10 research outputs found

    Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease

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    Alzheimer's disease (AD) is a lethal progressive neurological disorder affecting the memory. Recently, US Food and Drug Administration mitigated the standard for drug approval, allowing symptomatic drugs that only improve cognitive deficits to be allowed to accelerate on to clinical trials. Our study focuses on taurine, an endogenous amino acid found in high concentrations in humans. It has demonstrated neuroprotective properties against many forms of dementia. In this study, we assessed cognitively enhancing property of taurine in transgenic mouse model of AD. We orally administered taurine via drinking water to adult APP/PS1 transgenic mouse model for 6 weeks. Taurine treatment rescued cognitive deficits in APP/PS1 mice up to the age-matching wild-type mice in Y-maze and passive avoidance tests without modifying the behaviours of cognitively normal mice. In the cortex of APP/PS1 mice, taurine slightly decreased insoluble fraction of AÎČ. While the exact mechanism of taurine in AD has not yet been ascertained, our results suggest that taurine can aid cognitive impairment and may inhibit AÎČ-related damages.MIT International Science and Technology InitiativesKorea Health Industry Development Institute (H14C04660000)Korea Institute of Science and Technology (Open Research 2E24582)Korea Institute of Science and Technology (Flagship 2E25023

    A Cu2O-CuSCN Nanocomposite as a Hole-Transport Material of Perovskite Solar Cells for Enhanced Carrier Transport and Suppressed Interfacial Degradation

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    Interfacial degradation in perovskite solar cells is a critical issue affecting long-term stability for future commercialization. In particular, a perovskite and an organic hole-transport layer (HTL) react easily when the device is exposed to extreme operating conditions (heat, light, and air). To prevent degradation, an inorganic CuSCN HTL has emerged as an alternative, yet the interfacial reactivity is still not clearly elucidated. Herein, Cu2O and CuSCN are coutilized to form an efficient and stable HTL. While uniform film formation using Cu2O is difficult despite its high mobility, a Cu2O-CuSCN nanocomposite can be excellently synthesized as an effective HTL, exhibiting a power conversion efficiency (PCE) of 19.2% and sustaining its PCE over 90% for 720 h under extreme conditions (85 degrees C/85% of relative humidity, encapsulated). A chemical distribution analysis by secondary-ion mass spectroscopy (SIMS) suggests that a Cu2O nanoparticle layer protects the interface between the perovskite and CuSCN. The optoelectronic properties of the nanocomposite HTL and the improved solar cell performance are correlated with the recombination rate, electronic trap distribution in the band gap, and charge extraction efficiencies.N

    Intrathecal RGS4 inhibitor, CCG50014, reduces nociceptive responses and enhances opioid-mediated analgesic effects in the mouse formalin test

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    BACKGROUND: The regulator of G-protein signaling protein type 4 (RGS4) accelerates the guanosine triphosphatase activity of Gαi and Gαo, resulting in the inactivation of G-protein–coupled receptor signaling. An opioid receptor (OR), a Gαi-coupled receptor, plays an important role in pain modulation in the central nervous system. In this study, we examined whether (1) spinal RGS4 affected nociceptive responses in the formalin pain test, (2) this RGS4-mediated effect was involved in OR activation, and (3) the ÎŒ-OR agonist–induced antinociceptive effect was modified by RGS4 modulation. METHODS: Formalin (1%, 20 ÎŒL) was injected subcutaneously into the right hindpaws of male 129S4/SvJae×C57BL/6J (RGS4+/+ or RGS4−/−) mice, and the licking responses were counted for 40 minutes. The time periods (seconds) spent licking the injected paw during 0 to 10 minutes (early phase) and 10 to 40 minutes (late phase) were measured as indicators of acute nociception and inflammatory pain response, respectively. An RGS4 inhibitor, CCG50014, and/ or a ÎŒ-OR agonist, [D-Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO), were intrathecally injected 5 minutes before the formalin injection. A nonselective OR antagonist, naloxone, was intraperitoneally injected 30 minutes before the CCG50014 injection. RESULTS: Mice that received the formalin injection exhibited typical biphasic nociceptive behaviors. The nociceptive responses in RGS4-knockout mice were significantly decreased during the late phase but not during the early phase. Similarly, intrathecally administered CCG50014 (10, 30, or 100 nmol) attenuated the nociceptive responses during the late phase in a dose-dependent manner. The antinociceptive effect of the RGS4 inhibitor was totally blocked by naloxone (5 mg/kg). In contrast, intrathecal injection of DAMGO achieved a dose-dependent reduction of the nociceptive responses at the early and late phases. This analgesic effect of DAMGO was significantly enhanced by the genetic depletion of RGS4 or by coadministration of CCG50014 (10 nmol). CONCLUSIONS: These findings demonstrated that spinal RGS4 inhibited the endogenous or exogenous OR-mediated antinociceptive effect in the formalin pain test. Thus, the inhibition of RGS4 activity can enhance OR agonist–induced analgesia. The enhancement of OR agonist– induced analgesia by coadministration of the RGS4 inhibitor suggests a new therapeutic strategy for the management of inflammatory pain. (Anesth Analg 2015;120:671–7) © 2015 International Anesthesia Research Society101

    Genome editing for horticultural crop improvement

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    Annual Selected Bibliography

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