银川市冬、春季大气PM2.5中12种元素浓度差异及来源分析

目的 通过对银川市空气污染高发的冬、春季大气PM2.5中12种元素含量进行分析,研究冬、春季空气污染物来源特点,为银川市空气污染治理提供针对性的建议。方法 2017年11月至2018年5月每月定期采集大气PM2.5,采用称重法和电感耦合等离子质谱法测定大气PM2.5及其12种元素的质量浓度,分析季节差异,采用富集因子分析和主成分分析判断污染物来源。结果 银川市冬季大气PM2.5浓度及元素Pb和Tl的浓度分别为77μg/m3和50.40ng/m3、0.71ng/m3,显著高于春季,存在统计学差异,P＜0.05。无论冬、春季,元素Sb、Cd、Hg、Pb、Se和Tl的富集程度均较高,且主成分分析显示这些元素载荷较大,主要来自人为源,如燃料的燃烧、交通源、工业源和垃圾燃烧等。结论 银川市冬季大气污染较春季严重,冬季与春季有共同的污染物来源,但冬季受供暖的影响,污染较春季严重。     

速效救心丸治疗心肌缺血疾病的网络药理学研究

目的：借助网络药理学分析方法,研究速效救心丸主要活性成分对心肌缺血疾病的网络调控作用。方法：预测速效救心丸中生物利用度较好的化合物,整合PharmMapper和Mas等公共数据库提供的成分、靶点、通路信息,使用Cytoscape 3.1.0软件构建速效救心丸成分-靶点-通路的药理学网络。运用蛋白互作分析、子簇聚类算法和功能富集分析,来发现蛋白互作网络中的功能模块及其所参与的生物学过程。结果：速效 救心丸的化学成分-靶点-通路网络图包括145个点和374条边。MCODE算法提取出得分≥3的5个子簇经功能富集分析（BinGo）显示,这5个子簇参与的生物学过程主要有：脂质和固醇荷尔蒙的相关代谢、谷胱甘肽和氨 基酸的相关代谢、炎症反应和免疫功能、心肌功能和能量供应及血压调节等方面。结论：本研究运用网络药理学的方法和技术,从分子网络层面阐释了速效救心丸主要活性成分通过调节心脏能量供应、脂质紊乱、免疫反 应等方面发挥了多成分、多靶点、多途径相互协同治疗疾病的机制。     

基于PPI网络预测和验证结直肠癌相关Hub基因

目的:通过PPI网络分析确定CRC相关Hub基因,为CRC靶向治疗提供一定参考。方法:从OpenTargets数据库获得CRC相关基因,使用Metascape对基因集进行富集分析,确定基因集富集术语。采用STRING数据库及CytoScape构建PPI网络,采用MCODE寻找PPI网络中的功能模块（子网）。根据功能模块中节点的网络属性确定Hub基因,通过文献法和GEPIA数据库对Hub基因进行验证。结果:共得到CXCL8、ERBB2、CYCS 3个Hub基因,它们均与CRC的发生和发展有一定关系,。它们均在CRC组织与正常组织中存在差异表达,并与CRC患者的总体生存时间相关。结论:基于PPI的网络分析可准确预测CRC相关Hub基因和为CRC靶向治疗提供参考。     

Gene set enrichment ensemble using fold change data only

In a number of biological studies, the raw gene expression data are not usually published due to different causes, such as data privacy and patent rights. Instead, significant gene lists with fold change values are usually provided in most studies. However, due to variations in data sources and profiling conditions, only a small number of common significant genes could be found among similar studies. Moreover, traditional gene set based analyses that consider these genes have not taken into account the fold change values, which may be important to distinguish between the different levels of significance of the genes. Human embryonic stem cell derived cardiomyocytes (hESC-CM) is a good representative of this category. hESC-CMs, with its role as a potentially unlimited source of human heart cells for regenerative medicine, have attracted the attentions of biological and medical researchers. Because of the difficulty of acquiring data and the resulting expenses, there are only a few related hESC-CM studies and few hESC-CM gene expression data are provided. In view of these challenges, we propose a new Gene Set Enrichment Ensemble (GSEE) approach to perform gene set based analysis on individual studies based on significant up-regulated gene lists with fold change data only. Our approach provides both explicit and implicit ways to utilize the fold change data, in order to make full use of scarce data. We validate our approach with hESC-CM data and fetal heart data, respectively. Experimental results on significant gene lists from different studies illustrate the effectiveness of our proposed approach.     

Altering BDNF expression by genetics and/or environment: Impact for emotional and depression-like behaviour in laboratory mice

According to the “neurotrophin hypothesis”, brain-derived neurotrophic factor (BDNF) is an important candidate gene in depression. Moreover, environmental stress is known to represent a risk factor in the pathophysiology and treatment of this disease.To elucidate, whether changes of BDNF availability signify cause or consequence of depressive-like alterations, it is essential to look for endophenotypes under distinct genetic conditions (e.g. altered BDNF expression). Furthermore it is crucial to examine environment-driven BDNF regulation and its effect on depressive-linked features. Consequently, gene × environment studies investigating prospective genetic mouse models of depression in different environmental contexts become increasingly important.The present review summarizes recent findings in BDNF-mutant mice, which have been controversially discussed as models of depression and anxiety. It furthermore illustrates the potential of environment to serve as naturalistic stressor with the potential to modulate the phenotype in wildtype and mutant mice. Moreover, environment may exert protective effects by regulating BDNF levels as attributed to “environmental enrichment”. The effect of this beneficial condition will also be discussed with regard to probable “curative/therapeutic” approaches.     

富血小板血浆制备套装的评估研究

目的通过分析富血小板血浆(platelet-rich plasma,PRP)中血小板、白细胞和生长因子的浓度,计算回收率和富集系数,并做相关性分析,探讨PRP制备套装的实用性和稳定性。方法取30例符合纳入标准的自愿者自愿捐赠的外周血各40mL,应用山东威高集团医用高分子制品股份有限公司的PRP制备套装制备PRP各4mL。全自动血液分析仪计数全血和PRP中血小板和白细胞浓度,并计算血小板或白细胞回收率及富集系数;并分别测定男、女自愿者血小板及白细胞浓度。ELISA法定量分析激活后全血及PRP中PDGF、TGF-β、VEGF的浓度。结果全血和PRP中血小板浓度分别为(131.40±29.44)×109/L和(819.47±136.32)×109/L,比较差异有统计学意义(t=—27.020,P=0.000);PRP中血小板回收率为60.85%±8.97%,富集系数为6.40±1.06。全血和PRP中白细胞浓度分别为(5.57±1.91)×1012/L和(32.20±10.42)×1012/L,比较差异有统计学意义(t=—13.780,P=0.000);PRP中白细胞回收率为58.30%±19.24%,富集系数为6.10±1.93。PRP中血小板浓度和白细胞浓度分别与全血中血小板浓度(r=0.652,P=0.000)和白细胞浓度(r=0.460,P=0.011)成正相关。男性组和女性组PRP中血小板浓度和白细胞浓度比较差异均无统计学意义(P>0.05)。PRP中PDGF、TGF-β、VEGF浓度分别为(698.15±64.48)、(681.36±65.90)、(1071.55±106.04)ng/mL,是全血的(5.67±1.18)、(6.99±0.61)、(5.74±0.83)倍。PRP中PDGF浓度(r=0.832,P=0.020)、TGF-β浓度(r=0.835,P=0.019)、VEGF浓度(r=0.824,P=0.023)均与PRP中血小板浓度成正相关。结论 PRP制备套装可以稳定地制备出富含高浓度血小板、白细胞和生长因子的PRP。     

Preliminary evaluation of a procedure for improved detection of Shiga toxin-producing Escherichia coli in fecal specimens

Culture confirmation of Shiga toxin-producing Escherichia coli (STEC) is very important for epidemiologic analysis. However, isolation of non-O157 STEC on conventional selective media such as sorbitol–MacConkey agar (SMAC) can be difficult because of heavy growth of competing bacteria and its phenotypical similarity to commensal nonpathogenic E. coli. An acid enrichment procedure was introduced in this study to facilitate detection of STEC from patients who were symptomatic. Forty-seven clinical fecal broths, which tested positive for Shiga toxin by commercial immunoassay, were processed for the isolation of STEC by both conventional and the acid enrichment methods. The acid enrichment method and conventional culture recovered STEC from 91% (43/47) and 70% (33/47) of the fecal broths, respectively. Neither method retrieved STEC in 3 specimens. Thirty-six STEC were successfully serogrouped, which included O26 (n = 11), O157 (n = 9), O103 (n = 7), O121 (n = 3), O111 (n = 2 each), O28AC, O146, O76, and O undetermined (n = 1 each). The analysis of STEC isolates by real-time PCR indicated that all 9 E. coli O157 contained stx2 gene alone or in combination with stx1. Non-O157 STEC more frequently contained stx1 only, and about one-third possessed stx2. The novel acid enrichment protocol greatly reduced the growth of competitor colonies on RTN and TCSMAC. The study demonstrated that incorporation of an acid enrichment procedure in clinical testing improved the isolation of STEC in fecal specimens.     

Effects of age, dietary, and behavioral enrichment on brain mitochondria in a canine model of human aging

Dogs develop cognitive decline and a progressive accumulation of oxidative damage. In a previous longitudinal study, we demonstrated that aged dogs treated with either an antioxidant diet or with behavioral enrichment show cognitive improvement. The antioxidant diet included cellular antioxidants (vitamins E and C, fruits and vegetables) and mitochondrial cofactors (lipoic acid and carnitine). Behavioral enrichment consisted of physical exercise, social enrichment, and cognitive training. We hypothesized that the antioxidant treatment improved neuronal function through increased mitochondrial function. Thus, we measured reactive oxygen species (ROS) production and bioenergetics in mitochondria isolated from young, aged, and treated aged animals. Aged canine brain mitochondria show significant increases in ROS production and a reduction in NADH-linked respiration. Mitochondrial function (ROS and NADH-linked respiration) was improved selectively in aged dogs treated with an antioxidant diet. In contrast, behavioral enrichment had no effect on any mitochondrial parameters. These results suggest that an antioxidant diet improves cognition by maintaining mitochondrial homeostasis, which may be an independent molecular pathway not engaged by behavioral enrichment.