Octyltrimethoxysilane was synthesized by octane and trimethoxysilane, and octane was synthesized by grignard reagent. The main effects of reacting conditions on the yield were discussed and the optimum experimental conditions were studied. Used 3-bromopropene and 1-Brompentane as raw materials, the molar ratio of octane: magnesium was 1:1.2. Droplets time was 3 hours, the reacting time in 1 hour, and yield was 45.6%. Target compounds were analysised through GC-MS. Then, used choroplatinicacid isopropanol as catalyst, octane reacted with trimethoxysilane to gain octyltrimethoxysilane, the time of activation of catalyst was 1 hour ,reacting time 1 hour, and the yield was up to 65.4%. Study found that using 1-Brompentane Grignard reagent and 3-bromopropene could extend the carbon chain successfully. On the contrary, using 3-bromopropene Grignard reagent and 1-Brompentane to react, the rate of conversion was very low, a large number of decane generated, rather than octane.
Solid-state composite polymer electrolyte PEO 18 LiTFSI-xDMSO (CPE x ) are prepared by the casting process. An optimized freestanding electrolyte CPE x system yields a lithium ionic conductivity of 2.8×10 -4 Scm -1 at 60 oC with x =1.32. The interfacial resistances of Li/CPE x and Li/CPE x /H-LAGP are examined. The interfacial resistance between CPE 0 and lithium metal is reduced sharply by the addition of DMSO for CPE 1.32 at 60 oC after storage about 35 days. The aqueous lithium air battery consists of Li/CPE 1.32 /H-LAGP electrode as a lithium protected electrode is successfully operated with LiCl saturated LiOH aqueous solution as electrolyte and Pt black as reference electrode at current density of 0.2 mAcm -1 at 60 oC.
Abstract: Eucommia ulmoides Oliv. is a famous traditional Chinese medicine which exhibits anti-oxidative stress ability and neuro-protective effects. Aucubin is the predominant component of Eucommia ulmoides Oliv. Our present study is intended to investigate aucubin’s potential protective effects on neurons against epilepsy in the hippocampus by establishing the lithium-pilocarpine induced status epilepticus (SE) rat model in vivo. Aucubin (at a low dose and a high dose of 5[Formula: see text]mg/kg and 10[Formula: see text]mg/kg, respectively) was administered through gavage for two weeks before lithium-pilocarpine injection. Rats were sacrificed at 4, 24 and 72[Formula: see text]h after SE induction. Pretreatment with both low-dose and high-dose aucubin significantly reduced the number of death neurons ([Formula: see text]) and increased the number of surviving neurons ([Formula: see text]) in DG, Hilus, CA1 and CA3 hippocampal regions post SE. Meanwhile, it significantly inhibited necroptosis proteins (MLKL and RIP-1) ([Formula: see text] or [Formula: see text]) and enhanced autophagy protein (Beclin-1 and LC3BII/LC3BI) prevalence in the hippocampus ([Formula: see text] or [Formula: see text]). In conclusion, aucubin appeared to ameliorate damages in lithium-pilocarpine induced SE in hippocampus, reduce the number of apoptotic neurons, and increased the number of survival neurons by inducing autophagy and inhibiting necroptosis. These original findings might provide an important basis for the further investigation of the therapeutic role of aucubin in treatment or prevention of epilepsy-related neuronal damages.
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