616 research outputs found

    NEXAFS Chemical State and Bond Lengths of p-Aminobenzoic Acid in Solution and Solid State

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    Solid-state and solution pH-dependent NEXAFS studies allow direct observation of the electronic state of para-aminobenzoic acid (PABA) as a function of its chemical environment, revealing the chemical state and bonding of the chemical species. Variations in the ionization potential (IP) and 1s→π* resonances unequivocally identify the chemical species (neutral, cationic, or anionic) present and the varying local environment. Shifts in σ* shape resonances relative to the IP in the NEXAFS spectra vary with C-N bond length, and the important effect of minor alterations in bond length is confirmed with nitrogen FEFF calculations, leading to the possibility of bond length determination in solution

    Glucocorticoid receptor gene polymorphisms associated with progression of lung disease in young patients with cystic fibrosis

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    <p>Abstract</p> <p>Background</p> <p>The variability in the inflammatory burden of the lung in cystic fibrosis (CF) patients together with the variable effect of glucocorticoid treatment led us to hypothesize that <it>glucocorticoid receptor </it>(<it>GR</it>) gene polymorphisms may affect glucocorticoid sensitivity in CF and, consequently, may contribute to variations in the inflammatory response.</p> <p>Methods</p> <p>We evaluated the association between four <it>GR </it>gene polymorphisms, <it>TthIII</it>, <it>ER22/23EK</it>, <it>N363S </it>and <it>BclI</it>, and disease progression in a cohort of 255 young patients with CF. Genotypes were tested for association with changes in lung function tests, infection with <it>Pseudomonas aeruginosa </it>and nutritional status by multivariable analysis.</p> <p>Results</p> <p>A significant non-corrected for multiple tests association was found between <it>BclI </it>genotypes and decline in lung function measured as the forced expiratory volume in one second (FEV<sub>1</sub>) and the forced vital capacity (FVC). Deterioration in FEV<sub>1 </sub>and FVC was more pronounced in patients with the <it>BclI </it>GG genotype compared to the group of patients with <it>BclI </it>CG and CC genotypes (p = 0.02 and p = 0.04 respectively for the entire cohort and p = 0.01 and p = 0.02 respectively for F508del homozygous patients).</p> <p>Conclusion</p> <p>The <it>BclI </it>polymorphism may modulate the inflammatory burden in the CF lung and in this way influence progression of lung function.</p

    Glucocorticoid receptor gene polymorphisms do not affect growth in fetal and early postnatal life. The Generation R Study

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    Background: Glucocorticoids have an important role in early growth and development. Glucocorticoid receptor gene polymorphisms have been identified that contribute to the variability in glucocorticoid sensitivity. We examined whether these glucocorticoid receptor gene polymorphisms are associated with growth in fetal and early postnatal life.Methods: This study was embedded in a population-based prospective cohort study from fetal life onwards. The studied glucocorticoid receptor gene polymorphisms included BclI (rs41423247), TthIIII (rs10052957), GR-9β (rs6198), N363S (rs6195) and R23K (rs6789 and6190). Fetal growth was assessed by ultrasounds in second and third trimester of pregnancy. Anthropometric measurements in early childhood were performed at birth and at the ages of 6, 14 and 24 months postnatally. Analyses focused on weight, length and head circumference. Analyses were based on 2,414 healthy, Caucasian children.Results: Glucocorticoid receptor gene polymorphisms were not associated with fetal weight, birth weight and early postnatal weight. Also, no associations were found with length and head circumference. Neither were these polymorphisms associated with the risks of low birth weight or growth acceleration from birth to 24 months of age.Conclusions: We found in a large population-based cohort no evidence for an effect of known glucocorticoid receptor gene polymorphisms on fetal and early post

    Effectiveness of interventions to promote healthy diet in primary care: systematic review and meta-analysis of randomised controlled trials

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    Background A diet rich in fruit, vegetables and dietary fibre and low in fat is associated with reduced risk of chronic disease. This review aimed to estimate the effectiveness of interventions to promote healthy diet for primary prevention among participants attending primary care.&lt;p&gt;&lt;/p&gt; Methods A systematic review of trials using individual or cluster randomisation of interventions delivered in primary care to promote dietary change over 12 months in healthy participants free from chronic disease or defined high risk states. Outcomes were change in fruit and vegetable intake, consumption of total fat and fibre and changes in serum cholesterol concentration.&lt;p&gt;&lt;/p&gt; Results Ten studies were included with 12,414 participants. The design and delivery of interventions were diverse with respect to grounding in behavioural theory and intervention intensity. A meta-analysis of three studies showed an increase in fruit consumption of 0.25 (0.01 to 0.49) servings per day, with an increase in vegetable consumption of 0.25 (0.06 to 0.44) serving per day. A further three studies that reported on fruit and vegetable consumption together showed a pooled increment of 0.50 (0.13 to 0.87) servings per day. The pooled effect on consumption of dietary fibre, from four studies, was estimated to be 1.97 (0.43 to 3.52) gm fibre per day. Data from five studies showed a mean decrease in total fat intake of 5.2% of total energy (1.5 to 8.8%). Data from three studies showed a mean decrease in serum cholesterol of 0.10 (-0.19 to 0.00) mmol/L.&lt;p&gt;&lt;/p&gt; Conclusion Presently-reported interventions to promote healthy diet for primary prevention in primary care, which illustrate a diverse range of intervention methods, may yield small beneficial changes in consumption of fruit, vegetables, fibre and fat over 12 months. The present results do not exclude the possibility that more effective intervention strategies might be developed.&lt;p&gt;&lt;/p&gt

    Uromodulin concentrations are not associated with incident CKD among persons with coronary artery disease

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    <p>Abstract</p> <p>Background</p> <p>A common variant of the UMOD gene was linked with prevalent chronic kidney disease (CKD) in large, genomics consortia. One community-based study found that urine concentrations of the uromodulin protein forecast risk of incident CKD. This study within persons with known coronary artery disease (CAD) evaluated whether uromodulin concentrations could distinguish CKD risk.</p> <p>Methods</p> <p>In the Heart and Soul Study, the UMOD snp (12917707) was genotyped in 879 individuals with baseline creatinine clearance (CrCl) measured from a 24-hour urine collection. Uromodulin protein was measured from stored urine specimens among a subset of 120 participants, balanced by genotype. Incident CKD cases (N = 102) were defined by an initial CrCl > 70 ml/min and a 5-year follow-up CrCl <60 ml/min; controls (N = 94) were matched on age, sex, and race.</p> <p>Results</p> <p>Among 527 self-described White participants with DNA, 373 (71%) were homozygous for the dominant allele (G/G), 133 (25%) were heterozygous (G/T) and only 21 (4%) were homozygous for the minor allele (T/T). The T/T genotype had an approximately 11 ml/min higher CrCl than the other 2 groups, but this difference did not reach statistical significance (p = 0.20). The T/T genotype had significantly lower uromodulin levels than the common G/G genotype, and the G/T genotype had intermediate levels. However, uromodulin concentrations were similar between cases and controls (44 vs. 48 mg/dL, p = 0.88).</p> <p>Conclusions</p> <p>This study among a cohort of persons with established CAD found no association between urine uromodulin and incident CKD, although UMOD genotype was associated with urine uromodulin concentrations.</p

    Human papillomavirus prevalence among indigenous and non-indigenous Australian women prior to a national HPV vaccination program

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    <p>Abstract</p> <p>Background</p> <p>Indigenous women in Australia have a disproportionate burden of cervical cancer despite a national cervical screening program. Prior to introduction of a national human papilloma virus (HPV) vaccination program, we determined HPV genotype prevalence by Indigenous status and residence in remote areas.</p> <p>Methods</p> <p>We recruited women aged 17 to 40 years presenting to community-based primary health services for routine Pap screening across Australia. A liquid-based cytology (LBC) cervical specimen was tested for HPV DNA using the AMPLICOR HPV-DNA test and a PGMY09/11-based HPV consensus PCR; positive specimens were typed by reverse hybridization. We calculated age-adjusted prevalence by weighting to relevant population data, and determined predictors of HPV-DNA positivity by age, Indigenous status and area of residence using logistic regression.</p> <p>Results</p> <p>Of 2152 women (655 Indigenous), prevalence of the high-risk HPV genotypes was similar for Indigenous and non-Indigenous women (HPV 16 was 9.4% and 10.5%, respectively; HPV 18 was 4.1% and 3.8%, respectively), and did not differ by age group. In younger age groups, the prevalence of other genotypes also did not differ, but in those aged 31 to 40 years, HPV prevalence was higher for Indigenous women (35% versus 22.5%; <it>P </it>< 0.001), specifically HPV clades α5 (OR = 2.1, 95% CI 1.1 to 4.3) and α7, excluding type 18 (OR 1.9, 95% CI 1.1 to 3.3). In multivariate analysis, detection of any HPV genotype was strongly associated with smoking and Pap-test abnormalities, with both risk factors more common among Indigenous women.</p> <p>Conclusion</p> <p>Although we found no difference in the prevalence of HPV16/18 among Australian women by Indigenous status or, for Indigenous women, residence in remote regions, differences were found in the prevalence of risk factors and some other HPV genotypes. This reinforces the importance of cervical screening as a complement to vaccination for all women, and the value of baseline data on HPV genotype prevalence by Indigenous status and residence for the monitoring of vaccine impact.</p
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