18 research outputs found

    Preparation, characterization and antibacterial effects of eco-friendly gold nanorods

    Get PDF
    Purpose: To synthesize and characterize eco-friendly gold nanorods (Au-NRs) and to assess their effects against two bacterial strains.Methods: Synthesis of eco-friendly gold nanorods was done from an aqueous solution of chloroauric acid and cetyltrimethylammonium bromide by mixing Olea europaea fruit and Acacia nilotica husk extracts with the latter as a reducing agent. The synthesis was monitored by ultraviolet–visible (UV) spectrophotmetry and a zetasizer, while the morphology of the resulting nanorods was assessed by transmission electron microscopy (TEM) and scanning electron microscopy (SEM) coupled with an energy-dispersive spectrophotometer (EDS). The effect of the prepared eco-nanorods on growth of Escherichia coli and Staphylococcus aureus bacteria were investigated by agar diffusion method.Results: The synthesized Au-NRs were mostly rod-shaped, with mean size of 96 nm. They exhibited a potent antibacterial activity against Gram-positive and  Gram-negative microorganisms (Escherichia coli and Staphylococcus aureus).Conclusion: The findings suggest that the nanoformulation of the biomaterial mix of Olea europaea fruit and Acacia nilotica husk extracts is a cost-effective, eco-friendly, and non-toxic synthesis of Au- NRs which has therpeautic potential.Keywords: Olea europaea, Acacia nilotica, Gold nanorods, Eco-friendly synthesis, Gram-positive and Gram-negative microorganism

    Endocrine Disruptors and Obesity: An Examination of Selected Persistent Organic Pollutants in the NHANES 1999–2002 Data

    Get PDF
    Recent evidence suggests that endocrine disrupting chemicals (EDCs) may cause perturbations in endogenous hormonal regulation that predispose to weight gain. Using data from NHANES (1999–2002), we investigated the association between body mass index (BMI), waist circumference (WC) and selected persistent organic pollutants (POPs) via multiple linear regressions. Consistent interaction was found between gender, ln oxychlordane and ln p,p’ DDT. Also, we found an association between WC and ln oxychlordane and ln hpcdd in subjects with detectable levels of POPs, whereas an association between WC and ln p,p’ DDT was observed in all subjects. Furthermore, ln Ocdd showed an increase with higher WC and BMI, whereas, ln trans-nonachlor decreased with higher BMI. Hence, BMI and WC are associated with POPs levels, making the chemicals plausible contributors to the obesity epidemic

    An Examination of the Association of Selected Toxic Metals with Total and Central Obesity Indices: NHANES 99-02

    Get PDF
    It is conceivable that toxic metals contribute to obesity by influencing various aspects of metabolism, such as by substituting for essential micronutrients and vital metals, or by inducing oxidative stress. Deficiency of the essential metal zinc decreases adiposity in humans and rodent models, whereas deficiencies of chromium, copper, iron, and magnesium increases adiposity. This study utilized the NHANES 99-02 data to explore the association between waist circumference and body mass index with the body burdens of selected toxic metals (barium, cadmium, cobalt, cesium, molybdenum, lead, antimony, thallium, and tungsten). Some of the associations were significant direct relationships (barium and thallium), and some of the associations were significant inverse relationships (cadmium, cobalt, cesium, and lead). Molybdenum, antimony, and tungsten had mostly insignificant associations with waist circumference and body mass index. This is novel result for most of the toxic metals studied, and a surprising result for lead because high stored lead levels have been shown to correlate with higher rates of diabetes, and obesity may be a key risk factor for developing diabetes. These associations suggest the possibility that environmental exposure to metals may contribute to variations in human weight gain/loss. Future research, such as prospective studies rather than the cross-sectional studies presented here, is warranted to confirm these findings

    Missing Data in Randomized Clinical Trials for Weight Loss: Scope of the Problem, State of the Field, and Performance of Statistical Methods

    Get PDF
    BACKGROUND: Dropouts and missing data are nearly-ubiquitous in obesity randomized controlled trails, threatening validity and generalizability of conclusions. Herein, we meta-analytically evaluate the extent of missing data, the frequency with which various analytic methods are employed to accommodate dropouts, and the performance of multiple statistical methods. METHODOLOGY/PRINCIPAL FINDINGS: We searched PubMed and Cochrane databases (2000-2006) for articles published in English and manually searched bibliographic references. Articles of pharmaceutical randomized controlled trials with weight loss or weight gain prevention as major endpoints were included. Two authors independently reviewed each publication for inclusion. 121 articles met the inclusion criteria. Two authors independently extracted treatment, sample size, drop-out rates, study duration, and statistical method used to handle missing data from all articles and resolved disagreements by consensus. In the meta-analysis, drop-out rates were substantial with the survival (non-dropout) rates being approximated by an exponential decay curve (e(-lambdat)) where lambda was estimated to be .0088 (95% bootstrap confidence interval: .0076 to .0100) and t represents time in weeks. The estimated drop-out rate at 1 year was 37%. Most studies used last observation carried forward as the primary analytic method to handle missing data. We also obtained 12 raw obesity randomized controlled trial datasets for empirical analyses. Analyses of raw randomized controlled trial data suggested that both mixed models and multiple imputation performed well, but that multiple imputation may be more robust when missing data are extensive. CONCLUSION/SIGNIFICANCE: Our analysis offers an equation for predictions of dropout rates useful for future study planning. Our raw data analyses suggests that multiple imputation is better than other methods for handling missing data in obesity randomized controlled trials, followed closely by mixed models. We suggest these methods supplant last observation carried forward as the primary method of analysis

    Bisphenol A Induces Hepatotoxicity through Oxidative Stress in Rat Model

    Get PDF
    Reactive oxygen species (ROS) are cytotoxic agents that lead to significant oxidative damage. Bisphenol A (BPA) is a contaminant with increasing exposure to it and exerts both toxic and estrogenic effects on mammalian cells. Due to limited information concerning the effect of BPA on liver, this study investigates whether BPA causes hepatotoxicity by induction of oxidative stress in liver. Rats were divided into five groups: The first four groups, BPA (0.1, 1, 10, 50 mg/kg/day) were administrated orally to rats for four weeks. The fifth group was taken water with vehicle. The final body weights in the 0.1 mg group showed a significant decrease compared to control group. Significant decreased levels of reduced glutathione, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and catalase activity were found in the 50 mg BPA group compared to control groups. High dose of BPA (50 mg/kg) significantly increased the biochemical levels of ALT, ALP and total bilirubin. BPA effect on the activity of antioxidant genes was confirmed by real time PCR in which the expression levels of these genes in liver tissue were significantly decrease compared to control. Data from this study demonstrate that BPA generate ROS and reduce the antioxidant gene expression that causes hepatotoxicity

    Bisphenol A Detection in Various Brands of Drinking Bottled Water in Riyadh, Saudi Arabia Using Gas Chromatography/Mass Spectrometer

    No full text
    Purpose: To assess whether bisphenol A contamination occurred in seven brands of bottled drinking water in Riyadh, Saudi Arabia. Methods: Liquid-liquid extraction (using dichloromethane) was used to analytically extract bisphenol A from drinking water bottles and a gas chromatograph-mass spectrometer was employed for its detection using a splitless capillary column and helium as the carrier gas. Results: The concentration of bisphenol A (BPA) was high in all the bottled water brands tested. The mean concentration of BPA of the bottled water stored indoors (4.03 ng/L) was significantly lower than that stored outdoors (7.5 ng/L). Conclusion: Our results show that significant amounts of BPA leached from bottle containers into the water. Long storage of bottled water under direct sunlight should be avoided to reduce the risk of human exposure to BPA

    Bisphenol A Induces Hepatotoxicity through Oxidative

    No full text
    Reactive oxygen species (ROS) are cytotoxic agents that lead to significant oxidative damage. Bisphenol A (BPA) is a contaminant with increasing exposure to it and exerts both toxic and estrogenic effects on mammalian cells. Due to limited information concerning the effect of BPA on liver, this study investigates whether BPA causes hepatotoxicity by induction of oxidative stress in liver. Rats were divided into five groups: The first four groups, BPA (0.1, 1, 10, 50 mg/kg/day) were administrated orally to rats for four weeks. The fifth group was taken water with vehicle. The final body weights in the 0.1 mg group showed a significant decrease compared to control group. Significant decreased levels of reduced glutathione, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and catalase activity were found in the 50 mg BPA group compared to control groups. High dose of BPA (50 mg/kg) significantly increased the biochemical levels of ALT, ALP and total bilirubin. BPA effect on the activity of antioxidant genes was confirmed by real time PCR in which the expression levels of these genes in liver tissue were significantly decrease compared to control. Data from this study demonstrate that BPA generate ROS and reduce the antioxidant gene expression that causes hepatotoxicity
    corecore