An integrative analysis of miRNA and mRNA expression in the brains of Alzheimer's disease transgenic mice after real-world PM2.5 exposure

Fine particulatematter (PM2.5) is associated with increased risks of Alzheimer’s disease (AD),yet the toxicologicalmechanisms of PM2.5 promoting AD remain unclear. In this study,wildtype and APP/PS1 transgenic mice (AD mice) were exposed to either filtered air (FA) or PM2.5 for eight weeks with a real-world exposure system in Taiyuan, China (mean PM2.5 concentration in the cage was 61 μg/m3). We found that PM2.5 exposure could remarkably aggravate AD mice’s ethological and brain ultrastructural damage, along with the elevation of the pro-inflammatory cytokines (IL-6 and TNF-α), Aβ-42 and AChE levels and the decline of ChAT levels in the brains. Based on high-throughput sequencing results, some differentially expressed (DE) mRNAs and DE miRNAs in the brains of AD mice after PM2.5 exposure were screened.Using RT-qPCR, seven DEmiRNAs (mmu-miR-193b-5p, 122b-5p, 466h-3p, 10b-5p, 1895, 384–5p, and 6412) and six genes (Pcdhgb8, Unc13b, Robo3, Prph, Pter, and Tbata) were evidenced the and verified. Two miRNA-target gene pairs (miR-125b-Pcdhgb8 pair and miR-466h-3p-IL-17Rα/TGF-βR2/Aβ-42/AChE pairs) were demonstrated that they were more related to PM2.5-induced brain injury. Results of Gene Ontology (GO) pathways and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways predicted that synaptic and postsynaptic regulation, axon guidance, Wnt, MAPK, and mTOR pathways might be the possible regulatory mechanisms associated with pathological response. These revealed that PM2.5- elevated pro-inflammatory cytokine levels and PM2.5-altered neurotransmitter levels in AD mice could be the important causes of brain damage and proposed the promising miRNA andmRNA biomarkers and potentialmiRNA-mRNA interaction networks of PM2.5-promoted AD.     

Prenatal diagnosis of congenital Chagas' disease (American trypanosomiasis)

The prenatal diagnosis of congenital transmission of Chagas' disease in a pregnant woman with the indeterminate form of the disease is reported. Sonography revealed fetal hydrops at 31 weeks' gestation. Anti-Trypanosoma cruzi IgM and IgG antibodies were negative in the fetal blood sampled by cordocentesis, but T. cruzi trypomastigotes were found in its buffy coat. Owing to anemia, in utero exchange transfusion was undertaken, but fetal demise ensued. Labor was induced and a stillborn infant weighing 2030 g was delivered. The pathological examination revealed placentitis and meningoencephalitis, myocarditis and splenitis in the stillborn fetus. Amastigotes were found in the myocardium, brain and placenta. Copyright © 2004 John Wiley & Sons, Ltd.     

人群的自然和社会属性分类下PM2.5对心血管疾病的影响

为了研究人群在自然属性和社会属性分类下的效应修饰作用,利用2005~2011年北京市大气PM_2.5日均浓度、气象要素及循环系统疾病每日死亡人数数据,根据不同年龄、性别及学历将人群分组,采用时间序列的半参数广义相加模型（GAM）,定量评价大气PM_2.5对居民循环系统疾病死亡人数的影响.单污染物模型和多污染物模型结果表明,PM_2.5为影响循环系统疾病每日死亡人数的主要大气污染物.北京市空气中PM_2.5的浓度每增加10μg/m³,循环系统疾病总死亡人数增加0.50%（95% CI：0.36,0.63）.不同人群的易感程度不同,各人群死亡人数的增加范围为0.23~0.71%,女性、60~74岁人群、文盲人群的健康风险相对较高.在文盲人群中,老年（60+）女性占比为66.2%,为了分离社会属性人群分类中可能存在的自然属性因素干扰,本文去除其中老年、女性这两个混杂因素的影响,文盲人群健康风险仍然大于较高学历的人群.年龄和性别因素叠加在学历因素上,可能加大低学历人群的健康风险,对于这部分叠加了自然因素和社会因素双重敏感性的人群应给与重点关注.     

Diagnosis of cardiac defects: where we've been,where we are and where we're going

There has been tremendous development in the field of prenatal diagnosis of cardiac disease in the last 30 years. Early work centered on the technical aspects of providing an accurate assessment of cardiac structure and function. Techniques of fetal cardiac screening have been developed and utilized throughout the world. More recently, investigators have begun to explore the ramifications of fetal cardiac diagnosis by assessing measures of outcome. In this article, the field of fetal echocardiography, as a screening tool for identifying congenital heart disease, and its impact on disease outcome is reviewed. Copyright © 2002 John Wiley & Sons, Ltd.