6 research outputs found

    Interaction between SNPs and arsenic in drinking water on risk of type 2 diabetes in Dhaka, Bangladesh, 2001–2011.

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    a<p>Models were adjusted for age, sex, BMI, smoking, skin lesion, SNPs and arsenic in drinking water using piece-wise regression models.</p>b<p>Q-values were calculated using FDR method for p for interaction among whole population.</p>c<p>P for interactions were 0.613 for rs1051055 (<i>CDC123</i>), 0.048 for rs699780 (<i>NOTCH2</i>), and 0.219 for rs2688 (<i>TCF2</i>) among people exposed to water arsenic less than 148 μg/L.</p

    Distribution of Demographic, Lifestyle, and Arsenic Exposure Variables by Diabetes Status (n = 919) in Dhaka, Bangladesh, 2001–2003 (Baseline).

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    a<p>SD and IQR denoted standard deviation and interquartile range, respectively.</p>b<p>P-values from Fisher's exact test for sex, marital status, education attainment, BMI, cigarette smoking, and skin lesion; or from Wilcoxon rank sum test with continuity correction for age, and arsenic in drinking water. 1 participant was missing for education and 8 participants were missing for smoking status.</p

    Associations between SNPs and risks of type 2 diabetes in Dhaka, Bangladesh, 2001–2011.

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    a<p>Models were adjusted for age, sex, BMI, smoking, skin lesion, and arsenic in drinking water using penalized splines.</p>b<p>P-value for overall effects of three markers in <i>ADAMST9</i> was 0.006 (q-value = 0.066) using kernel machine regression adjusting for age, sex, BMI, smoking, skin lesion, and arsenic in drinking water.</p

    Translation of polymeric microneedles for treatment of human diseases: recent trends, progress, and challenges

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    The ongoing search for biodegradable and biocompatible microneedles (MNs) that are strong enough to penetrate skin barriers, easy to prepare, and can be translated for clinical use continues. As such, this review paper is focused upon discussing the key points (e.g., choice polymeric MNs) for the translation of MNs from laboratory to clinical practice. The review reveals that polymers are most appropriately used for dissolvable and swellable MNs due to their wide range of tunable properties and that natural polymers are an ideal material choice as they structurally mimic native cellular environments. It has also been concluded that natural and synthetic polymer combinations are useful as polymers usually lack mechanical strength, stability, or other desired properties for the fabrication and insertion of MNs. This review evaluates fabrication methods and materials choice, disease and health conditions, clinical challenges, and the future of MNs in public healthcare services, focusing on literature from the last decade. </p

    In <i>utero</i> arsenic exposure and epigenome-wide associations in placenta, umbilical artery, and human umbilical vein endothelial cells

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    <p>Exposure to arsenic early in life has been associated with increased risk of several chronic diseases and is believed to alter epigenetic programming <i>in utero</i>. In the present study, we evaluate the epigenome-wide association of arsenic exposure <i>in utero</i> and DNA methylation in placenta (n = 37), umbilical artery (n = 45) and human umbilical vein endothelial cells (HUVEC) (n = 52) in a birth cohort using the Infinium HumanMethylation450 BeadChip array. Unadjusted and cell mixture adjusted associations for each tissue were examined along with enrichment analyses relative to CpG island location and omnibus permutation tests of association among biological pathways. One CpG in artery (cg26587014) and 4 CpGs in placenta (cg12825509; cg20554753; cg23439277; cg21055948) reached a Bonferroni adjusted level of significance. Several CpGs were differentially methylated in artery and placenta when controlling the false discovery rate (q-value<0.05), but none in HUVEC. Enrichment of hypomethylated CpG islands was observed for artery while hypermethylation of open sea regions were present in placenta relative to prenatal arsenic exposure. The melanogenesis pathway was differentially methylated in artery (Max F <i>P</i> < 0.001), placenta (Max F <i>P</i> < 0.001), and HUVEC (Max F <i>P</i> = 0.02). Similarly, the insulin-signaling pathway was differentially methylated in artery (Max F <i>P</i> = 0.02), placenta (Max F <i>P</i> = 0.02), and HUVEC (Max F <i>P</i> = 0.02). Our results show that prenatal arsenic exposure can alter DNA methylation in artery and placenta but not in HUVEC. Further studies are needed to determine if these alterations in DNA methylation mediate the effect of prenatal arsenic exposure and health outcomes later in life.</p
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