Background:The loss of glenohumeral internal rotation range of motion in overhead athletes has been well documented in the literature. Several different methods of assessing this measurement have been described, making comparison between the results of studies difficult.Hypothesis:Significant differences in the amount of internal rotation range of motion exist when using different methods of stabilization.Study Design:Descriptive laboratory study.Methods:Three techniques were used bilaterally in random fashion to measure glenohumeral internal rotation range of motion: stabilization of the humeral head, stabilization of the scapula, and visual inspection without stabilization. An initial study on 20 asymptomatic participants was performed to determine the intrarater and interrater reliability for each measurement technique. Once complete, measurements were performed on 39 asymptomatic professional baseball players to determine if a difference existed in measurement techniques and if there was a significant side-to-side difference. A 2-way repeated-measures analysis of variance was used.Results:While interrater reliability was fair between all 3 methods, scapular stabilization provided the best intrarater reliability. A statistically significant difference was observed between all 3 methods (P < .001). Internal rotation was significantly less in the dominant shoulder than in the nondominant shoulder (P < .001).Conclusion:Differences in internal rotation range of motion measurements exist when using different methods. The scapula stabilization method displayed the highest intrarater reproducibility and should be considered when evaluating internal rotation passive range of motion of the glenohumeral joint.Clinical Relevance:A standardized method of measuring internal rotation range of motion is required to accurately compare physical examinations of patients. The authors recommend the use of the scapula stabilization method to assess internal rotation range of motion by allowing normal glenohumeral arthrokinematics while stabilizing the scapulothoracic articulation.

OBJECTIVES-We previously demonstrated that sphingosine 1-phosphate (S1P) bimodally regulates epithelial ovarian cancer (EOC) cell invasiveness: low-concentration S1P stimulates invasion similar to lysophophatidic acid (LPA), while high-concentration S1P inhibits invasion. In this study, we investigated the mechanisms through which S1P affects EOC cell proteolysis, invasion, and adhesion in two cultured epithelial ovarian cancer cell lines. METHODS-G-proteinGi was inhibited by pertussis toxin (PTX) and GTP binding protein Rac by NSC23766. S1P conditioned media of DOV13 and OVCA429 cells were evaluated via gel zymography, fluorometric gelatinase assay, urokinase plasminogen activator (uPA) activity assay, and Western Blot for MT1-MMP. Cell invasion was analyzed in Matrigel chambers. Membrane-N-cadherin was localized via fluorescence microscopy.RESULTS-Zymography revealed pro-MMP2 in conditioned media of EOC cells regardless of treatment. Gelatinase activity was increased by low-concentration S1P. In DOV13 cells this effect was Gi and Rac dependent. In all OVCA429 and control DOV13 cells, PTX enhanced gelatinolysis, suggesting an MMP2-inhibitory pathway via Gi. MT1-MMP was decreased Gidependently by high-concentration S1P. Rac inhibition significantly counteracted low-S1P enhancement and high-S1P reduction of DOV13 invasiveness; and uPA activity in conditioned media of invading cells correlated significantly. Immunohistochemistry revealed Gi-dependent clustering of membrane-N-cadherin in DOV13 cells treated with 0.5µM S1P or 10µM LPA.CONCLUSIONS-S1P influences EOC invasion by regulating ECM-proteolysis and cell-cell attachment via MMP2, uPA, and membrane-N-cadherin. Furthermore, this study illustrates that the net effect of S1P on each of these processes reflects a complex interplay of multiple GPCR pathways involving Gi and downstream Rac.

Articular cartilage lesions of the knee joint are common in patients of varying ages. Some articular cartilage lesions are focal lesions located on one aspect of the tibiofemoral or patellofemoral joint. Other lesions can be extremely large or involve multiple compartments of the knee joint and these are often referred to as osteoarthritis. There are numerous potential causes for the development of articular cartilage lesions: joint injury (trauma), biomechanics, genetics, activities, and biochemistry. Numerous factors also contribute to symptomatic episodes resulting from lesions to the articular cartilage: activities (sports and work), joint alignment, joint laxity, muscular weakness, genetics, dietary intake, and body mass index. Athletes appear to be more susceptible to developing articular cartilage lesions than other individuals. This is especially true with specific sports and subsequent to specific types of knee injuries. Injuries to the anterior cruciate ligament and/or menisci may increase the risk of developing an articular cartilage lesion. The treatment for an athletic patient with articular cartilage lesions is often difficult and met with limited success. In this article we will discuss several types of knee articular cartilage injuries such as focal lesions, advanced full-thickness lesions, and bone bruises. We will also discuss the risk factors for developing full-thickness articular cartilage lesions and osteoarthritis, and describe the clinical evaluation and nonoperative treatment strategies for these types of lesions in athletes.

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