40 research outputs found

    Observation of B̅0→D(*)0pp̅

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    Table_1_The effect of omega-3 fatty acids on alcohol-induced damage.DOCX

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    Alcohol is the most widely consumed psychoactive substance in the world that has a severe impact on many organs and bodily systems, particularly the liver and nervous system. Alcohol use during pregnancy roots long-lasting changes in the newborns and during adolescence has long-term detrimental effects especially on the brain. The brain contains docosahexaenoic acid (DHA), a major omega-3 (n-3) fatty acid (FA) that makes up cell membranes and influences membrane-associated protein function, cell signaling, gene expression and lipid production. N-3 is beneficial in several brain conditions like neurodegenerative diseases, ameliorating cognitive impairment, oxidative stress, neuronal death and inflammation. Because alcohol decreases the levels of n-3, it is timely to know whether n-3 supplementation positively modifies alcohol-induced injuries. The aim of this review is to summarize the state-of-the-art of the n-3 effects on certain conditions caused by alcohol intake, focusing primarily on brain damage and alcoholic liver disease.</p

    養護 子どもの心が動く健康教育をめざして : グローバルな視点で健康設計(IX. 教科研究)

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    2009-01-15急速にグローバル化が進む中で、生涯にわたって健康を保つには、個人の努力だけでなく、国際社会の一員としての視点で考えることも大切である。そこで、高校2年生の保健で国際理解教育を取り入れた授業実践を行った。グローバルな視点で、健康に結びつく適切な意思決定と、適切な行動選択ができるようになる力を養うためにも、また、健康教育を推進していくためにも、国際理解教育とコラボレーションする教育的意義は大きいと考えた。国立情報学研究所で電子化したコンテンツを使用している。departmental bulletin pape

    Inhibition of DGL-α, the enzyme that synthesizes 2-AG, blocked eCB-LTD.

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    <p>Averaged time courses of the experiments in which the 10 min at 10 Hz protocol was given in control ACSF (open circles) of after pre-treatment with tetrahydrolipstatin (THL, 10 µM, black circles), an inhibitor of the DGL-α.</p

    Presynaptic CB1R-mediated LTD in the PrPFC.

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    <p>(A) Left: A 10 min 10 Hz stimulation of layer II-III fibers (arrow) induced a profound long-term depression of evoked EPSCs recorded in patch-clamped layer V-VI pyramidal neurons. The induction of LTD was completely prevented when slices were preincubated and tetanized in the presence of the CB1R antagonist AM251 (4 µM). Traces represent the average of 12 consecutive EPSCs before and 25 minutes after LTD induction in the absence (upper left) or presence (upper right) of AM251. Right: The coefficient of variation, 1/CV<sup>2</sup>, was significantly reduced after induction of eCB-LTD (p = 0.0025 paired t-test). Calibration bars: x: 50 ms, y: 100 pA. (B) Representative continuous 3 seconds sweeps showing the spontaneous EPSCs (sEPSCs) recorded before (left) and after eCB-LTD induction (right). The distribution of sEPSCs inter-event intervals (left panel) but not of their amplitude (right panel) was modified following induction of LTD suggesting a presynaptic modulation (Kolmogorov-Smirnov test: inter event interval p<0.005, amplitude p = 0.507). Calibration bars: x: 100 ms, y: 10 pA. (C) Responses to hyperpolarizing and depolarizing somatic current pulses of a typical pyramidal neuron in the PFC before and after induction of eCB-LTD. Similar I–V curves were obtained suggesting that eCB-LTD induction did not change post-synaptic pyramidal neurons properties. Calibration bars: x: 100 ms, y: 25 mV.</p

    Effects of blocking eCB reuptake on sub threshold tetanus.

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    <p>Averaged time courses of the experiments in which the 5 min at 10 Hz protocol was given in control ACSF (open circles) of after pre-treatment with the eCB reuptake blocker AM404 (20 µM, black circles).</p

    Pharmacological characterization of presynaptic CB1R at layer V-VI synapses of the PrPFC.

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    <p>Layer V-VI pyramidal cells were voltage-clamped and held at -70mV. (A) CB1R-mediated inhibition of evoked transmission. The cannabimimetic CP55,940 (10 µM) reduced evoked EPSCs on average to 48±5 % (n = 6) of basal value. Traces represent the average of 10 consecutive EPSCs taken at the times indicated on the time-course graph. (B) The inhibitory effects of CP55,940 on evoked EPSCs were blocked by pre-treatment with the selective CB1R antagonist SR141716A (10 µM, t-test p = 0.0386) in agreement with the involvement of CB1R. (C) Dose response curve measured 20 min after beginning CP55,940 application. Each point is expressed as the percentage of inhibition of its basal value. The EC50 was 195±0.3 nM. (D) The coefficient of variation, expressed as 1/CV<sup>2</sup> was reduced following the CP55,940 (p = 0.0107 paired t-test). 1/CV<sup>2</sup> was calculated with 60 sweeps i.e. 10 min before and 20 min after CP55,940.</p

    Percentage of presynaptic and postsynaptic elements immunoreactive for CB1R, mGluR5 or DGL-α.

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    <p>The percentage of CB1R-labeled presynaptic compartments relative to postsynaptic mGluR5 and DGL-α is shown. Prelimbic prefrontal cortical sections used for counting were obtained from 3 adult mice. Electron micrographs were taken at a final magnification of x15,000.</p
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