Exploring the views of emergency department staff on the use of videoconferencing for mental health emergencies in southwestern Ontario.

Patients presenting to a rural emergency department (ED) with mental health symptoms have difficulty accessing services of mental health professionals [1,2]. Videoconferencing (VC) has been found to improve patient access to health services that require specialist care in rural EDs [3,4,5]. Although previous studies highlight the benefit of using VC for patients presenting with mental health emergencies, no study has investigated the current views and use of VC for mental health emergencies in EDs in Southwestern Ontario [3,5,6]. To explore the views of ED staff regarding the use of VC in mental health emergencies, structured telephone interviews were conducted with representatives from EDs in the Erie St. Clair and Southwest Local Health Integration Networks (LHIN). Participants noted that using VC for mental health emergencies may improve patient experience and benefit crisis response teams. VC was perceived by some participants as a means to expedite the direct assessment of a patient presenting with a mental health emergency by a mental health specialist. However several participants stated that using VC for mental health emergencies strains ED resources. Lack of use and difficulty accessing a psychiatrist were identified as potential barriers to implementing the use of VC for mental health emergencies.

Herpes simplex virus 2 infection impacts stress granule accumulation.

Interference with stress granule (SG) accumulation is gaining increased appreciation as a common strategy used by diverse viruses to facilitate their replication and to cope with translational arrest. Here, we examined the impact of infection by herpes simplex virus 2 (HSV-2) on SG accumulation by monitoring the localization of the SG components T cell internal antigen 1 (TIA-1), Ras-GTPase-activating SH3-domain-binding protein (G3BP), and poly(A)-binding protein (PABP). Our results indicate that SGs do not accumulate in HSV-2-infected cells and that HSV-2 can interfere with arsenite-induced SG accumulation early after infection. Surprisingly, SG accumulation was inhibited despite increased phosphorylation of eukaryotic translation initiation factor 2α (eIF2α), implying that HSV-2 encodes previously unrecognized activities designed to maintain translation initiation downstream of eIF2α. SG accumulation was not inhibited in HSV-2-infected cells treated with pateamine A, an inducer that works independently of eIF2α phosphorylation. The SGs that accumulated following pateamine A treatment of infected cells contained G3BP and PABP but were largely devoid of TIA-1. We also identified novel nuclear structures containing TIA-1 that form late in infection. These structures contain the RNA binding protein 68-kDa Src-associated in mitosis (Sam68) and were noticeably absent in infected cells treated with inhibitors of viral DNA replication, suggesting that they arise as a result of late events in the virus replicative cycle.