Social Media Use Among Hand Surgeons.

Background: Recently social media use within healthcare has increased significantly. Today, it is common for patients to browse the Internet, including physicians' social media pages, to learn about their medical conditions and search for providers. The purpose of this study is to analyze the use of social media among hand surgeons, and to compare this use between academic and private surgeons. Methods: Using the American Society for Surgery of the Hand's (ASSH) online directory, all active members practicing within the ten most populated U.S. cities were identified. Social media presence was determined by an Internet search of platforms. Members were stratified by practice model (academic vs. private). Chi-square and t-tests were used to compare categorical and continuous variables, and a multivariable logistic regression was performed for the binary variable practice model. Results: Two hundred and fifty-six hand surgeons were identified with 150 (59%) in academic and 106 (41%) in private practice. For ResearchGate accounts, 51 (82%) were academic and 11 (18%) were private. Mean PubMed publications was 38 for academic and 9 for private. YouTube presence was 69 (70%) in academic and 29 (30%) in private. On multivariable analysis, the odds of having ResearchGate and YouTube presence were higher for academic practice. There was no statistically significant difference by practice type for Facebook, Twitter, LinkedIn, and Instagram. Conclusions: With the recent social media expansion, surgeons have adopted social media platforms to reach patients. While the literature has shown that private practices are more active in social media, our results show they are not more active than academic practices in the ten most populated U.S. cities. Level of Evidence: IV.

Development of a Cx46 Targeting Strategy for Cancer Stem Cells.

Gap-junction-mediated cell-cell communication enables tumor cells to synchronize complex processes. We previously found that glioblastoma cancer stem cells (CSCs) express higher levels of the gap junction protein Cx46 compared to non-stem tumor cells (non-CSCs) and that this was necessary and sufficient for CSC maintenance. To understand the mechanism underlying this requirement, we use point mutants to disrupt specific functions of Cx46 and find that Cx46-mediated gap-junction coupling is critical for CSCs. To develop a Cx46 targeting strategy, we screen a clinically relevant small molecule library and identify clofazimine as an inhibitor of Cx46-specific cell-cell communication. Clofazimine attenuates proliferation, self-renewal, and tumor growth and synergizes with temozolomide to induce apoptosis. Although clofazimine does not cross the blood-brain barrier, the combination of clofazimine derivatives optimized for brain penetrance with standard-of-care therapies may target glioblastoma CSCs. Furthermore, these results demonstrate the importance of targeting cell-cell communication as an anti-cancer therapy.

Cx25 contributes to leukemia cell communication and chemosensitivity.

Leukemia encompasses several hematological malignancies with shared phenotypes that include rapid proliferation, abnormal leukocyte self-renewal, and subsequent disruption of normal hematopoiesis. While communication between leukemia cells and the surrounding stroma supports tumor survival and expansion, the mechanisms underlying direct leukemia cell-cell communication and its contribution to tumor growth are undefined. Gap junctions are specialized intercellular connections composed of connexin proteins that allow free diffusion of small molecules and ions directly between the cytoplasm of adjacent cells. To characterize homotypic leukemia cell communication, we employed in vitro models for both acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) and measured gap junction function through dye transfer assays. Additionally, clinically relevant gap junction inhibitors, carbenoxolone (CBX) and 1-octanol, were utilized to uncouple the communicative capability of leukemia cells. Furthermore, a qRT-PCR screen revealed several connexins with higher expression in leukemia cells compared with normal hematopoietic stem cells. Cx25 was identified as a promising adjuvant therapeutic target, and Cx25 but not Cx43 reduction via RNA interference reduced intercellular communication and sensitized cells to chemotherapy. Taken together, our data demonstrate the presence of homotypic communication in leukemia through a Cx25-dependent gap junction mechanism that can be exploited for the development of anti-leukemia therapies.