Revue d'histoire du Bas-Saint-Laurent, vol. 12 (3-4)

Mot de l'éditeur -- Au micro de CJBR -- La grande histoire de CJBR -- Jules-A. Brillant et le poste CJBR -- Avec CJBR, un bon en avant pour le Bas St-Laurent -- CJBR, l'école -- L'annonceur: un éducateur populaire -- Sandy Burgess : le journaliste que j'ai connu -- "Ce pays qui est le mien" -- Un demi-siècle d'information: que de nouvelles! -- Journaliste de père en fils à CJBR -- Le théâtre à CJBR -- 50 ans de musique à CJBR, le château fort de la mélodie française -- Poésie, théâtre, jazz et originalité avec Michel Garneau -- Les "Chroniques du dimanche", l'âge d'or de la critique culturelle à CJBR -- "Si CJBR m'était conté..." -- L'évolution technologique, un élément-clef de l'histoire des 50 ans de radiodiffusion -- La publicité à CJBR, quarante ans de croissance -- Des pionnières à CJBR -- 1958-1972, des années enrichissantes -- De Trois-Pistoles à Rimouski -- Le sport et son enracinement dans le milieu régional -- "Debout c'est l'heure", c'est Jean Brisson qui sonne le réveil -- "Par une belle journée de tempête" -- Et on repart vers la centain

Fish, docosahexaenoic acid and Alzheimer’s disease

Cognitive decline in the elderly, particularly Alzheimer’s disease (AD), is a major socio-economic and healthcare concern. We review here the literature on one specific aspect of diet affecting AD, that of the ω3 fatty acids, particularly the brain’s principle ω3 fatty acid – docosahexaenoic acid (DHA). DHA has deservedly received wide attention as a nutrient supporting both optimal brain development and for cardiovascular health. Our aim here is to critically assess the quality of the present literature as well as the potential of ω3 fatty acids to treat or delay the onset of AD. We start with a brief description of cognitive decline in the elderly, followed by an overview of well recognized biological functions of DHA. We then turn to epidemiological studies, which are largely supportive of protective effects of fish and DHA against risk of AD. However, biological studies, including blood and brain DHA analyses need careful interpretation and further investigation, without which the success of clinical trials with DHA may continue to struggle. We draw attention to some of the methodological issues that need resolution as well as an emerging mechanism that may explain how DHA could be linked to protecting brain function in the elderly

Revue d'histoire du Bas Saint-Laurent, vol.1 (2)

Le souvenir des gens et des choses -- La première église de pierre de Rimouski -- Le Collège-séminaire de Rimouski -- La maison-mère d'une communauté diocésaine -- Le Couvent gris -- Le Musée régional de Rimouski -- En fouillant les vieux papiers -- Cyprien Tanguay : du collège de Rimouski à l'érudition québécoise -- Un curé, la guerre et le monument aux Brave

Physostigmine and Methylphenidate Induce Distinct Arousal States During Isoflurane General Anesthesia in Rats

BACKGROUND: Although emergence from general anesthesia is clinically treated as a passive process driven by the pharmacokinetics of drug clearance, agents that hasten recovery from general anesthesia may be useful for treating delayed emergence, emergence delirium, and postoperative cognitive dysfunction. Activation of central monoaminergic neurotransmission with methylphenidate has been shown to induce reanimation (active emergence) from general anesthesia. Cholinergic neurons in the brainstem and basal forebrain are also known to promote arousal. The objective of this study was to test the hypothesis that physostigmine, a centrally acting cholinesterase inhibitor, induces reanimation from isoflurane anesthesia in adult rats. METHODS: The dose-dependent effects of physostigmine on time to emergence from a standardized isoflurane general anesthetic were tested. It was then determined whether physostigmine restores righting during continuous isoflurane anesthesia. In a separate group of rats with implanted extradural electrodes, physostigmine was administered during continuous inhalation of 1.0% isoflurane, and the electroencephalogram changes were recorded. Finally, 2.0% isoflurane was used to induce burst suppression, and the effects of physostigmine and methylphenidate on burst suppression probability (BSP) were tested. RESULTS: Physostigmine delayed time to emergence from isoflurane anesthesia at doses ≥0.2 mg/kg (n = 9). During continuous isoflurane anesthesia (0.9% ± 0.1%), physostigmine did not restore righting (n = 9). Blocking the peripheral side effects of physostigmine with the coadministration of glycopyrrolate (a muscarinic antagonist that does not cross the blood-brain barrier) produced similar results (n = 9 each). However, during inhalation of 1.0% isoflurane, physostigmine shifted peak electroencephalogram power from δ ( < 4 Hz) to θ (4-8 Hz) in 6 of 6 rats. During continuous 2.0% isoflurane anesthesia, physostigmine induced large, statistically significant decreases in BSP in 6 of 6 rats, whereas methylphenidate did not. CONCLUSIONS: Unlike methylphenidate, physostigmine does not accelerate time to emergence from isoflurane anesthesia and does not restore righting during continuous isoflurane anesthesia. However, physostigmine consistently decreases BSP during deep isoflurane anesthesia, whereas methylphenidate does not. These findings suggest that activation of cholinergic neurotransmission during isoflurane anesthesia produces arousal states that are distinct from those induced by monoaminergic activation.National Institutes of Health (U.S.) (Grant TR01-GM104948)National Institutes of Health (U.S.) (Grant DP1-OD003646)National Institutes of Health (U.S.) (Grant K08-GM094394