Monitoring lower limb biomechanical asymmetry and psychological measures in athletic populations - A scoping review

Background: Lower limb biomechanics, including asymmetry, are frequently monitored to determine sport performance level and injury risk. However, contributing factors extend beyond biomechanical and asymmetry measures to include psychological, sociological, and environmental factors. Unfortunately, inadequate research has been conducted using holistic bio-psycho-social models to characterize sport performance and injury risk. Therefore, this scoping review summarized the research landscape of studies concurrently assessing measures of lower limb biomechanics, asymmetry, and introspective psychological state (e.g., pain, fatigue, perceived exertion, stress, etc.) in healthy, competitive athletes. Methods: A systematic search of Medline, Embase, CINAHL, SPORT Discus, and Web of Science Core Collections was designed and conducted in accordance with PRISMA guidelines. 51 articles were included in this review. Results: Significant relationships between biomechanics (k = 22 studies) or asymmetry (k = 20 studies) and introspective state were found. Increased self-reported pain was associated with decreased range of motion, strength, and increased lower limb asymmetry. Higher ratings of perceived exertion were related to increased lower limb asymmetry, self-reported muscle soreness, and worse jump performance. Few studies (k = 4) monitored athletes longitudinally throughout one or more competitive season(s). Conclusion: This review highlights the need for concurrent analysis of introspective, psychological state, and biomechanical asymmetry measures along with longitudinal research to understand the contributing factors to sport performance and injury risk from bio-psycho-social modeling. In doing so, this framework of bio-psycho-social preventive and prognostic patient-centered practices may provide an actionable means of optimizing health, well-being, and sport performance in competitive athletes

Cyclic AMP induces IPC leukemia cell apoptosis via CRE-and CDK-dependent Bim transcription

The IPC-81 cell line is derived from the transplantable BNML model of acute myelogenic leukemia (AML), known to be a reliable predictor of the clinical efficiency of antileukemic agents, like the first-line AML anthracycline drug daunorubicin (DNR). We show here that cAMP acted synergistically with DNR to induce IPC cell death. The DNR-induced death differed from that induced by cAMP by (1) not involving Bim induction, (2) being abrogated by GSK3β inhibitors, (3) by being promoted by the HSP90/p23 antagonist geldanamycin and truncated p23 and (4) by being insensitive to the CRE binding protein (CREB) antagonist ICER and to cyclin-dependent protein kinase (CDK) inhibitors. In contrast, the apoptosis induced by cAMP correlated tightly with Bim protein expression. It was abrogated by Bim (BCL2L11) downregulation, whether achieved by the CREB antagonist ICER, by CDK inhibitors, by Bim-directed RNAi, or by protein synthesis inhibitor. The forced expression of BimL killed IPC-81WT cells rapidly, Bcl2-overexpressing cells being partially resistant. The pivotal role of CREB and CDK activity for Bim transcription is unprecedented. It is also noteworthy that newly developed cAMP analogs specifically activating PKA isozyme I (PKA-I) were able to induce IPC cell apoptosis. Our findings support the notion that AML cells may possess targetable death pathways not exploited by common anti-cancer agents

Gender differences in gait kinematics for patients with knee osteoarthritis

BACKGROUND: Females have a two-fold risk of developing knee osteoarthritis (OA) as compared to their male counterparts and atypical walking gait biomechanics are also considered a factor in the aetiology of knee OA. However, few studies have investigated sex-related differences in walking mechanics for patients with knee OA and of those, conflicting results have been reported. Therefore, this study was designed to examine the differences in gait kinematics (1) between male and female subjects with and without knee OA and (2) between healthy gender-matched subjects as compared with their OA counterparts. METHODS: One hundred subjects with knee OA (45 males and 55 females) and 43 healthy subjects (18 males and 25 females) participated in this study. Three-dimensional kinematic data were collected during treadmill-walking and analysed using (1) a traditional approach based on discrete variables and (2) a machine learning approach based on principal component analysis (PCA) and support vector machine (SVM) using waveform data. RESULTS: OA and healthy females exhibited significantly greater knee abduction and hip adduction angles compared to their male counterparts. No significant differences were found in any discrete gait kinematic variable between OA and healthy subjects in either the male or female group. Using PCA and SVM approaches, classification accuracies of 98–100 % were found between gender groups as well as between OA groups. CONCLUSIONS: These results suggest that care should be taken to account for gender when investigating the biomechanical aetiology of knee OA and that gender-specific analysis and rehabilitation protocols should be developed

Tracking the reliability of force plate-derived countermovement jump metrics over time in female basketball athletes: A comparison of principal component analysis vs. conventional methods

BACKGROUND: Establishing the reliability of countermovement jump (CMJ) metrics over multiple weeks can be important in understanding and tracking changes in jump performance over time. However, a limited number of key performance indicators are generally retained for ease of interpretation. Fortunately, CMJ metrics are often highly correlated, which offers the potential to summarize key jump aspects using principal component analysis 33 (PCA). PURPOSE: The objective of this study was to assess and compare the week-to-week (i.e., week 1 vs. week 2, week 2 vs. week 3, etc.) vs. preseason (i.e., nth-week vs. average of the 7-weeks) reliability of CMJ metrics, relative to principal components (PCs). METHODS: Thirteen varsity female basketball athletes completed 17 weeks of CMJ testing (i.e., off-season (4 weeks), pre-season (7 weeks), and in-season (6 weeks)). The PCA was developed from all data collected, but only results of the pre-season PC scores were examined for reliability purposes. RESULTS: It was 38 found that both methods displayed comparable reliability, such that 11/18 CMJ metrics and 3/6 PCs displayed excellent weekly reliability (ICC≥0.9), while 17/18 of the CMJ metrics and 5/6 of the PCS displayed excellent reliability when assessed longitudinally. PCs 1-4 explained 83% of the variance in the data relating to force measures, braking metrics, jump power measures, and between-limb differences, respectively. CONCLUSION: These findings support the use of PCA in routine longitudinal athletic monitoring, as this technique retains valuable performance information and summarizes distinct aspects of the jump, providing a more holistic assessment of performance and indication of injury susceptibility

Role of immune cells in animal models for inherited neuropathies: facts and visions*

Mice heterozygously deficient in the peripheral myelin adhesion molecule P0 (P0+/− mice) are models for some forms of Charcot–Marie–Tooth (CMT) neuropathies. In addition to the characteristic hallmarks of demyelination, elevated numbers of CD8-positive T-lymphocytes and F4/80-positive macrophages are striking features in the nerves of these mice. These immune cells increase in number with age and progress of demyelination, suggesting that they might be functionally related to myelin damage. In order to investigate the pathogenetic role of lymphocytes, the myelin mutants were cross-bred with recombination activating gene 1 (RAG-1)-deficient mice, which lack mature T-and B-lymphocytes. The immunodeficient myelin mutants showed a less severe myelin degeneration. The beneficial effect of lymphocyte-deficiency was reversible, since demyelination worsened in immunodeficient myelin-mutants when reconstituted with bone marrow from wild-type mice. Ultrastructural analysis revealed macrophages in close apposition to myelin and demyelinated axons. We therefore cross-bred the P0+/− mice with spontaneous osteopetrotic (op) mutants deficient in the macrophage colony-stimulating factor (M-CSF), hence displaying impaired macrophage activation. In the corresponding double mutants the numbers of macrophages were not elevated in the peripheral nerves, and the demyelinating phenotype was less severe than in the genuine P0+/− mice, demonstrating that macrophages are also functionally involved in the pathogenesis of genetically mediated demyelination. We also examined other models for inherited neuropathies for a possible involvement of immune cells. We chose mice deficient in the gap junction component connexin 32, a model for the X-linked form of CMT. Similar to P0-deficient mice, T-lymphocytes and macrophages were elevated and macrophages showed a close apposition to degenerating myelin. We conclude that the involvement of T-lymphocytes and macrophages is a common pathogenetic feature in various forms of slowly progressive inherited neuropathies