Healthcare Data-Based Prediction Algorithm for Potential Knee Joint Injury of Football Players

It is important to predict the potential harm to the knee joint in order to prevent football players from inflicting numerous injuries to the knee during activity. Numerous professionals have been drawn to this subject, and many viable prediction systems have been developed. Prediction of potential knee joint injury is critical to effectively avoid knee joint injury during exercise. The current prediction algorithms are mainly implemented through expert interviews, medical reports, and historical documents. The algorithms have problems with low prediction accuracy or precision values. There is a need to understand more knee injury factors and improve the prediction accuracy; hence, the intelligent prediction algorithm for potential injury of knee joints of football players is proposed in this paper. Firstly, the characteristics of the knee joint injury and the injury factors of the football players are gathered and analyzed. Then, the damage is predicted by the similarity measurement. The experimental results show that the proposed algorithm has higher prediction accuracy and shorter time. According to the findings of a survey that collected healthcare data, several key factors contribute to football knee injuries. To a degree, this algorithm can predict the likelihood of a football player’s knee injury.

Neutrophil Extracellular Traps Promote Joint Injury in Hemophilia

Epidemiological evidence suggests that recurring episodes of joint-bleeding contribute to the development of hemophilic arthropathy (H) in 70-85% of hemophilia patients. Despite major advances in the treatment to prevent joint bleeding, HA continues to be a major morbidity affecting hemophilia patients and the etiological mechanism contributing to the progression of HA remains poorly understood. Recent evidence suggests that the accumulation of blood in the joints may lead to the release of erythrocyte-derived DAMPs (eDAMPs) such as heme and hemoglobin that can promote sterile inflammation, however, the innate immune pathways contributing to this pathophysiology remain unknown. In the study, we used a model of puncture-induced knee joint injury in FVIII-total knockout (F8TKO) mice and blood samples from hemophilia-A patients diagnosed with HA. Intravital multi-photon-excitation fluorescence intravital (in vivo) microscopy of injured synovium in live F8TKO or control mice was conducted to assess neutrophil-platelet aggregation and NETs generation in the knee-joint. Imaging-flow-cytometry and ELISA assays were used to estimate the number of circulating NETs in plasma of patients diagnosed with HA and mice after the knee-injury procedure. Scoring of the bleeding severity, histology, IHC and confocal imaging of joints were conducted to quantify the joint injury in mice. F8TKO but not control mice manifested knee-joint injury and severity of bleeding 5-days post knee-injury. Progression of knee-joint injury was associated with increased neutrophil accumulation and NETs shedding within the synovium of F8TKO mice. Circulating NETs were significantly abundant in the plasma of hemophilia patients diagnosed with HA and F8TKO mice following knee-injury but not plasma of control humans or mice. These findings are the first to suggest that NETs contribute to pathogenesis of HA in hemophilia. Currently, experiments are underway to identify the innate immune pathways that promote NETs shedding, leading to joint-damage in hemophilia. Disclosures Ragni: Takeda Therapeutics: Membership on an entity's Board of Directors or advisory committees; Bioverativ (Sanofi): Membership on an entity's Board of Directors or advisory committees; BioMarin Pharmaceutical: Membership on an entity's Board of Directors or advisory committees; Alnylam (Sanofi): Membership on an entity's Board of Directors or advisory committees; University of Pittsburgh: Research Funding; Spark Therapeutics: Membership on an entity's Board of Directors or advisory committees. Sundd: CSL Behring Inc: Research Funding; Novartis: Membership on an entity's Board of Directors or advisory committees, Research Funding; Bayer: Research Funding.

Is There a Sex Difference in Trunk Neuromuscular Control among Recreational Athletes during Cutting Maneuvers?

Trunk motion is most likely to influence knee joint injury risk, but little is known about sex-related differences in trunk neuromuscular control during changes of direction. The purpose of the present study was to test whether differences in trunk control between males and females during changes of direction exist. Twelve female and 12 male recreational athletes (with at least 10 years of experience in team sport) performed unanticipated changes of direction with 30° and 60° cut angles, while 3D trunk and leg kinematics, ground reaction forces and trunk muscles electromyography were recorded. Trunk kinematics at the time of peak knee abduction moment and directed co-contraction ratios for trunk muscles during the pre-activation and weight acceptance phases were determined. None of the trunk kinematics and co-contraction ratio variables, nor peak knee abduction moment differed between sexes. Compared to the 30° cut, trunk lateral flexion remained unchanged and trunk external rotation was reduced (p < 0.001; η²p (partial eta squared for effect size) = 0.78), while peak knee abduction moment was increased (p < 0.001; η²p = 0.84) at 60°. The sharper cutting angle induced muscle co-contraction during the pre-activation directed less towards trunk flexors (p < 0.01; η²p = 0.27) but more towards trunk medial flexors and rotators opposite to the movement direction (p < 0.001; η²p > 0.46). However, muscle co-contraction during the weight acceptance phase remained comparable between 30° and 60°. The lack of sex-related differences in trunk control does not explain knee joint injury risk discrepancies between sexes during changes of direction. Trunk neuromuscular strategies during sharper cutting angles revealed the importance of external oblique muscles to maintain trunk lateral flexion at the expense of trunk rotation. This provides new information for trunk strength training purposes for athletes performing changes of direction.

Changes in anterior femoral articular cartilage structure in collegiate rugby athletes with and without a history of traumatic knee joint injury following a five-month competitive season

This study aimed to examine anterior femoral cartilage morphology before (pre-season) and after (post-season) a 5-month competitive season in collegiate ruby players with and without a previous history of traumatic injury to ligamentous, meniscus, and/or cartilage structures at the knee joint. Using a prospective cohort design, 42 male collegiate rugby players with a previous history of traumatic intracapsular knee joint injury and 124 players without knee injury history were included in this study. Ultrasonography assessments of anterior femoral cartilage were performed before (pre-season) and following a 5-month athletic season (post-season). Rugby players with a history of traumatic knee joint injury had greater lateral condylar thickness (2.37 ± 0.35 mm, p = 0.03), intercondylar thickness (2.51 ± 0.47 mm, p = 0.03), and partial area (44.67 ± 7.28mm2, p = 0.02) compared to control players (lateral = 2.23 ± 0.35 mm, intercondylar = 2.32 ± 0.47 mm, partial area = 41.60 ± 7.26 mm2), regardless of pre-and post-season assessment time points. Pre-season ultrasonography assessment of lateral condylar thickness (2.34 ± 0.47 mm, p = 0.02), medial condylar thickness (2.05 ± 0.43 mm, p = 0.03), and partial area (44.10 ± 9.23 mm2, p = 0.001) were significantly greater than the post-season ultrasonography assessment time point (lateral = 2.26 ± 0.43 mm, medial = 1.98 ± 0.43 mm, partial area = 42.17 ± 8.82 mm2), regardless of group membership. Rugby players with a history of intracapsular knee joint injury displayed altered anterior femoral cartilage size via ultrasonography assessments. Regardless of a presence of injury history, collegiate rugby players showed a decrease in cartilage thickness and partial area following a 5-month competitive season.

Platelet-targeted hyperfunctional FIX gene therapy for hemophilia B mice even with preexisting anti-FIX immunity

Gene therapy may lead to a cure for hemophilia B (HB) if it is successful. Data from clinical trials using adeno-associated virus (AAV)–mediated liver-targeted FIX gene therapy are very encouraging. However, this protocol can be applied only to adults who do not have liver disease or anti-AAV antibodies, which occur in 30% to 50% of individuals. Thus, developing a protocol that can be applied to all HB patients is desired. Our previous studies have demonstrated that lentivirus-mediated platelet-specific FIX (2bF9) gene therapy can rescue bleeding diathesis and induce immune tolerance in FIXnull mice, but FIX expression was only ∼2% to 3% in whole blood. To improve the efficacy, we used a codon-optimized hyperfunctional FIX-Padua (2bCoF9R338L) to replace the 2bF9 cassette, resulting in 70% to 122% (35.08-60.77 mU/108 platelets) activity levels in 2bCoF9R338L-transduced FIXnull mice. Importantly, sustained hyperfunctional platelet-FIX expression was achieved in all 2bCoF9R338L-transduced highly immunized recipients with activity levels of 18.00 ± 9.11 and 9.36 ± 12.23 mU/108 platelets in the groups treated with 11 Gy and 6.6 Gy, respectively. The anti-FIX antibody titers declined with time, and immune tolerance was established after 2bCoF9R338L gene therapy. We found that incorporating the proteasome inhibitor bortezomib into preconditioning can help eliminate anti-FIX antibodies. The bleeding phenotype in 2bCoF9R338L-transduced recipients was completely rescued in a tail bleeding test and a needle-induced knee joint injury model once inhibitors dropped to undetectable. The hemostatic efficacy in 2bCoF9R338L-transduced recipients was further confirmed by ROTEM and thrombin generation assay (TGA). Together, our studies suggest that 2bCoF9R338L gene therapy can be a promising protocol for all HB patients, including patients with inhibitors.