心脏晶体停搏液和冷血停搏液不同灌注方法对心肌保护的评价

目的：评估二种心脏停搏液不同灌注方法对心肌保护作用。方法：30例双瓣患者随机分为冷晶体停搏液间断灌注组(n=10),冷血停搏液间断灌注组(n=10),冷血停搏液持续灌注组(n=10),观察血浆心肌肌钙蛋白T(CnT)、肌酸激酶(CK)、肌酸激酶同工酶(CK—MB)。结果：体外循环后冷晶体停搏液间断灌注组血浆心肌肌钙蛋白T和肌酸激酶、肌酶激酶同工酶较其他2组明显增高;冷血停搏液间断灌注组和冷血停搏液持续灌注组血浆心肌肌钙蛋白T、肌酸激酶、肌酸激酶同工酶无明显差异。结论：冷血停搏液的心肌保护优于冷晶体停搏液,冷血停搏液间断灌注与持续灌注没有明显差异。     

几种草坪草的引种栽培试验研究

通过对引种栽培的8种草坪草的物候期、覆盖度、再生速度、品质特性及抗逆性等方面进行分析研究和综合评价,筛选出适合北方温带环境条件下栽培的几种优良草坪草品种——新哥来德(Poa pratensis cv．Nugtade)、枪手股(P.pratensis cv．BlueChip)、午夜(P．pratensis cv．Midnight)、帕特(Agrostis tenuis cv．Putter)、贝克(碧西)(Festuca arundinacea cv．Plxie)等。对陕西关中草坪草的引种和适地栽植提供一定的理论依据。     

广东新会维管植物区系的研究

新会市位于广东省中南部 ,地理位置为北纬 2 2°0 5′4 3″～ 2 2°4 8′2 4″,东经 1 1 2°4 7′0 3″～ 1 1 3°1 5′2 4″,南濒南海 .该地区共有维管植物 1 6 98种 ,隶属于 2 0 9科 81 6属 ,其中蕨类植物 32科 5 4属 82种 ,种子植物 1 78科 76 2属1 6 1 6种 .区系地理学研究表明 :蕨类植物地理成分以热带亚热带分布属居多 ,达 2 6属 ,占蕨类总属数的 4 8.1 3% ,而且是以单种属或少种属占优势 .种子植物地理成分以泛热带、热带亚洲分布占绝对优势 ,全部热带成分已达78.0 9% ;其特征科主要有 :山矾科、冬青科、壳斗科、桑科、金缕梅科、山茶科、樟科、萝摩科、大戟科、蝶形花科、野牡丹科、茜草科等 ;中国特有属杉木属、穗花杉属、石笔木属、四药门花属、马蹄参属、天星藤属、大血藤属、刚毛药花属、台闽苣苔属、酸竹属及广东特有属绣球茜草属、异枝竹属等 .与邻近的香港、惠东古田、鼎湖山和黑石顶的植物区系比较其相似性很高 ,体现出南亚热带地区植物区系成分的过渡性及热带区系的渗透性     

KITLG is a novel target of miR‐34c that is associated with the inhibition of growth and invasion in colorectal cancer cells

MiR‐34c is considered a potent tumour suppressor because of its negative regulation of multiple target mRNAs that are critically associated with tumorigenesis and metastasis. In the present study, we demonstrated a novel target of miR‐34c, KITLG, which has been implicated in colorectal cancer (CRC). First, we found a significant negative relationship between miR‐34c and KITLG mRNA expression levels in CRC cell lines, including HT‐29, HCT‐116, SW480 and SW620 CRC cell lines. In silico analysis predicted putative binding sites for miR‐34c in the 3′ untranslated region (3′UTR) of KITLG mRNA. A dual‐luciferase reporter assay further confirmed that KITLG is a direct target of miR‐34c. Then, the cell lines were infected with lentiviruses expressing miR‐34c or a miR‐34c specific inhibitor. Restoration of miR‐34c dramatically reduced the expression of KITLG mRNA and protein, while silencing of endogenous miR‐34c increased the expression of KITLG protein. The miR‐34c‐mediated down‐regulation of KITLG was associated with the suppression on proliferation, cellular transformation, migration and invasion of CRC cells, as well as the promotion on apoptosis. Knockdown of KITLG by its specific siRNA confirmed a critical role of KITLG down‐regulation for the tumour‐suppressive effects of miR‐34c in CRC cells. In conclusion, our results demonstrated that miR‐34c might interfere with KITLG‐related CRC and could be a novel molecular target for CRC patients.     

Molecular mechanism of ERK dephosphorylation by striatal‐enriched protein tyrosine phosphatase

Striatal‐enriched tyrosine phosphatase (STEP) is an important regulator of neuronal synaptic plasticity, and its abnormal level or activity contributes to cognitive disorders. One crucial downstream effector and direct substrate of STEP is extracellular signal‐regulated protein kinase (ERK), which has important functions in spine stabilisation and action potential transmission. The inhibition of STEP activity toward phospho‐ERK has the potential to treat neuronal diseases, but the detailed mechanism underlying the dephosphorylation of phospho‐ERK by STEP is not known. Therefore, we examined STEP activity toward para‐nitrophenyl phosphate, phospho‐tyrosine‐containing peptides, and the full‐length phospho‐ERK protein using STEP mutants with different structural features. STEP was found to be a highly efficient ERK tyrosine phosphatase that required both its N‐terminal regulatory region and key residues in its active site. Specifically, both kinase interaction motif (KIM) and kinase‐specific sequence of STEP were required for ERK interaction. In addition to the N‐terminal kinase‐specific sequence region, S245, hydrophobic residues L249/L251, and basic residues R242/R243 located in the KIM region were important in controlling STEP activity toward phospho‐ERK. Further kinetic experiments revealed subtle structural differences between STEP and HePTP that affected the interactions of their KIMs with ERK. Moreover, STEP recognised specific positions of a phospho‐ERK peptide sequence through its active site, and the contact of STEP F311 with phospho‐ERK V205 and T207 were crucial interactions. Taken together, our results not only provide the information for interactions between ERK and STEP, but will also help in the development of specific strategies to target STEP‐ERK recognition, which could serve as a potential therapy for neurological disorders.

     

罗布泊地区第四纪环境演化

新疆罗后干涸湖盆中的Ｋ１钻孔揭示,１００、２ｍ的沉积剖面共有９２个宙积层,划归１６同积旋回,包括了早更新世以来的各时期沉积。据划分的１５个孢粉组这及古地磁、１４＾Ｃ、岩石地层资料综合分析,早更新世该区曾发育森林－草原植被,早更民末,强烈的构造运动保留我下更充变形,上覆的中更统与下更新统间呈不整合接触。中更新世,荒漠和荒漠草原交替出现,地层中有大量膏质泥岩和石膏。晚更新世以来,在干旱气候的控制之下,     

小麦耐盐种质遗传多样性的RAPD分析

选用２２个引物对２４份小麦耐盐种质进行ＲＡＰＤ分析,共产生２００条扩增片段,多态性片段数为１７２条,扩增片段的多态性百分率为８６％,利用ＮＹＳＴＳ软件根据Ｊａｃｃａｒｄ系统分析ＲＡＰＤ结果,并按ＵＰＧＭＡ类平均法进行聚类。２４份材料相似系数在０．２１￣０．９７之间,其中含有多枝赖草、黑麦和偃麦草等外源染色体的多１７４、ＷＲ８３０和南前１２７被分别在３个独立的组,多１７４和南前１２７的亲关系最远,相     

人PSP94的分泌表达及其表达产物抗前列腺癌作用

将编码人 94个氨基酸的前列腺分泌蛋白 ( PSP94) c DNA与酵母整合载体 p PICZαA重组 ,构建的重组质粒线性化后转染酵母细胞 GS1 1 5,获得了 PSP94在酵母细胞中遗传性稳定表达酵母工程细胞 .诱导后的培养物中 ,rh PSP94表达量约为 0 .9mg/L,分子量约 1 6.5k D.培养上清经离子交换层析纯化后 ,目的蛋白的纯度为 92 % .体外在人前列腺癌细胞上活性分析表明 ,rh PSP94以1 0 0μg/L ,对该细胞的抑制率 2 0 .4% ;单纯新型 TNF,以 1 0 3 U/ml,抑制率 2 9.8% ;rh PSP94和新型 TNF以上述同样剂量联合应用 ,抑制率为 86.3% .提示 PSP94在体外对抗前列腺癌细胞有杀伤作用 ,但不明显 ;PSP94与新型 TNF联合应用 ,可使抑制率明显提高 ,可能 PSP94与新型 TNF有协同抗前列腺癌的作用 .     

基因组内碱基分布整体均衡与局部不均衡的研究进展

近年来,随着各种基因组计划的相继完成,发现在各种生物体单核苷酸链水平上存在着A≌T,G≌C的数量关系,但从几千个至十几万个碱基的范围来看,A≠T,G≠C。从数学上可以证明,如果DNA双链之间碱基的突变率一致,则A≌T,G≌C成立,但很多实验表明,双链之间的突变率并不一致,因此这个问题的解决仍有赖于数理科学和生物学的进一步结合。 Abstract:With more and more genome have been completely sequenced,scientists find the Partial Rule 2(PR2) in entire single strand that A≌T,G≌C.But from the scope of thousands to hundreds of thousand bases,A≠T,G≠C.Form the view of math,if the mutational rate of one strand is equal to others,it could be proved that A≌T,G≌C,but from the view of experience,that premise doesn't exist,so the solution of the problem needs the deeply combination of biology and math.     

EPO modified MSCs can inhibit asthmatic airway remodeling in an animal model

There was no effective measures can be obtained at present to reverse or prevent airway remodeling. We investigated the therapeutic effect of Erythropoietin (EPO) gene modified mesenchymal stem cells (MSCs) on asthmatic airway remodeling and the possible underlied molecular mechanisms. EPO gene was transfected into MSCs via lentivirus vector. The transfected cells (EPO‐MSCs) were identified by flow cytometry and the EPO secreting function was detected by PCR and Western blot. MSCs or EPO‐MSCs were administrated to albumin (OVA)‐induced chronic asthmatic mouse model via tail veins. The asthmatic phenotype was analyzed. Number of cells in bronchoalveolar lavage fluid (BALF) was counted using a hemocytometer. Histological findings of airways were evaluated by microscopic examination. The concentrations of interleukin 4(IL‐4), interleukin 5(IL‐5), and interleukin 13(IL‐13) in lung homogenate were determined by ELISA. The activation state of transforming growth factor‐β 1 (TGF‐β1), Transforming growth factor beta‐activated kinase 1 (TAK1), and p38 Mitogen Activated Protein Kinase (p38MAPK) signaling was detected by Real‐Time PCR and Western blotting. EPO‐MSCs were successfully constructed. EPO‐MSCs showed a more potently suppressive effect on local asthmatic airway inflammation and the level of IL‐4, IL‐5, and IL‐13 in lung tissue than MSCs. Moreover, the numbers of goblet cells, the thicknesses of smooth muscle layer, collagen density, percentage of proliferating cell nuclear antigen positive (PCNA⁺) mesenchymal cells, and von Willebrand factor positive(vWF⁺) vessels were also significantly inhibited by EPO‐MSCs. Furthermore, EPO‐MSCs could downregulate the expression of TGF‐β1, TAK1, and p38MAPK in lung tissue both in mRNA level and in protein level. EPO gene modified MSCs may more efficiently attenuate asthmatic airway remodeling, which maybe related with the downregulation of TGF‐β1‐TAK1‐p38MAPK pathway activity.