Implementation and value of a student-run volunteer clinical research program at an academic medical center.

Clinical research output in the emergency department (ED) continues to be constrained by limitations in funding for researchers, demands of patient care on ED providers, and difficulties in obtaining high-quality data. In response, several institutions have established programs in which student volunteers are integrated into department workflows to increase clinical research output and introduce pre-health students to careers in medicine. One such program, the student volunteer clinical research program, presently consists of over 40 undergraduate and post-baccalaureate student volunteers who screen, consent, and enroll patients into prospective studies in the ED of the University of California, Los Angeles (UCLA) Ronald Reagan Medical Center. The program is led by student coordinators who collaborate with departmental research staff and faculty. Our program is unique in that it is primarily run by the students themselves. Experienced student research associates facilitate recruitment through a competitive biannual application process, train new volunteers to perform on-shift research duties, and monitor participants for compliance with both hospital and program policies. Participation in the program provides students with exposure to frontline medical research, opportunities to observe clinical medicine, and access to a variety of program-specific resources including student-led committees, career development resources, and mentorship from peers, alumni, and faculty. This concept piece serves as a structural model for other institutions seeking to implement volunteer clinical research or bolster existing programs through increased student-led initiatives.

NMYC Amplification in Neuroblastoma: The Molecular Landscape.

OBJECTIVES: Neuroblastoma remains one of the most clinically diverse cancers common in pediatric patients. An important prognostic indicator for neuroblastoma involves the NMYC gene, which is the differentiating factor between high-risk and low-risk disease; the five-year survival rates for patients with and without NMYC mutations are 40% and 95%, respectively. This review assesses our current understanding of the molecular role and function of NMYC in risk stratification and disease progression and highlights key areas of research to improve existing and identify novel targets for neuroblastoma treatments.

Alterations in the gut microbiota contribute to cognitive impairment induced by the ketogenic diet and hypoxia.

Many genetic and environmental factors increase susceptibility to cognitive impairment (CI), and the gut microbiome is increasingly implicated. However, the identity of gut microbes associated with CI risk, their effects on CI, and their mechanisms remain unclear. Here, we show that a carbohydrate-restricted (ketogenic) diet potentiates CI induced by intermittent hypoxia in mice and alters the gut microbiota. Depleting the microbiome reduces CI, whereas transplantation of the risk-associated microbiome or monocolonization with Bilophila wadsworthia confers CI in mice fed a standard diet. B. wadsworthia and the risk-associated microbiome disrupt hippocampal synaptic plasticity, neurogenesis, and gene expression. The CI is associated with microbiome-dependent increases in intestinal interferon-gamma (IFNg)-producing Th1 cells. Inhibiting Th1 cell development abrogates the adverse effects of both B. wadsworthia and environmental risk factors on CI. Together, these findings identify select gut bacteria that contribute to environmental risk for CI in mice by promoting inflammation and hippocampal dysfunction.

A Complex Karyotype in a 68-Year-Old Patient With T-PLL.

OBJECTIVES: T-cell prolymphocytic leukemia, or T-PLL, is an extremely rare and highly metastatic neoplasm characterized by proliferating mature T-cells and genetic aberrations that often involve chromosome 14. While T-PLL is commonly accompanied by a complex karyotype, there is little analysis on such cases in existing literature and thorough discussions of the less "characteristic" cytogenetic mutations are particularly lacking. We present a case study of a 68-year-old male T-PLL patient with marked leukocytosis and a history of T-cell lymphoproliferative disorder. Chromosomal analysis revealed a complex karyotype that included a translocation of both copies of chromosome 14, rearrangements on 9p and 5p, isochromosome 8, deletion 11q, and monosomy 17. Molecular cytogenetic analysis indicated a rearrangement of TRD (14q11.2), loss of the ATM and CDKN2A signals, and gains of the RELN, TES and MYC signals. Many of these mutations have strongly corresponded to poor prognoses in patients with T-PLL and other leukemias, especially when appearing concurrently. However, there are still profound knowledge gaps in our understanding of many genetic aberrations and the significance of marker chromosomes in the context of T-PLL. Considering the lack of consensus on the improvement of patient outcomes in the past two decades as well as the frequency of a complex karyotype in T-PLL, this case study highlights the critical need of continued research efforts in profiling complex cases to provide potential avenues for novel therapeutic targets for T-PLL patients.