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Background: Brain concentrations of omega-3 docosahexaenoic acid (DHA, 22:6n-3) have been reported to positively correlate with seizure thresholds in rodent seizure models. It is not known whether brain DHA depletion, achieved by chronic dietary omega-3 polyunsaturated fatty acid (PUFA) deficiency, lowers seizure thresholds in rats. Objective: The present study tested the hypothesis that lowering brain DHA concentration with chronic dietary n-3 PUFA deprivation in rats will reduce seizure thresholds, and that compared to injected oleic acid (OA), injected DHA will raise seizure thresholds in rats maintained on n-3 PUFA adequate and deficient diets. Methods: Rats (60 days old) were surgically implanted with electrodes in the amygdala, and subsequently randomized to the AIN-93G diet containing adequate levels of n-3 PUFA derived from soybean oil or an n-3 PUFA-deficient diet derived from coconut and safflower oil. The rats were maintained on the diets for 37 weeks. Afterdischarge seizure thresholds (ADTs) were measured every 4-6 weeks by electrically stimulating the amygdala. Between weeks 35 and 37, ADTs were assessed within 1 h of subcutaneous OA or DHA injection (600 mg/kg). Seizure thresholds were also measured in a parallel group of non-implanted rats subjected to the maximal pentylenetetrazol (PTZ, 110 mg/kg) seizure test. PUFA composition was measured in the pyriform-amygdala complex of another group of non-implanted rats sacrificed at 16 and 32 weeks. Results: Dietary n-3 PUFA deprivation did not significantly alter amygdaloid seizure thresholds or latency to PTZ-induced seizures. Acute injection of OA did not alter amygdaloid ADTs of rats on the n-3 PUFA adequate or deficient diets, whereas acute injection of DHA significantly increased amygdaloid ADTs in rats on the n-3 PUFA adequate control diet as compared to rats on the n-3 PUFA deficient diet (P < 0.05). Pyriform-amygdala DHA percent composition did not significantly differ between the groups, while n-6 docosapentaenoic acid, a marker of n-3 PUFA deficiency, was significantly increased by 2.9-fold at 32 weeks. Conclusion: Chronic dietary n-3 PUFA deficiency does not alter seizure thresholds in rats, but may prevent the anti-seizure effects of DHA.

Introduction:Within the local context in Montréal, the elderly population makes up more than 50% of patient hours in emergency department. To meet ministerial targets for length of stay, our health technology assessment unit was requested to conduct an umbrella review to evaluate interventions aimed at reducing health care services use for this population. Within that context, our unit was asked to further evaluate the efficacy of advance practice nurse (APN)-led interventions. The objective of this rapid response was to summarize the scientific literature for APN-led interventions on hospital services use.Methods:An umbrella review using the PRISMA statement was conducted to review the scientific literature. Systematic searches were conducted in five databases, along with a grey literature search. Two reviewers performed the study selection, quality assessment using the ROBIS, and data extraction. The primary studies within the selected systematic reviews were extracted by two reviewers and a meta-analysis was conducted to analyze the efficacy of APN-involved in discharge planning and transitional care.Results:From the twenty-seven systematic reviews identified in the literature search, four reported data on APN-led interventions. In all, sixteen primary studies were included in the four systematic reviews. While most studies focused on transitional care, there was heterogeneity in the components of the interventions implemented. At six months post-discharge, a reduction of forty-one percent in relative risk of readmission was observed with APN-led discharge planning and transitional care with patient education, follow-up and services coordination. Studies with fewer components reported less significant results than studies with comprehensive discharge planning and transitional care. The few APN-led primary care studies identified in the systematic reviews reported inconsistent results.Conclusions:APN-led comprehensive discharge planning and transitional care can reduce hospital readmission rate. Several components were identified and should be considered in the discharge planning and transitional care.

The omega-3 polyunsaturated acids (n-3 PUFA) show great promise as a therapy for epileptic seizures. There has been considerable confusion, however, in the animal data related to the n-3 PUFAs’ anticonvulsant effects. Our own recent work has clarified this confusion, and led to a simple, reproducible animal preparation in which to study the n-3 PUFAs’ mechanism(s) of action. We first attempted to replicate the studies of Yehuda et al. (1994), who had reported dramatic seizure suppression after 21 days of 40 mg/kg injections of the “SR 3” formula i.p in rats. In our replication, we found no effect at all at this dose (Taha et al., 2006). We therefore tested the higher dose of 200 mg/kg of the SR-3 mixture. At 200 mg/kg, we found a significant increase in PTZ seizure latency, although no change in severity (Taha et al., 2009). We subsequently tried acute administration of a single dose in rats, switching from SR 3 to docosahexaenoic acid (DHA). Injecting subcutaneously (s.c.), we found a significant elevation in PTZ-seizure latency following after a single injection (Taha et al., 2010). Our dose–response curves in this study, however, were “inverted U” shaped. In parallel studies, we tested dietary (p.o.) administration. Working in rats with chronically implanted electrodes, we found that dietary PUFAs elevated thresholds in both the cortex and the amygdala of rats. These effects, however, took several months to occur (Taha et al., in preparation). To simplify the kinetics, we have moved to intravenous (i.v.) injections of DHA (tail vein in rats). Our i.v. experiments have now shown anticonvulsant effects 5 min after injection and plasma concentrations that rise rapidly, plateau at 5 min, and drop to baseline a minute after infusion (Trepanier et al., in preparation). We have therefore finally evolved a preparation in which anticonvulsant effects and plasma concentrations parallel the known kinetics of DHA. This preparation will now allow a meaningful study of DHA’s mechanisms of anticonvulsant action.