Online video-based resistance training improves the physical capacity of junior basketball athletes

ABSTRACT: Klusemann, MJ, Pyne, DB, Fay, T, and Drinkwater, EJ. Online Video-Based Resistance Training Improves the Physical Capacity of Junior Basketball Athletes. J Strength Cond Res 26(10): 2677-2684, 2012-Junior basketball athletes require a well-designed resistance training program to improve their physical development. Lack of expert supervision and resistance training in junior development pathways may be overcome by implementing an online video-based program. The aim of this study was to compare the magnitude of improvement (change) in physical performance and strength and functional movement patterns of junior basketball athletes using either a fully supervised or an online video-based resistance training program. Thirty-eight junior basketball athletes (males, n = 17; age, 14 ± 1 year; height, 1.79 ± 0.10 m; mass, 67 ± 12 kg; females, n = 21; age, 15 ± 1 year; height, 1.70 ± 0.07 m; mass, 62 ± 8 kg) were randomly assigned into a supervised resistance training group (SG, n = 13), video training group (VG, n = 13) or control group (CG, n = 12) and participated in a 6-week controlled experimental trial. Pre- and posttesting included measures of physical performance (20-m sprint, step-in vertical jump, agility, sit and reach, line drill, and Yo-Yo intermittent recovery level 1), strength (15 s push-up and pull-up), and functional movement screening (FMS). Both SG and VG achieved 3-5% ± 2-4% (mean ± 90% confidence limits) greater improvements in several physical performance measures (vertical jump height, 20-m sprint time, and Yo-Yo endurance performance) and a 28 ± 21% greater improvement in push-up strength compared with the CG. The SG attained substantially larger gains in FMS scores over both the VG (12 ± 10%) and CG (13 ± 8%). Video-based training appears to be a viable option to improve physical performance and strength in junior basketball athletes. Qualified supervision is recommended to improve functional movement patterns in junior athletes.     

Uncovering Wolbachia Diversity upon Artificial Host Transfer

The common endosymbiotic Wolbachia bacteria influence arthropod hosts in multiple ways. They are mostly recognized for their manipulations of host reproduction, yet, more recent studies demonstrate that Wolbachia also impact host behavior, metabolic pathways and immunity. Besides their biological and evolutionary roles, Wolbachia are new potential biological control agents for pest and vector management. Importantly, Wolbachia-based control strategies require controlled symbiont transfer between host species and predictable outcomes of novel Wolbachia-host associations. Theoretically, this artificial horizontal transfer could inflict genetic changes within transferred Wolbachia populations. This could be facilitated through de novo mutations in the novel recipient host or changes of haplotype frequencies of polymorphic Wolbachia populations when transferred from donor to recipient hosts. Here we show that Wolbachia resident in the European cherry fruit fly, Rhagoletis cerasi, exhibit ancestral and cryptic sequence polymorphism in three symbiont genes, which are exposed upon microinjection into the new hosts Drosophila simulans and Ceratitis capitata. Our analyses of Wolbachia in microinjected D. simulans over 150 generations after microinjection uncovered infections with multiple Wolbachia strains in trans-infected lines that had previously been typed as single infections. This confirms the persistence of low-titer Wolbachia strains in microinjection experiments that had previously escaped standard detection techniques. Our study demonstrates that infections by multiple Wolbachia strains can shift in prevalence after artificial host transfer driven by either stochastic or selective processes. Trans-infection of Wolbachia can claim fitness costs in new hosts and we speculate that these costs may have driven the shifts of Wolbachia strains that we saw in our model system.     

Caenorhabditis elegans RMI2 functional homolog-2 (RMIF-2) and RMI1 (RMH-1) have both overlapping and distinct meiotic functions within the BTR complex

Homologous recombination is a high-fidelity repair pathway for DNA double-strand breaks employed during both mitotic and meiotic cell divisions. Such repair can lead to genetic exchange, originating from crossover (CO) generation. In mitosis, COs are suppressed to prevent sister chromatid exchange. Here, the BTR complex, consisting of the Bloom helicase (HIM-6 in worms), topoisomerase 3 (TOP-3), and the RMI1 (RMH-1 and RMH-2) and RMI2 scaffolding proteins, is essential for dismantling joint DNA molecules to form non-crossovers (NCOs) via decatenation. In contrast, in meiosis COs are essential for accurate chromosome segregation and the BTR complex plays distinct roles in CO and NCO generation at different steps in meiotic recombination. RMI2 stabilizes the RMI1 scaffolding protein, and lack of RMI2 in mitosis leads to elevated sister chromatid exchange, as observed upon RMI1 knockdown. However, much less is known about the involvement of RMI2 in meiotic recombination. So far, RMI2 homologs have been found in vertebrates and plants, but not in lower organisms such as Drosophila, yeast, or worms. We report the identification of the Caenorhabditis elegans functional homolog of RMI2, which we named RMIF-2. The protein shows a dynamic localization pattern to recombination foci during meiotic prophase I and concentration into recombination foci is mutually dependent on other BTR complex proteins. Comparative analysis of the rmif-2 and rmh-1 phenotypes revealed numerous commonalities, including in regulating CO formation and directing COs toward chromosome arms. Surprisingly, the prevalence of heterologous recombination was several fold lower in the rmif-2 mutant, suggesting that RMIF-2 may be dispensable or less strictly required for some BTR complex-mediated activities during meiosis.     

Exportin T and Exportin 5: tRNA and miRNA biogenesis - and beyond

Abstract The biogenesis of most eukaryotic kinds of RNA requires nuclear export, which is mediated by a variety of specific nuclear transport receptors. The nuclear export receptors Exportin-t (Exp-t) and Exportin 5 (Exp5), and their homologues, are involved in the export of transfer RNA to the cytoplasm. Exp5 is further involved in additional nucleocytoplasmic transport pathways, which include nuclear export of microRNA precursors (pre-miRNAs) and pre-60S ribosomal subunits. Inactivation of Exp5 results in nuclear accumulation of pre-miRNAs and perturbation of gene expression, and its mutation was recently found in malignant diseases. Here, we compare the cellular function of Exp5 and Exp-t with focus on Exp5 substrates and its role in diseases.     

The ER membrane complex (EMC) can functionally replace the Oxa1 insertase in mitochondria

Two multisubunit protein complexes for membrane protein insertion were recently identified in the endoplasmic reticulum (ER): the guided entry of tail anchor proteins (GET) complex and ER membrane complex (EMC). The structures of both of their hydrophobic core subunits, which are required for the insertion reaction, revealed an overall similarity to the YidC/Oxa1/Alb3 family members found in bacteria, mitochondria, and chloroplasts. This suggests that these membrane insertion machineries all share a common ancestry. To test whether these ER proteins can functionally replace Oxa1 in yeast mitochondria, we generated strains that express mitochondria-targeted Get2–Get1 and Emc6–Emc3 fusion proteins in Oxa1 deletion mutants. Interestingly, the Emc6–Emc3 fusion was able to complement an Δoxa1 mutant and restored its respiratory competence. The Emc6–Emc3 fusion promoted the insertion of the mitochondrially encoded protein Cox2, as well as of nuclear encoded inner membrane proteins, although was not able to facilitate the assembly of the Atp9 ring. Our observations indicate that protein insertion into the ER is functionally conserved to the insertion mechanism in bacteria and mitochondria and adheres to similar topological principles.

Redirecting the core subunits of the protein membrane insertion complex EMC into mitochondria rescues cells deficient for the mitochondrial Oxa1 system; this supports the hypothesis that the machinery for protein insertion into the ER membrane is functionally analogous to the YidC/Oxa1/Alb3 family of bacteria, mitochondria and chloroplasts.     

Coexpression of acidic fibroblast growth factor enhances specific productivity and antibody titers in transiently transfected HEK293 cells

Recombinant proteins are of great commercial and scientific interest. However, most current production methods using mammalian cells involve the time- and labor-intensive step of creating stable cell lines. Although production methods based on transient gene expression could offer a significant improvement, transient transfection is currently still limited by low titers and low specific productivity compared to stable cell lines. To overcome these bottlenecks, we have explored the use of various growth factors to enhance specific productivity and titers in the context of transient gene expression. For that purpose, several growth factors were cloned and screened for their effect on transient gene expression in HEK293E and CHO-DG44 cells. In particular, acidic fibroblast growth factor (aFGF) was able to increase specific productivity by 60% and recombinant protein titers by 80% in HEK293E cells, while FGF9 increased titers by 250% in CHO-DG44 cells.     

Deposition within the vicinity of the Mid-Eifelian High: detailed sedimentological study and magnetic susceptibility of a mixed ramp-related system from the Eifelian Lauch and Nohn formations (Devonian; Ohlesberg,Eifel, Germany)

This study focuses on the base of the Eifelian stage and on the abandoned Ohlesberg quarry. The exposed section (92 m thick) is related to the Lauch and Nohn formations. Petrographic study leads to the definition of 11 microfacies which are integrated in a palaeogeographical model. It corresponds to a complex ramp setting where carbonate, mixed and siliciclastic deposits coexist. The microfacies evolution is interpreted in terms of bathymetric and lateral variations, showing a general shallowing-upward trend and transitions between carbonate-dominated and siliciclastic-dominated sedimentary domains. This interpretation is supported by trends in magnetic susceptibility data. Even if the proximity to emerged areas appears to be the major influence on magnetic susceptibility values, the influence of carbonate productivity and wave agitation is also noted. The Ohlesberg section clearly points to the local and regional complex facies architecture, and advocates to variegated depositional environments along the Mid-Eifelian High.     

Integrating Top-Down and Bottom-Up Sensory Processing by Somato-Dendritic Interactions

The classical view of cortical information processing is that of a bottom-up process in a feedforward hierarchy. However, psychophysical, anatomical, and physiological evidence suggests that top-down effects play a crucial role in the processing of input stimuli. Not much is known about the neural mechanisms underlying these effects. Here we investigate a physiologically inspired model of two reciprocally connected cortical areas. Each area receives bottom-up as well as top-down information. This information is integrated by a mechanism that exploits recent findings on somato-dendritic interactions. (1) This results in a burst signal that is robust in the context of noise in bottom-up signals. (2) Investigating the influence of additional top-down information, priming-like effects on the processing of bottom-up input can be demonstrated. (3) In accordance with recent physiological findings, interareal coupling in low-frequency ranges is characteristically enhanced by top-down mechanisms. The proposed scheme combines a qualitative influence of top-down directed signals on the temporal dynamics of neuronal activity with a limited effect on the mean firing rate of the targeted neurons. As it gives an account of the system properties on the cellular level, it is possible to derive several experimentally testable predictions.     

The heat shock protein HSP70 promotes mouse NK cell activity against tumors that express inducible NKG2D ligands

The stress-inducible heat shock protein (HSP) 70 is known to function as an endogenous danger signal that can increase the immunogenicity of tumors and induce CTL responses. We show in this study that HSP70 also activates mouse NK cells that recognize stress-inducible NKG2D ligands on tumor cells. Tumor size and the rate of metastases derived from HSP70-overexpressing human melanoma cells were found to be reduced in T and B cell-deficient SCID mice, but not in SCID/beige mice that lack additionally functional NK cells. In the SCID mice with HSP70-overexpressing tumors, NK cells were activated so that they killed ex vivo tumor cells that expressed NKG2D ligands. In the tumors, the MHC class I chain-related (MIC) A and B molecules were found to be expressed. Interestingly, a counter selection was observed against the expression of MICA/B in HSP70-overexpressing tumors compared with control tumors in SCID, but not in SCID/beige mice, suggesting a functional relevance of MICA/B expression. The melanoma cells were found to release exosomes. HSP70-positive exosomes from the HSP70-overexpressing cells, in contrast to HSP70-negative exosomes from the control cells, were able to activate mouse NK cells in vitro to kill YAC-1 cells, which express NKG2D ligands constitutively, or the human melanoma cells, in which MICA/B expression was induced. Thus, HSP70 and inducible NKG2D ligands synergistically promote the activation of mouse NK cells resulting in a reduced tumor growth and suppression of metastatic disease.