Andreasencampbell7121

Concurrent training incorporates dual exercise modalities, typically resistance and aerobic-based exercise, either in a single session or as part of a periodized training program, that can promote muscle strength, mass, power/force and aerobic capacity adaptations for the purposes of sports performance or general health/wellbeing. Despite multiple health and exercise performance-related benefits, diminished muscle hypertrophy, strength and power have been reported with concurrent training compared to resistance training in isolation. Dietary protein is well-established to facilitate skeletal muscle growth, repair and regeneration during recovery from exercise. The degree to which increased protein intake can amplify adaptation responses with resistance exercise, and to a lesser extent aerobic exercise, has been highly studied. In contrast, much less focus has been directed toward the capacity for protein to enhance anabolic and metabolic responses with divergent contractile stimuli inherent to concurrent training and potentially negate interference in muscle strength, power and hypertrophy. This review consolidates available literature investigating increased protein intake on rates of muscle protein synthesis, hypertrophy, strength and force/power adaptations following acute and chronic concurrent training. Acute concurrent exercise studies provide evidence for the significant stimulation of myofibrillar protein synthesis with protein compared to placebo ingestion. High protein intake can also augment increases in lean mass with chronic concurrent training, although these increases do not appear to translate into further improvements in strength adaptations. Similarly, the available evidence indicates protein intake twice the recommended intake and beyond does not rescue decrements in selective aspects of muscle force and power production with concurrent training.Resistance training (RT) is the only non-pharmacological intervention known to consistently improve, and therefore offset age-related declines in, skeletal muscle mass, strength, and power. Fedratinib RT is also associated with various health benefits that are underappreciated compared with the perceived benefits of aerobic-based exercise. For example, RT participation is associated with reduced all-cause and cancer-related mortality and reduced incidence of cardiovascular disease, hypertension, and symptoms of both anxiety and depression. Despite these benefits, participation in RT remains low, likely due to numerous factors including time constraints, a high-perceived difficulty, and limited access to facilities and equipment. Identification of RT strategies that limit barriers to participation may increase engagement in RT and subsequently improve population health outcomes. Across the lifespan, declines in strength and power occur up to eight times faster than the loss of muscle mass, and are more strongly associateng sedentary behaviour patterns associated with increased cardiometabolic risk. Compared to traditional approaches, minimal-dose RT may also limit negative affective responses, such as increased discomfort and lowered enjoyment, both of which are associated with higher training volumes and may negatively influence exercise adherence. A number of practical factors, including the selection of exercises that target major muscle groups and challenge both balance and the stabilising musculature, may influence the effectiveness of minimal-dose RT on outcomes such as improved independence and quality-of-life in older adults. This narrative review aims to summarise the evidence for minimal-dose RT as a strategy for preserving muscle strength and functional ability across the lifespan, and to discuss practical models and considerations for the application of minimal-dose RT approaches.

The aim of this study was to increase knowledge of genes associated with anorexia nervosa (AN) and their diagnostic offer, using a next generation sequencing (NGS) panel for the identification of genetic variants. The rationale underlying this test is that we first analyze the genes associated with syndromic forms of AN, then genes that were found to carry rare variants in AN patients who had undergone segregation analysis, and finally candidate genes intervening in the same molecular pathways or identified by GWAS or in mouse models.

We developed an NGS gene panel and used it to screen 68 Italian AN patients (63 females, 5 males). The panel included 162 genes. Family segregation study was conducted on available relatives of probands who reported significant genetic variants.

In our analysis, we found potentially deleterious variants in 2 genes (PDE11A and SLC25A13) associated with syndromic forms of anorexia and predicted deleterious variants in the following 12 genes CD36, CACNA1C, DRD4, EPHX2, ESR1, GRIN2A, GRIN3B, LRP2, NPY4R, PTGS2, PTPN22 and SGPP2. Furthermore, by Sanger sequencing of the promoter region of NNAT, we confirmed the involvement of this gene in the pathogenesis of AN. Family segregation studies further strengthened the possible causative role of CACNA1C, DRD4, GRIN2A, PTGS2, SGPP2, SLC25A13 and NNAT genes in AN etiology.

The major finding of our study is the confirmation of the involvement of the NNAT gene in the pathogenesis of AN; furthermore, this study suggests that NGS-based testing can play an important role in the diagnostic evaluation of AN, excluding syndromic forms and increasing knowledge of the genetic etiology of AN.

Level I, experimental study.

Level I, experimental study.

The purpose of this study was to investigate associations between the various definitions of adding-on identified in the literature and HRQoL at 10years following posterior spinal fusion (PSF) for adolescent idiopathic scoliosis (AIS) to identify a clinically relevant definition.

In this retrospective cohort study, patients with Lenke type 1 or 2 AIS with 10-year follow-up after PSF were identified in a multicenter registry. Adding-on was identified independently using 5 published definitions and expert spine surgeons' visual confirmation. Worsening of HRQoL was defined as a preoperative to 10-year postoperative decrease in SRS-22 domain score ≥ the minimal clinically important difference (MCID).

One hundred fifty patients were included, and 118 had HRQoL data available for the main analysis. Worsening pain was noted in 49 (41.5%) patients, appearance in 1 (0.8%), and activity in 70 (59.3%) from preoperative to postoperative. 4 of the 5 definitions of adding-on demonstrated no evidence of association with worsening HRQoL. By Cho's definition (either 1. ≥ 5° increase in Cobb angle AND increase in number of vertebrae in curve distally, or 2. ≥ 5° increase in angulation of 1st disc below LIV), adding-on (27 patients, 22.9%) was associated with an increased risk of worsening pain (59.3% vs. 36.3%, p = 0.033) and activity (77.8% vs. 53.8%, p = 0.026). There was no evidence of association with changes in appearance. Risk of worsening pain and activity was increased by 1.75 and 1.51 times (p = 0.023 and p = 0.002), respectively.

Cho's definition of adding-on was associated with worsening HRQoL at 10years following PSF for Lenke type 1 and 2 AIS. Consistent use of this definition will allow us to compare studies and obtain meaningful information in this population.

Level II.

Level II.MCM3AP-AS1 regulates the cartilage repair in osteoarthritis, but how it regulates osteogenic differentiation of dental pulp stem cells (DPSCs) remains to be determined. DPSCs were isolated and induced for osteogenic differentiation. MCM3AP-AS1 expression was increased along with the osteogenic differentiation of DPSCs, whose expression was positive correlated with those of OCN, alkaline phosphatase (ALP) and RUNX2. On contrary, miR-143-3p expression was decreased along with the osteogenic differentiation and was negatively correlated with those of OCN, ALP and RUNX2. Dual-luciferase reporter gene assay showed that miR-143-3p can be negatively regulated by MCM3AP-AS1 and can regulate IGFBP5. MCM3AP-AS1 overexpression increased the expression levels of osteogenesis-specific genes, ALP activity and mineralized nodules during DPSC osteogenic differentiation, while IGFBP5 knockdown or miR-143-3p overexpression counteracted the effect of MCM3AP-AS1 overexpression in DPSCs. Therefore, this study demonstrated the role of MCM3AP-AS1/miR-143-3p/IGFBP5 axis in regulating DPSC osteogenic differentiation.

Left ventricular (LV) reverse remodeling has been identified as a strong predictor of long-term survival in patients receiving CRT. Interestingly, CRT induces reverse remodeling in the left atrium (LA) as well. It is currently unknown to what extent LA reverse remodeling is correlated to long-term survival after CRT. This study aims to assess the long-term prognostic value of left atrium (LA) reverse remodeling in patients undergoing cardiac resynchronization therapy (CRT).

Baseline and 3-months follow-up echocardiograms after CRT implantation were prospectively assessed to determine changes in left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), left atrial volume (LAV), and left atrial reservoir strain (LAS

). Multivariate Cox regression analysis was performed to identify predictors for long-term survival.

In our study population of 99 patients with a mean follow-up of 6.3 ± 2.1years, 43 patients (43%) reached the end-point of all-cause mortality. More extensive LA reverse remodeling, as measured by a relative increase in LAS

, was observed in survivors compared to non-survivors (43 [29-64] % vs. 8 [2-28] %, P < 0.001, respectively). After multivariate analysis, delta LAS

remained the only significant predictor of mortality [HR per 5% 0.90 (0.86-0.95); AUC 0.78 (0.68-0.88)].

An increase in LAS

is associated with favorable long-term outcome after CRT. The observed clinical importance of LA reverse remodeling after CRT asks for further validation in larger prospective cohorts.

An increase in LASr is associated with favorable long-term outcome after CRT. The observed clinical importance of LA reverse remodeling after CRT asks for further validation in larger prospective cohorts.This study presents a method with high accuracy performance that aims to automatically detect schizophrenia (SZ) from electroencephalography (EEG) records. Unlike related literature studies using traditional machine learning algorithms, the features required for the training of the network are automatically extracted from the EEG records in our method. In order to obtain the time frequency features of the EEG signals, the signal was converted into 2D by using the Continuous Wavelet Transform method. This study has the highest accuracy performance in the relevant literature by using 2D time frequency features in automatic detection of SZ disease. It is trained with Visual Geometry Group-16 (VGG16), an advanced convolutional neural networks (CNN) deep learning network architecture, to extract key features found on scalogram images and train the network. The study shows a high success in classifying SZ patients and healthy individuals with a very satisfactory accuracy of 98% and 99.5%, respectively, using two different datasets consisting of individuals from different age groups.