Browsing by Author "Palmer B"

Now showing 1 - 3 of 3
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    Environmental drivers of antimicrobial resistance – cadmium contamination & antibiotic resistance in soil samples from a rural airstrip.
    (2023-12-05) Heydari A; Kim N; Biggs P; Horswell J; Gielen G; Siggins A; Bromhead C; Palmer B
    Environmental contamination with both inorganic and organic compounds is a growing problem globally. In this study we investigated links between heavy metal contamination of soil and selection for antibiotic resistance in soil bacteria. Soil samples taken at 10 m intervals along the length of a 70 m transect of a rural airstrip used for aerial topdressing located in Belmont Regional Park near Wellington were analysed for heavy metal content and resistance profiles of heterotrophic bacteria cultured were characterised. A gradient of cadmium contamination (a known contaminant of superphosphate fertiliser) ranging from 1.14 to 7.20 mg kg-1 of dry soil was detected in the samples. Total bacterial counts were significantly reduced at the most heavily contaminated subsites, with >60% of isolates resistant to 0.01 mM CdCl2. The ratio of antibiotic resistant isolates to total CFU was significantly higher at the most contaminated compared to the least contaminated subsite for five common antibiotics. Metagenomic analysis of total DNA from three subsites showed significantly different profiles at all taxonomic levels. This suggests environmental contamination with heavy metals may be a significant and under-appreciated driver of selection for antimicrobial resistance.
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    Monoamine oxidase (MAO) inhibitory effects of candidate MAO inhibitors found in cigarette smoke.
    (23/11/2021) Niraula P; Palmer B; Truman P; Page R
    There is strong evidence that tobacco smoke inhibits both MAO A and MAO B isoforms in the body. However, which components of cigarette smoke are responsible for MAO inhibition is not clear yet. Our group has identified six previously unidentified candidate MAO inhibitors from the tobacco smoke. The MAO inhibitory effects of these candidate inhibitors were compared with that of nicotine and TPM (Tobacco Particulate Matter). An SH-SY5Y cell line was exposed to different regimens of ethanol (control), nicotine, TPM and the cocktail of candidate inhibitors. A final concentration 0.2 μM nicotine was used and the concentration of each candidate inhibitor was relative to that originally found in TPM. We found that nicotine did not have any significant MAO inhibitory effect compared to the control. TPM inhibited overall MAO activity by 39%, while the MAO inhibition by cocktail of candidate inhibitors was 47%. The results suggest that the candidate inhibitors identified by our group are the major contributors to the total MAO inhibitory activity depicted by cigarette smoke and potentially unlocks the mystery behind the components responsible for MAO inhibition by cigarette smoke in smokers.
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    sFlt-1 and NTproBNP independently predict mortality in a cohort of heart failure patients.
    (2/12/2018) Paterson MA; Pilbrow AP; Frampton CM; Cameron VA; Pemberton CJ; Lund M; Devlin GP; Doughty RN; Richards AM; Palmer B
    Objective: Soluble fms-like tyrosine kinase-1 (sFlt-1) is a circulating receptor for VEGF-A. Recent reports of elevated plasma levels of sFlt-1 in coronary heart disease and heart failure (HF) motivated our study aimed at investigating the utility of sFlt-1 as a prognostic biomarker in heart failure patients. Methods: ELISA assays for sFlt-1 and NTproBNP were performed in n=858 patients from a prospective multicentre, observational study (the PEOPLE study) of outcome among patients after appropriate treatment for an episode of acute decompensated HF in New Zealand. Plasma was sampled at a baseline visit and stored at -80°C. Statistical tests were adjusted for patient age at baseline visit, skewed data were log-adjusted and the endpoint for clinical outcome analysis was all-cause death. Patients were followed for a median of 3.63 (range 0.74-5.50) years. Results: Mean baseline plasma sFlt-1 was 125 +/- 2.01 pg/ml. sFlt-1 was higher in patients with HF with reduced ejection fraction (HFrEF) (130 +/- 2.62 pg/ml, n=553) compared to those with HF with preserved EF (HFpEF) (117 +/-3.59 pg/ml, n=305; p=0.005). sFlt-1 correlated with heart rate (r=0.148, p<0.001), systolic blood pressure (r=-0.139, p<0.001) and LVEF (r=-0.088, p=0.019). A Cox proportional hazards model showed sFlt-1 was a predictor of all-cause death (HR=6.30, p<0.001) in the PEOPLE cohort independent of age, NTproBNP, ischaemic aetiology, and NYHA class (n=842, 274 deaths), established predictors of mortality in the PEOPLE cohort. Conclusion: sFlt-1 levels at baseline should be investigated further as a predictor of death; complementary to established prognostic biomarkers in heart failure.