Publications by authors named "J Gregory Hixon"
Script training is a speech-language intervention designed to promote fluent connected speech via repeated rehearsal of functional content. This type of treatment has proven beneficial for individuals with aphasia and apraxia of speech caused by stroke and, more recently, for individuals with primary progressive aphasia (PPA). In the largest study to-date evaluating the efficacy of script training in individuals with nonfluent/agrammatic primary progressive aphasia (nfvPPA; Henry et al.
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- Defects in DNA repair pathways, particularly in BRCA1 or BRCA2, contribute to tumor evolution and resistance to therapies like PARP inhibitors, creating vulnerabilities in tumors.
- Researchers identified USP1 as a key target in BRCA-mutant tumors and developed KSQ-4279, the first selective USP1 inhibitor being tested clinically.
- The combination of KSQ-4279 and PARP inhibitors showed promise by effectively reducing tumors resistant to PARP treatment, suggesting a new strategy for improving outcomes in patients with HR-deficient tumors.
Type 1 diabetes (T1D) affects gastrointestinal (GI) motility, favoring gastroparesis, constipation, and fecal incontinence, which are more prevalent in women. The mechanisms are unknown. Given the G-protein-coupled estrogen receptor's (GPER) role in GI motility, we investigated sex-related diabetes-induced epigenetic changes in GPER.
View Article and Find Full Text PDFSocial transmission of fear occurs in a subset of individuals, where an Observer displays a fear response to a previously neutral stimulus after witnessing or interacting with a conspecific Demonstrator during memory retrieval. The conditions under which fear can be acquired socially in rats have received attention in recent years, and suggest that social factors modulate social transmission of information. We previously found that one such factor, social rank, impacts fear conditioning by proxy in male rats.
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- G3BP1 and G3BP2 are proteins that help form stress granules in cells during stress, like viral infections, but SARS-CoV-2's nucleocapsid (N) protein stops this process.
- The study identifies a specific mutation (N-F17A) in the N protein that prevents its interaction with G3BP1/2, leading to an inability to inhibit stress granule formation.
- This disruption results in lower viral replication and reduced illness in experimental models, showing that the G3BP1-N interaction is crucial for SARS-CoV-2’s ability to replicate and cause disease.