Altered lower extremity biomechanics following anterior cruciate ligament reconstruction during single-leg and double-leg stop-jump tasks: A bilateral total support moment analysis.

BACKGROUND: Injury to the anterior cruciate ligament (ACL) can lead to long-lasting biomechanical alterations that put individuals at risk of a second ACL injury. Examining the total support moment may reveal between- and within-limb compensatory strategies. METHODS: Twenty-six participants who were cleared to return to sport following ACL reconstruction were recruited. Each participant completed the single-leg and double-leg stop jump tasks. These tasks were analyzed using force plates and a 3D motion analysis system. The total support moment was calculated by summing the internal moments of the hip, knee and ankle at peak vertical ground reaction force. FINDINGS: Internal knee extensor moment was lower in the involved limb compared to the uninvolved for both tasks (17.6%, P = 0.022; 18.4%, P = 0.008). No significant between-limb differences were found for the total support moment. The involved limb exhibited an 18.2% decrease in knee joint contribution (P = 0.01) and a 21.6% increase in ankle joint contribution (P = 0.016) to the total support moment compared to the uninvolved limb in the single-leg stop jump task. INTERPRETATION: Compensation for the involved knee is likely due to altered biomechanics that redistributes load to the uninvolved knee or to adjacent joints of the same limb. A partial shift in joint contribution from the knee to the ankle during the single-leg stop jump task demonstrates a tendency to decrease load to the knee. Further studies are needed to investigate how these adaptations impact the prevalence of subsequent injury and poor joint health.

Micro-Meta App: an interactive tool for collecting microscopy metadata based on community specifications.

For quality, interpretation, reproducibility and sharing value, microscopy images should be accompanied by detailed descriptions of the conditions that were used to produce them. Micro-Meta App is an intuitive, highly interoperable, open-source software tool that was developed in the context of the 4D Nucleome (4DN) consortium and is designed to facilitate the extraction and collection of relevant microscopy metadata as specified by the recent 4DN-BINA-OME tiered-system of Microscopy Metadata specifications. In addition to substantially lowering the burden of quality assurance, the visual nature of Micro-Meta App makes it particularly suited for training purposes.

Decreased inspired oxygen stimulates de novo formation of coronary collaterals in adult heart.

RATIONALE: Collateral vessels lessen myocardial ischemia when acute or chronic coronary obstruction occurs. It has long been assumed that although native (pre-existing) collaterals enlarge in obstructive disease, new collaterals do not form in the adult. However, the latter was recently shown to occur after coronary artery ligation. Understanding the signals that drive this process is challenged by the difficulty in studying collateral vessels directly and the complex milieu of signaling pathways, including cell death, induced by ligation. Herein we show that hypoxemia alone is capable of inducing collateral vessels to form and that the novel gene Rabep2 is required. OBJECTIVE: Hypoxia stimulates angiogenesis during embryonic development and in pathological states. We hypothesized that hypoxia also stimulates collateral formation in adult heart by a process that involves RABEP2, a recently identified protein required for formation of collateral vessels during development. METHODS AND RESULTS: Exposure of mice to reduced FiO2 induced collateral formation that resulted in smaller infarctions following LAD ligation and that reversed on return to normoxia. Deletion of Rabep2 or knockdown of Vegfa inhibited formation. Hypoxia upregulated Rabep2, Vegfa and Vegfr2 in heart and brain microvascular endothelial cells (HBMVECs). Knockdown of Rabep2 impaired migration of HBMVECs. In contrast to systemic hypoxia, deletion of Rabep2 did not affect collateral formation induced by ischemic injury caused by LAD ligation. CONCLUSIONS: Hypoxia induced formation of coronary collaterals by a process that required VEGFA and RABEP2, proteins also required for collateral formation during development. Knockdown of Rabep2 impaired cell migration, providing one potential mechanism for RABEP2's role in collateral formation. This appears specific to hypoxia, since formation after acute ischemic injury was unaffected in Rabep2-/- mice. These findings provide a novel model for studying coronary collateral formation, and demonstrate that hypoxia alone can induce new collaterals to form in adult heart.