经济全球化促进了跨境贸易的发展,跨境电商产业蕴含着巨大的发展机遇,但人才市场缺口较大.民办高校是培养应用型、技能型人才的重要教学机构,是为跨境电商输送创新创业人才的重要途径.该文以民办高校跨境电商创新创业人才孵化基地建设为研究对象,探讨民办高校孵化基地对跨境电商学科建设、人才培养、校企合作等方面的意义,分析民办高校跨境电商孵化基地的建设现状,提出跨境电商孵化基地建设的措施,以促进民办高校跨境电商人才的培养,满足市场的人才需求.

Thrombomodulin (TM) functions in coagulation, fibrinolysis and inflammation by its cofactor activity for protein C, thrombin-activatable fibrinolysis inhibitor (TAFI) activation and high mobility group box 1 (HMGB1) degradation induced by thrombin. It has been widely reported that mutations in TM are related to thromboembolic diseases but hardly in lectin domain. Here we report our findings about the functional deficiencies in TM caused by substitution of aspartate with tyrosine at residue 126. Three patients suffering from recurrent thromboembolic diseases were identified with this mutation and their plasma soluble TM levels were decreased. Transfected cells expressing wild-type TM or the variant and corresponding proteins were used to examine TM functions in vitro. The cofactor activity of the mutant for protein C, TAFI activation was reduced to approximately 50% and 60% respectively. Loss in anti-inflammation due to weakened HMGB1 degradation was also observed. And the study with thrombosis models of mice suggested the decreased inhibition of thrombus development of the mutant. Together the results showed deleterious changes on TM function caused by this mutation, which may explain the thrombophilia tendency of the patients. This work provided supportive evidence that mutation in lectin domain of TM might be related to thrombotic diseases and may help us better understand the physiological roles of TM.

Plasma levels of the anticoagulant cofactor protein S and PROS1 mutation are reported to impart increased risk of thromboembolism in European and south east Asian populations, but the relationship is not yet documented in Han Chinese in population-based study. Therefore, we undertook a case-control study of this relationship among patients with venous thromboembolism, and probed the genetic factors contributing to low protein S deficiency. Among the 603 consecutively recruited venous thromboembolism patients, 51 (8.5%) proved to be deficient in free protein S antigen (lower than 38.6 U/dl), among whom 30 cases were identified to have a causative mutation by direct sequencing. In contrast, six cases (1.0%) of the 584 healthy controls had low free antigen levels, among whom direct sequencing confirmed disease-causing gene mutations in four controls (0.7%). After adjusting for age and gender, the odds ratio of developing venous thromboembolism in individuals with protein S deficiency based on free protein S tests was 8.1 (95% CI = 3.6-19.9, P < 0.001). Gene sequencing yielded 24 different heterozygous mutations in the 34 participants, of which 13 were newly described. 17 (50%) of the 34 mutations in our study cohort occurred in exons 12 and 13, indicating the LGR2 domain to be a hotspot mutation region for the protein. These findings are conducive to the clinical application of protein S assays for the molecular diagnosis of thrombophilia.

The invention discloses a thrombus and hemorrhagic disease gene diagnosis method. All currently known 156 related genes which directly or indirectly influence blood coagulation can be comprehensivelyand systematically analyzed at a time, and key points can be placed in areas, closely related to diseases, in human genomes to find out pathogenic mutations. Most of gene variations such as point mutation, small fragment and large fragment insertion and deletion, copy number change and the like are widely screened, covered and mutated for genes involved in a blood coagulation factor system, a platelet system, a fibrinolytic system, an endothelial system, an inflammatory system, a metabolic system and an anticoagulation system at a time. Compared with other popular whole-genome sequencing technologies at present, the method is superior to whole-genome sequencing in indexes such as thrombus-related target area coverage, effective data volume, capture efficiency data utilization rate, averagesequencing depth and repetition rate, and can effectively improve the diagnosis rate of thrombotic diseases and hemorrhagic diseases.

作为组织创新和竞争优势的主要来源,创造力在近年来受到了学者们的广泛关注.然而,作为重要的组织环境因素,高绩效人力资源实践对个体创造力的影响机制却并未得到充分认识.通过对466名企业员工为样本进行问卷调查,探讨了高绩效人力资源实践对个体创造力的影响及其作用机制.结果 表明,高绩效人力资源实践能够促进员工个体创造力的提升,这种作用受到要求-能力匹配和需要-供给匹配的并行中介作用,同时会因个体特征表现出差异.对于高模糊容忍性的个体而言,高绩效人力资源实践对创造力的促进作用会更强;而对低模糊容忍性的个体而言,高绩效人力资源实践对创造力的影响则十分有限.

基于相对剥削理论和自我分类理论,考察了员工资质过高感对组织公民行为的影响机制.通过对110个团队的433份员工的调查数据进行分析,结果表明:员工的资质过高感与其组织公民行为显著负相关;内部人身份感知中介了资质过高感与员工组织公民行为的关系;团队资质过高感知调节员工资质过高感与内部人身份感知的负向关系.具体而言,当团队资质过高感知较高时,员工资质过高感与内部人身份感知变为正相关;团队资质过高感知调节内部人身份感知对资质过高感与组织公民行为之间关系的中介作用.

This study aimed to explore the mechanism of a novel mutation (p.Lys38Glu) in apolipoprotein H (APOH) gene causing hereditary beta2-glycoprotein I (β2GPI) deficiency and thrombosis in a proband with thrombophilia. The plasma level of β2GPI was measured by ELISA and Western blotting, and anti-β2GPI antibody by ELISA. Lupus anticoagulant (LA) was assayed using the dilute Russell viper venom time. Deficiency of the major natural anticoagulants including protein C (PC), protein S (PS), antithrombin (AT) and thrombomodulin (TM) was excluded from the proband. A mutation analysis was performed by amplification and sequencing of the APOH gene. Wild type and mutant (c.112A>G) APOH expression plasmids were constructed and transfected into HEK293T cells. The results showed that the thrombin generation capacity of the proband was higher than that of the other family members. Missense mutation p.Lys38Glu in APOH gene and LA coexisted in the proband. The mutation led to β2GPI deficiency and thrombosis by impairing the protein production and inhibiting the platelet aggregation. It was concluded that the recurrent thrombosis of the proband is associated with the coexistence of p.Lys38Glu mutation in APOH gene and LA in plasma.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">基于面子理论,本研究探讨了员工资质过高感与个体创造力的关系,并验证能力面子压力的中介作用和集体主义氛围对二者的调节作用。通过对92个团队379名企业员工进行配对问卷调查,统计分析结果表明,员工资质过高感与个体创造力呈U型关系,能力面子压力在二者之间起中介作用,集体主义氛围调节员工资质过高感与能力面子压力的U型关系。具体而言,相比低水平的集体主义氛围,当团队为高集体主义氛围时,在员工资质过高感与能力面子压力的负向关系和正向关系均更强。</span>

Objective To observe the expressions of leptin,insulin-like growth factor-1 (IGF-1),and insulin-like growth factorbinding protein-3 (IGFBP-3) in serum of postmenopausal women with osteoporosis,explore the clinical significance. Methods Sixty postmenopausal women with osteoporosis (observation group) were divided into non-fracture group (34 cases) and fracture group (26 cases) according to complicating with fracture or not. During the same period,40 postmenopausal women without osteoporosis were selected as control group. ELISA was used to detect the expression levels of serum leptin,IGF-1,ad IGFBP-3 in the three groups. Body mass density (BMD) detection equipment was used to detect BMD values of lumbar vertebra (L1-L4),femoral neck,and Wards triangle area in the three groups. The detection results were compared. The correlations between serum leptin,IGF-1,IGFBP-3 and BMD were analyzed. Results The expression levels of serum leptin,IGF-1,and IGFBP-3 in observation group were statistically significantly lower than those in control group (P＜0. 05). The expression levels of serum leptin,IGF-1,IGFBP-3 and BMD in fracture group were statistically significantly lower than those in non-fracture group (P＜0. 05). There were positive correlations among the four indexes (leptin,IGF-1, IGFBP-3,and BMD) (P＜0. 05). Conclusion Serum leptin,IGF-1,and IGFBP-3 can be used as sensitive laboratory indicators for early diagnosis of postmenopausal women with osteoporosis and assessment of the severity.

OBJECTIVES:To investigate the association between thrombomodulin c.1418C>T polymorphism and venous thrombosis.METHODS:Systematic searches of Pubmed, EMBASE, Chinese Biomedical Database, Chinese National Knowledge Infrastructure, the VIP Database and WANFANG Database were performed. Pooled odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated to assess the strength of the association. Subgroup analysis was conducted to seek for potential sources of heterogeneity.RESULTS:A total of 8 studies were collected in our analysis, including 2519 cases and 3196 controls. No significant association between thrombomodulin c.1418C>T polymorphism and venous thrombosis was shown under the five genetic models (T vs C: OR=1.02, 95% CI=0.82-1.26; TT vs CC: OR=0.90, 95% CI=0.52-1.56; CT vs CC: OR=1.07, 95% CI=0.84-1.37; CT+TT vs CC: OR=1.05, 95% CI=0.82-1.34; TT vs CT+CC: OR=0.81, 95% CI=0.59-1.11). Similar results were observed in the following subgroup analysis based on ethnicity and source of control. However, an increased risk of venous thrombosis was found in Asian populations under three genetic models (T vs C: OR=1.31, 95% CI=1.01-1.70; CT vs CC: OR=1.41, 95% CI=1.00-2.98; TT+CT vs CC vs CC: OR=1.41, 95% CI=1.02-1.95).CONCLUSION:Current studies on the thrombomodulin c.1418C>T polymorphism are of great heterogeneity. It might not be a risk factor for venous thromboembolism.

Despite the essential anticoagulant function of antithrombin and the high risk of thrombosis associated with its deficiency, the prevalence of antithrombin deficiency among patients with venous thromboembolism (VTE) is very low. However, increasing evidence suggests that antithrombin deficiency may be underestimated. The analysis of SERPINC1, the gene encoding antithrombin, in 1,304 consecutive Chinese VTE patients and 1,334 healthy controls revealed a hotspot involving residues 294 and 295 that severely increases the risk of VTE. We detected the c.883G > A (p. Val295Met) (rs201381904) mutation in 11 patients and just one control (OR = 13.6; 95% CI: 1.7-107.1); c.881G > T (p.Arg294Leu) (rs587776397) in six patients but no controls; and c.880C > T (p. Arg294Cys) (rs747142328) in two patients but no controls. In addition, c.881G > A (p. Arg294His) (rs587776397) was identified in one control. These mutations were absent in a Caucasian cohort. Carriers of these mutations had normal antithrombin levels and anticoagulant activity, consistent with results obtained in a recombinant model. However, mutation carriers had a significantly increased endogenous thrombin potential. Our results suggest the existence in the Chinese population of a hotspot in SERPINC1 that significantly increases the risk of VTE by impairing the anticoagulant capacity of the hemostatic system. This effect is not revealed by current antigen or in vitro functional antithrombin assays.

Researchers have found that high-performance human resource practices (HPHRP) are positively related to good firm performance and sustainable competitive advantage; however, there is not substantial evidence about their effect on individual creativity. We examined the relationship between HPHRP and individual creativity with a sample of 466 employees of high-tech industries in China. Findings showed that HPHRP had an inverse U-shaped relationship with individual creativity, which was positively moderated by proactive personality. When the employee had a very proactive personality, the positive relationship between human resource practices that were not high performance and individual creativity, and the negative relationship between HPHRP and individual creativity escalated. Evidence also supported a mediation effect of intrinsic motivation on the interaction effect of HPHRP, proactive personality, and individual creativity.

目的:探讨PROS1 5'非翻译区基因多态性c.-190C＞G和c.-189G＞C以及血浆蛋白S(PS)水平与华中地区静脉血栓栓塞症(VTE)的关系.方法:采用病例-对照研究,收集湖北省血栓与止血临床研究中心VTE患者外周血标本1 304例,收集与病例组年龄、性别相对应且无动静脉血栓栓塞病史的正常人外周血标本1 334例.提取全血基因组DNA,PCR扩增目的片段,采用限制性内切酶BsoBI酶切鉴定并测序验证,比较2组间PROS1 c.-190C＞G与c.-189G＞C突变的CC、CG、GG基因型比例.采用ELISA法测定血浆中游离PS抗原水平,对比突变型与野生型有无差异.结果:PROS1 c.-190C＞G等位基因G在病例组中发生率为1.34％,与对照组相比,OR=1.44(0.86-2.41,P=0.17),PROS1 c.-189G＞C等位基因C在病例组中发生率为0.31％,与对照组相比,OR=1.64(0.54-5.02,P=0.38).因此,PROS1的基因多态性c.-190C＞G及c.-189G＞C在病例组与对照组比较差异无统计学意义,2种突变型血浆游离PS抗原水平与野生型比较差异也无统计学意义(P＞0.05).结论:PROS1 5非编码区的基因多态性c.-190C＞G与c.-189G＞C可能不是华中地区VTE的危险因素.未来还需扩大样本量对PS缺乏的VTE患者进行更深入的研究.

目的:冠状动脉疾病(CAD)是威胁人类健康的主要疾病之一.血小板的活化及其与细胞外基质的粘附在CAD的发生、发展中发挥重要的作用.GPVI基因编码的GPα2β1是一种血小板膜蛋白,通过Ca2+离子通道传导信号引起血小板聚集而形成血栓.湖北地区汉族人群中关于CAD易感基因的分子特征尚不明确.因此,我们开展了编码GPα2β1血小板膜蛋白的GPVI基因与CAD易感性的相关研究.方法:将102例CAD患者GPVI基因的启动子区、外显子区、剪切区及非翻译区进行重测序,查找引起CAD的致病突变;采用病例-对照研究评价c.940C＞G(p.Pro314Ala)突变对CAD发生风险的优势比;并用生物信息学工具评价c.430G＞A(p.Ala144Thr),c.655C＞T(p.Pro219Ser),c.940C＞G(p.Pro314Ala)突变的危害性.结果:本研究发现,GPVIc·940C＞G(p.Pro314Ala)与CAD不存在明显的相关性(OR=0.984,95％CI 0.746-1.298,P=0.908 94).结论:本研究发现存在于湖北地区汉族人群中GPVI基因突变体c.940C＞G(p.Pro314Ala)可能不是导致CAD患病风险增加的遗传学因素.

绩效考核目的取向不仅是组织绩效考核过程能够得以顺利实施的关键,还是员工态度及行为的重要影响因素。目前,国内外关于绩效考核目的取向对员工工作卷入的影响还缺乏系统研究。本文通过问卷调查、数据分析等实证研究方法,对来自421位员工的数据进行分析,剖析了绩效考核目的取向对员工工作卷入的影响及其影响机制,结果表明:评估型绩效考核对员工工作卷入、内在激励均具有显著负向影响;发展型绩效考核对员工工作卷入、内在激励均具有显著正向影响;内在激励在绩效考核目的取向与员工工作卷入之间具有部分中介作用;而自主性倾向在绩效考核目的取向与内在激励之间不具有调节作用。

With the development of information technology, sharing economy emerged and showed a strong lifeblood. However, theoretical research is far behind the practical application. Based on the perspective of Transaction Cost Theory, a supply-demand framework of sharing economy was built to lead a more clear understanding of the nature of sharing economy. Findings showed that values created by sharing platform root in their ability to reduce transaction cost among users, which depends on the number of users. Through attracting more people to become their users, sharing platforms make the value they created come into reality. And by taking a commission on transactions among users, platforms distribute the benefit of the value created between themselves and their users. Monopoly sharing platform can maximize value creation, but the commission it takes can result in a low economic efficiency, which calls for a regulation of government. The complex relationship between platforms and their users also provides new challenges to the management of platform's users and the formulation of public policy. These understanding provides references for sharing platform managers and policy makers, and some future directions were proposed.

Hemophilia B (HB) is an X-linked recessive bleeding disorder caused by mutations in the coagulation factor IX (FIX) gene. Genotyping patients with HB is essential for genetic counseling and provides useful information for patient management. In this study, the F9 gene from 23 patients with HB was analyzed by direct sequencing. Nineteen point mutations were identified, including a novel missense variant (c.520G > C, p.Val174Leu) in a patient with severe HB and a previously unreported homozygous missense mutation (c.571C > T, p.Arg191Cys) in a female patient with mild HB. Two large F9 gene deletions with defined breakpoints (g.10413_11363del, g.12163_23369del) were identified in two patients with severe HB using a primer walking strategy followed by sequencing. The flanking regions of the two breakpoints revealed recombination-associated elements (repetitive elements, non-B conformation forming motifs) with a 5-bp microhomology in the breakpoint junction of g.12163_23369del. These findings imply that non-homologous end joining and microhomology-mediated break-induced replication are the putative mechanisms for the deletions of the F9 gene. Because the g.12163_23369del deletion caused exons to be absent without a frameshift mutation occurring, a smaller FIX protein was observed in western blot analyses.

During the past decades, many novel agents have improved response and survival of patients with multiple myeloma. Nevertheless, it remains challenging when they suffer relapsing. Thus, novel therapeutic agents are needed. We aimed to assess the efficacy and safety of a novel agent panobinostat for patients with relapsed or/and refractory MM. A systematic literature review identified studies for clinical trials about panobinostat in patients with relapsed or/and refractory MM. We searched studies published between January 2000 and December 2015 in Pubmed, Ovid, EBSCO and the Cochrane library. Random-effect pooled estimates were calculated for overall response rate and rates of common adverse effects. The results showed 11 clinical trials including 700 patients with relapsed or/and refractory MM treated with panobinostat were identified. The ORR varied between 0.08 and 0.67. Pooled analyses showed the results that the ORR was 0.45 (95% CI: 0.31–0.59, I 2 = 90.5%, P = 0.000) for panobinostat combined with any other kind of drugs. The most common Grade3/4 adverse effects were thrombocytopenia, neutropenia, lymphopenia, anemia, diarrhea, fatigue, nausea and so on. In conclusion, based on our analyses, the regimen of panobinostat combining with other agents seems to be well tolerated and efficacious in patients with relapsed or/and refractory MM.

Exposure to air pollution has been linked to cardiovascular and respiratory disorders. However, the effect of air pollution on venous thrombotic disorders is uncertain. We performed a meta-analysis to assess the association between air pollution and venous thrombosis. PubMed, Embase, EBM Reviews, Healthstar, Global Health, Nursing Database, and Web of Science were searched for citations on air pollutants (carbon monoxide, sulfur dioxide, nitrogen dioxide, ozone, and particulate matters) and venous thrombosis. Using a random-effects model, overall risk estimates were derived for each increment of 10 μg/m3 of pollutant concentration. Of the 485 in-depth reviewed studies, 8 citations, involving approximately 700,000 events, fulfilled the inclusion criteria. All the main air pollutants analyzed were not associated with an increased risk of venous thrombosis (OR = 1.005, 95% CI = 0.998–1.012 for PM2.5; OR = 0.995, 95% CI = 0.984–1.007 for PM10; OR = 1.006, 95% CI = 0.994–1.019 for NO2). Based on exposure period and thrombosis location, additional subgroup analyses provided results comparable with those of the overall analyses. There was no evidence of publication bias. Therefore, this meta analysis does not suggest the possible role of air pollution as risk factor for venous thrombosis in general population.

We empirically explored how creative self-efficacy acts as a mediator in the relationship between knowledge sharing and employee innovation and examined the moderating effects of job satisfaction on this relationship. Matched supervisor–subordinate pairs (N = 274) completed a survey. First, subordinates completed measures of their knowledge sharing, creative self-efficacy, and innovation. Then, the supervisors of these employees assessed their subordinates' responses in terms of innovation. Results showed that knowledge sharing and creative self-efficacy were positively related to employee innovation and that creative self-efficacy mediated the effects of both knowledge sharing and innovation. Finally, job satisfaction enhanced the relationship between creative self-efficacy and employee innovation. We have extended the existing research on individual innovation and we suggest several managerial implications in line with this.