Knee kinematics and kinetics in former soccer players with a 16-year-old ACL injury – the effects of twelve weeks of knee-specific training

BACKGROUND: Training of neuromuscular control has become increasingly important and plays a major role in rehabilitation of subjects with an injury to the anterior cruciate ligament (ACL). Little is known, however, of the influence of this training on knee stiffness during loading. Increased knee stiffness occurs as a loading strategy of ACL-injured subjects and is associated with increased joint contact forces. Increased or altered joint loads contribute to the development of osteoarthritis. The aim of the study was to determine if knee stiffness, defined by changes in knee kinetics and kinematics of gait, step activity and cross-over hop could be reduced through a knee-specific 12-week training programme. METHODS: A 3-dimensional motion analysis system (VICON) and a force plate (AMTI) were used to calculate knee kinetics and kinematics before and after 12 weeks of knee-specific training in 12 males recruited from a cohort with ACL injury 16 years earlier. Twelve uninjured males matched for age, sex, BMI and activity level served as a reference group. Self-reported patient-relevant data were obtained by the KOOS questionnaire. RESULTS: There were no significant changes in knee stiffness during gait and step activity after training. For the cross-over hop, increased peak knee flexion during landing (from 44 to 48 degrees, p = 0.031) and increased internal knee extensor moment (1.28 to 1.55 Nm/kg, p = 0.017) were seen after training, indicating reduced knee stiffness. The KOOS sport and recreation score improved from 70 to 77 (p = 0.005) and was significantly correlated with the changes in knee flexion during landing for the cross-over hop (r = 0.6, p = 0.039). CONCLUSION: Knee-specific training improved lower extremity kinetics and kinematics, indicating reduced knee stiffness during demanding hop activity. Self-reported sport and recreational function correlated positively with the biomechanical changes supporting a clinical importance of the findings. Further studies are needed to confirm these results in women and in other ACL injured populations

Primary Xenografts of Human Prostate Tissue as a Model to Study Angiogenesis Induced by Reactive Stroma

Characterization of the mechanism(s) of androgen-driven human angiogenesis could have significant implications for modeling new forms of anti-angiogenic therapies for CaP and for developing targeted adjuvant therapies to improve efficacy of androgen-deprivation therapy. However, models of angiogenesis by human endothelial cells localized within an intact human prostate tissue architecture are until now extremely limited. This report characterizes the burst of angiogenesis by endogenous human blood vessels in primary xenografts of fresh surgical specimens of benign prostate or prostate cancer (CaP) tissue that occurs between Days 6–14 after transplantation into SCID mice pre-implanted with testosterone pellets. The wave of human angiogenesis was preceded by androgen-mediated up-regulation of VEGF-A expression in the stromal compartment. The neo-vessel network anastomosed to the host mouse vascular system between Days 6–10 post-transplantation, the angiogenic response ceased by Day 15, and by Day 30 the vasculature had matured and stabilized, as indicated by a lack of leakage of serum components into the interstitial tissue space and by association of nascent endothelial cells with mural cells/pericytes. The angiogenic wave was concurrent with the appearance of a reactive stroma phenotype, as determined by staining for α-SMA, Vimentin, Tenascin, Calponin, Desmin and Masson's trichrome, but the reactive stroma phenotype appeared to be largely independent of androgen availability. Transplantation-induced angiogenesis by endogenous human endothelial cells present in primary xenografts of benign and malignant human prostate tissue was preceded by induction of androgen-driven expression of VEGF by the prostate stroma, and was concurrent with and the appearance of a reactive stroma phenotype. Androgen-modulated expression of VEGF-A appeared to be a causal regulator of angiogenesis, and possibly of stromal activation, in human prostate xenografts