Prediction of Leachate Level in Kimpo Metropolitan Landfill Site by Total Water Balance

Kimpo metropolitan landfill has received various kinds of wastessince January 1992. The leachate level was measured to be 10.3 m in May 1995 and the level increased to 12.2 m in August 1996. Therefore, to prove the reason for the increasing leachate level, we calibrated hydraulic conductivity of each waste andintermediate layer using the HELP (Hydrologic Evaluation ofLandfill Performance) model. The leachate generation data measured from February 1993 to October 1995 was used in the model calibration. As a result of a model calibration, we obtained anaverage infiltration ratio and used this in analysis of the total water balance to predict elevation of leachate level. Main causes of the elevation of the leachate level were the high water content of the waste and the degradation of the leachate-drainage system caused by the subsidence of a naturalbarrier layer.     

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.