Background and purpose: Ischaemia damages to the cardiac mitochondria by increasing generation of reactive oxygen species (ROS) and peroxidation of cardiolipin. The inhibited mitochondrial function leads to the cardiac injury during reperfusion. Propofol (2, 6-diisopropylphenol), an intravenous anaesthetic, has been shown to decrease cardiac ischaemia and reperfusion injury. In the present study, we propose that propofol protects mitochondrial function and decreases cardiac injury by prevention of cardiolipin peroxidation during ischaemia and reperfusion. Experimental approach: After isolation of mitochondria from isolated rat heart perfused on a Langendorff model, various mitochondrial bioenergetic parameters were evaluated such as rates of mitochondrial oxygen consumption, H 2 O 2 production, complex I and III activity as well as the degree of lipid peroxidation and cardiolipin content. The action of propofol was also explored in isolated mitochondria. And the effect of cardiolipin was evaluated by fusing cardiolipin liposome with mitochondria. Key results: Propofol treatment had strong dose-dependent protection attenuating these parameters alterations in reperfused rat heart and isolated mitochondria. Additionally, cardiolipin treatment had the same protective effect, compared with propofol treatment at high concentration. Conclusions and implications:The protective effect of propofol appears to be due, at least in part, as a chemical uncoupler, to the interruption of the vicious circle of ROS-cardiolipin-complexes of the respiratory chain-ROS through preserving the content and integrity of cardiolipin molecules by ROS attack. These findings may provide an explanation for some of the factors responsible for cardioprotection and one approach exploring an available antioxidant.

31Several studies have shown microRNAs (miRNAs) could regulate the placental 32 development, yet the role and mechanism of miRNAs in the development of 33 non-diabetic macrosomia (NDFMS) remains unclear. The key miRNA that abnormal 34 expressed in NDFMS placentas was screened out by miRNA microarray and verified 35 using qRT-PCR in 91 subjects. The effects of the key miRNA were verified by 36 proliferation assay and invasion assay in HTR-8/SVneo cell, and also in pregnant 37 C57BL/6J mice. miR-141-3p was determined as the key miRNA with the most 38 significant difference, which could promote the proliferation and invasion by 39 regulating the expression of target gene PLAG1. Overexpression of PLAG1 could 40 reverse the effect of cell proliferation and invasion ability caused by miR-141-3p 41 overexpression. Significant difference in fetal birth weight was observed between the 42 control group and treated group with miR-141-3p agomir in late pregnancy, but not in 43 early pregnancy. This study revealed miR-141-3p could increase the proliferation of 44 placenta to participate in the occurrence and development of NDFMS through 45 regulating PLAG1 expression.46

We investigated the first presence of qnrA among Shigella sonnei clinical isolates in Jiangsu Province, China. The qnrA-positive isolates coexisted with the mutation in gyrA at codon 83, these isolates were resistant to nalidixic acid and 22·2% (2 of 9) of them were resistant to norfloxacin.