Tao Huang

TL;DR: In this article, a wire saw guide plate structure for craniotomy is described, where buffering heads are installed on the two sides of the outer portion of the guide plate and an air cushion is attached to the outer part of the buffer head.

TL;DR: Increasing NLR obtained on admission is a powerful predictor for inpatient mortality, AKI, and ETI in COVID-19 patients.

Abstract: E-Mail karger@karger.com www.karger.com/jnn © 2015 S. Karger AG, Basel 1661–6499/15/0081–0002$39.50/0 1 Vitamin D Receptor Polymorphism Fok1 Alters Risk of Adenomatous Polyps in Australian Males E.L. Beckett1,2, K.C. le Gras1, M. Veysey3, L. Boyd1, X. Ng1, Z. Yates4, K. Duesing2, M. Lucock1 1School of Environmental and Life Sciences, University of Newcastle, Central Coast, Ourimbah, NSW, Australia; 2Food and Nutrition Flagship, CSIRO, North Ryde, NSW, Australia; 3Central Coast Local Health District, Gosford, NSW, Australia; 4School of Biomedical Sciences and Pharmacy, University of Newcastle, Central Coast, Ourimbah, NSW, Australia E-mail: emma.beckett@uon.edu.au Background/Aims: The vitamin D receptor (VDR) gene polymorphism, Fok1 (rs10735810), may influence risk of cancers via modulation of multiple vitamin D sensitive pathways, including angiogenesis, cell proliferation and differentiation, and protection from oxidative stress. In colorectal cancer (CRC) however, results have been mixed and any association remains contentious [1–7]. Failure to clinically exclude the presence of adenomatous polyps (AP), the benign precursor of CRC, in control cohorts may contribute to the lack of consensus. Insufficient adjustment for other potential risk factors (such as diet, smoking and alcohol intake) may also explain some of the discrepancies. Therefore, we assessed the role of the Fok1 polymorphism in modifying the risk for AP in clinically confirmed cases and controls, adjusting for a range of dietary and lifestyle variables. Methods: Blood was collected from patients undergoing routine colonoscopy (n = 258). Diagnosis of AP was used to classify cases and controls. Fok1 polymorphisms were assessed using RFLP-PCR (F = absence; f = presence of restriction site, early start codon, less transcriptionally active) [8–9]. Dietary habits were estimated from food frequency questionnaires. AP incidence (OR, 95% CI) were calculated by genotype, stratified by sex and corrected for age. Additional adjustments were made for life-style factors (smoking history and alcohol intake), objective markers of diet (blood B12 and folate), and reported markers of dietary habits (including estimated dietary fibre, iron, vitamin C, calcium, vitamin D and fat intake). Regression analysis was used to examine the relationship between vitamin D and AP risk. Results: Participants were aged 18–89 (mean 62.25 ± 0.75); 44% were male. AP were detected in 57 (22%) of participants. No statistically significant relationships were found between AP and Fok1 genotype in females. In males the ‘F’ allele was associated with increased incidence of AP. When adjusted for age only, AP incidence was increased in ‘F’ homozygotes, relative to ‘f’ homozygotes (OR = 6.43, 1.09–123.03). Additional adjustment for lifestyle factors revealed increased AP incidence in those possessing the ‘F’ allele (ORs: FF = 7.59, 1.23–148.70; Ff = 6.42, 1.07–124.68). Further adjustment for dietary variables revealed similar associations. Reported vitamin D intake did not correlate with risk of AP in males or females, regardless of correction for age, smoking status, alcohol consumption or dietary factors (p > 0.05). Conclusion: In Australian males, VDR-Fok1 polymorphisms may influence the risk of AP, the benign precursor to CRC, which in turn, is likely to influence the risk of CRC. Lifestyle & dietary habits influence the strength of this association and need to be fully considered in future studies. This study offers novel insight into the potential for VDR genetics to contribute to risk for adenomatous polyps, and is the first to demonstrate a sex-specific relationship between the VDR-Fok1 polymorphism and risk for adenomatous polyps.