ABSTRACT
CONTEXT: Just Say Know to Drugs! is a summer pharmacology enrichment program for high school students. First-year osteopathic medical students serve as teachers, introducing students to pharmacology while acquiring teaching skills. OBJECTIVE: To assess the effects of a pharmacology program on high school students and to understand the effects of teaching this program on first-year osteopathic medical students. METHODS: The influence of a pharmacology STEM (science, technology, engineering, and mathematics) enrichment program on high school students' career interests and student teacher preparedness was determined by a pre- and posttest, as well as a postprogram survey. RESULTS: Data from all 37 participating high school students and 10 of 16 student teachers (medical students and undergraduate assistants) were evaluated in the study. Survey findings suggested that this STEM program increased student awareness and knowledge of pharmacology, osteopathic medicine, and scientific research. Furthermore, student teachers thought that they developed the necessary skills to communicate and educate populations with diverse science backgrounds and comprehension levels. The immersion of high school students in the scientific content significantly increased student awareness of pharmacology (paired t test, P<.0001). CONCLUSION: The Just Say Know to Drugs! program delivered benefits for both high school students and student teachers.
Subject(s)
Health Education/organization & administration , Pharmacology/education , Schools/organization & administration , Substance-Related Disorders/prevention & control , Adolescent , Female , Humans , Male , Program Development , Program Evaluation , Rural Population , Students, Medical , West VirginiaABSTRACT
Huntington's disease (HD) is a hereditary neurodegenerative disease that leads to striatal degeneration and a severe movement disorder. We used a transgenic mouse model of HD (the R6/2 line with approximately 150 glutamine repeats) to test a new therapy for this disease. We treated HD mice with metformin, a widely used anti-diabetes drug, in the drinking water (0, 2 or 5mg/ml) starting at 5 weeks of age. Metformin treatment significantly prolonged the survival time of male HD mice at the 2mg/ml dose (20.1% increase in lifespan) without affecting fasting blood glucose levels. This dose of metformin also decreased hind limb clasping time in 11-week-old mice. The higher dose did not prolong survival, and neither dose of metformin was effective in female HD mice. Collectively, our results suggest that metformin may be worth further investigation in additional HD models.
Subject(s)
Huntington Disease/drug therapy , Hypoglycemic Agents/therapeutic use , Metformin/therapeutic use , AMP-Activated Protein Kinases , Age Factors , Animals , Behavior, Animal , Blood Glucose/drug effects , Disease Models, Animal , Dose-Response Relationship, Drug , Enzyme Activation/drug effects , Female , Glutamine/genetics , Male , Mice , Mice, Transgenic , Motor Activity/drug effects , Multienzyme Complexes/metabolism , Protein Serine-Threonine Kinases/metabolism , Sex Factors , Trinucleotide Repeats/geneticsABSTRACT
We have developed a simple and sensitive assay to quantify neuron-specific death in primary cell cultures that represents a significant improvement over more commonly used methods including manual cell counting and lactate dehydrogenase release. This new method selectively detects neuronal death by combining immunolabeling for a neuron-specific marker with the ease, sensitivity, and speed of an enzyme-linked fluorescence assay. Using microtubule associated protein 2 (MAP2) as a neuron-specific marker, we assessed glutamate-receptor mediated neurotoxicity in neuron-enriched cultures and in mixed neuronal/glial cultures established from mouse forebrain and compared these results to neuronal death measured by lactate dehydrogenase (LDH) release. We were able to achieve statistically significant differences in toxicity between intermediately toxic concentrations of glutamate (30, 50, and 100 microM) with the MAP2 assay, while we were not able to discriminate among these concentrations with the LDH assay. We were also able to measure hydrogen peroxide-induced neuronal death, and demonstrate neuroprotection by antioxidant addition. This new assay is easily adaptable to high-throughput in vitro screens of neurodegeneration and of neuroprotective therapies.
