Wrist Pain in Gymnasts: A Review of Common Overuse Wrist Pathology in the Gymnastics Athlete.

Injury rates among gymnasts are among the highest of any sport at the high school and collegiate level per athletic exposure. The wrist has increased injury risk due to repetitive physical stresses predisposing it to acute injury, overuse, and degenerative damage. This article will review the most common overuse wrist injuries seen in gymnasts. Prompt evaluation and management is necessary to avoid the negative sequelae that can often accompany these injuries. Little is known about effective sport-specific injury prevention strategies, but general guidelines for overuse injury prevention including limiting excessive loading of the wrist, maintaining wrist joint flexibility, an emphasis on proper technique, and incorporating wrist and general core strengthening seem beneficial. General return to play principles are similar for all gymnast-related wrist injuries, including resolution of pain, restoration of normal wrist joint function, completion of a progressive rehabilitation program, and use of proper technique.

Drowning episodes: prevention and resuscitation tips.

CPR for drowning survivors differs from that commonly used in cardiogenic cardiac arrest. Routine antibiotic prophylaxis is not indicated.

In vivo assessment of scapulohumeral rhythm during unconstrained overhead reaching in asymptomatic subjects.

BACKGROUND: The contribution of scapulothoracic and glenohumeral motion to overall shoulder motion remains difficult to determine. We sought to determine the exact ratio between these two motion components in order to better understand overall shoulder kinematics in asymptomatic individuals in unconstrained reaching. MATERIALS AND METHODS: This study assessed shoulder motion using bone-fixed sensors to quantify scapulohumeral motion during unconstrained raising and lowering of the arm. Electromagnetic tracking devices rigidly fixed to bone pins recorded active scapular and humeral motion. RESULTS: We found a significant difference in the ratio of glenohumeral elevation to scapular upward rotation during arm raising (2.3) and lowering (2.7). Each degree of glenohumeral elevation yielded scapular upward rotation of 0.43 degrees (raising) compared with downward rotation of 0.37 degrees (lowering), across the motion arc. Until 125 degrees of glenohumeral elevation, the scapula internally rotated and then externally rotated with further elevation. Scapular upward rotation and posterior tilting progressively increased until maximal elevation. Scapulohumeral rhythm was greatest in the first increment of raising the arm and higher overall when lowering the arm. DISCUSSION: Understanding these data allows improved evaluation of potential motion abnormalities in patients with shoulder pathology and may improve treatment for restoration of normal shoulder motion.

Inhibition of both mesothelioma cell growth and Cdk4 activity following treatment with a TATp16INK4a peptide.

UNLABELLED: Disruption of the 9p21 locus is common in mesothelioma and leads to loss of both the p16INK4a and the p14ARF gene products. This study tested the hypothesis that reexpression of p16INK4a carried out using the TAT delivery system that carries the protein transduction domain of the HIV TAT will result in mesothelioma cell death. MATERIALS AND METHODS: A synthetic TATp16INK4a peptide and a charge matched control were transduced into mesothelioma cells in vitro and in vivo. Cells were assayed for Cdk4 inhibition, cell cycle arrest, and cell death. RESULTS: Treatment of mesothelioma cells with TATp16INK4a for 48 hours resulted in cell death. Apoptosis and G1 cell cycle arrest was also observed. Following transduction of cells with TATp16INK4a there was complete but transient hypophosphorylation of pRb. Similar effects were observed in mesothelioma xenografts. CONCLUSION: Therapeutic strategies which introduce either TATp16INK4a peptide, or small molecule mimetic, could be an effective strategy for mesothelioma treatment.

Analysis of paired primary lung and lymph node tumor cells: a model of metastatic potential by multiple genetic programs.

BACKGROUND: The current paradigm of metastasis proposes that rare cells within primary tumors acquire metastatic capability via sequential mutations, suggesting that metastases are genetically dissimilar from their primary tumors. We tested this hypothesis by examining the molecular differences, if any, between primary tumor cells and matched lymph node metastatic cells in human non-small-cell lung carcinoma specimens. METHODS: We performed transcriptional profiling studies on malignant cells from 11 pairs of stage III tumors and their tumor-positive lymph nodes using multiple, complementary analytic techniques. To confirm the overall validity of microarray data, we used real-time polymerase chain reaction. RESULTS: The molecular signature of nodal metastasis was a composite of two paradoxical, but not mutually exclusive, expression patterns: metastatic cells are: (1) different from their primary tumor cells based on a few genes and (2) genetically similar, overall, to their primary tumor cells. Consequently, we found a 27-gene subset sufficient to differentiate nodal metastatic cells from primary tumor cells. CONCLUSIONS: Thus, we concluded that a more accurate model of metastatic potential is based on a global primary tumor expression pattern along with the appearance of distinct metastatic variants. The 27-gene signature differentiating primary tumors from their metastatic cells may define non-small-cell lung carcinoma nodal metastatic potential.