Staff Low Back Injury Risk During Assisted Falls Virtual Reality Simulations.

BACKGROUND: Assisted falls occur when staff try to minimize the impact of falls by slowing a patient's descent. Assisting a patient fall may decrease patient injury risk, but biomechanical risk of injury to staff has not been evaluated. Assisted falls virtual reality (VR) simulations were conducted to examine staff low back injury risk during common assisted falls scenarios. METHODS: VR simulations of a toilet to wheelchair transfer were developed with a male patient avatar for three assisted falls scenarios: standing up from toilet, sitting down on wheelchair, and ambulation. Patient avatar weight was modified to reflect normal, underweight, and overweight adult patients. The average spinal compression force at L5/S1 was calculated for each participant with five trials per three scenarios while utilizing physical ergonomic techniques and compared to the safe spinal compression limit of 3,400 Newtons (N). FINDINGS: Six staff participants completed 90 VR simulations in total. The average calculated spinal compression force ranged from 7,132 N to 27,901 N. All participant trials exceeded the safe spinal compression limit of 3,400 N for every assisted falls scenario and avatar weight despite application of ergonomic techniques including wide stance, knees bent, and backs straight. CONCLUSIONS/APPLICATION TO PRACTICE: Staff are at risk for low back injury if they assist falls regardless of the adult patient weight and application of ergonomic techniques. Safer alternatives like the implementation of mobility screening tools and safe patient handling and mobility technology are needed to help prevent assisted falls to decrease injury risk to both patients and staff.

Animal models of melanoma: a somatic cell gene delivery mouse model allows rapid evaluation of genes implicated in human melanoma.

The increasing incidence and mortality associated with advanced stages of melanoma are cause for concern. Few treatment options are available for advanced melanoma and the 5-year survival rate is less than 15%. Targeted therapies may revolutionize melanoma treatment by providing less toxic and more effective strategies. However, maximizing effectiveness requires further understanding of the molecular alterations that drive tumor formation, progression, and maintenance, as well as elucidating the mechanisms of resistance. Several different genetic alterations identified in human melanoma have been recapitulated in mice. This review outlines recent progress made in the development of mouse models of melanoma and summarizes what these findings reveal about the human disease. We begin with a discussion of traditional models and conclude with the recently developed RCAS/TVA somatic cell gene delivery mouse model of melanoma.

Ink4a/Arf loss promotes tumor recurrence following Ras inhibition.

Aberrant activation of rat sarcoma (Ras) signaling contributes to the development of a variety of human cancers, including gliomas. To determine the dependence of high-grade gliomas on continued Ras signaling, we developed a doxycycline-regulated Kirsten Ras (KRas) glioma mouse model. We previously demonstrated that KRas is required for the maintenance of glioblastoma multiforme tumors arising in the context of activated Akt signaling in vivo; inhibition of KRas expression resulted in apoptotic tumor regression and significantly increased survival. We utilized a well-established glioma mouse model to determine the reliance of gliomas on continued KRas signaling in the context of Ink4a/Arf deficiency, a common occurrence in human gliomas. Despite the dependency of primary gliomas on continued KRas signaling, a significant percentage of tumors progressed to a KRas-independent state in the absence of Ink4a/Arf expression, demonstrating that these tumor suppressors play a critical role in the suppression of glioma recurrence. While even advanced stages of gliomas may remain dependent upon KRas signaling for maintenance and growth, our findings demonstrate that loss of Ink4a/Arf facilitates the acquisition of oncogene independence and tumor recurrence. Furthermore, reactivation of the Ras mitogen-activated protein kinase pathway in the absence of virally delivered KRas expression is a common mechanism of recurrence in this context.

Akt signaling is required for glioblastoma maintenance in vivo.

Glioblastoma multiforme (GBM) can be induced in mice through the combined expression of activated forms of KRas and Akt in glial progenitor cells. We have previously demonstrated that KRas is required for the maintenance of these tumors in vivo as inhibition of KRas expression resulted in apoptotic tumor regression and significantly increased survival. To determine the reliance of these tumors on Akt signaling in vivo, we generated a viral vector that allows the expression of Akt to be controlled post-delivery. Survival rates were compared between those animals with continued Akt expression and animals in which expression of Akt was suppressed. Although a fifth of the tumors were refractory to treatment, inhibition of Akt significantly increased the survival of tumor-bearing mice and nearly a fourth of the mice remained in remission four months after the treatment period. These data suggest that Akt is required for glioblastoma maintenance in the context of activated Ras and that loss of Akt expression results in increased survival; therefore, the PI3K/AKT signaling pathway is a viable therapeutic target in this context.