Mattinglypehrson4159

Adolescent athletes can feature significantly greater muscle strength and tendon stiffness compared to untrained peers. However, to date, it is widely unclear if radial muscle and tendon hypertrophy may contribute to loading-induced adaptation at this stage of maturation. The present study compares the morphology of the vastus lateralis (VL) and the patellar tendon between early-adolescent athletes and untrained peers. In 14 male elite athletes (A) and 10 untrained controls (UC; 12-14 years of age), the VL was reconstructed from full muscle segmentations of magnetic resonance imaging (MRI) sequences and ultrasound imaging was used to measure VL fascicle length and pennation angle. The physiological cross-sectional area (PCSA) of the VL was calculated by dividing muscle volume by fascicle length. The cross-sectional area (CSA) of the patellar tendon was measured over its length based on MRI segmentations as well. Considering body mass as covariate in the analysis, there were no significant differences between ociated with imbalances of muscle strength and tendon stiffness and could have implications for the disposition towards tendon overuse injury.Background Recent studies indicate that aquaporin (AQP) water channels have a regulatory function in human platelet secretion and in procoagulant response of murine platelets. However, the engagement of AQPs in morphological changes, procoagulant response, and thrombus formation in human blood has never been investigated. Methods Confocal microscopy was used to study platelet spreading, filopodia formation, ballooning, and thrombus formation under flow. Flow cytometry was utilized to assess platelet phosphatidylserine (PS) exposure and microparticles shedding. Kinetics of clot formation in vitro was evaluated by thromboelastometry. Mouse model of ferric chloride (III) (FeCl3)-induced thrombosis was used to investigate thrombus formation in vivo. Results We found that chloroauric(III) acid (HAuCl4), a classical AQP inhibitor (10-100 μM), reduced spreading of human platelets on collagen-coated surfaces and inhibited filopodia formation in a fluid phase. Under flow conditions, HAuCl4 (100 μM) attenuated thrombi growth on collagen, platelet secretion, and PS exposure. Thrombus formation was restored by the addition of exogenous adenosine diphosphate (ADP). Protein Tyrosine Kinase inhibitor Collagen-evoked platelet procoagulant response (evaluated as PS exposure, shedding of microparticles, platelet-dependent thrombin generation, and membrane ballooning) was distinctly reduced by HAuCl4 (25-200 μM), as well as the dynamics of clot formation. In mouse model of thrombosis, reduction of surface of PS-positive cells within thrombus was observed in the presence of HAuCl4 (1-10 mg/kg). Conclusion These results suggest that in human platelets AQPs are crucial for agonist-evoked morphological changes, thrombus formation under flow, and in development of procoagulant response. Antithrombotic effect in vivo suggests that nontoxic inhibitors of AQPs may be considered as potential candidates for a novel class of antiplatelet drugs.

The passive stiffness of skeletal muscle can drastically affect muscle function

, such as the case for fibrotic tissue or patients with cerebral palsy. The two constituents of skeletal muscle that dominate passive stiffness are the intracellular protein titin and the collagenous extracellular matrix (ECM). However, efforts to correlate stiffness and measurements of specific muscle constituents have been mixed, and thus the complete mechanisms for changes to muscle stiffness remain unknown. We hypothesize that biaxial stretch can provide an improved approach to evaluating passive muscle stiffness.

We performed planar biaxial materials testing of passively stretched skeletal muscle and identified three previously published datasets of uniaxial materials testing. We developed and employed a constitutive model of passive skeletal muscle that includes aligned muscle fibers and dispersed ECM collagen fibers with a bimodal von Mises distribution. Parametric modeling studies and fits to experimental data (both ls testing data of passively stretched skeletal muscle and use of constitutive modeling and finite element analysis to explore the interaction between stiffness, constituent variability, and applied deformation in passive skeletal muscle. The results highlight the importance of biaxial stretch in evaluating muscle stiffness and in further considering the role of ECM collagen in modulating passive muscle stiffness.Long non-coding RNA (lncRNA) is involved in many biological processes, and it has been closely investigated. However, research into the role of lncRNA in ovine ovarian development is scant and poorly understood, particularly in relation to the molecular mechanisms of ovine oocyte maturation. In the current study, RNA sequencing was performed with germinal vesicle (GV) and in vitro matured metaphase II (MII) stage oocytes, isolated from ewes. Through the use of bioinformatic analysis, abundant candidate lncRNAs in stage-specific ovine oocytes were identified, and their trans- and cis-regulatory effects were deeply dissected using computational prediction software. Functional enrichment analysis of these lncRNAs revealed that they were involved in the regulation of many key signaling pathways during ovine oocyte development, which was reflected by their targeted genes. From this study, multiple lncRNA-mRNA networks were presumed to be involved in key signaling pathways regarding ovine oocyte maturation and meiotic resumption. In particular, one novel lncRNA (MSTRG.17927) appeared to mediate the regulation of phosphatidylinositol 3-kinase signaling (PI3K) signaling during ovine oocyte maturation. Therefore, this research offers novel insights into the molecular mechanisms underlying ovine oocyte meiotic maturation regulated by lncRNA-mRNA networks from a genome-wide perspective.

Exergaming may be a viable alternative to more traditional exercise. As high-intensity exercise can provide substantial health benefits, the purpose of this study was to investigate the long-term effectiveness of providing inactive adults with access to a high-intensity exergaming platform.

In this study, 52 inactive adults (<150 min of exercise per week), aged 18 years or older, were randomized (11) into an exergaming (

= 27) or a control group (

= 25). Exergaming participants were given access to the Playpulse exergaming platform for 6 months, where they decided how frequently they wanted to use the platform. The primary outcome measure, analyzed with a mixed model, was peak oxygen uptake (V̇O

). Secondary outcomes included body composition, blood pressure, and blood markers of cardiometabolic health.

Mean V̇O

at 6 months was 42.3 (SD 7.0) mL⋅kg

⋅min

and 41.9 (SD 7.4) mL⋅kg

⋅min

for the exergaming and control group, respectively with no significant between-group differences (-0.7, 95% CI -2.7 to 1.3,

= 0.49). Apart from increased moderate-intensity physical activity in the exergaming group at 3 months (21.9 min⋅day

, 95% CI 2.2 to 41.5,

= 0.03) compared to the control group, there were no significant between-group differences for any outcome at either 3 or 6 months. On average, participants in the exergaming group performed 12 (SD 13) exergaming sessions with an average heart rate of 74.5 (SD 7.5)% of maximum heart rate, throughout the intervention.

Due to low exergaming frequency over the 6-month intervention, exergaming participants showed no significant health benefits compared to control. Our study indicates that although the Playpulse exergaming platform is found enjoyable, this is not enough to motivate inactive adults to regularly engage in exercise and thereby improve health.

www.clinicaltrials.gov, identifier NCT03513380.

www.clinicaltrials.gov, identifier NCT03513380.Pain is a fundamental feature of inflammation. The immune system plays a critical role in the activation of sensory neurons and there is increasing evidence of neuro-inflammatory mechanisms contributing to painful pathologies. The inflammasomes are signaling multiprotein complexes that are key components of the innate immune system. They are intimately involved in inflammatory responses and their activation leads to production of inflammatory cytokines that in turn can affect sensory neuron function. Accordingly, the contribution of inflammasome activation to pain signaling has attracted considerable attention in recent years. NLRP3 is the best characterized inflammasome and there is emerging evidence of its role in a variety of inflammatory pain conditions. In vitro and in vivo studies have reported the activation and upregulation of NLRP3 in painful conditions including gout and rheumatoid arthritis, while inhibition of NLRP3 function or expression can mediate analgesia. In this review, we discuss painful conditions in which NLRP3 inflammasome signaling has been pathophysiologically implicated, as well as NLRP3 inflammasome-mediated mechanisms and signaling pathways that may lead to the activation of sensory neurons.Bicuspid aortic valve (BAV), the most frequent congenital heart malformation, is characterized by the presence of a two-leaflet aortic valve instead of a three-leaflet one. BAV disease progression is associated with valvular dysfunction (in the form of stenosis or regurgitation) and aortopathy, which can lead to aneurysm and aortic dissection. This morphological abnormality modifies valve dynamics and promotes eccentric blood flow, which gives rise to alterations of the flow pattern and wall shear stress (WSS) of the ascending aorta. Recently, evidence of endothelial dysfunction (ED) in BAV disease has emerged. Different studies have addressed a reduced endothelial functionality by analyzing various molecular biomarkers and cellular parameters in BAV patients. Some authors have found impaired functionality of circulating endothelial progenitors in these patients, associating it with valvular dysfunction and aortic dilation. Others focused on systemic endothelial function by measuring artery flow-mediated dila by many, it is not clear which its main cause may be. Comprehending the pathways that promote ED and its relevance in BAV could help further understand and maybe prevent the serious consequences of this disease. This review will discuss the ED present in BAV, focusing on the latest evidence, biomarkers for ED and potential therapeutic targets (Figure 1).To date, there has been no study on the long-term effects of resistance exercise on sarcopenia and obesity indices for people with sarcopenia. The present study thus aimed to determine the effect of 18 months of periodized, high-velocity/intensity/effort progressive resistance training (HIT-RT) on body composition and strength in older men with osteosarcopenia. Using a single-blind, two-group parallel design, 43 community-dwelling men, 72 years and older, with osteopenia and sarcopenia in Erlangen-Nürnberg, Germany, were randomly assigned to two study arms by drawing lots (1) an exercise group that conducted a consistently supervised periodized high-velocity/intensity/effort protocol (HIT-RT; n = 21) on machines twice a week for 18 months or (2) a control group (CG; n = 22) that maintained their physical activity/exercise habits. Both groups were supplied with protein, cholecalciferol, and calcium according to current recommendations. The study outcomes were lean body mass (LBM), total and abdominal body fat as determined by dual-energy X-ray absorptiometry and maximum hip/leg extensor strength as assessed on an isokinetic leg press at baseline and after 8, 12, and 18 months of follow-up.