Integrating a Personal Finance Workshop to Enhance Financial Literacy Among Senior Medical Students: A Single Institution's Experience.

Purpose: Graduating medical students frequently start their training burdened with substantial financial debt and minimal savings, especially in comparison to their peers in other professional fields. A lack of financial literacy can result in increased debt, decreased job satisfaction and contribute to physician burnout. Enhancing financial education could improve both the financial stability and emotional well-being of future medical professionals.

Senataxin deficiency disrupts proteostasis through nucleolar ncRNA-driven protein aggregation.

Senataxin is an evolutionarily conserved RNA-DNA helicase involved in DNA repair and transcription termination that is associated with human neurodegenerative disorders. Here, we investigated whether Senataxin loss affects protein homeostasis based on previous work showing R-loop-driven accumulation of DNA damage and protein aggregates in human cells. We find that Senataxin loss results in the accumulation of insoluble proteins, including many factors known to be prone to aggregation in neurodegenerative disorders.

Geriatric proximal femur fracture updates.

Proximal femur fractures in the aging population present a variety of challenges. Physiologically, patients incurring this fracture are typically frail, with significant medical comorbidities, yet require early surgical treatment to restore mobility to prevent deterioration. Socioeconomically, the occurrence of a fragility fracture may be the beginning of the loss of independence, and the burdens of rehabilitation and support are borne by the individual patient and health care systems.

Regulation of transcription patterns, poly(ADP-ribose), and RNA-DNA hybrids by the ATM protein kinase.

The ataxia telangiectasia mutated (ATM) protein kinase is a master regulator of the DNA damage response and also an important sensor of oxidative stress. Analysis of gene expression in ataxia-telangiectasia (A-T) patient brain tissue shows that large-scale transcriptional changes occur in patient cerebellum that correlate with the expression level and guanine-cytosine (GC) content of transcribed genes. In human neuron-like cells in culture, we map locations of poly(ADP-ribose) and RNA-DNA hybrid accumulation genome-wide with ATM inhibition and find that these marks also coincide with high transcription levels, active transcription histone marks, and high GC content.

A-T neurodegeneration and DNA damage-induced transcriptional stress.

Loss of the ATM protein kinase in humans results in Ataxia-telangiectasia, a disorder characterized by childhood-onset neurodegeneration of the cerebellum as well as cancer predisposition and immunodeficiency. Although many aspects of ATM function are well-understood, the mechanistic basis of the progressive cerebellar ataxia that occurs in patients is not. Here we review recent progress related to the role of ATM in neurons and the cerebellum that comes from many sources: animal models, post-mortem brain tissue samples, and human neurons in culture.