Shoulder posture and median nerve sliding

Background: Patients with upper limb pain often have a slumped sitting position and poorshoulder posture. Pain could be due to poor posture causing mechanical changes (stretch; localpressure) that in turn affect the function of major limb nerves (e.g. median nerve). This studyexamines (1) whether the individual components of slumped sitting (forward head position, trunkflexion and shoulder protraction) cause median nerve stretch and (2) whether shoulderprotraction restricts normal nerve movements.Methods: Longitudinal nerve movement was measured using frame-by-frame cross-correlationanalysis from high frequency ultrasound images during individual components of slumped sitting.The effects of protraction on nerve movement through the shoulder region were investigated byexamining nerve movement in the arm in response to contralateral neck side flexion.Results: Neither moving the head forward or trunk flexion caused significant movement of themedian nerve. In contrast, 4.3 mm of movement, adding 0.7% strain, occurred in the forearm duringshoulder protraction. A delay in movement at the start of protraction and straightening of thenerve trunk provided evidence of unloading with the shoulder flexed and elbow extended and thescapulothoracic joint in neutral. There was a 60% reduction in nerve movement in the arm duringcontralateral neck side flexion when the shoulder was protracted compared to scapulothoracicneutral.Conclusion: Slumped sitting is unlikely to increase nerve strain sufficient to cause changes tonerve function. However, shoulder protraction may place the median nerve at risk of injury, sincenerve movement is reduced through the shoulder region when the shoulder is protracted andother joints are moved. Both altered nerve dynamics in response to moving other joints and localchanges to blood supply may adversely affect nerve function and increase the risk of developingupper quadrant pain

Induction of anti-tumor immunity by vaccination with dendritic cells pulsed with anti-CD44 IgG opsonized tumor cells

Due to the pivotal role that dendritic cells (DC) play in eliciting and maintaining functional anti-tumor T cell responses, these APC have been exploited against tumors. DC express several receptors for the Fc portion of IgG (Fcγ receptors) that mediate the internalization of antigen-IgG complexes and promote efficient MHC class I and II restricted antigen presentation. In this study, the efficacy of vaccination with DC pulsed with apoptotic B16 melanoma cells opsonized with an anti-CD44 IgG (B16-CD44) was explored. Immature bone marrow derived DC grown in vitro with IL-4 and GM-CSF were pulsed with B16-CD44. After 48 h of pulsing, maturation of DC was demonstrated by production of IL-12 and upregulation of CD80 and CD40 expression. To test the efficacy of vaccination with DC+B16-CD44, mice were vaccinated subcutaneously Lymphocytes from mice vaccinated with DC+B16-CD44 produced IFN-γ in response to B16 melanoma lysates as well as an MHC class I restricted B16 melanoma-associated peptide, indicating B16 specific CD8 T cell activation. Upon challenge with viable B16 cells, all mice vaccinated with DC alone developed tumor compared to 40% of mice vaccinated with DC+B16-CD44; 60% of the latter mice remained tumor free for at least 8 months. In addition, established lung tumors and distant metastases were significantly reduced in mice treated with DC+B16-CD44. Lastly, delayed growth of established subcutaneous tumors was induced by combination therapy with anti-CD44 antibodies followed by DC injection. This study demonstrates the efficacy of targeting tumor antigens to DC via Fcγ receptors.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45862/1/262_2005_Article_104.pd