Asymmetry during Functional Movement Screening and injury risk in junior football players: A replication study.

An indicator of movement quality and potential injury risk during Functional Movement Screen (FMS) testing is the presence of asymmetry when comparing the left and right sides of the body. The aim of the study was to investigate the reproducibility of the injury risk model proposed in our previous research (Chalmers et al. 2017; derivation study) that showed an increased injury risk for elite junior Australian football players demonstrating ≥2 asymmetrical FMS subtests. We used a direct replication design. Players underwent pre-season FMS testing, and an injury surveillance system monitored 277 male participants during the subsequent regular season competition. Designated club officials monitored the weekly competition participation of players. The definition of an injury was "a trauma or medical condition which caused a player to miss a competitive game". Cox proportional hazards regression models were used to investigate the relationship between asymmetry and number of games played before first injury (ie, survival time). The level of reproducibility was determined according to statistical significance, effect size, and subjective assessment. Demonstrating asymmetry during FMS testing was not associated with a significant increase in prospective injury risk in the replication study (P > .05). Moreover, effect sizes (hazard ratios) from the derivation dataset were not within the 95% confidence intervals of the respective asymmetry predictor in the replication dataset. Subjectively, researchers were in agreement that the findings from the derivation data were not successfully reproduced. Clinicians and researchers should be cautious about using FMS asymmetry findings to derive injury risk for junior football players.

The m4 gene of murine gammaherpesvirus modulates productive and latent infection in vivo.

Murine gammaherpesvirus 68 (MHV-68) infection of mice represents a viable small-animal model for the study of gammaherpesvirus pathogenesis. MHV-76 is a deletion mutant of MHV-68, which lacks four MHV-68-specific genes (M1 to M4) and eight viral tRNA-like sequences at the 5' end of the genome. These genes are implicated in latency and/or immune evasion. Consequently, MHV-76 is attenuated in the acute phase of in vivo infection with respect to MHV-68. Little is known about the role of M4 in viral infection, except that it is expressed as an immediate-early/early transcript during lytic replication of MHV-68 in vitro. To elucidate the contribution M4 makes to in vivo pathogenesis, we created a novel MHV-76 mutant (MHV-76inM4), in which the region of MHV-68 coding for M4 and accompanying putative promoter elements were inserted into the 5' region of the MHV-76 genome. The growth of MHV-76inM4 in vitro was indistinguishable from that of MHV-76 and MHV-68. However, virus titers from MHV-76inM4-infected BALB/c mice were significantly increased with respect to MHV-76 at early times in the lung. In addition, at days 17 and 21 postinfection, there was a significant elevation in latent viral load in splenocytes of MHV-76inM4-infected mice compared to MHV-76. Like MHV-76-infected mice, MHV-76inM4-infected mice display no evidence of overt splenomegaly, a finding characteristic of MHV-68 infection. M4 expression in vivo was detectable during productive infection in the lung and during the establishment of latency in the spleen, but in general M4 was not detectable during long-term latency (day 100 postinfection).

Diversity of Tn1546 elements in clinical isolates of glycopeptide-resistant enterococci from Scottish hospitals.

The Tn1546-related elements of 48 Van glycopetide-resistant enterococci were compared. Ten distinct Tn1546 types were identified with variation primarily due to IS1542 and IS1216V-like insertions. Clonal isolates frequently differed in their Tn1546 type, indicating instability of Tn1546-related elements. A putative hybrid promoter was identified, generated upstream of vanR by the insertion of IS1542. The presence of this hybrid promoter was associated with constitutive expression of the van genes and elevated teicoplanin resistance.