香蕉MaASR1基因的抗干旱作用

ASR(ABA, stress, ripening induced protein)是一类响应植物干旱胁迫的关键转录因子, 在许多植物中已有报道, 然而尚未见香蕉(Musa acuminata)中ASR与抗旱作用的相关研究。该实验从香蕉果实cDNA文库中筛选出1个ASR基因, 即MaASR1(登录号为AY628102)。干旱胁迫下, 该基因在叶片中的表达量高于根部。将MaASR1转入拟南芥(Arabidopsis thaliana), Southern检测确定了两株独立表达的转基因株系(命名为L14和L38)。表型观察发现, 此两转基因株系的叶片变小且变厚; Northern和Western检测结果表明, MaASR1在L14和L38中表达。控水处理后, L14和L38的存活率及脯氨酸含量均高于野生型。经干旱胁迫和外源ABA处理后, 对MaASR1转基因株系中ABA/胁迫响应基因的表达分析, 发现MaASR1可增强转基因株系对ABA信号的敏感度, 但不能增强植株依赖于ABA途径的抗旱性。     

固脾消积饮诱导人肝癌HepG2细胞凋亡的分子机制*

目的: 探讨固脾消积饮对人肝癌细胞HepG2凋亡的分子机制。方法: 将HepG2细胞分为4组:对照组(Control)、空白血清组(Blank)、固脾消积饮血清组(GPXJY)和顺铂组(Positive),每组设置8个复孔。固脾消积饮含药血清和顺铂干预24 h后,检测细胞活性、活细胞数量、细胞凋亡状态、细胞周期以及线粒体膜电位状况,检测细胞的脂质过氧化(MDA)水平、糖酵解速率和凋亡Bax、Bcl-2、Caspase-3蛋白的表达,检测细胞上清液三酰甘油(TG)、胆固醇(TC)、丙酮酸和葡萄糖的含量。结果: 与Control组比较,GPXJY组(细胞的)抑制率增加、细胞数量减少、凋亡阳性细胞数增多(P＜0.01),G1期细胞数目显著增加(P＜0.05),细胞线粒体膜电位降低(P＜0.01),糖酵解功能显著抑制,细胞中MDA水平升高,细胞Bax、Caspase-3的表达升高、Bcl-2的表达下降(P＜0.05,P＜0.01),细胞上清液中TC、TG、葡萄糖含量显著减少、丙酮酸含量显著增加(P＜0.05,P＜0.01)。结论: 固脾消积饮可诱导HepG2细胞发生凋亡,可能对能量代谢发挥作用。     

EV71感染抗病毒药物及疫苗研究进展

手足口病在世界多个地区,尤其是亚洲爆发并流行,且其感染率和死亡率逐年增高,危害十分严重。肠道病毒71(Enterovirus 71,EV71)是手足口病(Hand,foot,andmouth disease,HFMD)的主要病原体,以感染婴幼儿为主,其感染常伴随神经系统并发症,严重可导致儿童死亡。近年来,分子生物学和抗病毒研究方面取得的进展为EV71感染的预防及治疗提供了新的途径。本文对EV71病毒学特点及抗EV71药物的筛选、疫苗开发、RNA干扰等进行了综述,以期为相关研究提供参考。     

黑龙江省金色蝗属一新种 (直翅目：蝗总科)

 报道了采自黑龙江省的蝗总科昆虫一新种：佳木斯金色蝗Chry sacris jiamusi sp.nov.,并与其近似种辽宁金色蝗Ch.liaoningensis Zheng和秦岭 金色蝗Ch.qinlingensis Zheng做了比较。模式标本保存于东北师范大学生命科学学院 动物标本室。     

阔叶红松林林冠空隙光强异质性对红松幼树生长的影响

利用Li-6400光合测定系统,研究了长白山阔叶红松林4个不同尺度林窗内光照强度的异质性,分析红松幼树在林窗内9个方位的光合作用日变化特征.结果表明：林窗内9个方位出现光合有效辐射(PAR)峰值顺序为:西实际林窗、北扩展林窗、林窗中心＞南实际林窗、南扩展林窗、东扩展林窗、东实际林窗＞西扩展林窗、北实际林窗,光照呈东-西、南-北不对称分布,光照梯度在西、北方向变化较大,但各方向距中心不同距离的日均PAR无显著差异.林窗Ⅰ～Ⅳ日均PAR分别为21.85、45.57、66.02和23.48 μmol·m^-2·s^-1,相互之间均达显著差异水平（P＜0.05）.PAR与净光合速率(P_n)呈显著正相关,且相关系数随PAR增大而增大.随林窗面积的增大,PAR和P_n均先增大后减小; 当林窗面积为267 m²时,二者同时达到最大值.     

A (13)C NMR study on the interactions of calcium chloride/potassium chloride with pyranosides in D(2)O

The (13)C NMR spectra of methyl beta-d-glucopyranoside, methyl beta-d-galactopyranoside, methyl beta-d-xylopyranoside, and methyl beta-l-arabinopyranoside were recorded in CaCl(2)/KCl+D(2)O mixtures and in D(2)O. The chemical shifts of C-1, C-3, and C-5 in the methyl beta-d-glucopyranoside and methyl beta-d-galactopyranoside decrease rapidly as molalities of CaCl(2)/KCl increase, while those of C-1, C-2, and C-3 in the methyl beta-d-xylopyranoside and methyl beta-l-arabinopyranoside decrease rapidly as molalities of CaCl(2)/KCl increase. Cations (Ca(2+)/K(+)) can weakly complex with O in OMe of the pyranosides studied. Results are discussed in terms of the stereochemistry of the pyranoside molecules and the structural properties of the ions.     

Fragile X mental retardation protein is required for chemically-induced long-term potentiation of the hippocampus in adult mice

Fragile X syndrome (FXS), a common form of inherited mental retardation, is caused by the lack of fragile X mental retardation protein (FMRP). The animal model of FXS, Fmr1 knockout mice, have deficits in the Morris water maze and trace fear memory tests, showing impairment in hippocampus-dependent learning and memory. However, results for synaptic long-term potentiation (LTP), a key cellular model for learning and memory, remain inconclusive in the hippocampus of Fmr1 knockout mice. Here, we demonstrate that FMRP is required for glycine induced LTP (Gly-LTP) in the CA1 of hippocampus. This form of LTP requires activation of post-synaptic NMDA receptors and metabotropic glutamateric receptors, as well as the subsequent activation of extracellular signal-regulated kinase (ERK) 1/2. However, paired-pulse facilitation was not affected by glycine treatment. Genetic deletion of FMRP interrupted the phosphorylation of ERK1/2, suggesting the possible role of FMRP in the regulation of the activity of ERK1/2. Our study provide strong evidences that FMRP participates in Gly-LTP in the hippocampus by regulating the phosphorylation of ERK1/2, and that improper regulation of these signaling pathways may contribute to the learning and memory deficits observed in FXS.     

Mechanism of folate deficiency-induced apoptosis in mouse embryonic stem cells: Cell cycle arrest/apoptosis in G1/G0 mediated by microRNA-302a and tumor suppressor gene Lats2

Deficiencies in maternal diet, such as inadequate intake of folate, can inhibit normal development and lead to developmental defects. MicroRNAs (miRNAs) may play a role in mediating the effects of folate deficiency in the growing mammalian embryo, although conclusive evidences to support that possibility are not yet available. The goal of the present study was to investigate whether and how folate deprivation alters the properties of mouse embryonic stem cells (mESCs) in culture. For this purpose, mESCs were cultured in folate-deficient or complete culture medium. The results show that folate-deficient mESCs have a significantly higher rate of apoptosis, accumulate in G0/G1 and fail to proliferate. Expression profiling revealed several miRs and many mRNAs are differently expressed in folate-deficient cells. RT-PCR data confirmed differential expressions of 12 miRNAs in folate-deficient cells. Furthermore, bioinformatics analyses and in vitro studies suggested that miR-302a plays a critical role in mediating the effects of folate on cell proliferation and cell cycle-specific apoptosis by targeting Lats2 gene. Together, these results suggest that the effects of folate deficiency on mammalian development may be mediated by miRNAs that regulate proliferation and/or cell cycle progression in ESCs.     

NPR1多肽抗体的制备和应用

根据NCBI GenBank中报道的NPR1一级结构信息,采用Blastn、Blastx、ExPASy和Protean等软件进行序列同源性和抗原性指数分析,获得三段序列特异性较高的多肽,并从中优选一段序列特异性多肽,采用9-氟甲氧羰基固相合成法获得序列特异性最好的多肽,采用HPLC和LC-MS测定合成多肽的浓度和分子量,试验表明目的多肽纯度达88%、目的多肽分子量为1.92234 kD。采用碳化二亚胺法将多肽与KLH进行偶联获得免疫原Pep-KLH,并将其免疫新西兰大白兔以获得抗血清和多克隆抗体,采用ELISA和Western blotting测定其效价和特异性,经ELISA检测表明抗血清和多克隆抗体可与Pep发生特异性免疫反应,经Western blotting试验表明抗血清和多克隆抗体可识别烟草叶片特异性条带,其相对分子量为65 kD,与预测分子量相符,表明利用该方法制备的NPR1多肽抗体具有较高特异性和灵敏度。