The reorganization of Fujian Huadian enterprises

本文试着结合所学知识企业实际情况，提出福建华电企业的改制重组方案，作为一种探索。第一章是环境和背景的介绍。通过对电力体制改革的回顾，分析了其对当前电力市场环境的影响，介绍了福建电力市场的态势和福建华电企业的基本情况。第二章重点分析了福建华电企业的优劣势及改制重组的必要性。通过分析，认为在当前福建激烈的发电市场竞争中，福建华电企业的改制重组有利于转换经营机制，强化经营管理，提高融资能力，增强企业生机与活力，最终实现可持续发展。第三章是华电福建公司的改制重组和可行性分析。阐述了华电福建公司改制重组的总体思路，对成立福建华电有限公司进行了可行性分析并提出了基本方案。第四章对福建华电下属企业的改制重组...Assets Restructuring (AR) is the necessary result and objective demand of allocating resources to their maximum advantages in the course of socialism marketing economy development. Facing the serious challenges in the markets, Fujian Huadian Enterprises should explore the path to a hopeful future of development. This paper consists of five chapters:The first part discusses the background of indust...学位：工商管理硕士院系专业：管理学院工商管理教育中心_工商管理硕士(MBA)学号：X20011504

Protein kinase C and JN K mediate lysophosphatidic acid-induced monocyte chemo-attractant protein-1 expression in human fetal lung fibroblasts

目的:; 研究蛋白激酶C(PKC)和c-Jun氨基末端激酶(JNK)在溶血磷脂酸(LPA)诱导人肺成纤维细胞(HLF-1)单核细胞趋化蛋白-1(MCP-1; )表达中的作用。方法:培养HLF-1细胞,以不同浓度(0、1、3和10 mumol/L)的LPA处理细胞不同时间(0.5、6、12和24; h)后,ELISA检测细胞培养基上清液中MCP-1的蛋白表达,荧光定量PCR检测MCP-1; mRNA的表达水平。用不同浓度的PKC抑制剂Bisindolylmaleimide I(0、0.1、1和10; mumol/L)或JNK抑制剂SP600125(0、0.1、1和10 mumol/L)预孵育细胞30 min后,用LPA(10; mumol/L)刺激2或6 h后,ELISA方法检测细胞培养基上清液中MCP-1的蛋白表达,荧光定量PCR检测MCP-1; mRNA的表达水平。用PKC抑制剂Bisindolylmaleimide I(1 mumol/L)预孵育30 min,以浓度为10; mumol/L的LPA处理细胞不同时间(0、5、30和60 min)后,Western; blot检测c-Jun蛋白磷酸化水平。结果:LPA可诱导HLF-1细胞MCP-1蛋白释放,并呈剂量效应和时间效应关系。LPA的浓度为10; mumol/L时,HLF-1细胞释放MCP-1蛋白的量是对照组的2.4倍(P<0.05);细胞在LPA处理24; h后,MCP-1蛋白的释放量较对照组增加约1倍(P<0.05)。LPA可诱导HLF-1细胞MCP-1 mRNA的表达并呈时间效应,LPA处理2; h后,MCP-1 mRNA表达水平是对照组的5.3倍(P<0.05)。PKC抑制剂Bisindolylmaleimide; I和JNK抑制剂SP600125均可显著抑制LPA诱导的HLF-1细胞MCP-1; mRNA表达及MCP-1蛋白释放。Bisindolylmaleimide I的浓度为1; mumol/L时可阻断LPA诱导的HLF-1细胞MCP-1蛋白释放量的60%(P<0.05),浓度为3 mumol/L时对MCP-1; mRNA表达有明显抑制效果,抑制率达40%(P<0.05);而SP600125的浓度为1; mumol/L时可阻断LPA诱导的HLF-1细胞MCP-1蛋白释放量的78%(P<0.05),对MCP-1; mRNA表达有明显抑制效果,抑制率达87%(P<0.05)。10; mumol/L的LPA可显著诱导HLF-1细胞c-Jun磷酸化,同时PKC抑制剂Bisindolylmaleimide I(1; mumol/L)可显著抑制LPA(10; mumol/L)诱导的HLF-1细胞c-Jun磷酸化。结论:PKC与JNK通路均参与LPA诱导HLF-1细胞MCP-1的表达。OBJECTIVE: To investigate the role of protein kinase C (PKC) and c-Jun; N-terminal kinase (JNK) in modulating lysophosphatidic acid; (LPA)-induced monocyte chemo-attractant protein-1 (MCP-1) expression in; human fetal lung fibroblasts (HLF-1). METHODS:Cultured human lung; fibroblasts (HLF-1) were incubated with LPA(0,1,3 and 10 mumol/L) for; 0.5,6,12 and 24 h. ELISA was used to detect MCP-1 protein levels in the; supernatants,and quantitative real-time PCR (qPCR) for MCP-1 mRNA levels; in the cell lysate. In addition,cells were pre-incubated with PKC; inhibitor bisindolylmaleimide I (0,0.1,1 and 10 mumol/L) or JNK; inhibitor SP600125 (0,0.1,1 and 10 mumol/L) for 30 min,and then treated; with LPA (10 mumol/L) for 2 or 6 h,and ELISA and qPCR assays were; conducted. Cells were also pre-incubated with PKC inhibitor; bisindolylmaleimide I (1 mumol/L) for 30 min,and then treated with LPA; (10 mumol/L) for 30 min. C-Jun N-terminal phosphorylation levels in the; cell lysate were measured by Western blot. RESULTS:LPA stimulated MCP-1; protein expression in dose-and time-dependent manners. The MCP-1 protein; production in the LPA (10 mumol/L) treated group was 2.4 times higher; than that in the untreated group (P<0.01). MCP-1 protein production in; the LPA (10 mumol/L) treated group for 24 h was 1 time higher than that; in the untreated group (P<0.01). LPA stimulated MCP-1 mRNA expression in; a time-dependent manner. The MCP-1 mRNA expression in the LPA (10; mumol/L) treated group for 2 h was 5.3 times higher than that in the; untreated group (P<0.01). PKC inhibitors bisindolylmaleimide I and JNK; SP600125 clearly inhibited LPA-induced MCP-l mRNA and protein; expressions. The LPA (10 mumol/L)-induced MCP-1 protein production was; reduced by 60% with bisindolylmaleimide I(1 mumol/L) compared with that; in the control group (P<0.05). With 3 mumol/L of bisindolylmaleimide; I,the induced MCP-1 mRNA expression was reduced by 40% (P<0.05). The LPA; (10 mumol/L)-induced MCP-1 protein production was reduced by 78% with; SP600125 (1 mumol/L) (P<0.05). The 10 mumol/L LPA-induced MCP-1 mRNA; expression was reduced by 40% with SP600125 (1 mumol/L) (P<0.05). The; activity of JNK was enhanced by LPA in HLF-1 while PKC inhibitors; bisindolylmaleimide I (1 mumol/L) suppressed the activity of JNK which; was induced by LPA(10 mumol/L). CONCLUSION:PKC and JNK mediated; LPA-induced MCP-1 expression in HLF-1.国家自然科学基金项目; 厦门大学中央高校基本业务费专项资金项目; 福建省自然科学基金青年项目; 福建省卫生系统中青年骨干人才培养项目;; 厦门市科技惠民计划项

慢病毒敲减质粒pLKO.1-hSRF的构建及鉴定

目的:构建敲减人血清反应因子SRF基因的慢病毒质粒,为进一步研究SRF在口腔鳞状细胞癌中的作用提供工具。方法:利用Thermo Fisher公司RNAi网站设计出针对SRF基因特异性敲减的片段,然后通过对pLKO.1载体进行双酶切,胶回收纯化后,经T4连接酶将双酶切线性化载体与设计的目的片段进行连接,转化和质粒提取,采用双酶切以及测序的方法对重组质粒进行序列鉴定。利用293T细胞对构建正确的pLKO.1-hSRF质粒进行病毒包装后感染SAS口腔鳞癌细胞,经嘌呤霉素筛选获得稳定株,并通过Western blot和实时荧光定量PCR对稳定转染细胞株的敲减效率进行验证。结果:构建出的慢病毒敲减质粒pLKO.1-hSRF经测序和酶切鉴定均正确,感染该慢病毒质粒的SAS细胞后,其SRF蛋白表达量和mRNA水平与对照组相比均显著下降(P<0.01)。结论:慢病毒敲减质粒pLKO.1-hSRF构建成功,获得SRF低表达的SAS细胞株。国家自然科学基金(81671001,81771079,207201);;福建省中青年骨干人才项目(2015-ZQN-ZD-35);;厦门医学院科研基金(K2015-06);;厦门市重大疾病联合攻关项目(3502Z20179051

虹鳟免疫诱导型基因Cathelicidin2启动子功能分析

本研究通过实时荧光定量PCR实验对虹鳟(Oncorhynchus mykiss)Cathelicidin2(Cath2)基因的转录模式进行了分析。结果显示,该基因在鳃、头肾等与机体免疫防御功能密切相关的组织内转录,在细菌和病毒感染后,转录水平均显著升高。对基因上游调控序列进行启动子和转录因子结合位点预测,发现该启动子具有真核生物典型的TATA盒和CAAT盒结构,基因上游直至第一内含子区域内,密集存在多个免疫相关转录因子结合位点,其中,2个核因子κB(Nuclear factor kappa B,NFκB)预测结合位点均位于核心启动子正链区域。在草鱼(Ctenopharyngodon idellus)肾组织细胞系内,绿色荧光蛋白和萤火虫荧光素酶基因都能够在该启动子驱动下表达,表明其具有启动子活性,且启动子活性在受到免疫诱导后增强,包括细菌脂多糖(Lipopolysaccharides,LPS)模拟的细菌感染和聚肌胞苷酸(Polyinosinic polycytidylic acid,Poly I:C)模拟的病毒感染。双荧光素酶报告基因检测显示,启动子活性在与NFκB转录因子表达时,增强至4.39倍,证明Cath2基因受NFκB通路调控。研究表明,虹鳟Cath2基因能够在多种免疫刺激诱导下表达,其启动子可以应用为免疫诱导型的基因工程元件,驱动外源免疫基因在鱼体内适时表达,抵御外界病原感染,同时,避免非必要条件下的过度表达形成生长负担。国家科技支撑计划项目(2015BAD25B01);;中国水产科学研究院基本科研业务费专项(2015C007)共同资助~

The effects of TGF-β and EGF signal on lysophosphatidic acid-induced human oral squamous cell carcinoma cell proliferation

目的:探讨转化生长因子(Tgf)及表皮生长因子(Egf)信号对溶血磷脂酸(lPA)诱导口腔鳞癌细胞增殖的影响。方法:口腔鳞癌SAS细胞接种于96孔板中,以含不同浓度(0、1、5和10μMOl/l)lPA的无血清dMEM分别处理细胞24和48 H后采用CCk-8法检测细胞增殖;免疫印迹检测10μMOl/l lPA分别处理细胞0、0.5、2和4 H后对Tgf-β下游信号分子SMAd2的影响;应用不同浓度(10、20和50μg/Ml)的Tgf-β阻断抗体1d11和100 nMOl/l Egfr阻断剂Ag1478分别预孵育细胞2和4 H后,再加入lPA诱导,检测SAS细胞增殖情况。结果:lPA呈剂量效应和时间效应诱导SAS细胞增殖,lPA浓度增加到10μMOl/l时SAS细胞数是对照组的近1.7倍(P<0.01),细胞在lPA处理24 H后增殖速率较对照组增加22%(<0.05)。lPA可活化Tgf-β,但Tgf-β阻断抗体1d11并不能阻断lPA诱导的SAS增殖;相反,Egfr阻断剂Ag1478能够抑制lPA诱导的SAS增殖,抑制率达到近77%。结论:lPA诱导的口腔鳞癌SAS细胞的增殖与Egfr活化信号有关,而与lPA诱导的Tgf-β活化无关。OBJECTIVE: To investigate the effects of transforming growth factor-β(TGF-β) activation and epidermal growth factor receptor(EGFR) transactivation on lysophosphatidic acid(LPA)-induced human oral squamous cell carcinoma(OSCC) SAS cell proliferation.METHODS:SAS cells were seeded in 96-well plates and treated with LPA(0,1,5 and 10 μmol/L) for 24 h and 48 h,and CCK-8 method was used to detect cell proliferation; Western blotting was used to detect the effect of LPA(10 μmol/L) on TGF-β activation by examining the expression of p-Smad2.Preincubation of SAS cells with TGF-β blocking antibody 1D11(10,20 and 50 μg/mL) and EGFR inhibitor AG1478(100 μmol/L) for 2 and 4 h were used to measure the effects of TGF-β activation and EGFR transactivation on LPA-induced SAS proliferation.RESULTS:LPA stimulated SAS cell proliferation in dose- and time-dependent manners.The cell number in LPA(10 μmol/L) treated group was 1.7 times higher than the number in untreated group(P<0.01).After 24 h incubation,the proliferation rate of LPA(10 μmol/L)treated group increased by 22% compared with the control group(P<0.05).LPA activated TGF-β.However,TGF-β blocking antibody 1D11 could not block LPA-induced SAS cell proliferation.In contrast,EGFR inhibitor AG1478 blocked LPA-induced SAS cell proliferation by 77%.CONCLUSION: LPA-induced SAS cell proliferation was dependent on EGFR transactivation and independent of TGF-β activation.国家自然科学基金(81370160;30900661;81072208); 教育部留学回国人员科研启动基金; 汕头大学医学院基础与临床科研基

Association of a single nucleotide polymorphism in 8q24 rs1530300 and nonsyndromic cleft lip with or without cleft palate in Guangdong

目的:探讨8Q24 rS1530300单核苷酸多态性(SnP)与广东籍汉族人群非综合征性唇腭裂(nSCl/P)的相关性。方法:收集广东籍nSCl/P患儿168名及健康对照者127名的外周血,提取基因组dnA,应用高分辨率熔解曲线(HrM)技术检测rS1530300位点基因多态性,采用卡方检验进行病例组及其父母与正常对照组基因型、等位基因频率的比较分析和传递不平衡(TdT)分析。结果:成功建立8Q24 rS1530300位点基因多态性检测方法。病例组及正常对照组8Q24 rS1530300位点基因型频率分布均符合HArdyWEInbErg平衡。病例组及其父母的rS1530300位点基因型和等位基因的分布频率与正常对照组比较差异均无统计学意义(P均>0.05),等位基因也不存在传递不平衡(P>0.05)。结论:8Q24 rS1530300位点多态性与中国广东人群nSCl/P无明显相关性。OBJECTIVE: To explore the association between nonsyndromic cleft lip with or without cleft palate(NSCL/P) and genetic polymorphism of 8q24 rs1530300 in Chinese Han population located in Guangdong province.METHODS:Blood samples from 168 NSCL/P patients and 127 unrelated healthy individuals of the Chinese Guangdong population were collected.DNA was extracted and high resolution melting(HRM) was used to identify single nucleotide polymorphism of rs 1530300 in all samples.Chi square test was used to analyze the genotype and allele distribution between case group,father group,mother group and control group.Transmission-disequilibrium test was also carried out.RESULTS:The method for genotyping 8q24 rs1530300 was set up.The genotypic distribution of rs1530300 in case and control group did not deviate from the Hardy-Weinberg equilibrium.There were no significant differences in the frequency distributions of both genotypes and alleles when case group,or father group,or mother group was compared with control group at the rs1530300(P>0.05).We found no evidence of allele transmission-disequilibrium at rs1530300 in cleft caseparent trios(P>0.05).CONCLUSION:In our study,the genetic polymorphism of 8q24 rs1530300 was not associated with the development of NSCL/P in Chinese Han population located in Guangdong province.“重生行动-全国贫困家庭唇腭裂儿童手术康复计划”项

鲑鳟通用型低通量单核苷酸多态性芯片的开发

为开发常见鲑鳟养殖物种通用的遗传分析工具,本研究利用Affymetrix虹鳟（Oncorhynchus mykiss） 57K高通量单核苷酸多态性（Single nucleotide polymorphism,SNP）芯片,对国内代表性鲑鳟养殖群体开展了分型检测,包括山女鳟（Oncorhynchus masou masou）、银鲑（Oncorhynchus kisutch）、美洲红点鲑（Salvelinus fontinalis）、白斑红点鲑（Salvelinus leucomaenis） 4个物种,从57,501个SNP标记中筛选出96个共享多态性标记,应用Fluigidm 96.96动态芯片平台,构建了大麻哈鱼属（Oncorhynchus）和红点鲑属（Salvelinus）通用型低通量SNP芯片。该芯片分型结果准确性较高,与Affymetrix高通量芯片分型一致性达到96.55%。使用该芯片对来自6个家系的48尾银鲑个体及其候选亲本进行检测,应用Cervus 3.0.7软件进行亲权鉴定,结果能够准确重现复杂家系的真实系谱。在用于单亲本亲权鉴定时,第一亲本非排除率（Non-exclusion probability for first parent, NE-1P）为4.120×10–4;用于双亲本亲权鉴定时,双亲非排除率（Non-exclusion probability for parent pair, NE-PP）低至6.219×10–12,表明该芯片在鲑鳟养殖群体系谱鉴定应用中具有较高的准确性。使用该芯片开展4个鲑鳟养殖群体遗传结构分析,样本分群聚类结果与其所属的分类阶元相符,能够准确反映群体遗传组分构成和遗传关系。本研究构建的低通量SNP芯片在常见鲑鳟养殖物种中具有良好的通用性,将其应用于养殖群体遗传分析,能够为鲑鳟制种、育种和引种等科学决策提供基因组信息参考。国家科技支撑计划项目(2015BAD25B01);;中国水产科学研究院基本科研业务费专项(2015C007)共同资助~

The expression and clinical relevance of integrin αvβ6 and JunB in oral squamous cell carcinoma

目的:探讨整合素αVβ6、Junb在口腔鳞癌组织中的表达及其临床意义。方法:采用免疫组化方法检测120例口腔鳞癌及15例口腔正常黏膜组织中整合素αVβ6和Junb的表达情况,并分析两者表达与口腔鳞癌患者临床病理指标及预后的关系。结果:整合素αVβ6表达于口腔鳞癌组织的细胞质和胞膜,而Junb定位在口腔鳞癌组织和口腔正常黏膜组织的细胞核内。整合素αVβ6、Junb在口腔鳞癌组织中的表达强度显著高于口腔正常黏膜组织(P<0.01)。整合素αVβ6在口腔鳞癌组织中的表达与浸润深度(T分期)、组织分化程度、是否有淋巴结转移(n分期)密切相关(P<0.05),而Junb在口腔鳞癌组织中的表达与浸润深度、是否有淋巴结转移密切相关(P<0.05)。单因素生存分析表明,整合素αVβ6高表达患者的预后较低表达的患者差(P=0.021)。COX回归多因素分析表明是否有淋巴结转移是影响患者预后的独立危险因素(P<0.05)。结论:整合素αVβ6和Junb在口腔鳞癌组织中表达增加,并与口腔鳞癌的浸润、转移密切相关;整合素αVβ6表达可作为判断口腔鳞癌患者预后判断的指标。OBJECTIVE:This study aimed to investigate the expression of integrin αvβ6 and JunB in oral squamous cell carcinoma(OSCC) and the correlation with clinicopathologic characteristics and prognosis.METHODS:The expression of integrin αvβ6 and JunB protein was detected with immunohistochemical staining assay in 120 cases of OSCC and 15 samples of normal oral mucosa.The correlation with clinicopathologic characteristics and prognosis of the patients were evaluated.RESULTS:Integrin αvβ6 was detected in both cytoplasm and cellular membrane of OSCC,but JunB protein was localized in the nuclei of both OSCC and normal oral mucous tissues.The expressions of integrin αvβ6 and JunB protein in OSCC were significantly higher than that in normal oral mucosa(P<0.01).The expression of integrin αvβ6 was positively related to depth of invasion(T stage),tumor differentiation degree and lymph node metastasis(N stage)(P<0.05).The expression of JunB was positively related to depth of invasion and lymph node metastasis(P<0.05).Survival as a single factor analysis revealed that patients with over-expression of integrin αvβ6 had a shorter overall survival(OC)(P=0.021).Through Cox multivariate regression analysis,lymph node metastasis(N stage) was an independent risk factor that affected the prognosis.CONCLUSION:The over-expressions of integrin αvβ6 and JunB were common in OSCC and closely correlated with tumor invasion and metastasis.Integrin αvβ6 may be used as a prognostic marker for therapy.国家自然科学基金项目(30900661;81072208;81370160); 中央高校基本业务费专项资金项目(厦门大学); 福建省医学创新科研项目(2014-CXB-47); 福建省自然科学基金青年项

鱿鱼顶骨β-甲壳素的化学反应活性及其与α-甲壳素的比较

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