悬铃木属植物果皮毛性状及其对小鼠肺部的致炎作用

观察了3种悬铃木聚合果的形态、坚果形态、聚合果上坚果数量、坚果上果皮毛数量、聚合果总果皮毛数量,比较了3种悬铃木聚合果的形态学差异,发现二球悬铃木的聚合果最大,聚合果上的坚果数量与坚果的果皮毛数量最多;采用石蜡切片染色观察和NaOH处理证明悬铃木果皮毛主要有果胶质、纤维素和木质素3种主要成分;通过用不同浓度粒级符合PM10大小的果皮毛对小白鼠进行支气管染毒试验,证明染毒后小鼠肺泡灌洗液中磷酸还原酶(ACP)含量升高,显示肺细胞受损;GSH-Px含量下降,显示小鼠肺部氧化和抗氧化系统失衡.试验结果证明,悬铃木果皮毛破碎后所形成的可吸入颗粒物PM10对小鼠的呼吸道具有致炎作用.     

Nitidine chloride inhibited the expression of S phase kinase-associated protein 2 in ovarian cancer cells

Nitidine chloride (NC) has been reported to exert its anti-tumor activity in various types of human cancers. However, the molecular mechanism of NC-mediated tumor suppressive function is largely unclear. In the current study, we used several approaches such as MTT, FACS, RT-PCR, Western blotting analysis, invasion assay, transfection, to explore the molecular basis of NC-triggered anti-cancer activity. We found that NC inhibited cell growth, induced cell apoptosis, caused cell cycle arrest in ovarian cancer cells. Emerging evidence has demonstrated that Skp2 plays an important oncogenic role in ovarian cancer. Therefore, we also explored whether NC exerts its biologic function via downregulation of Skp2 in ovarian cancer cells. We observed that NC significantly inhibited the expression of Skp2 in ovarian cancer cells. Notably, overexpression of Skp2 abrogated the anti-cancer activity induced by NC in ovarian cancer cells. Consistently, downregulation of Skp2 expression enhanced the sensitivity of ovarian cancer cells to NC treatment. Thus, inactivation of Skp2 by NC could be a novel strategy for the treatment of human ovarian cancer.     

Autocrine tumor necrosis factor alpha links endoplasmic reticulum stress to the membrane death receptor pathway through IRE1alpha-mediated NF-kappaB activation and down-regulation of TRAF2 expression

NF-kappaB is critical for determining cellular sensitivity to apoptotic stimuli by regulating both mitochondrial and death receptor apoptotic pathways. The endoplasmic reticulum (ER) emerges as a new apoptotic signaling initiator. However, the mechanism by which ER stress activates NF-kappaB and its role in regulation of ER stress-induced cell death are largely unclear. Here, we report that, in response to ER stress, IKK forms a complex with IRE1alpha through the adapter protein TRAF2. ER stress-induced NF-kappaB activation is impaired in IRE1alpha knockdown cells and IRE1alpha(-/-) MEFs. We found, however, that inhibiting NF-kappaB significantly decreased ER stress-induced cell death in a caspase-8-dependent manner. Gene expression analysis revealed that ER stress-induced expression of tumor necrosis factor alpha (TNF-alpha) was IRE1alpha and NF-kappaB dependent. Blocking TNF receptor 1 signaling significantly inhibited ER stress-induced cell death. Further studies suggest that ER stress induces down-regulation of TRAF2 expression, which impairs TNF-alpha-induced activation of NF-kappaB and c-Jun N-terminal kinase and turns TNF-alpha from a weak to a powerful apoptosis inducer. Thus, ER stress induces two signals, namely TNF-alpha induction and TRAF2 down-regulation. They work in concert to amplify ER-initiated apoptotic signaling through the membrane death receptor.     

利用癌功能类从癌基因组突变谱中识别癌基因

从大规模癌样本基因突变扫查数据中识别癌基因具有重要的意义. 一些重要功能的改变对于癌的发生发展是必需的, 因此将它们定义为癌功能类, 并从GO(Gene Ontology)中选择一组显著富集已知癌基因的细致功能类来代表它们. 为了评价以癌相关功能类作为特征识别癌基因的效果, 将已知的蛋白激酶癌基因定义为阳性金标准, 而将其他的蛋白激酶基因定义为阴性金标准. 结果表明, 与利用选择压力作为特征的方法比较, 利用癌相关功能类作为特征的方法可以更有效地识别癌基因. 进一步结合癌相关功能类与基因非同义突变个数可以产生更可靠的预测结果. 最后, 将46个注释到癌相关功能类并且其非同义突变个数至少为3的蛋白激酶基因预测为癌基因, 预测精确率达到0.42.     

栓皮栎体细胞胚胎发生的细胞组织学观察

以栓皮栎未成熟合子胚为外植体,在添加0.25mg/L 2,4-D和0.5mg/L 6-BA的MS培养基上6周可诱导产生2种类型的胚性愈伤组织,一种表面具光泽、白色;另一种表面光滑湿润具光泽,色泽淡黄或无色透明。组织切片表明,胚性愈伤组织的细胞体积小,细胞核大,细胞质浓,细胞排列紧密;非胚性愈伤组织细胞的体积大,细胞核小,细胞质稀薄。胚性细胞团培养在不含激素的培养基上可诱导产生体细胞胚。体细胞胚直接起源于胚性细胞团表皮或近表皮的单细胞,经历与合子胚相似的球形胚、心形胚、鱼雷胚和子叶胚发育阶段。所有发育时期的体细胞胚的胚轴、子叶均产生次生体胚,它们起源于细胞质较浓的表皮单细胞。     

中国栉眼蚤属两新亚种记述(蚤目:多毛蚤科)

根据１９８８年以来,人采自浙江省景宁,永嘉等县的标本,记述了栉眼蚤属两新亚各,即台湾栉眼蚤浙江亚种Ｃｔｅｎｏｐｈｔｈａｌｍｕｓ（Ｓｉｎｏｃｔｅｎｏｐｈｔｈａｌｍｕｓ）ｔａｉｗａｎｕｓｚｈｅｊｉａｎｇｅｎｓｉｓＬｕｅｔＱｉｕ,ｓｓｐ．ｎｏｖ和短突栉眼蚤永嘉亚种Ｃｔｅｎｏｐｈｔｈａｌｍｕｓ（Ｓｉｎｏｃｔｅｎｏｐｈｔｈａｌｍｕｓ）ｂｒｅｖｉｐｒｏｊｉｃｉｅｎｓｙｏｎｇｊｉａｅｎｓｉｓ,Ｌｕ,Ｚｈａｎｇ,     

Adenosine kinase regulation of cardiomyocyte hypertrophy

There is evidence that extracellular adenosine can attenuate cardiac hypertrophy, but the mechanism by which this occurs is not clear. Here we investigated the role of adenosine receptors and adenosine metabolism in attenuation of cardiomyocyte hypertrophy. Phenylephrine (PE) caused hypertrophy of neonatal rat cardiomyocytes with increases of cell surface area, protein synthesis, and atrial natriuretic peptide (ANP) expression. These responses were attenuated by 5 μM 2-chloroadenosine (CADO; adenosine deaminase resistant adenosine analog) or 10 μM adenosine. While antagonism of adenosine receptors partially blocked the reduction of ANP expression produced by CADO, it did not restore cell size or protein synthesis. In support of a role for intracellular adenosine metabolism in regulating hypertrophy, the adenosine kinase (AK) inhibitors iodotubercidin and ABT-702 completely reversed the attenuation of cell size, protein synthesis, and expression of ANP by CADO or ADO. Examination of PE-induced phosphosignaling pathways revealed that CADO treatment did not reduce AKT(Ser??3) phosphorylation but did attenuate sustained phosphorylation of Raf(Ser33?) (24-48 h), mTOR(Ser2???) (24-48 h), p70S6k(Thr3??) (2.5-48 h), and ERK(Thr2?2/Tyr2??) (48 h). Inhibition of AK restored activation of these enzymes in the presence of CADO. Using dominant negative and constitutively active Raf adenoviruses, we found that Raf activation is necessary and sufficient for PE-induced mTORC1 signaling and cardiomyocyte hypertrophy. CADO treatment still blocked p70S6k(Thr3??) phosphorylation and hypertrophy downstream of constitutively active Raf, however, despite a high level phosphorylation of ERK(Thr202/Tyr204) and AKT(Ser??3). Reduction of Raf-induced p70S6k(Thr3??) phosphorylation and hypertrophy by CADO was reversed by inhibiting AK. Together, these results identify AK as an important mediator of adenosine attenuation of cardiomyocyte hypertrophy, which acts, at least in part, through inhibition of Raf signaling to mTOR/p70S6k.     

混凝复配剂的制备及其污水处理效果

采用静态实验遴选不同种硅藻土,进而研究其与常用混凝剂的最佳组合及复配比,考察其中几种复配剂在一定条件对城市污水的处理效果。实验结果表明:硅藻土和混凝剂组成的复配剂具有强化混凝作用;氯化铝、硫酸亚铁和高分子絮凝剂与硅藻土分别在1:9,1:11,和1:9的配比时制备复配剂处理生活污水的效果最佳。     

细胞生物活性肽-蛋氨酸脑啡肽对小鼠CD4~+T细胞mRNA的影响

从基因水平探讨蛋氨酸脑啡肽对小鼠CD4'T细胞mRNA转录的影响。6～8周龄BALB/c雌性小鼠体内、外不同浓度MEK刺激。采用RT-PCR技术检测mRNA,所得不同浓度MEK刺激的CD4+T细胞mRNA和β-actin条带密度比值作为相对表达强度,所得数据采用SPSS11.5软件进行统计分析。4mg/mLMEK体内刺激及10-9～10-12mol/mL的MEK体外刺激促进小鼠CD4'T细胞mRNA转录;10-1～10-8mol/mL的MEK抑制小鼠CD4+T细胞mRNA的转录。10-13～10-14mol/mL的MEK对小鼠CD4'T细胞mRNA的转录无明显变化。适量浓度的MEK体内、外刺激能促进小鼠CD4+T细胞mRNA转录的高效表达。     

基因组原位杂交的新进展及其在植物中的应用

基因组原位杂交 ( Genomic in situ hybridization GISH)是 2 0世纪 80年代末发展起来的一种原位杂交技术。它最初应用于动物方面的研究[1 ] ,但很快被植物方面所借用 ,并且使用频率高于动物方面的研究。它采用来自一个物种的总基因组 DNA作为标记探针 ,用另一物种的总基因组 DNA以适当的浓度进行封阻 ,在靶染色体上进行原位杂交。在封阻DNA和标记 DNA探针之间 ,封阻 DNA优先与一般序列杂交 ,剩下的特异性序列主要被标记探针所杂交。在此基础上 ,人们先后发展了荧光基因组原位杂交、多色基因组原位杂交和比较基因组原位杂交等技术 ,…