Peroxynitrite, a highly oxidative molecule, plays a role in neuronal cell death following traumatic brain injury (TBI). A peptide comprised of the HIV-1 tat transduction domain fused to nine cysteine residues (Tat-9c) was previously designed to act as an exogenous target for nitrosylation by peroxynitrite. The present study’s aim was to explore the efficacy of Tat-9c in maintaining neurological function following TBI. Rats treated with Tat-9c exhibited significant improvement in performance compared to controls 24 hrs following TBI in the Beam-Walk task but not in the Rota-Rod task. Injured animals, given the drug, show a recovery as indicated by similar performance on the Morris Water Maze task compared to sham controls. These findings suggest Tat-9c may constitute a potential therapy for improving motor and cognitive function following TBI.

Peroxynitrite, a highly oxidative molecule, plays a role in neuronal cell death following traumatic brain injury (TBI). A peptide comprised of the HIV-1 tat transduction domain fused to nine cysteine residues (Tat-9c) was previously designed to act as an exogenous target for nitrosylation by peroxynitrite. The present study’s aim was to explore the efficacy of Tat-9c in maintaining neurological function following TBI. Rats treated with Tat-9c exhibited significant improvement in performance compared to controls 24 hrs following TBI in the Beam-Walk task but not in the Rota-Rod task. Injured animals, given the drug, show a recovery as indicated by similar performance on the Morris Water Maze task compared to sham controls. These findings suggest Tat-9c may constitute a potential therapy for improving motor and cognitive function following TBI.

Peroxynitrite, a highly oxidative molecule, plays a role in neuronal cell death following traumatic brain injury (TBI). A peptide comprised of the HIV-1 tat transduction domain fused to nine cysteine residues (Tat-9c) was previously designed to act as an exogenous target for nitrosylation by peroxynitrite. The present study’s aim was to explore the efficacy of Tat-9c in maintaining neurological function following TBI. Rats treated with Tat-9c exhibited significant improvement in performance compared to controls 24 hrs following TBI in the Beam-Walk task but not in the Rota-Rod task. Injured animals, given the drug, show a recovery as indicated by similar performance on the Morris Water Maze task compared to sham controls. These findings suggest Tat-9c may constitute a potential therapy for improving motor and cognitive function following TBI.

Peroxynitrite, a highly oxidative molecule, plays a role in neuronal cell death following traumatic brain injury (TBI). A peptide comprised of the HIV-1 tat transduction domain fused to nine cysteine residues (Tat-9c) was previously designed to act as an exogenous target for nitrosylation by peroxynitrite. The present study’s aim was to explore the efficacy of Tat-9c in maintaining neurological function following TBI. Rats treated with Tat-9c exhibited significant improvement in performance compared to controls 24 hrs following TBI in the Beam-Walk task but not in the Rota-Rod task. Injured animals, given the drug, show a recovery as indicated by similar performance on the Morris Water Maze task compared to sham controls. These findings suggest Tat-9c may constitute a potential therapy for improving motor and cognitive function following TBI.

Vascular endothelial growth factor (VEGF) may play a role in neuroprotection after traumatic brain injury (TBI) in addition to being a regulator of angiogenesis. Gene therapy using an adenovirus carrying an engineered zinc-finger protein (Adv-ZFP) and transcription factor construct targeted to the VEGF gene, has been shown to upregulate genomic expression of VEGF-A isoforms in skeletal muscle. Our objective was to use this gene therapy to explore cell survival in TBI. Rats were subjected to a unilateral fluid percussion injury (FPI) in the cortex. Groups consisted of control, injured and injured-treated animals. Adv-ZFP-VEGF was injected into the cortex and hippocampus. Engineered ZFP-VEGF increases VEGF-A protein levels and correlates with increased CA2 hippocampal cell survival and reduction in apoptotic cell death following TBI. NF200 expression in TBI+VEGF animals was comparable to levels in naive animals. This study suggests a therapeutic strategy to treat delayed cell death in a model of TBI.

Brain injury has become a more topical issue over the past decade, however limited research has been done on experiences of university students and few are specific to female students. The research question became: “How has having an acquired brain injury impacted the experience of female students within postsecondary education?” Narrative and auto-ethnographic methodologies were employed; semi-structured interviews with five participants were conducted, and text boxes were utilized to weave the researcher’s voice as a student with a brain injury into the narrative. Findings indicate brain injury has diverse implications depending on severity. Some participants spoke of accessing (dis)Ability resource centres, while others did not utilize formal accommodations. Findings revealed that participants navigate the academy in isolation yet wanted to connect with fellow students who have acquired brain injuries. Social workers can facilitate this process and provide counselling, challenge negative social implications and work toward building an inclusive educational environment.

Background: Traumatic brain injury (TBI) is devastating to patients and their family members who are left trying to understand and cope with this diagnosis. This is especially true for family members of patients with TBI who are treated in the intensive care unit (ICU), which presents additional challenges. Family members are often present at the bedside and desire information about the patient and diagnosis. However, this can be a stressful event for family members as they attempt to understand the complexities of TBI. This DNP project analyzed the quality of education and information delivery from ICU staff members to family members of patients with moderate to severe TBI and used the findings to create a standardized education program for future implementation. Methods: A mixed-model, descriptive design with both qualitative and quantitative components was used to conduct a needs assessment at an urban, Level II trauma center within the ICU. Patients with moderate to severe TBI, as measured as Glasgow Coma Scale of 12 or less, were selected. From these patients, family members and close friends who were 18 years of age and older were asked to complete surveys and interviews about their experiences with education and information delivery in the ICU. ICU staff nurses also completed surveys about their opinions of delivering education and information to family members. Results: Over a time period of 5 months, 6 patients who met criteria were selected, and 5 family members completed surveys and interviews. Of the 56 staff nurses who received surveys, 17 participated in the surveys. Based on quantitative data, family members did not demonstrate a need for improvement in the method of education and information delivery, but provided a rich description of many needed improvements through qualitative responses. On the other hand, staff nurses reported dissatisfaction in current method of education and information delivery in all aspects except for one. Conclusion: Based on the results, the TBI Family Education Model was developed as an education tool that can be implemented in the future to standardize education and information delivery to family members of patients with moderate to severe TBI.

Research has shown that health promotion programs (HPP) that incorporate education about physical activity (PA) are one mode of rehabilitation that can improve the health of individuals with disabilities. However, education-based PA curriculum is not included in the rehabilitation program for individuals with a brain injury, indicating a gap in services provided. Consequently, the purpose of this study was to create and deliver a physical activity centered education (PACE) program that supplemented the existing rehabilitation program for brain injury. PACE consists of an 8-week (16 session) program aimed to (1) increase self-efficacy for being physically active of PACE program participants, (2) increase PA stage of change in PACE program participants or the maintenance of adequate level of PA, and (3) improve the rehabilitation outcomes (i.e., abilities, participation, adjustment) of PACE program participants. Based on previous research, it is hypothesized that participation in PACE will result in (1A) increased self-efficacy for PA, (1B) greater self-efficacy for PA than the standard of care group, (2A) increased readiness to be physically active, (2B) greater readiness to change their PA behavior than the standard of care group, (3A) improved rehabilitation outcomes, and (3B) greater rehabilitation outcomes than the standard of care group. the PACE program resulted in: (1) an average increase of 19.36% in participants’ PA self-efficacy (effect size [ES] = 0.37), (2) 15 of the 22 PACE participants (68.18%) reported readiness to engage in regular PA , and (3) an increase in rehabilitation outcomes (i.e., abilities, adjustment, and participation)In conclusion, the PACE program can improve PA self-efficacy, readiness for regular PA behavior, and improved short-term rehabilitation outcomes.

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