楠竹材表面硅烷化及防水/油润湿和渗透的特性

目的斥油材料表面通常采用氟化合物来修饰,为了减小氟化合物对人体健康和生态环境带来的潜在危害,探索研究含氟化合物的替代品,采用无氟化合物制备防水、防油润湿和渗透的功能化竹材。方法以甲基三甲氧基硅烷(MTMS)为功能化单体,将浓度为0.1 mol/L的盐酸与MTMS按照体积比1∶4混合,在盛有冰浴的超声波中进行水解,将竹材试样放入水解后的溶液中浸渍5 min,取出放置30 min后在103℃条件下烘干。采用傅里叶红外光谱仪(FT-IR)、X射线光电子能谱仪(XPS)、场发射扫描电子显微镜(SEM)分析改性竹材的表面性能。采用接触角测量仪分析功能化竹材的润湿性,考察随着浸泡时间的延长,其吸水率和吸油率的变化规律。通过动态热机械分析仪(DMA)分析改性竹材的动态热力学性能。结果处理后竹材表面出现了较强的Si-CH_(3)特征吸收峰,-OH吸收峰强度与对照样相比有所减弱。采用水解时间不同的MTMS溶液浸渍处理竹材,竹材表面的Si元素含量均保持在24%左右,但C元素含量随着水解时间的增加而增加,而O元素含量则略有减小。当MTMS的水解时间由5 min延长至240 min时,改性竹材的水接触角由65.3°±2.2°增加到81.5°±0.9°,水接触角的静置稳定性随着水解时间的延长而提高。油接触角和静置稳定性受水解时间的影响较小,采用不同水解时间改性竹材样品后其油接触角为(49.0°±1.0°)~(53.1°±0.4°),静置480 min后,其值的降幅在2.6°以内,表明改性竹材表面具有极为稳定的防油渗透性能。竹材表面形成了均匀致密的硅氧聚合物涂层,其吸水率和吸油率会随着水解时间的延长而减小。动态热机械分析结果表明,改性竹材的储能模量和耐高温性得到增强。结论在酸性条件下将水解的MTMS溶液浸渍处理竹材后,竹材表面具有防水、防油润湿的特性,同时提高了竹材的储能模量和耐高温性能。

IcarisideⅡ alleviates oxygen-glucose deprivation and reoxygenation-induced PC12 celloxidative injury by activating Nrf2 / SIRT3signaling pathway

OBJECTIVE To investigate icariside(ICS)Ⅱ protects against PC12 cel damage induced by oxygen-glucose deprivation and reoxygenation and explore its mechanism.METHODS The oxidative stress injury model was induced by oxygen-glucose deprivation/reoxygenation(OGD/R) 2 h/24 h in PC12 cells.N-acetyl-lcysteine(NAC),a classical anti-oxidant,was used as positive control.Pharmacodynamic experimental study groups as follows:control,control+ICS Ⅱ50 μmol·L^(-1),OGD/R,OGD/R+ICSⅡ 12.5 μmol·L^(-1),OGD/R + ICS Ⅱ 25 μmol·L^(-1),OGD/R + ICS Ⅱ50 μmol·L^(-1),and OGD/R+NAC 100 μmol·L^(-1) groups.Cell viability and lactate dehydrogenase(LDH) leakage rate were measured by MTT assay and LDH ELISA kit,respectively.Moreover,reactive oxygen species(ROS) ELISA kit was used for detection of intracellular ROS generation,Mito-SOX fluorescence staining was used for detecting production of ROS in mitochondria and mitochondrial membrane potential(MMP)was detected by rhodamine 123 dye.In addition,PC12 cells apoptosis was detected by one-step TUNEL assay.Furthermore,the expressions of nuclear factor erythroid 2-related factors(Nrf2),Keap1,HO^(-1),NQO^(-1),silent information regulator 3(SIRT3),IDH2,Bax,Bcl-2 and caspase 3 were detected by Western blotting analysis.RESULTS The results of MTT and LDH assay showed that OGD/R reduced the cell viability and improved LDH release compared with the control or ICSⅡ 50 μmol·L^(-1) alone(P<0.01).Meanwhile,OGD/R not only increased intracellular and mitochondrial ROS generation,but also elevated the fluorescence intensity of TUNEL staining,at the same time,the MMP was declined when challenged by OGD/R.Furthermore,the Western blotting results showed that OGD/R induced the increase in the expression of cytoplasm-Nrf2,Keap1,Bax and cleaved-caspase 3 level,while the decrease in the expression of nucleus-Nrf2,HO^(-1),NQO^(-1),SIRT3,IDH2 and Bcl-2(P<0.05).However,ICS Ⅱ significantly increased the viability of PC12 cells and reduced LDH leakage(P<0.01).Notably,ICS Ⅱ also suppressed ROS generation both in the intracellular and mitochondria,as well as restored MMP.It was also worthy to note that ICS Ⅱ decreased the expressions of cytoplasmNrf2,Keap1,Bax and the level of cleaved-caspase3,whereas,it increased the expressions of nucleus-Nrf2,HO^(-1),NQO^(-1),SIRT3,IDH2 and Bcl-2(P<0.05).CONCLUSION ICSⅡ reduced OGD/Rinduced oxidative damage in PC12 cells under the laboratory conditions,and its underlying mechanism may be related to the regulation of Nrf2/SIRT3 signaling pathway.

基于灰色预测模型的福建省建筑垃圾产量预测

随着建筑业发展进程的加快,福建省建筑垃圾产生量呈现逐年不断上升趋势,为了推进福建省能够科学有效实现建筑垃圾资源化,采用建筑面积估算法对2010~2017年的建筑垃圾产生量进行估算,通过灰色预测模型对2018~2022年未来五年的建筑垃圾产生量进行预测.采用Matlab编写程序计算得出2022年的建筑垃圾产生量为1.4523×10^8t,是2010年的3倍,结果表明,采用灰色预测模型能够很精确的预测福建省中短期内的建筑垃圾产生量,从而为建筑垃圾资源化提供思路.

Icariside Ⅱ, a PDE5 inhibitor, attenuates cerebral ischemia/reperfusion injury through activating BDNF/TrkB/CREB signaling pathway

OBJECTIVE To explore the effects and mechanism of icariside Ⅱ(ICS Ⅱ),a pharmacologically active compound derived from herbal Epimedii with previous study-proved phosphodiesterase 5(PDE5) inhibitors,was investigated in vivo using a middle cerebral artery occlusion/reperfusion(MCAO/R) model in rats and in vitro using an oxygen-glucose deprivation/reperfusion(OGD/R) model in primary hippocampal neurons.METHODS Laser Doppler flowmeter was introduced to examine the cerebral blood flow of MCAO/R rats.The neurological deficits scores,brain water content and infarction volume were assessed after MCAO/R.OGD/R-induced primary hippocampal neuronal injury and apoptosis were examined by MTT,lactate dehydrogenase(LDH) release,TUNEL staining and flow cytometry,respectively.Expressions of PDE5 A and memory-related signaling pathways were measured using Western blotting analysis.The direct interaction between ICS Ⅱand PDE5 was further evaluated by molecular docking.RESULTS ICS Ⅱ significantly decreased the infraction volume in MCAO/R rats.Furthermore,ICS Ⅱ significantly abrogated OGD/R-induced hippocampal neuronal death.Moreover,ICSⅡ not only effectively restored the 3′ 5′-cyclic guanosine monophosphate(cGMP) level and protein kinase G(PKG) activity both in vivo and in vitro,but also increased brain-derived neurotrophic factor(BDNF),tyrosine protein kinase B(TrkB) and cAMP response element-binding protein(CREB) expressions,thereby inhibited hippocampal neuronal apoptosis.Mechanistically,the beneficial effects of ICS Ⅱ was attributed to its activation of the PKG/TrkB/BDNF via increasing BDNF expression,evidenced by that the inhibition effects of ICSⅡ was abrogated by Rp-8-BrcGMPS,a PKG inhibitor,or ANA-12,a TrkB inhibitor.ICSⅡ also decreased both protein level and activity of PDE5.Notably,ICSⅡ might effectively bind and inhibite PDE5 as demonstrated by relatively high binding score.CONCLUSION ICSⅡ significantly protect against cerebral ischemia/reperfusion injury in rats and rescues OGD/Rinduced hippocampal neuronal injury,and the underling mechanisms are,at least partly,due to inhibition of PDE5 and activation of BDNF/TrkB/CREB signaling pathway.Hence ICS Ⅱ may be an effective agent for combating cerebral ischemia/reperfusion injury.