Proctorgiles0393

© 2020 The Authors. Published under the terms of the CC BY 4.0 license.WHAT IS KNOWN AND OBJECTIVE Polypharmacy is common, and many medications have cognitive side effects. Such effects can be transient and subside when the drug in question is discontinued or can be long-lasting with effects present for years afterwards. Although formal assessment of cognition is feasible and often undertaken in neuropsychiatric trials, these effects are usually neglected in the evaluation of any non-neuropsychiatric health intervention. Medication effects can be assessed within a cognitive footprint framework, to account for the magnitude and the duration of cognitive side effects, with some likely to have a greater and more lasting effect than others. COMMENT Adverse event reporting suggests that many medications may be indirectly associated with cognitive effects, for example due to headaches, somnolence and 'dizziness'; however, inferring causation from adverse event reporting can be problematic. In order to better understand the impact of investigational drug and concomitant medications effen different drug regimens. © 2020 The Authors. Journal of Clinical Pharmacy and Therapeutics published by John Wiley & Sons Ltd.BACKGROUND Trace elements' (TEs) contamination of parenteral nutrition (PN) solutions is an ongoing concern. The aims of this study were 1) to measure actual TE concentrations in PN admixtures compared with ordered concentrations and 2) compare TE intake with current recommendations. METHODS PN admixtures from discarded bags were collected from patients receiving home PN and on inpatient wards. Samples were collected from 72 patients (39 inpatients, 33 receiving home PN). Age, percentage energy intake from PN, and PN orders were collected from patients' charts. PN samples were analyzed for TEs, including chromium (Cr) and manganese (Mn), and concentration measurements compared with ordered concentrations and current recommendations. RESULTS Measured Cr and Mn concentrations were higher than ordered concentrations 5.3 ± 1.7 vs 2.8 ± 1.5 µg/L; P 1 year. Manganese should also be excluded from PN admixture for pediatric patients but plasms monitoring 2-3 times per year is recommended for those on long-term PN. © 2020 American Society for Parenteral and Enteral Nutrition.PURPOSE To investigate the dosimetric robustness of dynamically collimated proton therapy (DCPT) treatment plans delivered using a dynamic collimation system (DCS) with respect to random uncertainties in beam spot and collimator position as well as systematic offsets in the DCS mounting alignment. This work also demonstrates a technique that can increase plan robustness while preserving target conformity. METHODS Variability in beam spot and collimator positioning can result in changes to a beam-let's dose distribution and incident fluence. The robustness of the DCPT treatment plans were evaluated for three intracranial treatment sites by modeling treatment variability as normally distributed random variables with standard deviations reflecting a clinical system. The simulated treatment plans were then re-calculated and compared against their nominal, idealized dose distribution among several trials. It was hypothesized that a plan's robustness to these delivery variables could be reduced by restricting a triainties associated with this new treatment modality. A simple approach utilizing a minimum trimmer offset was able to preserve the majority of the target conformity and healthy tissue sparing the DCS technology affords while minimizing the uncertainties in this treatment approach. This article is protected by copyright. All rights reserved.Previous studies on the association of adiposity with endometrial cancer risk have mostly used body mass index (BMI) as the main exposure of interest. Whether more precise measures of body fat, such as body fat percentage and fat mass estimated by bioimpedance analyses, are better indicators of risk than BMI is unknown. The role of central adiposity and fat-free mass in endometrial cancer development remains unclear. selleckchem We used Cox regression models to estimate hazard ratios (HR) and corresponding 95% confidence intervals (CI) for the associations of various measures of body size/composition with the risk of endometrial cancer among 135 110 postmenopausal women enrolled in UK Biobank. During a mean follow up of 6.8 years, 706 endometrial cancers were diagnosed, with a mean age at diagnosis of 65.5 years. The HRs (95% CIs) for endometrial cancer per 1 SD increase in BMI, body fat percentage and fat mass were broadly comparable, being 1.71 (1.61-1.82), 1.92 (1.75-2.11) and 1.73 (1.63-1.85), respectively. There was an indication of positive association between central adiposity, as reflected by waist circumference (HRper 1-SD increase = 1.08, 95% CI 1.00-1.17) and waist to hip ratio (HRper 1-SD increase = 1.13, 95% CI 1.01-1.26), and endometrial cancer risk after accounting for BMI. Fat-free mass was not an independent predictor of risk in this cohort. These findings suggest that body fat percentage and fat mass are not better indicators of endometrial cancer risk than BMI. Further studies are needed to establish whether central adiposity contributes to risk beyond overall adiposity. © 2020 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.Few genetic risk factors have been demonstrated to be specifically associated with aggressive prostate cancer (PrCa). Here, we report a case-case study of PrCa comparing the prevalence of germline pathogenic/likely pathogenic (P/LP) genetic variants in 787 men with aggressive disease and 769 with nonaggressive disease. Overall, we observed P/LP variants in 11.4% of men with aggressive PrCa and 9.8% of men with nonaggressive PrCa (two-tailed Fisher's exact tests, P = .28). The proportion of BRCA2 and ATM P/LP variant carriers in men with aggressive PrCa exceeded that observed in men with nonaggressive PrCa; 18/787 carriers (2.3%) and 4/769 carriers (0.5%), P = .004, and 14/787 carriers (0.02%) and 5/769 carriers (0.01%), P = .06, respectively. Our findings contribute to the extensive international effort to interpret the genetic variation identified in genes included on gene-panel tests, for which there is currently an insufficient evidence-base for clinical translation in the context of PrCa risk. © 2020 UICC.