Biomechanical Changes During a 90º Cut in Collegiate Female Soccer Players With Participation in the 11+

# Background Valgus collapse and high knee abduction moments have been identified as biomechanical risk factors for ACL injury. It is unknown if participation in the 11+, a previously established, dynamic warm-up that emphasizes biomechanical technique and reduces ACL injury rates, reduces components of valgus collapse during a 90º cut. # Hypothesis/Purpose To determine whether participation in the 11+ during a single soccer season reduced peak knee abduction moment and components of valgus collapse during a 90º cut in collegiate female soccer players. # Study Design Prospective cohort study # Methods Forty-six participants completed preseason and postseason motion analysis of a 90º cut. During the season, 31 players completed the 11+ and 15 players completed their typical warm-up (control group). Peak knee abduction moment, components of valgus collapse (hip adduction, internal rotation, and knee abduction angles), and a novel measure of knee valgus collapse were analyzed with repeated-measures ANOVAs to determine differences between preseason and postseason. Smallest detectable change (SDC) and minimal important difference (MID) values were applied to contextualize results. # Results There was a significant main effect of time for non-dominant knee valgus collapse (p=0.03), but decreases in non-dominant knee valgus collapse only exceeded the SDC in the intervention team. # Conclusions Clinically meaningful decreases in knee valgus collapse may indicate a beneficial biomechanical effect of the 11+. Participation in the 11+ may lower ACL injury risk by reducing valgus collapse during a 90º cut. # Level of Evidence 2

Superior 2-Year Functional Outcomes Among Young Female Athletes After ACL Reconstruction in 10 Return-to-Sport Training Sessions: Comparison of ACL-SPORTS Randomized Controlled Trial With Delaware-Oslo and MOON Cohorts

Background: Outcomes after anterior cruciate ligament reconstruction (ACLR) are not uniformly good and are worse among young female athletes. Developing better rehabilitation and return-to-sport training programs and evaluating their outcomes are essential. Purpose: (1) Test the effect of strength, agility, plyometric, and secondary prevention (SAPP) exercises with and without perturbation training (SAPP + PERT) on strength, hops, function, activity levels, and return-to-sport rates in young female athletes 1 and 2 years after ACLR and (2) compare 2-year functional outcomes and activity levels among young female athletes in the Anterior Cruciate Ligament Specialized Post-Operative Return-to-Sports (ACL-SPORTS) trial to homogeneous cohorts who completed criterion-based postoperative rehabilitation alone (Multicenter Orthopaedic Outcomes Network [MOON]) and in combination with extended preoperative rehabilitation (Delaware-Oslo). Study Design: Randomized controlled trial, Level of evidence, 1; and cohort study, Level of evidence, 3. Methods: A total of 40 level 1 and level 2 female athletes were enrolled after postoperative impairment resolution 3 to 9 months after primary ACLR. Participants were randomized to 10 SAPP or SAPP + PERT sessions and were tested 1 and 2 years after ACLR on quadriceps strength, hop tests, functional outcomes, and return-to-sport rates. Participants were then compared with homogeneous cohorts of young (<25 years) female athletes who completed criterion-based postoperative rehabilitation alone (MOON) and in combination with extended preoperative rehabilitation (Delaware-Oslo) on 2-year functional outcomes. Results: No significant or meaningful differences were found between SAPP and SAPP + PERT, so groups were collapsed for comparison with the other cohorts. At 2-year follow-up, ACL-SPORTS had the highest scores (P < .01) on the Marx activity rating scale (ACL-SPORTS, 13.5 ± 3.3; Delaware-Oslo, 12.5 ± 2.7; MOON, 10.6 ± 5.1); International Knee Documentation Committee Subjective Knee Evaluation Form (96 ± 7, 92 ± 9, and 84 ± 14, respectively); and Knee injury and Osteoarthritis Outcome Score (KOOS) subscales for Pain (98 ± 4, 94 ± 9, and 90 ± 10, respectively), Symptoms (94 ± 6, 90 ± 9, and 83 ± 14, respectively), Activities of Daily Living (100 ± 1, 99 ± 4, and 96 ± 7, respectively), Sports and Recreation (94 ± 8, 86 ± 15, and 82 ± 17, respectively), and Quality of Life (89 ± 14, 78 ± 18, and 76 ± 19, respectively). The Patient Acceptable Symptom State threshold on the KOOS–Sports and Recreation was achieved by 100% of the ACL-SPORTS cohort compared with 90% of Delaware-Oslo and 78% of MOON (P = .011). Conclusion: Although perturbation training provided no added benefit, 10 sessions of return-to-sport training, compared with criterion-based postoperative rehabilitation alone, yielded statistically significant and clinically meaningfully higher 2-year functional outcomes among young, high-level female athletes after ACLR

MST1 Promotes Apoptosis through Phosphorylation of Histone H2AX*

MST1 (mammalian STE20-like kinase 1) is a serine/threonine kinase that is cleaved and activated by caspases during apoptosis. Overexpression of MST1 induces apoptotic morphological changes such as chromatin condensation, but the mechanism is not clear. Here we show that MST1 induces apoptotic chromatin condensation through its phosphorylation of histone H2AX at Ser-139. During etoposide-induced apoptosis in Jurkat cells, the cleavage of MST1 directly corresponded with strong H2AX phosphorylation. In vitro kinase assay results showed that MST1 strongly phosphory-lates histone H2AX. Western blot and kinase assay results with a mutant S139A H2AX confirmed that MST1 phos-phorylates H2AX at Ser-139. Direct binding of MST1 and H2AX can be detected when co-expressed in HEK293 cells and was also confirmed by an endogenous immunoprecipitation study. When overexpressed in HeLa cells, both the MST1 full-length protein and the MST1 kinase domain (MST1-NT), but not the kinase-negative mutant (MST1-NT-KN), could induce obvious endogenous histone H2AX phosphorylation. The caspase-3 inhibitor benzyloxycarbonyl-DEVD-fluoromethyl ketone (Z-DEVD-fmk) attenuates phosphorylation of H2AX by MST1 but cannot inhibit MST1-NT-induced histone H2AX phosphorylation, indicating that cleaved MST1 is responsible for H2AX phosphory-lation during apoptosis. Histone H2AX phosphorylation and DNA fragmentation were suppressed in MST1 knockdown Jurkat cells after etoposide treatment. Taken together, our data indicated that H2AX is a substrate of MST1, which functions to induce apoptotic chromatin condensation and DNA fragmentation