Significant longevity-extending effects of EGCG on Caenorhabditis elegans under stress

Epigallocatechin gallate (EGCG), a main active ingredient of green tea, is believed to be beneficial in association with anticarcinogenesis, antiobesity, and blood pressure reduction. Here we report that EGCG extended Caenorhabditis elegans longevity under stress. Under heat stress (35°C), EGCG improved the mean longevity by 13.1% at 0.1 μg/ml, 8.0% at 1.0 μg/ml, and 11.8% at 10.0 μg/ml. Under oxidative stress, EGCG could improve the mean longevity of C. elegans by 172.9% at 0.1 μg/ml, 177.7% at 1.0 μg/ml, and 88.5% at 10.0 μg/ml. However, EGCG could not extend the life span of C. elegans under normal culture conditions. Further studies demonstrated that the significant longevity-extending effects of EGCG on C. elegans could be attributed to its in vitro and in vivo free radical-scavenging effects and its up-regulating effects on stress-resistance-related proteins, including superoxide dismutase-3 (SOD-3) and heat shock protein-16.2 (HSP-16.2), in transgenic C. elegans with SOD-3∷green fluorescent protein (GFP) and HSP-16.2∷GFP expression. Quantitative real-time PCR results showed that the up-regulation of aging-associated genes such as daf-16, sod-3, and skn-1 could also contribute to the stress resistance attributed to EGCG. As the death rate of a population is closely related to the mortality caused by external stress, it could be concluded that the survival-enhancing effects of EGCG on C. elegans under stress are very important for antiaging research.     

天然杀伤细胞在受照射小鼠中的造血调控作用

研究了天然杀伤（ＮＫ）细胞对受致死剂量γ线照射的同系小鼠的造血调控作用。ＡＭＳ／５小鼠经９Ｇｙγ线全身照射后立即经尾静脉注射ＮＫ细胞（５×１０５）,可明显提高受照小鼠３０ｄ活存率,照后８ｄ小鼠骨髓中ＣＦＵ－ＧＭ数量明显高于对照和脾细胞注射组,照射后３０ｄ,ＮＫ细胞注射组活存小鼠的骨髓有核细胞数和ＣＦＵ－ＧＭ数已恢复到正常的７６％─９６％。病理组织学观察显示,输注ＮＫ细胞可使小鼠骨髓、脾脏的组织损伤程度减轻,造血功能增强,表现为造血灶数增多,造血细胞功能活跃,核分裂相增多,且涉及红系、粒系、巨核细胞系造血。ＮＫ细胞可能通过直接与造血干细胞相互作用或改善造血微环境等促进“内源性”造血功能,从而发挥对造血的正调控作用。提示ＮＫ细胞在小鼠造血功能的平衡维持中起重要作用。     

HPLC测定灵芝子实体水提物及相关产品中三萜的含量

灵芝药品大多以灵芝子实体水提物为原料,为快速准确测定灵芝子实体水提物及相关产品中三萜的含量,建立了具有较好分离效果的HPLC分析测定方法。通过优化色谱柱和洗脱条件,优选出Agilent Zorbax SB-Aq C18色谱柱(250 mm×4.6 mm,5μm),以乙腈-乙酸水溶液(0.01%)为流动相梯度洗脱,流速为1.0 mL/min,检测波长252 nm,柱温30℃,该条件下灵芝酸A、灵芝酸F等10种灵芝酸得到较好的分离。方法学考察显示该分析方法精密度、重复性、稳定性和加样回收率的RSD值均小于5%,可以用于灵芝酸C2、灵芝酸G、灵芝烯酸B、灵芝酸B等10种灵芝酸的定量检测。通过对灵芝子实体原料、水提物和市售灵芝产品中10种三萜类成分分析发现,灵芝子实体水提物中均含有这10种三萜,含量为2.52%–6.83%,较子实体原料大幅提高,市售的灵芝产品中的三萜含量为0.27%–0.84%。该方法的建立为灵芝水提物及其产品质量标准的建立奠定基础。     

学习经历在平腹小蜂寄主选择过程中的作用

研究了已经交配与未经交配的平腹小蜂在羽化后不同时间对中间寄主柞蚕卵信息记忆的持效性,比较了经学习训练与未经学习训练的平腹小蜂在不同时间对其自然寄主荔枝蝽卵和中间寄主柞蚕卵的选择性。结果表明：交配过的平腹小蜂在大量羽化后96h检验柞蚕卵的时间和数量都显著增多,而未经交配的平腹小蜂在此时搜索寄主的时间也显著延长,说明平腹小蜂在此时对柞蚕卵信息的记忆开始明显减弱。经学习训练的和未经学习训练的平腹小蜂在大量羽化后96h对荔枝蝽卵的第一选择数和刺卵数都明显提高,并且前者较后者在各个时段对荔枝蝽卵的第一选择数、检验卵数以及刺卵数都多,说明经学习训练的平腹小蜂对荔枝蝽卵的趋性较高,并且随着时间的延长受柞蚕卵信息的干扰逐渐减小,对荔枝蝽卵的学习效果不断增强。     

Breeding bacterial blight-resistant hybrid rice with the cloned bacterial blight resistance gene Xa21

The cloned bacterial blight (BB) resistance gene Xa21 was transferred into Minghui63, a widely used restorer line of indica hybrid rice in China, through an Agrobacterium-mediated system. Molecular and resistance analyses revealed that the Xa21 gene was integrated in the genomes of transgenic plants and their progeny inherited resistance stably. For the purpose of hybrid breeding, Xa21 transgenic homozygous restorer lines were selected through `within-lane' dosage comparison of hybridization signal in combination with PCR and resistance analyses. The selected transgenic restorer lines were then crossed with a commonly used sterile line, Zhenshan97A, to produce Xa21 transgenic hybrid rice, Shanyou63-Xa21. The hybrid rice plants with Xa21 displayed high broad-spectrum resistance to Xanthomonas oryzae pv. oryzae (Xoo) races and maintained elite agronomic characters of Shanyou63. The propagation of this BB-resistant hybrid variety with Xa21 will benefit rice production.     

Genome-wide regulation of 5hmC, 5mC, and gene expression by Tet1 hydroxylase in mouse embryonic stem cells

DNA methylation at the 5 position of cytosine (5mC) in the mammalian genome is a key epigenetic event critical for various cellular processes. The ten-eleven translocation (Tet) family of 5mC-hydroxylases, which convert 5mC to 5-hydroxymethylcytosine (5hmC), offers a way for dynamic regulation of DNA methylation. Here we report that Tet1 binds to unmodified C or 5mC- or 5hmC-modified CpG-rich DNA through its CXXC domain. Genome-wide mapping of Tet1 and 5hmC reveals mechanisms by which Tet1 controls 5hmC and 5mC levels in mouse embryonic stem cells (mESCs). We also uncover a comprehensive gene network influenced by Tet1. Collectively, our data suggest that Tet1 controls DNA methylation both by binding to CpG-rich regions to prevent unwanted DNA methyltransferase activity, and by converting 5mC to 5hmC through hydroxylase activity. This Tet1-mediated antagonism of CpG methylation imparts differential maintenance of DNA methylation status at Tet1 targets, ultimately contributing to mESC differentiation and the onset of embryonic development.     

In situ observation of elementary growth processes of protein crystals by advanced optical microscopy

To start systematically investigating the quality improvement of protein crystals, the elementary growth processes of protein crystals must be first clarified comprehensively. Atomic force microscopy (AFM) has made a tremendous contribution toward elucidating the elementary growth processes of protein crystals and has confirmed that protein crystals grow layer by layer utilizing kinks on steps, as in the case of inorganic and low-molecular-weight compound crystals. However, the scanning of the AFM cantilever greatly disturbs the concentration distribution and solution flow in the vicinity of growing protein crystals. AFM also cannot visualize the dynamic behavior of mobile solute and impurity molecules on protein crystal surfaces. To compensate for these disadvantages of AFM, in situ observation by two types of advanced optical microscopy has been recently performed. To observe the elementary steps of protein crystals noninvasively, laser confocal microscopy combined with differential interference contrast microscopy (LCM-DIM) was developed. To visualize individual mobile protein molecules, total internal reflection fluorescent (TIRF) microscopy, which is widely used in the field of biological physics, was applied to the visualization of protein crystal surfaces. In this review, recent progress in the noninvasive in situ observation of elementary steps and individual mobile protein molecules on protein crystal surfaces is outlined.     

离散广义Logistic模型的稳定性和浑沌现象

文[1]提出了单种生长的连续性文广义Logistic dx/dt=γx({K-x}/(K+px))其中γ>ο为种群的内禀生长率,K>0为环境容纳量,ν>-1表示种群对环境(包括营     

雷公藤红素抑制Cd2+诱导的神经毒性北大核心CSCD

镉(cadmium,Cd)是环境中常见的一种重金属,Cd^(2+)可以通过穿透血脑屏障,产生神经毒性,从而诱发各种神经退行性疾病,雷公藤红素是雷公藤的一种有效成分,具有抗癌、抗炎等一系列药理作用,本文探究雷公藤红素对Cd^(2+)诱导的相应神经毒性的影响作用。通过细胞增殖实验、细胞膜完整性实验、细胞形态实验探索了Cd^(2+)对小胶质细胞HMC3活力的影响;通过一氧化氮(NO)检测实验、脂质过氧化(malondialdehyde,MDA)检测实验、蛋白免疫印迹实验分析了Cd^(2+)的神经毒性以及雷公藤红素对Cd^(2+)诱导的相应神经毒性的影响。结果表明:与对照组相比,当Cd^(2+)浓度达到40μmol/L时,对HMC3细胞增殖抑制率为(57.17±8.23)%(P<0.01,n=5),继续增大Cd^(2+)浓度,细胞活性将进一步降低;当Cd^(2+)浓度达到40μmol/L以上时,HMC3的细胞膜明显受到破坏,并且破坏作用与浓度呈剂量依赖性关系;随着Cd^(2+)浓度的增加,细胞形态开始变化,贴壁效果变差。Cd^(2+)使HMC3细胞释放的NO量显著增加,而雷公藤红素能够有效地抑制Cd^(2+)诱导的HMC3细胞NO的释放;Cd^(2+)使HMC3细胞脂质过氧化水平显著增加,加入10^(-7) mol/L雷公藤红素后,MDA的释放量显著减少;Cd^(2+)会使p-PI3K蛋白含量增加,而加入了雷公藤红素(10^(-7)、10^(-6) mol/L)后,p-PI3K蛋白和p-AKT蛋白的激活均被抑制,从而抑制了细胞凋亡。综上所述,雷公藤红素能够抑制Cd^(2+)诱导的小胶质细胞毒性,从而起到神经保护作用。     

MazF cleaves cellular mRNAs specifically at ACA to block protein synthesis in Escherichia coli

Escherichia coli contains operons called "addiction modules," encoding toxin and antitoxin, which are responsible for growth arrest and cell death. Here, we demonstrate that MazF toxin encoded by "mazEF addiction module" is a sequence-specific (ACA) endoribonuclease functional only for single-stranded RNA. MazF works as a ribonuclease independent of ribosomes, and is, therefore, functionally distinct from RelE, another E. coli toxin, which assists mRNA cleavage at the A site on ribosomes. Upon induction, MazF cleaves whole cellular mRNAs to efficiently block protein synthesis. Purified MazF inhibited protein synthesis in both prokaryotic and eukaryotic cell-free systems. This inhibition was released by MazE, the labile antitoxin against MazF. Thus, MazF functions as a toxic endoribonuclease to interfere with the function of cellular mRNAs by cleaving them at specific sequences leading to rapid cell growth arrest and cell death. The role of such endoribonucleases may have broad implication in cell physiology under various growth conditions.