First-generation college students (students whose parents did not complete a bachelor’s degree) are a growing population within U.S. colleges. These students often belong to historically underrepresented populations including racial and ethnic minority groups and those with lower socioeconomic status. This paper discusses a project to redesign introductory anthropology courses to be more “first-generation friendly.” Changes discussed include creating a welcoming classroom climate, providing clear expectations and feedback, integrating Universal Design for Learning, rethinking course content, and creating plans for critical self-reflection. We conclude by discussing the impact of our changes and plans for future work.

Huntington's disease (HD), an adult-onset, dominantly-inherited neurodegenerative disease primarily affecting the striatum and deep cortical regions of the brain, is caused by a polyglutamine expansion in the N-terminal region of a 350 kD protein called huntingtin (htt). Huntingtin normally contains an N-terminal polyglutamine stretch of less than 36 amino acids, but if and when the stretch exceeds this number, the protein misfolds and aggregates into protein plaques called inclusion bodies. Concurrently, the protein becomes toxic. As polyglutamine repeat number increases, disease emerges at an earlier age while the protein tends to aggregate faster in vitro. To understand pathogenic mechanisms in HD at the cellular level, various molecular risk factors need to be linked to the fate of individual neurons, much like individual health characteristics in human patients can be linked to outcomes like recovery, illness, or death. In this dissertation, we employ automated microscopy technology to track thousands of individual neurons and precisely relate a range of molecular risk factors we can measure to outcomes we are interested in, thereby suggesting pathogenic mechanisms and pathways in which therapeutic intervention may prove effective. We establish critical limits on how the basic molecular characteristics of the disease, including htt levels, polyglutamine expansion length, and inclusion body formation, relate to neuronal death. We then evaluate the prognostic significance of various misfolded conformations of htt and discover that a conformation with a two-stranded, compact, hairpin configuration of the polyglutamine region is strongly predictive of death. This conformation is recognized by monoclonal antibody 3B5H10, which could serve in the future as an intermediate marker for neurotoxicity in high-throughput small molecule therapeutic screens. We then employ our newly acquired knowledge of HD cellular pathogenesis to therapeutically evaluate the effect of a series of small molecules and proteins impinging on several different putative pathogenic or therapeutic pathways. Several therapies we test show initial potential as therapeutics and should be investigated further.

Application of pulsed radiofrequency (PRF) currents to the dorsal root ganglia (DRG) has been reported to produce relief from certain pain states without causing thermal ablation. In this study, we examined the direct correlation between PRF application to DRG associated with spinal nerve injury and reversal of injury-induced behavioral hypersensitivity in a rat neuropathic pain model.

Neuropathic lesioning was performed via left L5 spinal nerve ligation on male adult Sprague-Dawley rats. Once the injured rats had developed tactile allodynia, one group was then assigned to PRF treatment of the L5 DRG and another group was assigned to the sham treatment to the DRG. Behavioral testing was performed on both the control and treated paws using the von Frey filament test before the surgery and at indicated days. The resulting data were analyzed using a linear mixed model to assess the overall difference between the treatment groups and the overall difference among the study days. Cohen's d statistic was computed from paired difference-from-baseline scores for each of the 14 study days after treatment and these measures of effect size were then used to descriptively compare the recovery patterns over time for each study group.

Spinal nerve injury resulted in the development of behavioral hypersensitivity to von Frey filament stimulation (allodynia) in the hindpaw of the left (injury) side. Mixed linear modeling showed a significant difference between the treatment groups (P = 0.0079) and a significant change of paw withdrawal threshold means over time (P = 0.0006) for all 12 animals. Evaluation of Cohen's d (effect size) revealed that the PRF-treated animals exhibited better recovery and recorded larger effect sizes than the sham-treated animals on 10 of the 14 post-PRF treatment days and exhibited moderate-to-strong effects posttreatment at days 8 to 10 and at and beyond day 32.

Findings from this study support that PRF of the DRG causes reversal of nerve injury (spinal nerve ligation)-induced tactile allodynia in rats. This allodynia reversal indicates that nonablative PRF acting via modulation of the DRG can speed recovery in nerve injury-induced pain.