山西马身猪及其杂交后代H-FABP基因的PCR-RFLP检测

运用PCR-RFLP法检测马身猪及其杂交后代H-FABP基因多态性。结果表明,马身猪在Hinf Ⅰ-RFLP位点上有HH和Hh两种基因型,在HaeⅢ-RFLP位点上只有DD基因型,在HinfⅠ*-RFLP位点上有BB和Bb两种基因型,等位基因以h、D、B占优势,其频率分别为0．958、1．000和0．968。其杂交后代在HaeⅢ-RFLP位点上只检测到两种基因型DD和Dd。     

Elastin overexpression by cell-based gene therapy preserves matrix and prevents cardiac dilation

After a myocardial infarction, thinning and expansion of the fibrotic scar contribute to progressive heart failure. The loss of elastin is a major contributor to adverse extracellular matrix remodelling of the infarcted heart, and restoration of the elastic properties of the infarct region can prevent ventricular dysfunction. We implanted cells genetically modified to overexpress elastin to re‐establish the elastic properties of the infarcted myocardium and prevent cardiac failure. A full‐length human elastin cDNA was cloned, subcloned into an adenoviral vector and then transduced into rat bone marrow stromal cells (BMSCs). In vitro studies showed that BMSCs expressed the elastin protein, which was deposited into the extracellular matrix. Transduced BMSCs were injected into the infarcted myocardium of adult rats. Control groups received either BMSCs transduced with the green fluorescent protein gene or medium alone. Elastin deposition in the infarcted myocardium was associated with preservation of myocardial tissue structural integrity (by birefringence of polarized light; P < 0.05 versus controls). As a result, infarct scar thickness and diastolic compliance were maintained and infarct expansion was prevented (P < 0.05 versus controls). Over a 9‐week period, rats implanted with BMSCs demonstrated better cardiac function than medium controls; however, rats receiving BMSCs overexpressing elastin showed the greatest functional improvement (P < 0.01). Overexpression of elastin in the infarcted heart preserved the elastic structure of the extracellular matrix, which, in turn, preserved diastolic function, prevented ventricular dilation and preserved cardiac function. This cell‐based gene therapy provides a new approach to cardiac regeneration.     

Targeted overexpression of inducible 6-phosphofructo-2-kinase in adipose tissue increases fat deposition but protects against diet-induced insulin resistance and inflammatory responses

Increasing evidence demonstrates the dissociation of fat deposition, the inflammatory response, and insulin resistance in the development of obesity-related metabolic diseases. As a regulatory enzyme of glycolysis, inducible 6-phosphofructo-2-kinase (iPFK2, encoded by PFKFB3) protects against diet-induced adipose tissue inflammatory response and systemic insulin resistance independently of adiposity. Using aP2-PFKFB3 transgenic (Tg) mice, we explored the ability of targeted adipocyte PFKFB3/iPFK2 overexpression to modulate diet-induced inflammatory responses and insulin resistance arising from fat deposition in both adipose and liver tissues. Compared with wild-type littermates (controls) on a high fat diet (HFD), Tg mice exhibited increased adiposity, decreased adipose inflammatory response, and improved insulin sensitivity. In a parallel pattern, HFD-fed Tg mice showed increased hepatic steatosis, decreased liver inflammatory response, and improved liver insulin sensitivity compared with controls. In both adipose and liver tissues, increased fat deposition was associated with lipid profile alterations characterized by an increase in palmitoleate. Additionally, plasma lipid profiles also displayed an increase in palmitoleate in HFD-Tg mice compared with controls. In cultured 3T3-L1 adipocytes, overexpression of PFKFB3/iPFK2 recapitulated metabolic and inflammatory changes observed in adipose tissue of Tg mice. Upon treatment with conditioned medium from iPFK2-overexpressing adipocytes, mouse primary hepatocytes displayed metabolic and inflammatory responses that were similar to those observed in livers of Tg mice. Together, these data demonstrate a unique role for PFKFB3/iPFK2 in adipocytes with regard to diet-induced inflammatory responses in both adipose and liver tissues.     

Expressions and purification of a mature form of recombinant human Chemerin in Escherichia coli

Chemerin is a novel chemokine that binds to the G protein-coupled receptor (GPCR) ChemR23, also known as chemokine-like receptor 1 (CMKLR1). It is secreted as a precursor and executes pro-inflammatory functions when the last six amino acids are removed from its C-terminus by serine proteases. After maturation, Chemerin attracts dendritic cells and macrophages through binding to ChemR23. We report a new method for expression and purification of mature recombinant human Chemerin (rhChemerin) using a prokaryotic system. After being expressed in bacteria, rhChemerin in inclusion bodies was denatured using 6 M guanidine chloride. Soluble rhChemerin was prepared by the protein-specific renaturation solution under defined conditions. It was subsequently purified using ion-exchange columns to more than 95% purity with endotoxin level <1.0 EU/μg. We further demonstrated its biological activities for attracting migration of human dendritic cells and murine macrophages in vitro using established chemotaxis assays.     

A catalogue of Burmite inclusions

Burmite (Burmese amber) from the Hukawng Valley in northern Myanmar is a remarkable valuable and obviously the most important amber for studying terrestrial diversity in the mid-Cretaceous.The diversity of Burmite inclusions is very high and many new taxa were found,including new order,new family/subfamily,and new genus.Till the end of 2016,14 phyla,21 classes,65 orders,279 families,515 genera and 643 species of organisms are recorded,which are summized and complied in this catalogue.Among them,587 species are arthropods.In addtion,the specimens which can not be identified into species are also listed in the paper.The information on type specimens,other materials,host and deposition of types are provided.     

美常安治疗老年人抗生素相关性腹泻的疗效观察

目的:观察美常安治疗老年人抗生素相关性腹泻的疗效.方法:将79例老年人抗生素相关性腹泻患者随机分为2组,对照组为常规治疗,治疗组在常规治疗的基础上加用美常安治疗.结果:治疗组患者的总有效率明显高于对照组,2组有显著差异(P＜0.05).结论:美常安治疗老年人抗生素相关性腹泻疗效显著.     

不同光强对吴茱萸生长动态和光合日变化的影响

报道了不同生长光强(透光率分别为15%、30%、50%、100%)对吴茱萸的生长和光合日变化的影响。结果表明:生长环境光强对吴茱萸苗期株高、地径和冠面积的影响较大,100%RI下的株高、地径和冠面积明显小于各遮荫处理,其中30%RI下吴茱萸的株高、地径和冠面积最大,这表明苗期强光不利于吴茱萸的生长。随着光强的减弱,吴茱萸增大冠面积与株高有利于截获更多光能。10月下旬,100%RI下吴茱萸净光合速率(Pn)日变化曲线呈"双峰型",11:30～14:30,吴茱萸的Pn、胞间二氧化碳浓度与气孔导度均下降,表明此时的光合午休现象是由气孔部分关闭造成的。各遮荫处理下,吴茱萸的Pn日变化均呈"单峰型",并无第二峰的出现,可能与遮荫条件下,下午光强较弱,环境温度较高,空气相对湿度较低有关。     

莳萝蒿适应盐渍环境的Na~+区域化方式和生理特征

莳萝蒿是广泛分布在我国北方的一种特殊类型的菊科盐生植物,阐明莳萝蒿特殊的耐盐机制和生理特征有助于丰富植物抗盐性研究的内容。用0、100、200、300、400 mmol/L Na Cl处理莳萝蒿7 d后,比较莳萝蒿盐处理植株与对照植株在生长和生理方面的差异,并详细分析了Na+在莳萝蒿体内的积累水平和区域化方式。结果显示:莳萝蒿虽然能够耐受400 mmol/L Na Cl,但盐处理显著抑制了莳萝蒿的生长,整株鲜重随着盐处理浓度的升高逐渐减小。在水分生理方面,随着盐处理浓度的升高,莳萝蒿叶片细胞的渗透调节能力逐渐增强,其叶片肉质化程度却呈逐渐降低的趋势。分析盐处理对光合作用的影响发现,盐处理后莳萝蒿叶片光合速率与气孔导度显著下降,而其PSⅡ光化学活性并未受到抑制,叶绿素含量甚至逐渐增大,说明盐处理后莳萝蒿叶片光合速率的降低主要是由于气孔因素造成的,而不是由于光合结构被破坏。莳萝蒿体内的Na+含量随着盐处理浓度的升高显著增加,400 mmol/L Na Cl条件下叶、茎、根中的Na+含量分别高达321.4、242.1和182.3μmol/g鲜重;莳萝蒿体内的Na+70%以上积累在叶片内,而叶片内98%左右的Na+积累在叶片原生质体中,叶片原生质体中的Na+平均浓度是质外体1.2—1.8倍,推测其叶片细胞内存在着有效的Na+区域化机制。盐处理后莳萝蒿叶片液泡膜V-H+-ATPase的质子泵活性比对照增加了30%—50%,液泡膜Na+/H+逆向转运活性则增加至对照的4—7倍,进一步证实莳萝蒿叶片具有较强的液泡Na+区域化能力。随着盐处理浓度的升高,Na+在叶片中的分布比例相对减少,V-H+-ATPase的质子泵活性和Na+/H+逆向转运活性增幅也减缓。这种Na+区域化能力使莳萝蒿获得了较强的耐盐性,有效保护了其光系统,降低了细胞汁液渗透势。但是盐处理后这种耐盐方式并不能阻止莳萝蒿叶片肉质化程度和光合活性下降,莳萝蒿生长仍然受盐抑制,说明Na+区域化是莳萝蒿适应盐渍环境的必要条件而非充分条件。