微囊藻毒素研究的当前进展和未来方向

蓝藻是一种广泛分布于全世界水体中的光能自养型微生物,其特点之一是所产生的特殊次级代谢产物藻毒素对于许多物种都有毒性作用。在正常生态环境中,水体中蓝藻数量维持在正常范围。人类活动的加剧以及对于水环境管理的缺乏造成了全球范围内的水体污染,其中以水体富营养化尤为严重,且有不断增加的趋势。水体富营       

Exosomes derived from umbilical cord mesenchymal stem cells alleviate viral myocarditis through activating AMPK/mTOR‐mediated autophagy flux pathway

Human umbilical cord mesenchymal stem cell‐derived exosomes (hucMSC‐exosomes) have been implicated as a novel therapeutic approach for tissue injury repair and regeneration, but the effects of hucMSC‐exosomes on coxsackievirus B3 (CVB3)‐induced myocarditis remain unknown. The object of the present study is to investigate whether hucMSC‐exosomes have therapeutic effects on CVB3‐induced myocarditis (VMC). HucMSC‐exosomes were identified using nanoparticle tracking analysis (NTA), transmission electron microscopy (TEM) and Western blot. The purified hucMSC‐exosomes tagged with PKH26 were tail intravenously injected into VMC model mice in vivo and used to administrate CVB3‐infected human cardiomyocytes (HCMs) in vitro, respectively. The effects of hucMSC‐exosomes on myocardial pathology injury, proinflammatory cytokines and cardiac function were evaluated through haematoxylin and eosin (H&E) staining, quantitative polymerase chain reaction (qPCR) and Doppler echocardiography. The anti‐apoptosis role and potential mechanism of hucMSC‐exosomes were explored using TUNEL staining, flow cytometry, immunohistochemistry, Ad‐mRFP‐GFP‐LC3 transduction and Western blot. In vivo results showed that hucMSC‐exosomes (50 μg iv) significantly alleviated myocardium injury, shrank the production of proinflammatory cytokines and improved cardiac function. Moreover, in vitro data showed that hucMSC‐exosomes (50 μg/mL) inhibited the apoptosis of CVB3‐infected HCM through increasing pAMPK/AMPK ratio and up‐regulating autophagy proteins LC3II/I, BECLIN‐1 and anti‐apoptosis protein BCL‐2 as well as decreasing pmTOR/mTOR ratio, promoting the degradation of autophagy flux protein P62 and down‐regulating apoptosis protein BAX. In conclusion, hucMSC‐exosomes could alleviate CVB3‐induced myocarditis via activating AMPK/mTOR‐mediated autophagy flux pathway to attenuate cardiomyocyte apoptosis, which will be benefit for MSC‐exosome therapy of myocarditis in the future.     

金沙江河谷特有单种属植物丁茜的染色体数目报道

报道茜草科植物丁茜（Trailliaedoxa gracilis）的染色体数目,2n=22,基数x=11。     

绵羊肌肉中FAS基因和HSL基因的发育性变化及其对肌内脂肪含量的影响

选取不同日龄的雄性哈萨克羊和新疆细毛羊共54只,屠宰后取背最长肌,用索氏抽提法检测肌内脂肪(intramuscular fat,IMF)含量,用荧光实时定量PCR法检测肌肉脂肪酸合成酶(fatty acid synthase,FAS)和激素敏感脂肪酶(hormone-sensitive lipase,HSL)基因表达的发育性变化,并分析基因表达对肌内脂肪沉积的影响。结果表明:1)随着日龄的增加,雄性哈萨克羊的IMF含量持续上升,各生长时期差异显著(P<0.05),而新疆细毛羊的IMF含量在各生长时期无显著差异(P>0.05)。雄性哈萨克羊的IMF含量30~90日龄期间极显著高于新疆细毛羊(P<0.01)。2)FAS基因mRNA水平在哈萨克羊肌肉中初生时最高(P<0.05),然后随日龄的增加呈下降趋势;在新疆细毛羊肌肉中,FAS mRNA水平表现出"下降-上升-下降-上升"的发育模式,其中60日龄显著高于90日龄(P<0.05),其余日龄之间差异不显著。HSL基因在2品种绵羊肌肉中的表达模式基本类似,在哈萨克羊肌肉中随年龄的增加而下降,初生时的水平显著高于60~90日龄(P<0.05);在新疆细毛羊中30日龄时达到最高(P<0.01),到60日龄时下降到最低(P<0.05),随后保持这种低表达水平。3)FAS和HSL基因mRNA的表达量均与哈萨克羊IMF含量呈负相关,相关系数分别为:r=-0.485(P=0.02),r=-0.423(P=0.05);在哈萨克羊中两基因表达量水平比值(FAS:HSL)与IMF呈极显著负相关r=-0.552(P=0.01)。在新疆细毛羊中两基因的表达水平及比值均与IMF无显著相关性(P>0.05)。     

采用BS-Ⅱ大孔离子交换树脂分离低分子肝素

采用HNO2降解法,通过控制降解过程中的pH和时间裂解低分子肝素,并经大孔离子交换树脂BS-Ⅱ对其进行分离纯化,用质谱法对其相对分子质量进行分析。结果表明:在pH3.5、4 h的降解条件下,降解得到低分子肝素。在0.34 mol/L NaCl、pH8.5的条件下吸附,4 mol/L NaCl、pH8.5条件下洗脱,其吸附率达97.2%,纯化后的低分子肝素抗凝活性为34.41 U/mg,比纯化前提高1.36倍,效价回收率达到85.24%。质谱分析表明,纯化所得低分子肝素的平均相对分子质量为8 411,67.45%集中分布在7 000~9 000段。     

大肠杆菌中表达关键基因产异丁醇的研究

目的:改造大肠杆菌的代谢途径,使非生产菌株大肠杆菌具备产异丁醇的能力.方法:将乳脂乳球菌NIZO B1157的2-酮酸脱羧酶基因kdcA克隆到大肠杆菌中,使大肠杆菌产异丁醇;另外,采取两种方法过量表达alsS、ilvC、ilvD基因,增加前体物质酮酸的供应,以提高异丁醇的产量:一是与kdcA串联表达;二是在另一个相容质粒中表达.结果:大肠杆菌工程菌具备产异丁醇的能力,其中相关基因在一个质粒中串联表达的产量比其在两个相容质粒中共表达的产量高30倍,达到3g/L.结论:导入的酮酸合成途径与醇类生产途径结合,能使非生产菌株大肠杆菌生产异丁醇,并且单质粒表达代谢途径相关基因的效果优于双质粒表达.     

基于多目标灰色局势决策的三峡库区防护林类型空间优化配置

基于2007年Landsat TM遥感影像和影响防护林的主导环境因子,对三峡库区的森林立地进行分类,并通过选取水源涵养量、生物量和林分生产力3个指标,利用多目标灰色局势决策模型对库区现有的针叶林、阔叶林、针阔混交林和灌木林4种防护林类型进行空间优化配置.结果表明： 2007年,三峡库区森林立地可划分为40种类型;空间配置优化后,研究区针叶林、阔叶林、针阔混交林和灌木林的面积比例分别为32.55%、29.43%、34.95%和3.07%.与优化前相比,优化后针叶林和灌木林的面积比例分别减少了8.79%和28.55%,阔叶林和针阔混交林分别增加了10.23%和27.11%.通过防护林类型的空间优化,三峡库区整体的水源涵养能力、生物量和林分生产力分别增加14.09×10⁸ m³、0.35×10⁸ t和1.08×10⁶ t.     

水氮运筹对膜下滴灌棉花光合特性及产量形成的影响

以不同基因型棉花品种为材料,在土柱栽培条件下研究膜下滴灌条件下水氮运筹方式对新疆棉花光合性能和产量构成的影响.结果表明： 播前灌溉+盛花期前限量滴灌+盛花期后充分滴灌,并配合氮肥基施20%+追施80%的水氮运筹方式（W₄N₂）下,盛花期叶片叶绿素含量、气孔导度（g_s）、净光合速率（P_n）、PSⅡ实际光化学效率（Φ_PSⅡ）和光化学猝灭系数（q_P）均显著低于全生育期常规滴灌处理,非光化学猝灭系数（NPQ）增加,地上部干物质累积量受到限制;盛铃期至吐絮期叶绿素含量、g_s、P_n、Φ_PSⅡ、q_P均随水氮供应量的提高而增大,地上部干物质产生超补偿积累,且有利于光合产物向棉铃的运转与分配.在氮肥基施20%+追施80%的施氮方式下,新陆早13号以播前灌溉+全生育期常规滴灌（W₃）处理的籽棉产量较高,新陆早43号以播前灌溉+盛花期前限量滴灌+盛花期后充分滴灌（W₄）处理籽棉产量最高.因此,在播前灌溉条件下适当减少盛花期前、增加生育中后期水氮供应,可以延长冠层叶片光合功能期,促进光合物质优先向生殖器官分配,充分发挥膜下滴灌棉花的增产潜力.     

NOX4-Derived Reactive Oxygen Species Drive Apelin-13-Induced Vascular Smooth Muscle Cell Proliferation via the ERK Pathway

Apelin is the endogenous ligand of the G-protein-coupled receptor, apelin–angiotensin receptor-like 1 (APJ). Vascular smooth muscle cells express both apelin and APJ, which are important regulatory factors in the cardiovascular system. Apelin-13 significantly stimulated vascular smooth muscle cell proliferation. However, little is known about the precise cellular mechanisms responsible for vascular smooth muscle cell proliferation induced by apelin-13. Here, we present novel data that indicate the key role of NADPH oxidase 4-derived reactive oxygen species in proliferation of vascular smooth muscle cells treated with apelin-13. Apelin-13 stimulated reactive oxygen species production in a concentration- and time-dependent manner. Furthermore, DPI impaired apelin-13-induced reactive oxygen species generation and vascular smooth muscle cell proliferation. Apelin-13-treatment increased the expression of NADPH oxidase 4 in a dose-dependent manner. Down-regulation of NADPH oxidase 4 using siRNA prevented apelin-13-induced reactive oxygen species generation and vascular smooth muscle cell proliferation. An increase in reactive molecules can trigger the activation of ERK stress-sensitive signaling pathways. Additionally, siRNA-NOX4 and DPI reversed the phosphorylation of ERK induced by apelin-13. Apelin-13 induced vascular smooth muscle cell proliferation by NOX4-derived ROS via the ERK signaling pathway.