MIS3阶段以来黄骅北部地区潮坪地层中的微体生物群

依据渤海湾湾顶南侧、古黄河三角洲河北省黄骅市北部地区13个钻孔岩芯材料微体古生物学研究,以及地球化学背景、沉积构造分析,本文确定了自相当海洋氧同位素MIS3阶段以来中潮坪、高潮坪、淡水注入的潮坪、潮汐通道、分支河道及边滩、牛轭湖、贫营养湖、滨海湿地与富营养湖、泛滥平原一泛滥盆地等不同沉积地层中的微体生物(有孔虫、海相与非海相介形类)分布特征.在MIS3阶段高潮坪一低地沉积之后,河口与相邻低地依然持续或断续出现海相微体生物,个别钻孔中其分布甚至延续到末次盛冰期低海面地层中,但是基本都是广盐种和低盐种.这一现象与沿海构造沉降背景下河口位置长期向陆迁移,微体生物随短暂的强潮及突发的风暴潮搬运、甚至与风、水和鸟的搬运作用有关;远离古河道地点则无此现象.这些海侵事件与全球海面变化和古海面高度无关.与渤海湾顶北侧天津沿海相比,黄骅北部未见天津沿海确定的全新世早期潮下带砂质沉积单元,以及相应的微体生物群,应与当时天津沿海构造沉降速率较高有关.在三角洲与潮坪研究中,微体古生物学发挥了重要作用,而不仅是记述内容之一.     

宁波地区斜纹夜蛾幼虫寄生蜂调查研究

2007—2008年的6～11月对宁波地区重要害虫斜纹夜蛾的寄生性天敌进行了调查,发现寄生蜂有18种,主要种类有：马尼拉陡胸茧蜂Snellenius manilae、侧沟茧蜂Microplitis sp、棉铃虫齿唇姬蜂Carnpoletis chlorideae和斑痣悬茧蜂Meteorus pulchricornis,并对主要寄生蜂与斜纹夜蛾幼虫的田间消长动态进行了系统观察。     

颌面部血管瘤和血管畸形的整形手术治疗模式研究

目的:探讨口腔颌面部软组织血管瘤和血管畸形以整形外科手术为原则的治疗效果.方法:对科室26例采用整形外科手术治疗口腔颌面部血管瘤和血管畸形的患者进行回溯性研究,其中男性15例,女性11例.术前通过B超、MRI和CT等影像学检查明确病变部位及性质,为手术治疗模式提供帮助,手术方法为肿瘤手术切除同时用邻位皮辩或血管化皮辩移植修复;治疗后经6个月至3年随访,评价疗效效果.结果:治疗后无严重并发症发生;疗效分析表明患者都有一定的改善,其中治愈率、显效率分别为61.5%和34.6%.结论:制定完善的诊断和序列治疗方案是保证血管瘤和血管畸形治疗效果和减少并发症的关键,整形外科为原则进行手术治疗在外形和功能均可获满意疗效而且安全.     

第一类肽链释放因子C端结构域参与调控终止密码子的识别过程

真核生物蛋白质翻译终止过程中,第一类肽链释放因子（eukaryotic polypeptide release factor, eRF1）利用其N端结构域识别终止密码子。eRF1的N结构域中的GTS、NIKS和YxCxxxF模体对于终止密码子的识别发挥重要作用。但至目前为止,eRF1识别终止密码子的机制,尤其是对于终止密码子的选择性识别机制仍不清楚。我们构建了四膜虫（Tetrahymena thermophilia）eRF1的N端结构域与酿酒酵母（Saccharomyces cerevisiae）或裂殖酵母（Schizosaccharomyces pombe）eRF1的M和C结构域组成的杂合eRF1,即Tt/Sc eRF1 和Tt/Sp eRF1。双荧光素酶检测结果证实,两种杂合eRF1在细胞中识别终止密码子的活性具有显著差异。Tt/Sc eRF1仅识别UGA密码子,与四膜虫eRF1一致,具有密码子识别特异性;而Tt/Sp eRF1可以识别3个终止密码子,无密码子识别特异性。为解释这一现象,将Sp eRF1的C结构域中的1个关键的小结构域中的氨基酸进行突变,与Sc eRF1相应位点的氨基酸一致。分析结果显示,突变体Tt/Sp eRF1识别密码子UAA和UAG的性质发生显著变化,说明第一类肽链释放因子的C端结构域参与了终止密码子的识别过程。这提示,四膜虫eRF1识别终止密码子的特异性可能依赖于eRF1分子内的结构域间相互作用。本研究结果为揭示肽链释放因子识别终止密码子的分子机制提供了数据支持。     

狐、貉和水貂犬瘟热病毒受体SLAM 的基因克隆及其真核表达

信号淋巴激活分子(SLAM)为犬瘟热病毒(CDV) 感染其宿主动物识别的细胞受体。本试验应用RT -PCR 从狐狸、貉和水貂的外周血淋巴细胞中克隆到其相应SLAM 基因。基因测序比较发现,狐狸、貉与同科的犬SLAM 基因编码区长度均为1 029 bp,核苷酸同源性高于98.6% ;而水貂SLAM 基因编码区长度为1 020 bp,与以上三种动物遗传关系较远(核苷酸同源性< 83.7%),但与海豹SLAM 基因遗传关系较近(核苷酸同源性为91.4% )。基于不同动物SLAM 基因序列的系统进化树分析显示,犬、狐狸、貉、水貂和海豹在进化树上构成了以CDV 为感染宿主的遗传分支。氨基酸序列比较显示,该5 种动物SLAM 分子上均存在一个长度为26 个氨基酸的信号肽序列,且在空间结构上影响宿主--病毒特异性的8 个关键氨基酸均完全保守。通过构建表达该狐狸、貉、水貂SLAM 基因的三种真核表达质粒,分别转染CRFK 细胞后,应用CDV 强毒感染试验证实,CDV 均能在三种转染细胞上产生明显的细胞病变效应(CPE),而未转染CRFK 细胞对照无CPE 产生,由此证实作为CDV细胞受体的狐、貉和水貂的SLAM,体外表达后能明显增强犬瘟热强毒株对非敏感细胞的感染能力。     

春小麦对不同灌水处理的气孔反应及其影响因子

选用3个春小麦品种（系）,采用大田试验方法,在冬灌1800 m³·hm^-2的基础上,在生育期设3次灌水处理（T₁）、2次灌水处理（T₂）和1次灌水处理（T₃）,每次灌水1050 m³·hm^-2,研究土壤水分对春小麦生育期气孔导度的影响及气孔导度与相关环境因素的关系.结果表明：灌水处理对春小麦生育期气孔导度的影响较大,气孔导度随着灌溉次数的减少逐渐降低,同时不同基因型间存在差异.从拔节期到开花期,不同处理春小麦气孔导度变化一致,都呈先升高后降低趋势, 在抽穗期达到峰值;开花期之后各处理出现差异,T₁各品种气孔导度先下降后上升,T₂品种间表现不同,T₃一直呈下降趋势.各环境因子中,大气相对湿度对春小麦气孔导度的影响最大,两者的相关系数在T₂和T₃中分别达显著(0.82^*)和极显著水平(0.92^**).春小麦适应水分亏缺的气孔调节机理为反馈式调节.     

Complete genome sequence of Staphylococcus aureus T0131, an ST239-MRSA-SCCmec type III clone isolated in China

We report here the complete genome sequence of Staphylococcus aureus T0131, which is a multiresistant clinical isolate recovered in China and the first sequenced epidemic ST239-MRSA-SCCmec type III strain obtained in Asia. Comparison with two published genomes of ST239 reveals the polymorphism among strains of this type from different continents.     

Complete genome sequence of Lactobacillus helveticus H10

Lactobacillus helveticus strain H10 was isolated from traditional fermented milk in Tibet, China. We sequenced the whole genome of strain H10 and compared it to the published genome sequence of Lactobacillus helveticus DPC4571.     

Modification of Sialylation Mediates the Invasive Properties and Chemosensitivity of Human Hepatocellular Carcinoma

Aberrant sialylation is closely associated with malignant phenotypes of tumor cells, including invasiveness and metastasis. This study investigated sialylation with regard to the modification of invasive properties and chemosensitivity in human hepatocellular carcinoma (HCC) cell lines and the association between the sialyltransferase gene family and clinicopathological characteristics in HCC patients. Using mass spectrometry analysis, we found that the composition profiling of sialylated N-glycans differed between MHCC97H and MHCC97L cells with different metastatic potential. The expressional profiles of 20 sialyltransferase genes showed differential expression in two cell lines, transitional and tumor tissues, from the same patients. Two genes, ST6GAL1 and ST8SIA2, were detected as overexpressed in MHCC97H and MHCC97L cells. The altered expression levels of ST6GAL1 and ST8SIA2 corresponded to a changed invasive phenotype and chemosensitivity of MHCC97H and MHCC97L cells both in vitro and in vivo. Further data indicated that manipulation of the expression of the two genes led to altered activity of the phosphoinositide-3 kinase (PI3K)/Akt signaling pathway. Targeting the PI3K/Akt pathway by its specific inhibitor wortmannin or by Akt RNA interference resulted in a reduced capacity for invasion and chemoresistance of MHCC97H cells. Our results imply that sialylation may function as an internal factor, regulating the invasion and chemosensitivity of HCC, probably through ST6GAL1 or ST8SIA2 regulation of the activity of the PI3K/Akt pathway.Metastasis of tumor cells and the development of resistance to antitumor therapies are the major causes of death in cancer patients. Specific changes in the glycosylation patterns of cell surface glycoproteins have been shown to enhance the metastatic efficiency of tumor cells, in particular that of terminal sialylation (1). It is well known that alterations in cell surface sialylated antigens affect many cellular properties—for example, cell–cell adhesion, cell–extracellular matrix adhesion, immune defense, cell metastasis, and invasion abilities (2–5). Sialyltransferases catalyze the transfer of sialic acid from cytidine 5′-monophospho-N-acetylneuraminic acid to terminal positions of glycoprotein and glycolipid carbohydrate groups (6).The sialyltransferase (ST)¹ family is a family of anabolic enzymes consisting of 20 members that are divided into three subfamilies (7). α-2,3-sialyltransferases mediate the transfer of sialic acid with an α-2,3-linkage to it with terminal Gal residues (ST3GalI-VI). α-2,6-sialyltransferases mediate the transfer of sialic acid with an α-2,6-linkage to it with terminal Gal (ST6GalI-II) (8, 9) or GalNAc residues (ST6GalNAcI-VI). α-2,8-sialyltransferases mediate the transfer of sialic acid with an α-2,8-linkage (ST8SiaI-VI). Changes in specific sialyltransferase expression in several tumors have been reported. ST3GalIII modulates pancreatic cancer cell motility and adhesion in vitro and enhances its metastatic potential in vivo (10). The high expression of ST3GalIV is associated with the malignant behavior of gastric cancer cells (11). ST6GalI is up-regulated in colon adenocarcinoma, and its expression is positively correlated with tumor cell invasiveness and metastasis (12–14). ST6GalNAcI expression is sufficient to enhance the tumorigenicity of MDA-MB-231 breast cancer cells (15). Overexpression of ST6GalNAcII has been correlated with poor patient survival (16). ST6GalNAcV has recently been reported to mediate brain metastasis of breast cancer cells (17). ST8Sia I is also overexpressed in neuroectoderm-derived malignant tumors such as melanoma, glioblastoma, and neuroblastoma, as well as in estrogen receptor negative breast cancer, where it plays a role in cell proliferation, migration, adhesion, and angiogenesis (18).The phosphoinositide 3 kinase (PI3K)/Akt pathway is involved in many cellular processes, including proliferation, differentiation, apoptosis, cell cycle progression, cell motility, tumorigenesis, tumor growth, and angiogenesis (19, 20). In addition, several reports highlight that the PI3K/Akt pathway is responsible for the proliferation, invasion, metastasis, and drug resistance of hepatocellular carcinoma (HCC), and targeting PI3K/AKT inhibits the proliferation and tumorigenesis of HCC cells (21, 22). MicroRNA-7 plays a substantial role in inhibiting the tumorigenesis and reversing the metastasis of HCC through the PI3K/Akt/mTOR signaling pathway in vitro and in vivo (23). The proliferation and invasion of HCC cells are inhibited by lipocalin 2 through the blockade of PI3K/Akt signaling (24). Activation of the PI3K/Akt pathway mediates rapamycin and sorafenib resistance in HCC cells (25, 26). However, little is known about the ST family and its signaling pathway in relation to malignant phenotypes of human HCC.Therefore, the aims of the present study were to determine sialylated oligosaccharide alteration and expression levels of ST genes among the MHCC97H and MHCC97L cell lines and HCC patient cells by using MS and real-time PCR. In addition, we investigated whether the ST gene family participates in the regulation of tumor invasion and chemosensitivity via the PI3K/Akt pathway and the possible mechanisms.     

Cyclin D1 G870A Polymorphism and Risk of Nasopharyngeal Carcinoma: A Case-Control Study and Meta-Analysis

Background

Cyclin D1 (CCND1) plays a key role in cell cycle regulation. It is a well-established human oncogene which is frequently amplified or overexpressed in cancers. The association between CCND1 G870A polymorphism and cancer risk has been widely assessed. However, a definitive conclusion between CCND1 G870A polymorphism and risk of nasopharyngeal carcinoma (NPC) remains elusive.

Methods

We firstly performed a hospital-based case-control study involving 165 NPC cases and 191 cancer-free controls in central-south China, and then conducted a meta-analysis with six case-control studies to evaluate the association between NPC risk and CCND1 G870A polymorphism.

Results

The case-control study found a significant association between CCND1 G870A polymorphism and NPC risk in various comparison models (AA vs. GG: OR = 2.300, 95% CI 1.089–4.857, p = 0.029; AG vs. GG: OR = 2.832, 95% CI 1.367–5.867, p = 0.005; AA/AG vs. GG: OR = 2.597, 95% CI 1.288–5.237, p = 0.008; AA vs. AG/GG: OR = 0.984, 95% CI 0.638–1.518, p = 0.944). Further meta-analysis showed that there was no significant association between CCND1 G870A polymorphism and NPC risk in overall analysis. In the stratified analysis by race, however, significant associations were only found in Caucasians (for the allele model A vs. G: OR = 0.75, 95% CI 0.59–0.97, p = 0.03; for the co-dominant model AA vs. GG: OR = 0.52, 95% CI 0.32–0.86, p = 0.01; for the dominant model AA/AG vs. GG: OR = 0.49, 95% CI 0.32–0.74, p<0.01; for the recessive model AA vs. AG/GG: OR = 0.90, 95% CI 0.61–1.34, p = 0.60).

Conclusions

A significant association between CCND1 G870A polymorphism and NPC risk was found in the central-southern Chinese population. The meta-analysis indicated that CCND1 G870A polymorphism may contribute to the development of NPC in Caucasians.