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Background: Current illustrations of the carpal tunnel vary greatly. The relative positions of the components such as the median nerve and flexor pollicis longus (FPL) tendon seem often arbitrarily chosen. The purpose of this study was to determine the locations of the median nerve and FPL in the carpal tunnel using ultrasound (US) and to determine whether the position of the median nerve changes in carpal tunnel syndrome (CTS). Method: Patients with and without CTS underwent US examination of the wrist. A 4 × 10 grid was fitted to each saved cross-sectional image. The center points of the median nerve and FPL were identified, and their horizontal and vertical coordinates were recorded. Results: The median nerve was identified in 115 wrists (average x = 0.70, y = 0.82), and FPL was identified in 90 wrists (average x = 0.86, y = 0.59). A scatter plot was created by stacking all US images to demonstrate the average positions of the median nerve and FPL. There were 97 wrists without CTS (No CTS) and 17 wrists with CTS. There was a significant difference in the vertical position of the median nerve between No CTS and CTS wrists (P =.0006). Conclusions: The locations of the median nerve and FPL within the carpal tunnel were determined using US of 115 wrists, and a heat map was created to illustrate these locations. The median nerve was found to be more superficial in the setting of CTS. [ABSTRACT FROM AUTHOR]

Background: The goal of proximal phalangeal fracture management is to allow for fracture healing to occur in acceptable alignment while maintaining gliding motion of the extensor and flexor tendons. Methods: We reviewed the most current literature on various treatment methods of proximal phalanx fractures, focusing on the indications and outcomes of nonoperative as well as operative interventions. Results: Stable fractures can be successfully treated nonoperatively, whereas unstable injuries benefit from surgery. Regardless of the surgical intervention employed, the overriding goal is to restore anatomy and impart enough stability to allow for early motion. The surgical dissection contributes to soft tissue scarring and should be minimized. Conclusions: Clinical success is achieved when acceptable fracture alignment and stability occur in the setting of unobstructed tendon gliding and early active range of motion. [ABSTRACT FROM AUTHOR]

Cdx2 is an intestine-specific transcription factor known to regulate proliferation and differentiation. We have reported previously that Cdx2 limits the proliferation of human colon cancer cells by inhibiting the transcriptional activity of the β-catenin–T-cell factor (TCF) bipartite complex. Herein we further elucidate this mechanism. Studies with a classic Cdx2 target gene and a canonical Wnt/β-catenin/TCF reporter suggest that Cdx2 regulates these promoters by distinctly different processes. Specifically, inhibition of β-catenin/TCF activity by Cdx2 does not require Cdx2 transcriptional activity. Instead, Cdx2 binds β-catenin and disrupts its interaction with the DNA-binding TCF factors, thereby silencing β-catenin/TCF target gene expression. Using Cdx2 mutants, we map the Cdx2 domains required for the inhibition of β-catenin/TCF activity. We identify a subdomain in the N-terminus that is highly conserved and when mutated significantly reduces Cdx2 inhibition of β-catenin/TCF transcriptional activity. Mutation of this subdomain also abrogates Cdx2’s anti-proliferative effects in colon cancer cells. In summary, we conclude that Cdx2 binds β-catenin and disrupts the β-catenin–TCF complex. Considering the pivotal role of β-catenin/TCF activity in driving proliferation of normal intestinal epithelial and colon cancer cells, our findings suggest a novel mechanism for Cdx2-mediated regulation of Wnt/β-catenin signaling and cell proliferation. [ABSTRACT FROM PUBLISHER]

We examined whether treatment utilization for Dupuytren's contracture varied with the presence of adverse socioeconomic determinants of health in the United States. After propensity score matching, the presence of adverse socioeconomic determinants of health was associated with decreased treatment utilization., Competing Interests: Declaration of conflicting interestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Objective: Strategies to improve cartilage repair tissue quality after bone marrow cell-based procedures may reduce later development of osteoarthritis. Doxycycline is inexpensive, well-tolerated, and has been shown to reduce matrix-metalloproteinases (MMPs) and osteoarthritis progression. This study tests the hypotheses that doxycycline reduces MMP, enhances chondrogenesis of human bone marrow-derived mesenchymal stem cells (hMSC), and improves in vivo cartilage repair., Design: Ninety hMSC pellets were cultured in chondrogenic media with either 0-, 1- or 2-μg/mL doxycycline. Pellets were evaluated with stereomicroscopy, proteoglycan assay, qRT-PCR, and histology. Osteochondral defects (OCDs) were created in the trochlear grooves of 24-Sprague-Dawley rats treated with/without oral doxycycline. Rats were sacrificed at 12-weeks and repair tissues were examined grossly and histologically., Results: hMSC pellets with 1-μg/mL (P = 0.014) and 2-μg/mL (P = 0.002) doxycycline had larger areas than pellets without doxycycline. hMSC pellets with 2-μg/mL doxycycline showed reduced mmp-13 mRNA (P = 0.010) and protein at 21-days. Proteoglycan, DNA contents, and mRNA expressions of chondrogenic genes were similar (P > 0.05). For the in vivo study, while the histological scores were similar between the two groups (P = 0.116), the gross scores of the OCD repair tissues in doxycycline-treated rats were higher at 12-weeks (P = 0.017), reflective of improved repair quality. The doxycycline-treated repairs also showed lower MMP-13 protein (P = 0.029)., Conclusions: This study shows that doxycycline improves hMSC chondrogenesis and decreases MMP-13 in pellet cultures and within rat OCDs. Doxycycline exerted no negative effect on multiple measures of chondrogenesis and cartilage repair. These data support potential use of doxycycline to improve cartilage repair to delay the onset of osteoarthritis., (Copyright © 2012 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.)

Joint injuries are very common in the athletic population, especially professional soccer players, with an incidence of 10 to 35.5 injuries per 1000 hours. Most soccer-related joint injuries occur in the lower extremities, with 16% to 46% occurring in the knee and 17% to 40% occurring in the ankle. Because of the limited healing capacity of cartilage and other intra-articular soft tissue structures, such as anterior cruciate ligament (ACL) and meniscus, joint injuries often lead to the development of early disabling osteoarthritis. Osteoarthritis in soccer players is 5 to 12 times more frequent than in the general population and diagnosed 4 to 5 years earlier. It remains a major cause of disability from this sport. This review focuses on the epidemiology of soccer-related joint injuries and subsequent development of osteoarthritis in the hip, knee, and ankle joints. As well, two different pathways for pathogenesis are described: (1) primary osteoarthritis via direct trauma to the articular cartilage and (2) secondary osteoarthritis that occurs indirectly through injury to the soft tissue structures that subsequently result in articular cartilage degeneration and loss.

Cdx2 is an intestine-specific transcription factor known to regulate proliferation and differentiation. We have reported previously that Cdx2 limits the proliferation of human colon cancer cells by inhibiting the transcriptional activity of the beta-catenin-T-cell factor (TCF) bipartite complex. Herein we further elucidate this mechanism. Studies with a classic Cdx2 target gene and a canonical Wnt/beta-catenin/TCF reporter suggest that Cdx2 regulates these promoters by distinctly different processes. Specifically, inhibition of beta-catenin/TCF activity by Cdx2 does not require Cdx2 transcriptional activity. Instead, Cdx2 binds beta-catenin and disrupts its interaction with the DNA-binding TCF factors, thereby silencing beta-catenin/TCF target gene expression. Using Cdx2 mutants, we map the Cdx2 domains required for the inhibition of beta-catenin/TCF activity. We identify a subdomain in the N-terminus that is highly conserved and when mutated significantly reduces Cdx2 inhibition of beta-catenin/TCF transcriptional activity. Mutation of this subdomain also abrogates Cdx2's anti-proliferative effects in colon cancer cells. In summary, we conclude that Cdx2 binds beta-catenin and disrupts the beta-catenin-TCF complex. Considering the pivotal role of beta-catenin/TCF activity in driving proliferation of normal intestinal epithelial and colon cancer cells, our findings suggest a novel mechanism for Cdx2-mediated regulation of Wnt/beta-catenin signaling and cell proliferation.