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T Fraser

Publications and source records attributed to T Fraser.

At least 19 recordsLinked to original sources

Bacteriocin T8, a novel class IIa sec-dependent bacteriocin produced by Enterococcus faecium T8, isolated from vaginal secretions of children infected with human immunodeficiency virus.

Enterococcus faecium T8, isolated from vaginal secretions of children with human immunodeficiency virus, produces a class IIa sec-dependent bacteriocin that is structurally different from three other class IIa sec-dependent bacteriocins, i.e., enterocin P and an enterocin P-like bacteriocin, produced by Enterococcus faecium, and bacteriocin 31, produced by Enterococcus faecalis, and from a class III bacteriocin produced by E. faecalis. The genes encoding the bacteriocin, immunity protein, mobilization protein, and relaxase nuclease are located on a 7-kb plasmid. Bacteriocin T8 has a molecular mass of 5.1 kDa based on its DNA sequence, similar to the 5.0 kDa recorded for bacteriocin 31 but larger than the 4.6 kDa reported for enterocin P. At the amino acid level, bacteriocin T8 is 69% homologous to bacteriocin 31 and 47% homologous to enterocin P. Bacteriocin T8 is active against E. faecalis isolated from patients diagnosed with vaginosis, against Lactobacillus sakei, and against a Propionibacterium sp. The peptide is heat stable (60 min at 100 degrees C) and remains active in phosphate buffer from pH 4.0 to 10.0. The mode of activity is bactericidal, as determined with E. faecalis.

Amino Acid Sequence↗

Hand rolling cigarette papers as the reference point for regulating cigarette fire safety.

AIM: To compare the burning characteristics of the tobacco and paper of manufactured and hand rolled cigarettes, and set a fire safety standard of manufacture to largely reduce the fire risk from discarded cigarettes. METHODS: (1) Cigarette extinction test of ignition strength: 40 cigarettes per brand, lit and placed on 15 layers of filter paper, in accordance with ASTM test standard E2187-02. (2) Citrate extracted by 0.1N hydrochloric acid from cigarette papers and from tobacco in manufactured cigarettes, the supernatant analysed by high performance liquid chromatography using ultraviolet visual light spectrophotometer. (3) Survey of 750 nationally representative adults age 18 years and over, by telephone, including 184 smokers. MATERIALS: (a) New Zealand made Holiday, and Horizon, and US made Marlboro manufactured cigarettes; (b) US manufactured Merit with banded paper; (c) Holiday, Horizon and Marlboro hand rolling tobaccos, hand rolled in Rizla cigarette papers; (d) manufactured cigarettes as in (a), reconstructed using Rizla hand rolling cigarette papers. RESULTS: 1. (a) For each brand of manufactured cigarettes, 40/40 burnt full length; (b) for Merit banded paper cigarettes 29/40 (73%) burnt full length; (c) for each brand of hand rolled cigarettes 0/40 burnt full length; (d) 0/40 manufactured cigarettes reconstructed with Rizla hand rolling paper burnt full length. 2. Citrate content: (a) In manufactured cigarette papers: 0.3-0.8 mg; in tobacco of manufactured cigarettes: Holiday 0, Horizon 0, Marlboro 8.8 mg; (b) Merit: in banded paper 0.418 mg; in tobacco 10.23 mg; (c) In hand rolled cigarettes: in the papers < 0.08 mg; in hand rolled tobacco 13.3-15.0 mg; (d) In hand rolling papers of reconstructed cigarettes: < 0.018 mg. 3. Requiring manufactured cigarettes to compulsorily self-extinguish when left unattended was supported by 67% of smokers, 61% of manufactured cigarette smokers, 82% of hand rolled smokers, and by 68% of non-smokers. CONCLUSION: The wrapping paper is a key determinant of whether or not unpuffed cigarettes burn their full length. Using international test methods, popular brands of manufactured cigarettes all burnt full length, but none did so when re-wrapped in hand rolling cigarette paper. This provides a ready-to-hand smoker acceptable standard for reducing ignition potential from manufactured cigarettes, as a basis for regulation or litigation.

Adolescent↗

Nicotine in hair of bar and restaurant workers.

AIM: To measure the relation between workplace smoking policies and exposures to Environmental Tobacco Smoke (ETS) of workers in bars and restaurants. METHODS: 114 workers in Wellington and Auckland were questioned about sources of exposure to ETS and smoking habits, and details of the smoke-free policy in their work place were recorded. A hair sample was collected from each participant and tested for nicotine. RESULTS: Among non-smoking workers, hair nicotine levels varied strongly according to the smoke free policy at their place of work (Kruskall-Wallis, chi2 = 26.38, p < 0.0001). Those working in 100% smoke free restaurants had much lower levels than staff working in bars with no restrictions on smoking, and levels were intermediate for staff working in places with a partial smoking ban. These findings were not changed when adjustments were made for other sources of ETS exposure. Hair nicotine levels among nonsmokers working in places with no restriction on smoking were similar to hair nicotine levels of active smokers. CONCLUSION: The present New Zealand Smoke Free Environment Act does not protect workers in the hospitality industry from exposure to ETS. The findings from this study highlight the substantial levels of exposure of bar and restaurant staff from patrons' smoking.

Adolescent↗

Weathering the storm: beta-blockade and the potential for disaster in severe hyperthyroidism.

Some patients with advanced thyrotoxicosis have occult cardiac dysfunction. The use of long-acting beta-blockers, traditional in the management of thyrotoxicosis, may have disastrous consequences in this setting. The following report documents the cardiovascular collapse and asystolic arrest of a patient with hyperthyroidism when treated with sotolol. Though the patient was successfully resuscitated, the long duration of action of sotolol necessitated prolonged inotropic and vasopressor support. A shorter acting beta-blocker, such as esmolol, theoretically may be a safer option.

Adrenergic beta-Antagonists↗

Characteristics of fungal growth in soft contact lenses.

Six fungal species (Fusarium sp, Exophiala jeanselmei, Penicillium spp, Aspergillus niger, Paecilomyces spp, and Alternaria spp) were used to inoculate soft contact lenses. Four types of soft lenses were used: high-water (58%) and low-water (38%) content lenses and lenses that were unworn or worn for 1 day. The fungi displayed a range of macroscopic and microscopic features that allowed differentiation of species. There was no statistically significant effect of lens water content on growth rate and only Penicillium spp showed significantly higher growth for worn versus unworn lenses. A number of the fungi showed secretions, thought to be enzymes, which potentially aid in the process of lens penetration.

Journal Article↗

L-arginine partially reverses established adrenocorticotrophin-induced hypertension and nitric oxide deficiency in the rat.

BACKGROUND: L-arginine treatment prevents adrenocorticotrophin (ACTH) induced hypertension in the rat. This study examined whether L-arginine treatment could reverse established ACTH hypertension and its effects on markers of decreased NO activity. METHODS: Sixty-four male Sprague-Dawley rats were randomly divided into 6 groups given 12 days of treatment: (1) sham (0.9% NaCl, 0.5 ml/kg, subcutaneously, sc, n = 16); (2) ACTH (0.5 mg/kg/day, sc, n = 16); (3) sham + L-arginine (0.6% in food, from treatment day 8 onwards, n = 10); (4) ACTH + L-arginine (n = 10); (5) sham + D-arginine (0.6% in food, from T 8 onwards) (n = 6); and (6) ACTH + D-arginine (n = 6). Systolic blood pressure, water intake, urine volume, and body weight were measured every second day. At the end of the experiments, plasma and urinary nitrate/nitrite (NOx), plasma amino acid concentrations (in groups 1-4), and urinary cyclic guanosine monophosphate (cGMP) concentrations were measured. RESULTS: Sham, sham + L-arginine, and sham + D-arginine treatments did not affect blood pressure. ACTH increased systolic blood pressure (from 121 +/- 1 to 147 +/- 2 mmHg, p < 0.001, pooled control vs treatment day 12, mean +/- sem), and this was partially reversed by L-arginine (group 4: from 141 +/- 2 on day 8 to 133 +/- 1 mmHg on day 12, n = 10, p < 0.001). In contrast, D-arginine did not affect blood pressure in ACTH-treated rats (group 6). ACTH increased water intake and urine volume and decreased body weight, and L-arginine administration did not alter these parameters. ACTH decreased plasma citrulline (group 1 vs 2: 115 +/- 7 vs 67 +/- 6 micro M/L, n = 16, p < 0.001) and NOx concentrations (group 1 vs 2: 8.3 +/- 0.8 vs 4.5 +/- 0.6 microM/L, n= 10, p < 0.001) and these decreases were reversed by L-arginine treatment (group 4: citrulline 98 +/- 9 micro M/L, NOx 9.1 +/- 1.6 micro M/L, group 2 vs 4, both p < 0.05). ACTH produced marked increases in urinary cGMP excretion (group 1 vs 2: 0.5 +/- 0.1 vs 1.9 +/- 0.4 nmol/24 h, p < 0.01). CONCLUSION: Supplementation with L-arginine partly reversed established ACTH-induced hypertension and restored plasma NOx and citrulline concentrations to levels seen in sham-treated rats. These data are consistent with previous studies suggesting that functional NO deficiency has a role in ACTH-induced hypertension in rats.

Adrenocorticotropic Hormone↗

Naturally acquired and vaccine-elicited antibodies block erythrocyte cytoadherence of the Plasmodium vivax Duffy binding protein.

Malaria merozoites require the presence of specific surface receptors on the red blood cell for invasion. Plasmodium vivax, requires the Duffy blood group antigen as an obligate receptor for invasion. The parasite Duffy binding protein (DBP) is the ligand involved in this process, making the DBP a potential vaccine candidate. A preliminary objective was to study whether people exposed to vivax malaria acquire antibodies that have the ability to block erythrocyte cytoadherence to the PvDBP. In comparison, we studied the immunogenicity of various recombinant DBP vaccines and investigated their potential to induct antifunctional antibodies. In order to do so, recombinant proteins to different regions of the putative ectodomain of the DBP and a DNA vaccine were used to immunize laboratory animals. An in vitro cytoadherence assay was used to investigate the presence of antifunctional antibodies in plasmas from people naturally exposed to vivax malaria, as well as in antisera obtained by animal vaccination. Our results showed that human plasma from populations naturally exposed to vivax malaria, as well as antisera obtained by vaccination using recombinant proteins, a DNA vaccine, and a synthetic peptide to DBP, inhibited in vitro binding of human erythrocytes to the DBP ligand domain (DBP(II)) in correlation to their previously measured antibody titer. Our results provide further evidence for the vaccine potential of this essential parasite adhesion molecule.

Animals↗

Cloning of a palmitoyl-acyl carrier protein thioesterase from oil palm.

A palmitoyl-acyl carrier protein (ACP) thioesterase cDNA clone was isolated from an oil palm cDNA library. The cDNA was expressed in Escherichia coli as a glutathione S-transferase fusion protein and a crude bacterial extract was assayed for acyl-CoA-hydrolysing activity. The recombinant enzyme was able to hydrolyse medium- and long-chain acyl-CoAs. Northern-blot analysis showed a high level of gene expression in leaf, flower and 15-, 17- and 18-week mesocarp tissues. Low-level gene expression was detected in germinated seedlings and 8- and 12-week mesocarp tissues, but no transcript was detected in any kernel tissues. Southern-blot analysis indicated the presence of a single gene and we have also isolated a genomic clone using the cDNA as a probe. Two genomic fragments were subcloned and a 7 kb contiguous stretch of the oil palm genome was sequenced. Comparison of this sequence with the cDNA sequence identified a putative 93 amino acid transit peptide, most of which is missing from the cDNA. The coding region of the gene consisted of seven exons and six introns.

Cloning, Molecular↗

Does triacylglycerol biosynthesis require diacylglycerol acyltransferase (DAGAT)?

Microsomal membrane preparations from the developing seeds of sunflower (Helianthus annuus L.) catalyse the conversion of sn-glycerol-3-phosphate and acyl-CoA to triacylglycerol via phosphatidic acid and diacylglycerol. The formation of diacylglycerol from phosphatidic acid was Mg2+ dependent and in the presence of EDTA phosphatidic acid accumulated. This property was used to generate large quantities of endogenous radioactive phosphatidic acid in the membranes. On addition of Mg2+ the phosphatidic acid was used in triacylglycerol formation. Acyl-CoA had little effect on the label which accumulated in triacylglycerol from phosphatidic acid. Diacylglycerol acyltransferase, therefore, may not play a major role in oil formation as originally envisaged and other enzymes, including diacylglycerol:diacylglycerol transacylase [Stobart, Mancha, Lenman, Dahlqvist and Stymne (1997) Planta 203, 58-66] may have important biosynthetic functions.

Acyl Coenzyme A↗

Oil biosynthesis in microsomal membrane preparations from Mortierella alpina.

Microsomal membrane preparations from Mortierella alpina catalysed the conversion of sn-glycerol 3-phosphate and [(14)C]oleoyl-CoA to radioactive phosphatidic acid, diacylglycerol and triacylglycerol. Experiments with lysophosphatidic acid and [(14)C]oleoyl-CoA gave a similar pattern of radioactivity in the complex lipids. The specific activity of lysophosphatidate acyltransferase was almost eight times greater than sn-glycerol-3-phosphate acyltransferase, indicating that the first acylation step was limiting in oil assembly in the microsomal membranes. Little conversion of radioactive oleate into phosphatidylcholine occurred, suggesting that triacylglycerol assembly and its relationship to phosphatidylcholine metabolism differed to that found in oilseeds.

Acyl Coenzyme A↗

Partial purification and photoaffinity labelling of sunflower acyl-CoA:lysophosphatidylcholine acyltransferase.

Previous attempts to purify acyl-CoA:1-acyl-lysophosphatidylcholine acyltransferase (EC 2.3.1.23) have been frustrated by difficulties in solubilizing the enzyme without inactivation. Microsomal preparations, from the developing cotyledons of sunflower, in high concentrations of urea retain activity. Gel-filtration liquid chromatography followed by trypsin treatment (minus urea) resulted in the removal of many contaminating proteins without loss of enzyme activity. SDS/PAGE showed the presence of two major peptides with apparent molecular masses of 52 and 59 kDa. These polypeptides cross-reacted with the radiolabelled photoreactive substrate 1-azido-oleoyl-sn-lysophosphatidyl-[N-methyl-(3)H]choline.

1-Acylglycerophosphocholine O-Acyltransferase↗

Sesamin inhibits lysophosphatidylcholine acyltransferase in Mortierella alpina.

The filamentous fungus, Mortierella alpina, accumulates complex lipids relatively rich in arachidonic acid (C(20:4) Delta(5,8,11,14)). The lignan, sesamin, has been used to reduce arachidonic acid production by specifically inhibiting Delta(5)-desaturation [Shimizu, Akimoto, Shinmen, Kawashima, Sugano and Yamada (1991) Lipids 26, 512-516]. Microsomal membrane preparations from M. alpina exhibit acyl-CoA:1-acyl lysophosphatidylcholine acyltransferase (LPCAT) activity. LPCAT is an enzyme involved in channelling fatty acid substrates to phosphatidylcholine for subsequent desaturation. Sesamin was found to inhibit this enzyme as measured in both spectrophotometric and radioactive assays. The inhibitory effect of sesamin on LPCAT was only evident in species of Mortierella and could not be demonstrated in other organisms.

1-Acylglycerophosphocholine O-Acyltransferase↗

Adrenocorticotrophin-induced hypertension: effects of mineralocorticoid and glucocorticoid receptor antagonism.

OBJECTIVE: To examine whether the increase of blood pressure in adrenocorticotrophin-treated rats is mediated through mineralocorticoid or glucocorticoid receptors or corticosterone 6 beta-hydroxylation inhibition. DESIGN: Rats were randomly allocated to 14 treatment groups for 10 days. The treatments included sham injection (n = 35), adrenocorticotrophin (5, 100, 500 micrograms/kg per day, subcutaneously, n = 5, 15 and 15, respectively), spironolactone (100 mg/kg per day, subcutaneously, n = 15), standard-dose or high-dose RU 486 (70 mg/kg every 3 days or 70 mg/kg per day, subcutaneously, n = 5 and 10, respectively), spironolactone + adrenocorticotrophin (100 micrograms/kg per day, n = 5, or 500 micrograms/kg per day, n = 10), standard-dose RU 486 + adrenocorticotrophin (500 micrograms/kg per day, n = 5), high-dose RU 486 + adrenocorticotrophin (100 micrograms/kg per day, n = 10), troleandomycin (40 mg/kg per day, subcutaneously, n = 5) and troleandomycin + adrenocorticotrophin (5 micrograms/kg per day, n = 5). Systolic blood pressure and metabolic parameters were measured every second day. RESULTS: Adrenocorticotrophin treatment increased systolic blood pressure dose-dependently (5 micrograms/kg per day: +14 +/- 2 mmHg; 100 micrograms/kg per day: +20 +/- 2 mmHg; 500 micrograms/kg per day: +28 +/- 2 mmHg, all P < 0.001). Adrenocorticotrophin at 100 and 500 micrograms/kg per day increased plasma sodium and decreased plasma potassium concentrations. Spironolactone did not block adrenocorticotrophin-induced systolic blood pressure changes but did block changes in plasma sodium and potassium levels. Standard-dose RU 486 did not modify the adrenocorticotrophin-induced (500 micrograms/kg per day) systolic blood pressure rise but blocked the effect of adrenocorticotrophin on body weight. High-dose RU 486 partially blocked the adrenocorticotrophin-induced (100 micrograms/kg per day) systolic blood pressure increase (adrenocorticotrophin at 100 micrograms/kg per day: 143 +/- 3 mmHg; high-dose RU 486 + adrenocorticotrophin at 100 micrograms/kg per day: 128 +/- 5 mmHg, P < 0.001) and body-weight loss. Troleandomycin did not alter the development of adrenocorticotrophin-induced hypertension. CONCLUSIONS: Spironolactone and standard-dose RU 486 did not modify adrenocorticotrophin-induced hypertension despite demonstrable antimineralocorticoid and antiglucocorticoid actions. High-dose RU 486 partially blocked adrenocorticotrophin-induced (100 micrograms/kg per day) hypertension, suggesting either a permissive effect of glucocorticoid on blood pressure or other antihypertensive actions of RU 486. Inhibition of glucocorticoid 6 beta-hydroxylation by troleandomycin did not modify adrenocorticotrophin-induced hypertension, suggesting that effects of corticosterone 6 beta-hydroxylation in adrenocorticotrophin-induced hypertension are negligible.

Adrenocorticotropic Hormone↗

Haemodynamic mechanisms of corticotropin (ACTH)-induced hypertension in the rat.

OBJECTIVES: To investigate the roles of cardiac output and systemic and regional resistances in corticotropin (ACTH)-induced hypertension in the rat METHODS: This study consisted of three series of experiments with eight groups of male Sprague-Dawley rats (n = 132). Series 1 comprised groups 1-4, where group 1 = sham (0.9% NaCl, subcutaneous (s.c.) injection); group 2 = ACTH (0.5 mg/kg per day, s.c.); group 3 = atenolol + sham; group 4 = atenolol + ACTH treatments. Series 2 comprised groups 5 and 6, where group 5 = minoxidil + sham and group 6 = minoxidil + ACTH treatments. Series 3 comprised groups 7 and 8, where group 7 = ramipril + sham and group 8 = ramipril + ACTH treatments. Systolic blood pressure, water and food intakes, urine volume, and body weight were measured every second day. After 10 days of treatment, mean arterial blood pressure was measured by intra-arterial cannulation, and cardiac output (CO), and renal, mesenteric and hindquarter blood flows (RBF, MBF and HBF) determined using transonic small animal flowmeters. RESULTS: ACTH treatment increased blood pressure (P < 0.001) with a rise in CO (P < 0.01) and renal vascular resistance (RVR, P < 0.05), but did not affect total peripheral resistance (TPR). Atenolol blocked the rise in CO without affecting the rise in blood pressure produced by ACTH treatment Minoxidil lowered TPR, but did not prevent the rise in blood pressure or renal vascular resistance. Ramipril blunted the rise in RVR and blood pressure without significantly affecting TPR. CONCLUSION: Neither preventing rise in CO nor lowering TPR altered the ACTH-induced rise in blood pressure in the rat However, both the hypertension and rise in RVR were prevented by ramipril. These data suggest that increase in RVR may play a role in the pathogenesis of ACTH-induced hypertension in the rat.

Adrenocorticotropic Hormone↗

Hemodynamic profile of corticotropin-induced hypertension in the rat.

OBJECTIVES: To examine hemodynamic variables in corticotropin-induced hypertension in rats and the effects of reversal of the hypertension by L-arginine on the hemodynamic profile. METHODS: Sixty male Sprague-Dawley rats were randomly divided into four groups: sham treatment (0.9% NaCl, injected subcutaneously); 0.5 mg/kg corticotropin per day, subcutaneously; 0.6% L-arginine in food plus sham; and L-arginine plus corticotropin. Systolic blood pressure, water and food intakes, urine volume, and body weight were measured every second day. After 10 days mean arterial blood pressure was measured by intra-arterial cannulation, and cardiac output, and renal, mesenteric, and hindquarter blood flows were determined using transonic small animal flowmeters. RESULTS: Injection of corticotropin increased blood pressure, water intake, urine volume, and plasma sodium concentration, and decreased body weight and plasma potassium concentration. It increased cardiac output (P < 0.01), mesenteric blood flow (P < 0.05), and renal vascular resistance (P < 0.05), and decreased renal blood flow (P < 0.05), but did not change calculated total peripheral resistance, hindquarter blood flow, mesenteric or hindquarter vascular resistance. L-arginine prevented corticotropin-induced rises in blood pressure (P < 0.001) and renal vascular resistance (P < 0.05), and a fall in renal blood flow (P < 0.05), but did not affect other hemodynamic variables. CONCLUSION: The hemodynamic profile of corticotropin-induced hypertension in the rat is characterized by a rise in cardiac output and renal vascular resistance, a fall in renal blood flow, but no change in total peripheral resistance, hindquarter blood flow, mesenteric vascular resistance, or hindquarter vascular resistance. L-arginine prevented corticotropin-induced rises both in blood pressure and in renal vascular resistance in the rat. These data suggest that the increase in renal vascular resistance might play a role in corticotropin-induced hypertension in the rat.

Adrenocorticotropic Hormone↗

Serologic responses to recombinant Plasmodium vivax Duffy binding protein in a Colombian village.

The Plasmodium vivax Duffy binding protein (DBP) is essential during merozoite invasion into human erythrocytes. Because of its biological importance, the DBP is also seen to have potential use as a malaria blood-stage vaccine. We have used a soluble recombinant DBP (rDBP) containing the functional ligand domain to assess the natural immunogenicity of DBP in a low-endemic vivax malaria region. Human sera from adult residents from a Colombian village with unstable vivax malaria transmission reacted specifically with the rDBP as determined by ELISA. There was a significant positive correlation between increased antibody response (average, median, and percent positives) and age of patients, although the level of responses did vary considerably in their reactivity to the rDBP from negative to very high level within each age group. These data confirm previous findings on the serologic reactivity of the DBP in exposed populations and that immunologic boosting to the DBP occurs in malaria-endemic regions even with low-level transmission.

Adolescent↗

Expression and serologic activity of a soluble recombinant Plasmodium vivax Duffy binding protein.

Plasmodium vivax Duffy binding protein (DBP) is a conserved functionally important protein. P. vivax DBP is an asexual blood-stage malaria vaccine candidate because adhesion of P. vivax DBP to its erythrocyte receptor is essential for the parasite to continue development in human blood. We developed a soluble recombinant protein of P. vivax DBP (rDBP) and examined serologic activity to it in residents of a region of high endemicity. This soluble rDBP product contained the cysteine-rich ligand domain and most of the contiguous proline-rich hydrophilic region. rDBP was expressed as a glutathione S-transferase (GST) fusion protein and was isolated from GST by thrombin treatment of the purified fusion protein bound on glutathione agarose beads. P. vivax rDBP was immunogenic in rabbits and induced antibodies that reacted with P. vivax and Plasmodium knowlesi merozoites. Human sera from adult residents of a region of Papua New Guinea where malaria is highly endemic or P. vivax-infected North American residents reacted with rDBP in an immunoblot and an enzyme-linked immunosorbent assay. The reactivity to reduced, denatured P. vivax rDBP and the cross-reactivity with P. knowlesi indicated the presence of immunogenic conserved linear B-cell epitopes. A more extensive serologic survey of Papua New Guinea residents showed that antibody response to P. vivax DBP is common and increases with age, suggesting a possible boosting of the antibody response in some by repeated exposure to P. vivax. A positive humoral response to P. vivax DBP correlated with a significantly higher response to P. vivax MSP-1(19). The natural immunogenicity of this DBP should strengthen its usefulness as a vaccine.

Adolescent↗