vanadate, oligomycin, NEM, NBD-Cl, azide and Cl-). 4. The third, pH optimum 8.0, was activated by Ca2+, was latent and the most stable, reacted equally well with nucleotide tri- or diphosphates, and was the least susceptible to inhibitors (vanadate and NEM). 5. All exhibited proton-translocating ability.

Adenosine Triphosphatases↗
PubMed1991

Setting up HIV serology for the Karonga leprosy vaccine trial in Malaŵi.

As part of the leprosy vaccine trial taking place in Karonga District, Northern Malaŵi, it is essential to establish whether the presence of HIV infection in the population is affecting the incidence rate or clinical presentation of leprosy or the effectiveness of the trial vaccines. To obtain the appropriate information, a rapid and economical HIV testing protocol, which could be performed in a rural laboratory and would be robust under variable environmental conditions, had to be developed. This paper reports on the development/evaluation phase of a multitest protocol based on commercially available particle agglutination and ELISA anti-HIV antibody detection kits. The protocol was devised by first evaluating a range of kits in London using a battery of African and non-African sera and then field testing 1455 sera in Malaŵi, which included 184 sera from leprosy patients and 60 sera from syphilis patients to check for cross-reactivity. According to the protocol developed, all sera are screened initially both by indirect ELISA (Organon) and using a rapid and economical modification of the Serodia particle agglutination test. Positives are retested using both a competitive ELISA (Wellcome or Behring) and the standard Serodia particle agglutination test. The validity of this multitest protocol was confirmed by Western blotting a large sample of the positive and negative Malaŵian sera in London. Factors affecting kit selection, and problems associated with individual kits, are discussed. While the specific multitest protocol developed for Malaŵi might not be suitable for every project, the principle of developing economical alternatives to Western blotting is an important consideration for any field investigation of HIV.

AIDS Serodiagnosis↗
PubMed1991

Is HIV infection a risk factor for leprosy?

A case control study was undertaken during 1988 and 1989 within the framework of the LEPRA Evaluation Project (LEP)/Karonga Prevention Trail (KPT) in Karonga District, northern Malawi, to investigate whether HIV infection is a risk factor for clinical leprosy. Cases were newly ascertained, biopsy-confirmed, incident leprosy patients older than 14 years of age. Controls were selected from the computer data base on over 170,000 people who form the basis of LEP/KPT. They were matched for sex, age, and area of residence. HIV seropositivity rates were 1.8% (2/112) for incident leprosy cases and 2.4% (24/1011) for controls. The Mantel Haenszel odds ratio is 0.6 (95% confidence interval 0.1-3.3). Thus, no evidence for an association between HIV infection and leprosy incidence has been observed in this population. In a parallel investigation, an odds ratio of 7.4% (95% confidence interval 3.3-16.7) was found for 102 microscopy- and/or culture-confirmed, incident pulmonary tuberculosis cases in the same population during 1989, a result similar to those obtained elsewhere in Africa. Among leprosy relapses, 16.7% (2/12) were HIV positive.

Adult↗
PubMed1989

Characterization of a secreted cytoactive factor from Trichomonas vaginalis.

Trichomonas vaginalis, grown in Dulbecco's modified Eagle's medium with or without serum, produced a factor (TVF) which altered the morphology of certain mammalian cells in vitro. TVF had a Mr of approximately 250 kDa by gel filtration, approximately 50 kDa by SDS-PAGE, and was heat (56 degrees C, 30 min) and pH (greater than 6 or less than 8) labile. Co-incubation of TVF with adherent target cells caused a marked rounding and clumping of BHK-21 or CHO-K1 cells, but had no effect on RK-13 or WEHI-3 cells. These morphologic changes were concentration, time, and energy dependent. Reversibility was attained by exogenous serum addition (greater than 10%) or TVF washout. Target cell perturbations were not accompanied by significant changes in growth (as measured by nuclei counts, DNA content, or 3H-thymidine incorporation), in cell leakage (as assessed by lactate dehydrogenase release), or in cell viability (by trypan blue dye exclusion). TVF-induced effects were independent of cyclic AMP and cyclic GMP levels in BHK cells exposed for 5 min-24 hr.

Agglutination↗
PubMed1988

Trichomonas vaginalis: characterization of its glutamate dehydrogenase.

An NADP-linked glutamate dehydrogenase (EC 1.4.1.4) was found in the soluble fraction of Trichomonas vaginalis. Its molecular weight was about 230,000 (gel filtration). The enzyme, partially purified by diafiltration and hydroxyapatite column chromatography, was heat stable (1 hr at 57 C). It catalyzed both the amination of alpha-ketoglutarate (mean Km 0.6 mM) and the deamination of glutamate (mean Km 1.2 mM) The optimum pH of the amination reaction was 6.7, and that of the deamination reaction was 8. Glutamate was a competitive inhibitor of the amination reaction (mean Ki 5.6 mM) and alpha-ketoglutarate a partially competitive inhibitor of the deamination reaction (mean Ki 0.45 mM). Both guanosine and inosine diphosphates (1 mM) increased the Km alpha-ketoglutarate fivefold (mean Ki's 0.3 and 0.4 mM, respectively). Guanosine diphosphate reduced the Km glutamate 40%. Adenosine di- and triphosphate (1 mM) were ineffective. Because the amination reaction displayed substrate inhibition, guanosine and inosine diphosphates were potent natural inhibitors, and ammonia released by deamination reactions would tend to raise pH (amination operative at acid pH), we hypothesize that the deamination reaction may predominate in the living organism.

Amination↗
PubMed1986

Dirofilaria immitis: comparison of cytosolic and mitochondrial glutamate dehydrogenases.

Two membrane-bound glutamate dehydrogenases were found in adult Dirofilaria immitis, an NAD-linked enzyme (EC 1.4.1.2) in the cytosol (C-GDH) and an enzyme equally reactive with NAD or NADP (EC 1.4.1.3) in the mitochondria (M-GDH). The cytosolic enzyme had a pH optimum of 7.8-8.0 and exhibited 30% more activity at 25 C than at 37 C (pH 8.0). The mitochondrial enzyme had a pH optimum at 8.4 and exhibited 27% more activity at 37 C than at 25 C (pH 8.4); it was also more sensitive to heat denaturation. Gel filtration of worm subfractions separated four peaks of C-GDH activity with molecular weights of approximately 610, 285, 180, and less than 100 thousand, and a single major peak of M-GDH activity with a molecular weight of about 335,000. When assayed at pH 8, 37 C, and 200 microM NADH, the Km for the substrate, alpha-ketoglutarate, was equivalent for the two enzymes, but the Km for ADP (activator) was five times greater for M-GDH. When the two enzymes were assayed at pH 8.0, 37 C, and 100 microM NADH, 1 mM ADP approximately doubled and 1 mM ATP halved the velocity observed for each enzyme with no effector present. Under these assay conditions AMP, IDP, GDP, and GTP had opposite effects on the reaction velocities for the two enzymes. When the assay conditions were changed, the effects of added purine nucleotides varied, even directionally. Addition of up to 5 mM glutamate (product) had no significant effect on C-GDH kinetics, nor on the substrate Km of M-GDH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Travellers' diarrhoea: prevention by chemoprophylaxis.

The chemoprophylaxis of travellers' diarrhoea by iodochlorhydroxyquinoline combinations, neomycin and phthalsulphathiazole, furazolidone, bismuth salicylates and streptotriad is reviewed. Streptotriad is regarded as a highly effective prophylactic against travellers' diarrhoea. Some elementary food hygiene precautions are detailed.

Adult↗
PubMed1982

Oxidative decarboxylation reactions in Dirofilaria immitis glucose metabolism.

1. Malic enzyme (EC 1.1.1.39) activity was demonstrated in the mitochondrial fraction of dog heartworm extracts. 2. Data published earlier together with those presented here confirm the presence of all the enzymes of the pentose shunt. 3. 14C from uniformly labelled glucose was incorporated into the nucleic acids, and methylene blue increased production of xylose-5-phosphate and of 14CO2 from [1-14C]glucose indicating a functioning pathway. 4. The oxidative decarboxylation of malate and of 6-phosphogluconate may account for the observed labelled CO2 formed when labelled glucose is metabolized since a functional tricarboxylic acid cycle is doubtful in this parasitic helminth.

Animals↗
PubMed1979

Glycolytic end products of the adult dog heartworm, Dirofilaria immitis.

1. Adult dog heartworms remained alive and motile for 24 hr without oxygen present and with only glucose available as a substrate. 2. Lactate accounted for 55% of the carbon from the 1-14C-glucose utilized in 1 hr and 14CO2 for 1.9%. 3. Only traces of 14C were found in glycogen and no net accumulation of acetate was demonstrated. 4. Dirofilaria immitis resembles Litomosoides carinii in the percent of utilized glucose appearing as lactate but is more akin to Brugia pahangi and Dipetalonema viteae in survival under anaerobic conditions and in negligible acetate production.

Acetates↗
PubMed1979

Glycerol metabolism in the adult dog heartworm, Dirofilaria immitis.

1. When adult Dirofilaria immitis were incubated up to 60 min in a medium containing physiological concentrations of glycerol and glucose, the mean amount of free glycerol present did not change significantly. 2. [14C]2-glycerol disappeared from media in which 1 g heartworms were incubated at a linear rate of about 0.7 mumol/hr/g during the first hour. 3. 85-95% of the radioactivity in the Folch extract remained in the aqueous phase. 4. Phosphoglycerides and diacylglycerols accounted for better than 90% of the 14C in the lipids. 5. The rate of glycerol conversion to lactate was only about 0.02% of the rate of glucose conversion under experimental conditions. 6. The data indicate that, although dog heartworms do utilize glycerol as a substrate in glycolysis, it is probably of more importance in lipid synthesis.

Animals↗
PubMed1979

Lipid synthesis in the adult dog heartworm, Dirofilaria immitis.

1. Incorporation studies with three labelled substrates--[14C]2-glycerol, [14C]1-acetate and [14C]1-oleic acid--demonstrated that adult dog heartworms can synthesize all classes of complex lipids present, including free cholesterol. 2. Diacylglycerols and phosphoglycerides were most rapidly labelled regardless of the precursor employed. 3. 14C from glycerol was found in the aqueous phase of saponified lipids, whereas that from oleic acid was in the fatty acid portion. 4. Tag from acetate was predominantly in the fatty acid portion of saponified lipids and also occurred in the unesterified fatty acids. 5. Acetate and unesterified fatty acids, as represented by oleic acid, were more readily used for lipid synthesis than was glycerol.

Absorption↗
PubMed1977

Hexokinase of the adult dog heartworm, Dirofilaria immitis.

1. Dirofilaria immitis hexokinase was relatively heat stable and had a pH optimum range between 7.8 and 8.2. 2. Mean Vmax was 0.40 +/- 0.10 (S.D.) mumole/min/100 mg of worm. 3. Mean Km values were 0.32 mM for glucose, 0.86 mM for fructose and 0.39 mM for ATP. 4. Glucose-6-phosphate was not a strong product inhibitor. 5. Starch gel electrophoresis demonstrated at least three isozymes.

Animals↗