Research on Acidic Stability of Immobilized Heavy Metals in Sediment from Polluted River

The heavy metals can accumulate in sediment after discharged into surface water bodies. Before the sediment can be further landfilled or recycled,a large amount of heavy metal in it needs to be treated,known as solidification/stabilization. The properties of treated sediment may change with environment such as acid rain and landfill time,which may lead to the release of heavy metals from treated sediment into environment,posing great risks to environment and human health. In this study,the quantitative relationship has been tested between the dissolution of heavy metals from treated sediment and the p H of the leaching solution,by changing the p H of the treated sediment-leaching solution continuously. The results showed that when the p H of the treated sediment-leaching solution was higher than 5. 5,the heavy metals released from the treated sediment into solution were relatively low;when the p H of the treated sediment-leaching solution dropped to about 5. 5,a large amount of Cu,Zn,Ni and other heavy metals were released. The solidification of Cu,Zn,Cr and Cd in the treated sediment is relatively stable,while that of Ni and Pb still need to be improved. The buffer capacity of the treated sediment to acid is 0. 999 meq/g,which means it has relatively high capacity to buffer the pH change caused by external acid.

MZF1(Myeloid Zinc Finger 1)activates transcriptional activity of p53 and suppresses breast cancer cell proliferation via acetyltransferase PCAF(P300/CBP associated factor)

p53 is an important tumor suppressor gene.The p53 pathway is activated in response to cellular stress stimulation.However,in more than 50%of breast cancers,p53 is mutated or inactivated,which permits cancer growth.1 Although a large number of co-regulators of p53 have been identified,the integrated molecular network of p53 and the key co-factors that could transactivate p53 remain unclear.2 Myeloid Zinc Finger 1(MZF1),a member of the SCAN-ZFP(SCAN-Zinc finger protein)family,has been involved in the occurrence and development of various types of malignant tumors,including breast cancer.3 However,the exact mechanism of action remains unclear.Our study aims to investigate the cross-regulatory loop between MZF1 and p53 in breast cancer cells.

Zebrafish Foxc1a controls ventricular chamber maturation by directly regulating wwtr1 and nkx2.5 expression

Chamber maturation is a significant process in cardiac development. Disorders of this crucial process lead to a range of congenital heart defects. Foxc1a is a critical transcription factor reported to regulate the specification of cardiac progenitor cells. However, little is known about the role of Foxc1a in modulating chamber maturation. Previously, we reported that foxc1a-null zebrafish embryos exhibit disrupted heart structures and functions. In this study, we observe that ventricle structure and cardiomyocyte proliferation are abolished during chamber maturation in foxc1a-null zebrafish embryos. To observe the endogenous localization of Foxc1a in the hearts of living embryos, we insert eyfp at the foxc1a genomic locus using TALEN. Analysis of the knockin zebrafish show that foxc1a is widely expressed in ventricular cardiomyocytes during chamber development. Cardiac RNA sequencing analysis reveals the downregulated expression of the Hippo signaling effector wwtr1. Dual-luciferase and chromatin immunoprecipitation assays reveal that Foxc1a can bind directly to three sites in the wwtr1 promoter region. Furthermore, wwtr1m RNA overexpression is sufficient to reverse the ventricle defects during chamber maturation. Conditional overexpression of nkx2.5 also partially rescues the ventricular defects during chamber development. These findings demonstrate that wwtr1 and nkx2.5 are direct targets of Foxc1a during ventricular chamber maturation.