Social Media Growth at Annual Medical Society Meetings: A Comparative Analysis of Diagnostic and Interventional Radiology to Other Medical Specialties.

OBJECTIVE: To understand social media growth in both diagnostic and interventional radiology compared to other related specialties by quantifying and comparing hashtag utilization at annual medical conferences. METHODS: Official annual conference hashtags for Society of Interventional Radiology (SIR), American College of Radiology (ACR), Radiological Society of North America, American College of Cardiology, American Heart Association, and American Society of Clinical Oncology were analyzed from 2015 to 2019, along with the IR hashtag #IRad. Twitter analytics were obtained with the use of Symplur Signals, a healthcare social media analytics platform. Linear regression analysis was performed on the number of tweets and users for each hashtag. RESULTS: For annual ACR meetings, the number of tweets/user (6.96 in 2019), retweets/user (4.39 in 2019), and impressions/user (40,051 in 2019) were among the highest of all the specialties studied. This trend was observed despite a smaller number of users among ACR than most other conferences. SIR tweets increased significantly at a rate of 1032.8 tweets/year (P = 0.008) while users also significantly grew at a rate of 212.5 users/years (P = 0.007). #IRad tweets are also growing at a rate of 13,234.8 tweets/year (P = 0.026) while #IRad users are growing at a rate of 1309.5 users/year (P = 0.003). Radiological Society of North America users were significantly decreasing at -1207.1 users/year (P = 0.018). CONCLUSION: ACR consistently had one of the highest counts of tweets/user, retweets/user, and impressions/user compared to the other studied specialties, suggesting that ACR's Twitter users are more active than users outside of the field of radiology. SIR was the only studied specialty conference that had statistically significant increases in the number of tweets and users.

BCG Vaccinations Upregulate Myc, a Central Switch for Improved Glucose Metabolism in Diabetes.

Myc has emerged as a pivotal transcription factor for four metabolic pathways: aerobic glycolysis, glutaminolysis, polyamine synthesis, and HIF-1α/mTOR. Each of these pathways accelerates the utilization of sugar. The BCG vaccine, a derivative of Mycobacteria-bovis, has been shown to trigger a long-term correction of blood sugar levels to near normal in type 1 diabetics (T1D). Here we reveal the underlying mechanisms behind this beneficial microbe-host interaction. We show that baseline glucose transport is deficient in T1D monocytes but is improved by BCG in vitro and in vivo. We then show, using RNAseq in monocytes and CD4 T cells, that BCG treatment over 56 weeks in humans is associated with upregulation of Myc and activation of nearly two dozen Myc-target genes underlying the four metabolic pathways. This is the first documentation of BCG induction of Myc and its association with systemic blood sugar control in a chronic disease like diabetes.

Optimizing TNFR2 antagonism for immunotherapy with tumor microenvironment specificity.

Most approved cancer immunotherapies lack T-regulatory (Treg) or tumor specificity. TNF receptor 2 (TNFR2) antibody antagonism is emerging as an attractive immunotherapy due to its tumor microenvironment (TME) specificity. Here we show that the human TNFR2 receptor is overexpressed on both human tumor cells and on human tumor-residing Tregs, but negligibly expressed on beneficial T effectors (Teffs). Further, we found widespread, if variable, TNFR2 expression on 788 human tumor cell lines from diverse cancer tissues. These findings provided strong rationale for developing a targeted immunotherapy using a TNFR2 antibody antagonist. We designed a novel, human-directed TNFR2 antibody antagonist and tested it for function using three cell-based TME assays. The antagonist showed TME specificity by killing of TNFR2-expressing tumor cells and Tregs, but sparing Teffs, which proliferated. However, the antagonist shuffled between five isoforms, only one of which showed the desirable function. We designed and tested several new chimeric human versions of the antagonist, finding that the IgG2 isotype functioned better than the IgG1 isotype. To further improve function, we introduced targeted mutations to its amino acid sequence to stabilize the natural variability of the IgG2 isotype's hinge. Altogether, our findings suggest that optimal TNFR2 antagonists are of the human IgG2 isotype, have hinge stabilization, and have wide separation of antibody arms to bind to newly synthesized TNFR2 on rapidly growing tumor cells. Antagonistic antibodies with these characteristics, when bound to TNFR2, can form a nonsignaling cell surface dimer that functions with high TME specificity.