Payal
Hegde
Sponsor: Elizabeth Vasile, Ph.D. MED: Clin & Trans Science Ctr Community member participation is critical for shaping health research but the barriers to participating are great. One way to reduce barriers for community participation in health research is to compensate community members for their time and expertise. The purpose of this research is to examine how compensation of community members works within the Clinical Translational Science Award (CTSA) network by investigating sample community-engagement programs. To address this question, multiple research methods were utilized, including an environmental scan of community engaged research program offering within the CTSA network, a literature review of peer- reviewed journals, a survey of CTSA community engagement managers, and information collected from interviews. Our study shows that the compensation system for community partners research is different within each CTSA hub. In addition, the range and rate of compensation varies significantly. The aims of this research are to uncover barriers, make the compensation process less difficult and have community participation increase within the CTSA network. Development of a DNA methylation assay for the Mecp2 locus in the mouse genome
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Authors:
Payal Hegde
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Rett's syndrome (RTT) is a progressive neurodevelopmental disorder that occurs almost exclusively in females, affecting about 1 in 10,000 individuals. Following a brief period of normal infancy, patients experience a regression in developmental markers including difficulty feeding, impaired speech, mobility problems, jerky hand movements, and seizures. RTT is caused by a loss-of- function mutation of the Mecp2 gene on the X chromosome. The normal copy of Mecp2 is turned off in neurons by a process called X chromosome inactivation (Xi). A potential treatment for RTT is to reactivate Mecp2 from Xi by demethylating the promoter region of this gene using CRISPR-based epigenome editing. As such, developing a suitable assay to detect DNA methylation in the Mecp2 promoter will optimize preclinical therapy development. A promoter DNA methylation pattern analysis was determined by extracting DNA from mouse cells and brain tissue treated with CRISPR epigenome editors. This was followed by a bisulfite conversion, PCR amplification of bisulfite converted DNA, and Sanger sequencing. The development of an epigenome editor that targets hypermethylation of Mecp2 in the brain has the potential to reverse clinical deficits and ultimately treat patients with RTT. Developing Anti-Racist Curricula: Exploring Liver Disease in Latiné Populations through Justice- Oriented Case Studies for Pre-health Students Sanjna Hegde
Source:
UC Davis / MED: Neurology / 2024
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Co-authors:
Payal Hegde