Elder abuse and neglect: detection, reporting, and intervention.

Dental providers are in an excellent position to identify elder abuse and neglect (EAN), yet they are often reluctant to report or intervene in cases of suspected elder maltreatment. This problem is widespread, and the negative impact of this dilemma cannot be ignored. In 1999, the American Dental Association's House of Delegates, through Resolution 44H-1999, urged constituent dental societies to educate their members about abuse and neglect and individual states' legal reporting requirements. The American Society for Geriatric Dentistry (ASGD), responding to a need to inform its members about this issue, requested this literature review on elder abuse and neglect. This paper emphasizes the role of the dental profession in ameliorating EAN and offers ASGD members recommendations to aid individual practitioners and staff in educating and assisting the profession in recognizing and reporting EAN.

Src deficiency or blockade of Src activity in mice provides cerebral protection following stroke.

Vascular endothelial growth factor (VEGF), an angiogenic factor produced in response to ischemic injury, promotes vascular permeability (VP). Evidence is provided that Src kinase regulates VEGF-mediated VP in the brain following stroke and that suppression of Src activity decreases VP thereby minimizing brain injury. Mice lacking pp60c-src are resistant to VEGF-induced VP and show decreased infarct volumes after stroke whereas mice deficient in pp59c-fyn, another Src family member, have normal VEGF-mediated VP and infarct size. Systemic application of a Src-inhibitor given up to six hours following stroke suppressed VP protecting wild-type mice from ischemia-induced brain damage without influencing VEGF expression. This was associated with reduced edema, improved cerebral perfusion and decreased infarct volume 24 hours after injury as measured by magnetic resonance imaging and histological analysis. Thus, Src represents a key intermediate and novel therapeutic target in the pathophysiology of cerebral ischemia where it appears to regulate neuronal damage by influencing VEGF-mediated VP.