Graphene Layers‐Wrapped Fe/Fe5C2 Nanoparticles Supported on N‐doped Graphene Nanosheets for Highly Efficient Oxygen Reduction

Synthesis of highly efficient nonprecious metal electrocatalysts for the oxygen reduction reaction (ORR) superior to platinum (Pt) is still a big challenge. Herein, a new highly active ORR electrocatalyst is reported based on graphene layers‐wrapped Fe/Fe₅C₂ nanoparticles supported on N‐doped graphene nanosheets (GL‐Fe/Fe₅C₂/NG) through simply annealing a mixture of bulk graphitic carbon nitride (g‐C₃N₄) and ferrocene. An interesting exfoliation–denitrogen mechanism underlying the conversion of bulk g‐C₃N₄ into N‐doped graphene nanosheets is revealed. Owing to the high graphitic degree, optimum N‐doping level and sufficient active sites from the graphene layers‐wrapped Fe/Fe₅C₂ nanoparticles, the as‐prepared GL‐Fe/Fe₅C₂/NG electrocatalyst obtained at 800 °C exhibits outstanding ORR activity with a 20 mV more positive half‐wave potential than the commercial Pt/C catalyst in 0.1 m KOH solution and a comparable onset potential of 0.98 V. This makes GL‐Fe/Fe₅C₂/NG an outstanding electrocatalyst for ORR in alkaline solution.     

Effect of Urea on the Enzymatic Hydrolysis of Lignocellulosic Substrate and Its Mechanism

Effect of hydrogen bond breaker (urea) addition on the enzymatic hydrolysis of Avicel and eucalyptus pretreated by dilute acid (Eu-DA) was investigated. Urea enhanced the enzymatic hydrolysis of Eu-DA at 50 or 30 °C when the concentration of urea was below 60 g/L, while it inhibited the hydrolysis of Avicel. Low concentration urea (<?240 g/L) had little effect on the cellulase spatial structure and its activity. But it decreased cellulase binding to cellulose surface to inhibit the cellulose hydrolysis. Meanwhile, urea obviously prevented the adsorption of cellobiohydrolase I (CBHI) on the lignin in spite of little effect on the adsorption of β-glucosidase (BGL) and two endoglucanases (EGIII and EGV) on lignin. It was proposed that urea enhanced the enzymatic efficiency of Eu-DA by decreasing the cellulase adsorption on lignin surface.     

The complete chloroplast genome of the green algae <Emphasis Type="Italic">Hariotina reticulata</Emphasis> (Scenedesmaceae,Sphaeropleales, Chlorophyta)

In this study, the chloroplast genome of Hariotina reticulata was fully sequenced and compared to other Sphaeropleales chloroplast genomes. It is 210,757 bp larger than most Sphaeropleales cpDNAs. It presents a traditional chloroplast structure, and contains 103 genes, including 68 protein-coding genes, six rRNA genes and 29 tRNA genes. The coding region constitutes of 43% of the whole cpDNA. Eighteen introns are found in 11 genes and six introns are unique for Hariotina. 11 open reading frames are identified among these introns. The synteny between Hariotina and Acutodesmus cpDNAs is in general identical, while within Sphaeropleales order, high variability in cpDNA architecture is indicated by general high DCJ distances. Ankyra judayi exhibits the greatest dissimilarity in gene synteny to the others and share some unique gene clusters with Treubaria triappendiculata. The phylogenomic analyses show that A. judayi is clustered with Treubariaceae species and sister to Chlorophyceae incertae sedis and other Sphaeropleales species. The monophyly of Sphaeropleales is rejected.     

Salidroside attenuates neuroinflammation and improves functional recovery after spinal cord injury through microglia polarization regulation

Spinal cord injury (SCI) is a severe neurological disease; however, few drugs have been proved to treat SCI effectively. Neuroinflammation is the major pathogenesis of SCI secondary injury and considered to be the therapeutic target of SCI. Salidroside (Sal) has been reported to exert anti‐inflammatory effects in airway, adipose and myocardial tissue; however, the role of Sal in SCI therapeutics has not been clarified. In this study, we showed that Sal could improve the functional recovery of spinal cord in rats as revealed by increased BBB locomotor rating scale, angle of incline, and decreased cavity of spinal cord injury and apoptosis of neurons in vivo. Immunofluorescence double staining of microglia marker and M1/M2 marker demonstrated that Sal could suppress M1 microglia polarization and activate M2 microglia polarization in vivo. To verify how Sal exerts its effects on microglia polarization and neuron protection, we performed the mechanism study in vitro in microglia cell line BV‐2 and neuron cell line PC12. The results showed that Sal prevents apoptosis of PC12 cells in coculture with LPS‐induced M1 BV‐2 microglia, also the inflammatory secretion phenotype of M1 BV‐2 microglia was suppressed by Sal, and further studies demonstrated that autophagic flux regulation through AMPK/mTOR pathway was involved in Sal regulated microglia polarization after SCI. Overall, our study illustrated that Sal could promote spinal cord injury functional recovery in rats, and the mechanism may relate to its microglia polarization modulation through AMPK‐/mTOR‐mediated autophagic flux stimulation.     

人参总皂甙对海马神经元核仁组织者区和苔藓纤维末梢发芽的…

本文研究人参总皂甙在海马齿状回颗粒细胞层诱发ＬＴＰ效应和促进大鼠记忆保持能力时,对海马神经元核仁组织者区和苔藓纤维末梢出芽的影响。给人参总皂甙第７天可显著提高群峰电位幅度。缩短ＰＳ起始和峰潜伏期,并可显著提高大鼠记忆保持能力,此时人参总皂甙可使海马ＣＡ３区锥体细胞和齿状回颗粒细胞Ａｇ－ＮＯＲ数较盐水组大鼠的平均提高６６．１７±２．３２％和７２．０７±０．９３％（Ｐ〈０．０１）。同时还可使大鼠的海马     

中国斯赤眼蜂属一新种(膜翅目:赤眼蜂科)(英文)

本文记述赤眼蜂科Trichogrammatidae斯赤眼蜂属SoikiellaNowicki一新种,亚洲斯赤眼蜂Soikiellaasiaticasp.nov.,新种与S．mongibelli相似,主要区别为：新种为褐色,体长0．9－1．0mm;雌虫触角棒节显著膨大呈卵圆形,长为宽的2倍;前翅翅面纤毛规则排列成行;而后者为黑色,体长1．13mm;棒节较细长,长为宽的2．5倍;前翅翅面仅有13列纤毛排列成行,其余散乱分布;两者易于区别。     

水稻品种对稻虱缨小蜂发育、存活及繁殖的影响

水稻品种既能直接地经物理结构,亦能间接地通过改变褐飞虱Niladarvatalugens(Stal)卵的适宜性,影响稻虱缨小蜂Anagrus nilaparvatae Pang et Wang的发育、存活和繁殖。稻虱缨小蜂的羽化率、怀卵量分别与其寄主褐飞虱卵所处水稻品种叶鞘鞘脊的硅细胞密度呈极显著和显著负相关;同时,怀卵量和虫体大小还与受水稻品种影响的褐飞虱卵粒大小呈极显著正相关。稻虱缨小蜂种群增长能力指数的组分分析表明,不同水稻品种影响稻虱缨小蜂种群增长能力的主要因子不同,显示了水稻品种对稻虱缨小蜂影响的多因子作用。     

Enhancement of Neurite Outgrowth Following Calpain Inhibition Is Mediated by Protein Kinase C

Abstract: We examined the interdependence of calpain and protein kinase C (PKC) activities on neurite outgrowth in SH-SY-5Y human neuroblastoma cells. SH-SY-5Y cells elaborated neurites when deprived of serum or after a specific thrombin inhibitor, hirudin, was added to serum-containing medium. The extent of neurite outgrowth under these conditions was enhanced by treatment of cells with the cell-permeant cysteine protease inhibitors N-acetyl-leucyl-leucyl-norleucinal (“C1”) and calpeptin or by the phospholipid-mediated intracellular delivery of either a recombinant peptide corresponding to a conserved inhibitory sequence of human calpastatin or a neutralizing anti-calpain antisera. Calpain inhibition in intact cells was confirmed by immunoblot analysis showing inhibition of calpain autolysis and reduced proteolysis of the known calpain substrates fodrin and microtubule-associated protein 1. The above inhibitory peptides and antiserum did not induce neurites in medium containing serum but lacking hirudin, suggesting that increased surface protein adhesiveness is a prerequisite for enhancement of neurite outgrowth by calpain inhibition. Treatment of cells with the PKC inhibitor H7, staurosporine, or sphingosine induced neurite outgrowth independently of serum concentration. Because calpain is thought to regulate PKC activity, we examined this potential interrelationship during neurite outgrowth. Simultaneous treatment with calpain and PKC inhibitors did not produce additive or synergistic effects on neurite outgrowth. PKC activation by 2-O-tetradecanoylphorbol 13-acetate (TPA) prevented and reversed both neurite initiation by serum deprivation and its enhancement by calpain inhibitors. Treatment of cells with the calpain inhibitor C1 retarded PKC down-regulation following TPA treatment. Cell-free analyses demonstrated the relative specificity of various protease and kinase inhibitors for calpain and PKC and confirmed the ability of millimolar calcium-requiring calpain to cleave the SH-SY-5Y PKC regulatory subunit from the catalytic subunit, yielding a free catalytic subunit (protein kinase M). These findings suggest that the influence of PKC on neurite outgrowth is downstream from that of surface adhesiveness and calpain activity.     

Arachidonic Acid, but Not Sodium Nitroprusside, Stimulates Presynaptic Protein Kinase C and Phosphorylation of GAP-43 in Rat Hippocampal Slices and Synaptosomes

Abstract: Activation of protein kinase C (PKC) and phosphorylation of its presynaptic substrate, the 43-kDa growth-associated protein GAP-43, may contribute to the maintenance of hippocampal long-term potentiation (LTP) by enhancing the probability of neurotransmitter release and/or modifying synaptic morphology. Induction of LTP in rat hippocampal slices by high-frequency stimulation of Schaffer collateral-CA1 synapses significantly increased the PKC-dependent phosphorylation of GAP-43, as assessed by quantitative immunoblotting with a monoclonal antibody that recognizes an epitope that is specifically phosphorylated by PKC. The stimulatory effect of high-frequency stimulation on levels of immunoreactive phosphorylated GAP-43 was not observed when 4-amino-5-phosphonovalerate (50 µM), an N-methyl-d -aspartate (NMDA) receptor antagonist, was bath-applied during the high-frequency stimulus. This observation supports the hypothesis that a retrograde messenger is produced postsynaptically following NMDA receptor activation and diffuses to the presynaptic terminal to activate PKC. Two retrograde messenger candidates—arachidonic acid and nitric oxide (sodium nitroprusside was used to generate nitric oxide)—were examined for their effects in hippocampal slices on PKC redistribution from cytosol to membrane as an indirect measure of enzyme activation and PKC-specific GAP-43 phosphorylation. Bath application of arachidonic acid, but not sodium nitroprusside, at concentrations that produce synaptic potentiation (100 µM and 1 mM, respectively) significantly increased translocation of PKC immunoreactivity from cytosol to membrane as well as levels of immunoreactive, phosphorylated GAP-43. The stimulatory effect of arachidonic acid on GAP-43 phosphorylation was also observed in hippocampal synaptosomes. These results indicate that arachidonic acid may contribute to LTP maintenance by activation of presynaptic PKC and phosphorylation of GAP-43 substrate. The data also suggest that nitric oxide does not activate this signal transduction system and, by inference, activates a distinct biochemical pathway.     

紫云英根瘤菌结瘤因子的初步研究

最近的研究结果表明,豆科植物与根瘤菌的共生识别是一种双向的信号物质交换过程.首先是豆科植物的根或种子分泌类黄酮物质,诱导根瘤菌的结瘤基因(nod genes)产生结瘤因子(nod factors),分泌到胞外,为植物所接受,从而引发植物某些基因表达,细胞分化,细胞壁形成,最终导致根毛变形等一系列变化.已经测定了几种苜蓿根瘤菌(Rhizobium meliloti)和豌豆根瘤菌(R.leguminosarum bv.viciae)结瘤因子的分子结构式,它们均属于寡糖胺类物质,在没有根瘤菌存在的条件下,结瘤因子能独立地促使根毛发生变形,这是检测结瘤因子是否存在的重要手段,即根毛变形试验(Root hairdeformation assay,简称Had试验).高浓度的结瘤因子甚至能诱导植物产生空瘤,其组织结构与典型的根瘤相同.