Using service-learning to encourage community health advocacy among high school students

The project outlined throughout this program management plan aims to develop a health-focused student advocacy group in the San Antonio Independent School District (SAISD). At its core, this project will be an opportunity for SAISD students to engage in service-learning, through which they will learn and develop by designing, organizing and participating in meaningful public health service experiences. ^ This program management plan addresses the genuine need for public health community education by using the service-learning model as a framework to engage students to effect change. The plan delineates the process by which the student advocacy group is to be assembled, selection of service-learning project, project objectives, technical objectives, and communication requirements. Ideally, the plan should help to facilitate project coordination, communication, and planning, and to support the direction of resources. The appendices that follow also provide useful tools with which to follow through with project implementation. ^ The plan is about more than providing a tool to educate students about the health issues in their community. It is about providing a way to teach health advocacy and self-interest and encourage civic engagement via public health. Students have the potential to positively effect lasting change among their peers, in their schools and in the community.^

Advances in Teaching & Learning Day Abstracts 2004

Proceedings of the Advances in Teaching & Learning Day Regional Conference held at The University of Texas Health Science Center at Houston in 2004.

Advances in Teaching & Learning Day Abstracts 2003

Proceedings of the Advances in Teaching & Learning Day Regional Conference held at The University of Texas Health Science Center at Houston in 2003.

Advances in Teaching & Learning Day Abstracts 2005

Proceedings of the Advances in Teaching & Learning Day Regional Conference held at The University of Texas Health Science Center at Houston in 2005.

Advances in Teaching & Learning Day Abstracts 2006

Proceedings of the Advances in Teaching & Learning Day Regional Conference held at The University of Texas Health Science Center at Houston in 2006.

Learning -dependent plasticity of movement representations in the primate primary motor cortex

Primary motor cortex (M1) is involved in the production of voluntary movement and contains a complete functional representation, or map, of the skeletal musculature. This functional map can be altered by pathological experiences, such as peripheral nerve injury or stroke, by pharmacological manipulation, and by behavioral experience. The process by which experience-dependent alterations of cortical function occur is termed plasticity. In this thesis, plasticity of M1 functional organization as a consequence of behavioral experience was examined in adult primates (squirrel monkeys). Maps of movement representations were derived under anesthesia using intracortical microstimulation, whereby a microelectrode was inserted into the cortex to electrically stimulate corticospinal neurons at low current levels and evoke movements of the forelimb, principally of the hand. Movement representations were examined before and at several times after training on behavioral tasks that emphasized use of the fingers. Two behavioral tasks were utilized that dissociated the repetition of motor activity from the acquisition of motor skills. One task was easy to perform, and as such promoted repetitive motor activity without learning. The other task was more difficult, requiring the acquisition of motor skills for successful performance. Kinematic analysis indicated that monkeys used a consistent set of forelimb movements during pellet extractions. Functional mapping revealed that repetitive motor activity during the easier task did not produce plastic changes in movement representations. Instead, map plasticity, in the form of selective expansions of task-related movement representations, was only produced following skill acquisition on the difficult task. Additional studies revealed that, in general, map plasticity persisted without further training for up to three months, in parallel with the retention of task-related motor skills. Also, extensive additional training on the small well task produced further improvements in performance, and further changes in movement maps. In sum, these experiments support the following three conclusions regarding the role of M1 in motor learning. First, behaviorally-driven plasticity is learning-dependent, not activity-dependent. Second, plastic changes in M1 functional representations represent a neural correlate of acquired motor skills. Third, the persistence of map plasticity suggests that M1 is part of the neural substrate for the memory of motor skills. ^

CHARACTERIZING AND TREATING THE NEUROPATHOLOGY OF TUBEROUS SCLEROSIS COMPLEX IN THE MOUSE

Tuberous sclerosis complex (TSC) is a multisystem, autosomal dominant disorder affecting approximately 1 in 6000 births. Developmental brain abnormalities cause substantial morbidity and mortality and often lead to neurological disease including epilepsy, cognitive disabilities, and autism. TSC is caused by inactivating mutations in either TSC1 or TSC2, whose protein products are known inhibitors of mTORC1, an important kinase regulating translation and cell growth. Nonetheless, neither the pathophysiology of the neurological manifestations of TSC nor the extent of mTORC1 involvement in the development of these lesions is known. Murine models would greatly advance the study of this debilitating disorder. This thesis will describe the generation and characterization of a novel brain-specific mouse model of TSC, Tsc2flox/ko;hGFAP-Cre. In this model, the Tsc2 gene has been removed from most neurons and glia of the cortex and hippocampus by targeted Cre-mediated deletion in radial glial neuroprogenitor cells. The Tsc2flox/ko;hGFAP-Cre mice fail to thrive beginning postnatal day 8 and die from seizures around 23 days. Further characterization of these mice demonstrated megalencephaly, enlarged neurons, abnormal neuronal migration, altered progenitor pools, hypomyelination, and an astrogliosis. The similarity of these defects to those of TSC patients establishes this mouse as an excellent model for the study of the neuropathology of TSC and testing novel therapies. We further describe the use of this mouse model to assess the therapeutic potential of the macrolide rapamycin, an inhibitor of mTORC1. We demonstrate that rapamycin administered from postnatal day 10 can extend the life of the mutant animals 5 fold. Since TSC is a neurodevelopmental disorder, we also assessed in utero and/or immediate postnatal treatment of the animals with rapamycin. Amazingly, combined in utero and postnatal rapamycin effected a histologic rescue that was almost indistinguishable from control animals, indicating that dysregulation of mTORC1 plays a large role in TSC neuropathology. In spite of the almost complete histologic rescue, behavioral studies demonstrated that combined treatment resulted in poorer learning and memory than postnatal treatment alone. Postnatally-treated animals behaved similarly to treated controls, suggesting that immediate human treatment in the newborn period might provide the most opportune developmental timepoint for rapamycin administration.

ROLE OF SYNAPSIN IN LONG-TERM SYNAPTIC FACILITATION IN APLYSIA

Enhanced expression of the presynaptic protein synapsin has been correlated with certain forms of long-term plasticity and learning and memory. However, the regulation and requirement for enhanced synapsin expression in long-term memory remains unknown. In the present study the technical advantages of the marine mollusc Aplysia were exploited in order to address this issue. In Aplysia, learning-induced enhancement in synaptic strength is modulated by serotonin (5-HT) and treatment with 5-HT in vitro of the sensorimotor synapse induces long-term facilitation (LTF) of synaptic transmission, which lasts for days, as well as the formation of new connections between the sensory and motor neuron. Results from immunofluorescence analysis indicated that 5-HT treatment upregulates synapsin protein levels within sensory neuron varicosities, the presumed site of neurotransmitter release. To investigate the mechanisms underlying increased synapsin expression, the promoter region of the Aplysia synapsin gene was cloned and a cAMP response element (CRE) was identified, raising the possibility that the transcriptional activator cAMP response element-binding protein-1 (CREB1) mediates the 5-HT-induced regulation of synapsin. Results from Chromatin Immunoprecipitation (ChIP) assays indicated that 5-HT treatment enhanced association of CREB1 surrounding the CRE site in the synapsin promoter and led to increased acetylation of histones H3 and H4 and decreased association of histone deacetylase 5 surrounding the CRE site in the synapsin promoter, a sign of transcriptional activation. In addition, sensory neurons injected with an enhanced green fluorescent protein (EGFP) reporter vector driven by the synapsin promoter exhibited a significant increase in EGFP expression following treatment with 5-HT. These results suggest that synapsin expression is regulated by 5-HT in part through transcriptional activation of the synapsin gene and through CREB1 association with the synapsin promoter. Furthermore, RNA interference that blocks 5-HT-induced elevation of synapsin expression also blocked long-term synaptic facilitation. These results indicate that 5-HT-induced regulation of synapsin is necessary for LTF and that synapsin is part of the cascade of synaptic events involved in the consolidation of memory.

Cerebellar cortex involvement in classical eyelid conditioning

A model for cerebellar involvement in motor learning was tested using classical eyelid conditioning in the rabbit. Briefly, we assume that modifications of the strength of granule cell synapses at Purkinje cells in the cerebellar cortex and mossy fiber (MF) synapses at cerebellar interpositus nuclei are responsible for the acquisition, adaptively-timed expression, and extinction of conditioned eyelid responses (CRs). A corollary of these assumptions is that the cerebellar cortex is necessary for acquisition and extinction. This model also suggests a mechanism whereby the cerebellar cortex can discriminate different times during a conditioned stimulus (CS) and thus mediate the learned timing of CRs. Therefore, experiments were done to determine the role of the cerebellar cortex in the timing, extinction, and acquisition of CRs. Lesions of the cerebellar cortex that included the anterior lobe disrupted the learned timing of CRs such that they occurred at extremely short latencies. Stimulation of MFs in the middle cerebellar peduncle as the CS could support differently timed CRs in the same animal. These data indicate that synaptic plasticity in the cerebellar cortex mediates the learned timing of CRs. These short-latency CRs which resulted from anterior lobe damage did not extinguish, while CRs in animals receiving lesions which did not include the anterior lobe extinguished normally. Preliminary data suggests that lesions of the anterior lobe which produce short-latency responses prevent the acquisition of CRs to a novel CS. These findings indicate that the anterior lobe of cerebellar cortex is necessary for eyelid conditioning. The involvement of the anterior lobe in eyelid conditioning has not been previously reported, however, the anterior lobe has generally been spared in lesion studies examining cerebellar cortex involvement in eyelid conditioning due to its relatively inaccessible location. The observation that the anterior lobe of the cerebellar cortex is not always required for the basic expression of CRs, but is necessary for response timing, extinction, and acquisition, is consistent with the hypothesis that eyelid conditioning can involve plasticity in both the cerebellar cortex and interpositus nucleus and that plasticity in the nucleus is controlled by Purkinje cell activity. ^

Volunteering: Demographic characteristics, motives and potential benefits from service

Volunteering is intricately woven into the fabric of our society. In 2009 alone, approximately 63.4 million Americans participated in volunteer activities, collectively donating over 8.1 billion service-hours (Corporation for National and Community Service [CNCS], 2010). Each service-hour is determined by the U.S. Bureau of Labor Statistics (2010) to be valued at $20.85/hr which translates to a national savings of $169 billion. Thus, we can clearly observe the significance of volunteer contribution to the overall benefit of society. In addition, there is now evidence that voluntary service may also benefit the actual volunteer, especially individuals who are 65+ years. As we reach 2020 this elderly class, composed of nearly 13 million (CNCS, 2010) Americans, will be of much consequence. Their potential to contribute in community-related efforts may save the U.S. billions in labor costs, and may also help reduce healthcare-related expenditures if volunteering proves to be a protective factor. In this literature review, we set out to explore the potential relationship between volunteer participation and increased mental and physical wellness. We also examined volunteer demographic characteristics and common motives for engaging in service-related activities. Analysis showed that volunteer work often combined low-impact physical activity and mental satisfaction from serving others, resulting in overall health benefit. Demographic characteristics displayed were consistent with previous studies and found that a majority of volunteers were female, White, married status, having received college degree or higher, employed, middle-high SES. In addition, age was seen to be a key characteristic in forecasting volunteer motivation and self-reported perceived health benefits.^