"The Gluten-Free Diet and Its Relationship with Metabolic Syndrome: Dietary Friend or Foe?"

PURPOSE OF REVIEW: Celiac disease (CD) is a prevalent digestive illness as well as a budding area of research in the field of gastroenterology. While investigations are underway to find new and improved pharmacological therapies for CD, the gluten-free diet (GFD) remains the only option to effectively manage the condition. RECENT FINDINGS: While the GFD is recommended for patients diagnosed with CD and other gluten-related conditions, studies show the number of individuals on the GFD surpasses the projected number of patients with these medical indications (1). The implications of widespread adoption of this dietary approach are still being determined, with many patients believing this diet will improve overall health and cardiovascular risk. This review analyzes the relationship between a GFD and metabolic syndrome in both non-celiac and celiac patients, concluding that although the diet may slightly improve overall cardiac risk factors, weight, and/or insulin resistance, its use in the absence of a gluten-related disorder is controversial.

PubMed-Indexed Research Productivity of Students Matching at Top Urology Programs: 2017-2020.

OBJECTIVE: To evaluate the number of PubMed-indexed research projects of medical students matching at top-ranked urology programs as compared to the average publications reported in the Electronic Residency Applicant Service (ERAS). METHODS: Doximity Residency Navigator was used to generate the top 50 residency programs when sorted by reputation. Residents were then found using program websites. PubMed was queried for peer-reviewed publications of incoming interns through post graduate year 3 residents as of February 2020. All PubMed-indexed research was recorded before September 15th of the residents' fourth year of medical school. We recorded the number of publications, first/last author publications, and urology-specific publications. RESULTS: The average number of publications across all 4 years was 2.38 ± 4.19. The average for urology-specific publications was 1.05 ± 3.19 and for first/last author publications was 0.80 ± 1.77. Most matched applicants had at least one PubMed-indexed publication (61.2%) and having over 3 placed them in the 75th percentile. It is uncommon for students to have urology specific or first/last author publications (34.0%, 36.5%). Top 10 programs matched applicants with significantly more research in each of the aforementioned categories and as program reputation declined, so did the publications of the applicants they matched. CONCLUSION: Most research that matched urology applicant's report in ERAS is not PubMed Indexed. Most had at least one PubMed-indexed publication by the time they submitted ERAS and those at top programs had more. It would be helpful to students and faculty advisors if ERAS published research metrics for matched and unmatched applicants separating PubMed-indexed work from posters and presentations.

Enhancer of Polycomb and the Tip60 complex repress hematological tumor initiation by negatively regulating JAK/STAT pathway activity.

Myeloproliferative neoplasms (MPNs) are clonal hematopoietic disorders that cause excessive production of myeloid cells. Most MPN patients have a point mutation in JAK2 (JAK2V617F ), which encodes a dominant-active kinase that constitutively triggers JAK/STAT signaling. In Drosophila, this pathway is simplified, with a single JAK, Hopscotch (Hop), and a single STAT transcription factor, Stat92E. The hopTumorous-lethal [hopTum ] allele encodes a dominant-active kinase that induces sustained Stat92E activation. Like MPN patients, hopTum mutants have significantly more myeloid cells, which form invasive tumors. Through an unbiased genetic screen, we found that heterozygosity for Enhancer of Polycomb [E(Pc)], a component of the Tip60 lysine acetyltransferase complex (also known as KAT5 in humans), significantly increased tumor burden in hopTum animals. Hematopoietic depletion of E(Pc) or other Tip60 components in an otherwise wild-type background also induced blood cell tumors. The E(Pc) tumor phenotype was dependent on JAK/STAT activity, as concomitant depletion of hop or Stat92E inhibited tumor formation. Stat92E target genes were significantly upregulated in E(Pc)-mutant myeloid cells, indicating that loss of E(Pc) activates JAK/STAT signaling. Neither the hop nor Stat92E gene was upregulated upon hematopoietic E(Pc) depletion, suggesting that the regulation of the JAK/STAT pathway by E(Pc) is dependent on substrates other than histones. Indeed, E(Pc) depletion significantly increased expression of Hop protein in myeloid cells. This study indicates that E(Pc) works as a tumor suppressor by attenuating Hop protein expression and ultimately JAK/STAT signaling. Since loss-of-function mutations in the human homologs of E(Pc) and Tip60 are frequently observed in cancer, our work could lead to new treatments for MPN patients.This article has an associated First Person interview with the first author of the paper.