In-Season Hip Thrust vs. Back Squat Training in Female High School Soccer Players

International Journal of Exercise Science 13(4): 49-61, 2020. The barbell back squat provides a highly effective training stimulus to improve lower body strength, speed, and power, which are considered key components of athletic performance in many sports. The barbell hip thrust exercise utilizes similar musculature, and is popular among practitioners, but has received far less scientific examination. The purpose of this study was to evaluate the effects of an in-season resistance training program with hip thrusts or back squats on physical performance in adolescent female soccer players. Fourteen players completed identical whole-body resistance training twice per week for 6 weeks, except one group used the barbell hip thrust (HT) (n = 6) and the other the back squat (SQ) (n = 8). Improvements were observed for both groups in hip thrust 3RM (HT = 34.0%, SQ = 23.8%), back squat 3RM (HT = 34.6%, SQ = 31.0%), vertical jump (HT = 5.4%, SQ = 4.9%), broad jump (HT = 10.5%, SQ = 8.1%), ball kicking distance (HT = 13.2%, SQ = 8.1%), and pro-agility (HT = -1.5%, SQ = -1.5%; faster), but not 36.6-m dash (HT = 2.9%, SQ = 1.9%; slower) with no significant between-group differences. These data indicate that both the hip thrust and the squat provide an effective stimulus to improve these sport-specific performance measures. Practitioners should consider these findings in combination with other factors (equipment availability, ability to coach the movement, training goals, injuries, etc.) when selecting exercises

A test of the effort equalization hypothesis in children with cerebral palsy who have an asymmetric gait

Healthy people can walk nearly effortlessly thanks to their instinctively adaptive gait patterns that tend to minimize metabolic energy consumption. However, the economy of gait is severely impaired in many neurological disorders such as stroke or cerebral palsy (CP). Moreover, self-selected asymmetry of impaired gait does not seem to unequivocally coincide with the minimal energy cost, suggesting the presence of other adaptive origins. Here, we used hemiparetic CP gait as a model to test the hypothesis that pathological asymmetric gait patterns are chosen to equalize the relative muscle efforts between the affected and unaffected limbs. We determined the relative muscle efforts for the ankle and knee extensors by relating extensor joint moments during gait to maximum moments obtained from all-out hopping reference test. During asymmetric CP gait, the unaffected limb generated greater ankle (1.36 +/- 0.15 vs 1.17 +/- 0.16 Nm/kg, p = 0.002) and knee (0.74 +/- 0.33 vs 0.44 +/- 0.19 Nm/kg, p = 0.007) extensor moments compared with the affected limb. Similarly, the maximum moment generation capacity was greater in the unaffected limb versus the affected limb (ankle extensors: 1.81 +/- 0.39 Nm/kg vs 1.51 +/- 0.34 Nm/kg, p = 0.033; knee extensors: 1.83 +/- 0.37 Nm/kg vs 1.34 +/- 0.38 Nm/kg, p = 0.021) in our force reference test. As a consequence, no differences were found in the relative efforts between unaffected and affected limb ankle extensors (77 +/- 12% vs 80 +/- 16%, p = 0.69) and knee extensors (41 +/- 17% vs 38 +/- 23%, p = 0.54). In conclusion, asymmetric CP gait resulted in similar relative muscle efforts between affected and unaffected limbs. The tendency for effort equalization may thus be an important driver of self-selected gait asymmetry patterns, and consequently advantageous for preventing fatigue of the weaker affected side musculature.Peer reviewe

Bayesian modeling of recombination events in bacterial populations

Background: We consider the discovery of recombinant segments jointly with their origins within multilocus DNA sequences from bacteria representing heterogeneous populations of fairly closely related species. The currently available methods for recombination detection capable of probabilistic characterization of uncertainty have a limited applicability in practice as the number of strains in a data set increases. Results: We introduce a Bayesian spatial structural model representing the continuum of origins over sites within the observed sequences, including a probabilistic characterization of uncertainty related to the origin of any particular site. To enable a statistically accurate and practically feasible approach to the analysis of large-scale data sets representing a single genus, we have developed a novel software tool (BRAT, Bayesian Recombination Tracker) implementing the model and the corresponding learning algorithm, which is capable of identifying the posterior optimal structure and to estimate the marginal posterior probabilities of putative origins over the sites. Conclusion: A multitude of challenging simulation scenarios and an analysis of real data from seven housekeeping genes of 120 strains of genus Burkholderia are used to illustrate the possibilities offered by our approach. The software is freely available for download at URL http://web.abo.fi/fak/ mnf//mate/jc/software/brat.html

Cluster analysis to estimate the risk of preeclampsia in the high-risk Prediction and Prevention of Preeclampsia and Intrauterine Growth Restriction (PREDO) study

Objectives Preeclampsia is divided into early-onset (delivery before 34 weeks of gestation) and late-onset (delivery at or after 34 weeks) subtypes, which may rise from different etiopathogenic backgrounds. Early-onset disease is associated with placental dysfunction. Late-onset disease develops predominantly due to metabolic disturbances, obesity, diabetes, lipid dysfunction, and inflammation, which affect endothelial function. Our aim was to use cluster analysis to investigate clinical factors predicting the onset and severity of preeclampsia in a cohort of women with known clinical risk factors. Methods We recruited 903 pregnant women with risk factors for preeclampsia at gestational weeks 12(+0)-13(+6). Each individual outcome diagnosis was independently verified from medical records. We applied a Bayesian clustering algorithm to classify the study participants to clusters based on their particular risk factor combination. For each cluster, we computed the risk ratio of each disease outcome, relative to the risk in the general population. Results The risk of preeclampsia increased exponentially with respect to the number of risk factors. Our analysis revealed 25 number of clusters. Preeclampsia in a previous pregnancy (n = 138) increased the risk of preeclampsia 8.1 fold (95% confidence interval (CI) 5.711.2) compared to a general population of pregnant women. Having a small for gestational age infant (n = 57) in a previous pregnancy increased the risk of early-onset preeclampsia 17.5 fold (95%CI 2.160.5). Cluster of those two risk factors together (n = 21) increased the risk of severe preeclampsia to 23.8-fold (95%CI 5.160.6), intermediate onset (delivery between 34(+0)-36(+6) weeks of gestation) to 25.1-fold (95%CI 3.179.9) and preterm preeclampsia (delivery before 37(+0) weeks of gestation) to 16.4-fold (95%CI 2.052.4). Body mass index over 30 kg/m(2) (n = 228) as a sole risk factor increased the risk of preeclampsia to 2.1-fold (95%CI 1.13.6). Together with preeclampsia in an earlier pregnancy the risk increased to 11.4 (95%CI 4.520.9). Chronic hypertension (n = 60) increased the risk of preeclampsia 5.3-fold (95%CI 2.49.8), of severe preeclampsia 22.2-fold (95%CI 9.941.0), and risk of early-onset preeclampsia 16.7-fold (95%CI 2.057.6). If a woman had chronic hypertension combined with obesity, gestational diabetes and earlier preeclampsia, the risk of term preeclampsia increased 4.8-fold (95%CI 0.121.7). Women with type 1 diabetes mellitus had a high risk of all subgroups of preeclampsia. Conclusion The risk of preeclampsia increases exponentially with respect to the number of risk factors. Early-onset preeclampsia and severe preeclampsia have different risk profile from term preeclampsia.Peer reviewe

Comprehensive self-tracking of blood glucose and lifestyle with a mobile application in the management of gestational diabetes : a study protocol for a randomised controlled trial (eMOM GDM study)

IntroductionGestational diabetes (GDM) causes various adverse short-term and long-term consequences for the mother and child, and its incidence is increasing globally. So far, the most promising digital health interventions for GDM management have involved healthcare professionals to provide guidance and feedback. The principal aim of this study is to evaluate the effects of comprehensive and real-time self-tracking with eMOM GDM mobile application (app) on glucose levels in women with GDM, and more broadly, on different other maternal and neonatal outcomes.Methods and analysisThis randomised controlled trial is carried out in Helsinki metropolitan area. We randomise 200 pregnant women with GDM into the intervention and the control group at gestational week (GW) 24-28 (baseline, BL). The intervention group receives standard antenatal care and the eMOM GDM app, while the control group will receive only standard care. Participants in the intervention group use the eMOM GDM app with continuous glucose metre (CGM) and activity bracelet for 1 week every month until delivery and an electronic 3-day food record every month until delivery. The follow-up visit after intervention takes place 3 months post partum for both groups. Data are collected by laboratory blood tests, clinical measurements, capillary glucose measures, wearable sensors, air displacement plethysmography and digital questionnaires. The primary outcome is fasting plasma glucose change from BL to GW 35-37. Secondary outcomes include, for example, self-tracked capillary fasting and postprandial glucose measures, change in gestational weight gain, change in nutrition quality, change in physical activity, medication use due to GDM, birth weight and fat percentage of the child.Ethics and disseminationThe study has been approved by Ethics Committee of the Helsinki and Uusimaa Hospital District. The results will be presented in peer-reviewed journals and at conferences.Peer reviewe

The impact of host metapopulation structure on the population genetics of colonizing bacteria

Many key bacterial pathogens are frequently carried asymptomatically, and the emergence and spread of these opportunistic pathogens can be driven, or mitigated, via demographic changes within the host population. These inter-host transmission dynamics combine with basic evolutionary parameters such as rates of mutation and recombination, population size and selection, to shape the genetic diversity within bacterial populations. Whilst many studies have focused on how molecular processes underpin bacterial population structure, the impact of host migration and the connectivity of the local populations has received far less attention. A stochastic neutral model incorporating heightened local transmission has been previously shown to fit closely with genetic data for several bacterial species. However, this model did not incorporate transmission limiting population stratification, nor the possibility of migration of strains between subpopulations, which we address here by presenting an extended model. We study the consequences of migration in terms of shared genetic variation and show by simulation that the previously used summary statistic, the allelic mismatch distribution, can be insensitive to even large changes in microepidemic and migration rates. Using likelihood-free inference with genotype network topological summaries we fit a simpler model to commensal and hospital samples from the common nosocomial pathogens Staphylococcus aureus, Staphylococcus epidermidis, Enterococcus faecalis and Enterococcus faecium. Only the hospital data for E. faecium display clearly marked deviations from the model predictions which may be attributable to its adaptation to the hospital environment

Plasmids Shaped the Recent Emergence of the Major Nosocomial Pathogen Enterococcus faecium

Enterococcus faecium is a gut commensal of humans and animals but is also listed on the WHO global priority list of multidrug-resistant pathogens. Many of its antibiotic resistance traits reside on plasmids and have the potential to be disseminated by horizontal gene transfer. Here, we present the first comprehensive population-wide analysis of the pan-plasmidome of a clinically important bacterium, by whole-genome sequence analysis of 1,644 isolates from hospital, commensal, and animal sources of E. faecium. Long-read sequencing on a selection of isolates resulted in the completion of 305 plasmids that exhibited high levels of sequence modularity. We further investigated the entirety of all plasmids of each isolate (plasmidome) using a combination of short-read sequencing and machine-learning classifiers. Clustering of the plasmid sequences unraveled different E. faecium populations with a clear association with hospitalized patient isolates, suggesting different optimal configurations of plasmids in the hospital environment. The characterization of these populations allowed us to identify common mechanisms of plasmid stabilization such as toxin-antitoxin systems and genes exclusively present in particular plasmidome populations exemplified by copper resistance, phosphotransferase systems, or bacteriocin genes potentially involved in niche adaptation. Based on the distribution of k-mer distances between isolates, we concluded that plasmidomes rather than chromosomes are most informative for source specificity of E. faecium. IMPORTANCE Enterococcus faecium is one of the most frequent nosocomial pathogens of hospital-acquired infections. E. faecium has gained resistance against most commonly available antibiotics, most notably, against ampicillin, gentamicin, and vancomycin, which renders infections difficult to treat. Many antibiotic resistance traits, in particular, vancomycin resistance, can be encoded in autonomous and extrachromosomal elements called plasmids. These sequences can be disseminated to other isolates by horizontal gene transfer and confer novel mechanisms to source specificity. In our study, we elucidated the total plasmid content, referred to as the plasmidome, of 1,644 E. faecium isolates by using short- and long-read whole-genome technologies with the combination of a machine-learning classifier. This was fundamental to investigate the full collection of plasmid sequences present in our collection (pan-plasmidome) and to observe the potential transfer of plasmid sequences between E. faecium hosts. We observed that E. faecium isolates from hospitalized patients carried a larger number of plasmid sequences compared to that from other sources, and they elucidated different configurations of plasmidome populations in the hospital environment. We assessed the contribution of different genomic components and observed that plasmid sequences have the highest contribution to source specificity. Our study suggests that E. faecium plasmids are regulated by complex ecological constraints rather than physical interaction between hosts.Peer reviewe

Presynaptic vesicle protein SEPTIN5 regulates the degradation of APP C-Terminal fragments and the levels of Aβ

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).Alzheimer's disease (AD) is a neurodegenerative disease characterized by aberrant amyloid-β (Aβ) and hyperphosphorylated tau aggregation. We have previously investigated the involvement of SEPTIN family members in AD-related cellular processes and discovered a role for SEPTIN8 in the sorting and accumulation of β-secretase. Here, we elucidated the potential role of SEPTIN5, an interaction partner of SEPTIN8, in the cellular processes relevant for AD, including amyloid precursor protein (APP) processing and the generation of Aβ. The in vitro and in vivo studies both revealed that the downregulation of SEPTIN5 reduced the levels of APP C-terminal fragments (APP CTFs) and Aβ in neuronal cells and in the cortex of Septin5 knockout mice. Mechanistic elucidation revealed that the downregulation of SEPTIN5 increased the degradation of APP CTFs, without affecting the secretory pathway-related trafficking or the endocytosis of APP. Furthermore, we found that the APP CTFs were degraded, to a large extent, via the autophagosomal pathway and that the downregulation of SEPTIN5 enhanced autophagosomal activity in neuronal cells as indicated by altered levels of key autophagosomal markers. Collectively, our data suggest that the downregulation of SEPTIN5 increases the autophagy-mediated degradation of APP CTFs, leading to reduced levels of Aβ in neuronal cells.This research was supported by the Academy of Finland (grant numbers 307866 and 315459), the Sigrid Jusélius Foundation, the Strategic Neuroscience Funding of the University of Eastern Finland, and the National Institute of Mental Health of the National Institutes of Health (grant numbers R01MH099660, R01DC015776, R21HD053114, and U54HD090260). Catarina B. Ferreira is a PhD Fellow (NeurULisboa - Integrated Neurosciences PhD program, supported by an individual grant from Fundação para a Ciência e Tecnologia (FCT), (PD/BD/128390/2017, SFRH/PD/BD/114441/2016, PD/BD/128091/2016). Work was also supported by Santa Casa da Misericórdia de Lisboa (MB37-2017) and SynaNet (LISBOA-01-0145-FEDER-0073919), under the grant agreement no. 692340, and the project was co-financed by FEDER, POR Lisboa 2020, Programa Operacional Regional de Lisboa, from PORTUGAL 2020 and by Fundação para a Ciência e a Tecnologia.info:eu-repo/semantics/publishedVersio

DHCR24 exerts neuroprotection upon inflammation-induced neuronal death

Abstract Background DHCR24, involved in the de novo synthesis of cholesterol and protection of neuronal cells against different stress conditions, has been shown to be selectively downregulated in neurons of the affected brain areas in Alzheimer’s disease. Methods Here, we investigated whether the overexpression of DHCR24 protects neurons against inflammation-induced neuronal death using co-cultures of mouse embryonic primary cortical neurons and BV2 microglial cells upon acute neuroinflammation. Moreover, the effects of DHCR24 overexpression on dendritic spine density and morphology in cultured mature mouse hippocampal neurons and on the outcome measures of ischemia-induced brain damage in vivo in mice were assessed. Results Overexpression of DHCR24 reduced the loss of neurons under inflammation elicited by LPS and IFN-γ treatment in co-cultures of mouse neurons and BV2 microglial cells but did not affect the production of neuroinflammatory mediators, total cellular cholesterol levels, or the activity of proteins linked with neuroprotective signaling. Conversely, the levels of post-synaptic cell adhesion protein neuroligin-1 were significantly increased upon the overexpression of DHCR24 in basal growth conditions. Augmentation of DHCR24 also increased the total number of dendritic spines and the proportion of mushroom spines in mature mouse hippocampal neurons. In vivo, overexpression of DHCR24 in striatum reduced the lesion size measured by MRI in a mouse model of transient focal ischemia. Conclusions These results suggest that the augmentation of DHCR24 levels provides neuroprotection in acute stress conditions, which lead to neuronal loss in vitro and in vivo