Publications by authors named "J C Martindale"
Article Synopsis
- Longitudinal patient relationships can enhance medical students' professional identity formation and understanding of illness, but implementing a traditional longitudinal integrated clerkship (LIC) may not always be possible.
- The Patient Student Partnership (PSP) program at the University of Virginia School of Medicine pairs students with chronic illness patients over four years, blending experiential learning with the existing block curriculum.
- Student feedback indicates that the PSP program fosters connections between classroom theory and clinical practice, improves communication skills, and enhances self-reflection on their future roles, with 80.6% agreeing it allowed them to observe the impact of chronic illness on patients' lives.
- Future research is needed to assess the program’s effectiveness in promoting professional identity formation similar to LICs and to improve student
Cells react to stress by triggering response pathways, leading to extensive alterations in the transcriptome to restore cellular homeostasis. The role of RNA metabolism in shaping the cellular response to stress is vital, yet the global changes in RNA stability under these conditions remain unclear. In this work, we employ direct RNA sequencing with nanopores, enhanced by 5' end adapter ligation, to comprehensively interrogate the human transcriptome at single-molecule and -nucleotide resolution.
View Article and Find Full Text PDFAttention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental condition that often results in poor academic performance. Little is known about how ADHD manifests in residents and fellows. To describe the prevalence and phenotype of ADHD among residents and fellows referred to a centralized remediation program.
View Article and Find Full Text PDFArticle Synopsis
- Senescence is when cells stop dividing, linked to aging and diseases like cancer, and is characterized by a weakened ability to respond to stress.
- Senescent cells show signs of stress response activation, like high eIF2α phosphorylation, but still fail to produce the stress response factor ATF4 due to ineffective regulatory mechanisms.
- When stressed, these cells not only struggle to respond effectively but also increase inflammation, which seems to be influenced by the levels of ATF4 mRNA that lack specific regulatory elements.