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Dosimetric Impact of Inter-Fraction Anatomical Changes in Carbon Improve Treatment for High-Risk Cancer of the prostate (AIRC IG 14300).
Purpose To investigate the effect of refractive error on the physiologic thinning rate of the retinal nerve fiber layer (RNFL) in healthy eyes. Materials and Methods. This study analyzed 223 eyes of 141 healthy subjects followed for more than 5 years and underwent at least five serial spectral domain optical coherence tomography (SD-OCT) examinations. Longitudinal RNFL measurements were analyzed by linear mixed models incorporating follow-up duration, baseline RNFL thickness, spherical equivalent (SE), age, intraocular pressure, and visual field mean deviation. Selleck WP1066 Thinning rates were classified according to SE into three groups nonmyopic (NM; >0 D), mild-to-moderately myopic (MM; >-6 D and ≤0 D), and highly myopic (HM; ≤-6 D). Results The overall slopes of change in RNFL thickness over time in the NM, MM, and HM groups were -0.305 ± 0.128, -0.294 ± 0.068, and -0.208 ± 0.097 μm/yr, respectively. Slopes of RNFL thickness changes in these groups were -0.514 ± 0.248, -0.520 ± 0.133, and -0.528 ± 0.188 μm/yr, respectively. Slopes of RNFL thickness changes in these groups were -0.514 ± 0.248, -0.520 ± 0.133, and -0.528 ± 0.188 μm/yr, respectively. Slopes of RNFL thickness changes in these groups were -0.514 ± 0.248, -0.520 ± 0.133, and -0.528 ± 0.188 μm/yr, respectively. Slopes of RNFL thickness changes in these groups were -0.514 ± 0.248, -0.520 ± 0.133, and -0.528 ± 0.188 μm/yr, respectively. Slopes of RNFL thickness changes in these groups were -0.514 ± 0.248, -0.520 ± 0.133, and -0.528 ± 0.188 . Conclusions Refractive error did not affect the physiologic thinning rate of RNFL when assessed by SD OCT. Copyright © 2020 Daun Jeong et al.Construction of an ensemble model is a process of combining many diverse base predictive learners. It arises questions of how to weight each model and how to tune the parameters of the weighting process. The most straightforward approach is simply to average the base models. However, numerous studies have shown that a weighted ensemble can provide superior prediction results to a simple average of models. The main goals of this article are to propose a new weighting algorithm applicable for each tree in the Random Forest model and the comprehensive examination of the optimal parameter tuning. Importantly, the approach is motivated by its flexibility, good performance, stability, and resistance to overfitting. The proposed scheme is examined and evaluated on the Physionet/Computing in Cardiology Challenge 2015 data set. It consists of signals (electrocardiograms and pulsatory waveforms) from intensive care patients which triggered an alarm for five cardiac arrhythmia types (Asystole, Bradycardia, Tachycardia, Ventricular Tachycardia, and Ventricular Fultter/Fibrillation). The classification problem regards whether the alarm should or should not have been generated. It was proved that the proposed weighting approach improved classification accuracy for the three most challenging out of the five investigated arrhythmias comparing to the standard Random Forest model.Improved hygiene leading to reduced exposure to microorganisms has been implicated as one possible cause for the recent "epidemic" of chronic inflammatory diseases (CIDs) in industrialized countries. That is the essence of the hygiene hypothesis that argues that rising incidence of CIDs may be, at least in part, the result of lifestyle and environmental changes that have made us too "clean" for our own good, so causing changes in our microbiota. Apart from genetic makeup and exposure to environmental triggers, inappropriate increase in intestinal permeability (which may be influenced by the composition of the gut microbiota), a "hyper-belligerent" immune system responsible for the tolerance-immune response balance, and the composition of gut microbiome and its epigenetic influence on the host genomic expression have been identified as three additional elements in causing CIDs. During the past decade, a growing number of publications have focused on human genetics, the gut microbiome, and proteomics, suggesting that loss of mucosal barrier function, particularly in the gastrointestinal tract, may substantially affect antigen trafficking, ultimately influencing the close bidirectional interaction between gut microbiome and our immune system. This cross-talk is highly influential in shaping the host gut immune system function and ultimately shifting genetic predisposition to clinical outcome. This observation led to a re-visitation of the possible causes of CIDs epidemics, suggesting a key pathogenic role of gut permeability. Pre-clinical and clinical studies have shown that the zonulin family, a group of proteins modulating gut permeability, is implicated in a variety of CIDs, including autoimmune, infective, metabolic, and tumoral diseases. These data offer novel therapeutic targets for a variety of CIDs in which the zonulin pathway is implicated in their pathogenesis. Copyright © 2020 Fasano A.Chronic infection by the obligate intracellular pathogen Mycobacterium leprae may lead to the development of leprosy. Of note, in the lepromatous clinical form of the disease, failure of the immune system to constrain infection allows the pathogen to reproduce to very high numbers with minimal clinical signs, favoring transmission. The bacillus can modulate cellular metabolism to support its survival, and these changes directly influence immune responses, leading to host tolerance, permanent disease, and dissemination. Among the metabolic changes, upregulation of cholesterol, phospholipids, and fatty acid biosynthesis is particularly important, as it leads to lipid accumulation in the host cells (macrophages and Schwann cells) in the form of lipid droplets, which are sites of polyunsaturated fatty acid-derived lipid mediator biosynthesis that modulate the inflammatory and immune responses. In Schwann cells, energy metabolism is also subverted to support a lipogenic environment. Furthermore, effects on tryptophan and iron metabolisms favor pathogen survival with moderate tissue damage. This review discusses the implications of metabolic changes on the course of M. leprae infection and host immune response and emphasizes the induction of regulatory T cells, which may play a pivotal role in immune modulation in leprosy. Copyright © 2020 de Macedo CS et al.
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