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Abstract Normal veins could develop to varicose vein (VV) by some risk factors, and might further progress to shallow vein thrombosis (SVT). However, the molecular mechanism of key genes associated with the progression and regression of VV are still not thorough enough. In this study, the healthy control (HC), VV, and SVT vascular samples were collected for transcriptome sequencing. The differentially expressed genes (DEGs) were screened by “DESeq2”, including DEGs1 (HC vs. VV), DEGs2 (HC vs. SVT) and DEGs3 (VV vs. SVT). And their functional enrichment analyses were conducted by “ClusterProfiler”. The receiver operating characteristic (ROC) curve was used to obtain the key genes (KGs) of the pathogenesis of VV and SVT. The qRT-PCR assay was performed to validate the expressions of KGs. Immune cell infiltration analyses were conducted based on ssGSEA method. The competitive endogenous RNAs (ceRNAs) regulatory network was constructed. The target drugs of KGs were predicted using DrugBank database. The biofunctions of DACT3 were further investigated through a series of experiments in vitro. All of these DEGs were associated with inflammation and immunity related functions. Immune cell infiltration was significantly different between VV and SVT. Six key genes including PLP2, DACT3, LRRC25, PILRA, MSX1 and APOD that were associated with the progression and regression of VV were screened. The expression of LRRC25 and PILRA was significantly negatively associated with central memory T cell, and significantly positively associated with B cell. Besides, XIST was the critical regulator of multiple KGs. Cimetidine was potential drug for VV and SVT therapy. Overexpression of DACT3 significantly inhibited the proliferation and migration of vascular smooth muscle cells (VSMCs), and affected their cell cycle and phenotypic transition. This study identified six key genes associated with the progression and regression of VV. Among them, DACT3 was proved to hinder VV progression. These findings may help to deepen understanding its underlying mechanisms.

Abstract Lower limb ischemia–reperfusion is a common pathological process during clinical surgery. Because lower limb ischemia–reperfusion usually aggravates ischemia-induced skeletal muscle tissue injury after lower limb ischemia–reperfusion, it also causes remote organ heart, intestine, liver, lung and other injuries, and there is no effective clinical treatment for lower limb ischemia–reperfusion injury, so it is urgent to study its injury mechanism. In this study, the rat model of lower limb ischemia–reperfusion was established by clamping the femoral artery with microarterial clips, and the wall destruction such as intimal injury, cell edema, collagen degeneration, neutrophil infiltration, and elastic fiberboard injury of the femoral artery wall was detected. The expression of inflammatory factors was detected by immunohistochemistry. miR-206 preconditioning was used to observe the expression of inflammatory factors, redox status and apoptosis in the vascular wall of rats after acute limb ischemia–reperfusion. Our findings suggest that vascular endothelial cell edema increases, wall thickening, neutrophil infiltration, and elastic fiber layer damage during IRI. Inflammatory factor expression was increased in femoral artery tissue, and miR-206 expression levels were significantly down-regulated. Further studies have found that miR-206 attenuates lower limb IRI by regulating the effects of phase inflammatory factors. In this study, we investigated the effect of miR-206 on inflammatory factors and its possible role in the development of lower limb IRI, providing new research ideas for the regulatory mechanism of lower limb IRI, and providing a certain theoretical basis for the treatment of lower limb ischemia–reperfusion injury after surgery or endovascular intervention.

Abstract To assess the response of lichen elemental compositions to road traffic and species difference in the context of high dust input and anthropogenic emissions, two foliose epiphytic lichens (Phaeophyscia hirtuosa, PHh; Candelaria fibrosa, CAf) were sampled near a road adjacent to Dolon Nor Town (Duolun County, Inner Mongolia, China). Twenty elements (Ba, Ca, Cd, Co, Cr, Cu, Fe, K, Mg, Mn, Mo, Na, Ni, P, Pb, Sb, Sr, Ti, V and Zn) in lichen and surface soil samples were analysed using inductively coupled plasma mass spectrometer (ICP-MS). The results demonstrate that lichen elemental compositions are highly influenced by both their natural environment and anthropogenic input. Windblown dust associated with sand dunes and degraded/desertified steppes represents the predominant source of lichen elements. Road traffic can enhance the lichen elemental burden by increasing the number of soil particles. Anthropogenic emissions from the town and road traffic have also led to the enrichment of Cd and Zn in lichens. PHh was higher than CAf in concentrations of 14 terrigenous metals. Both lichens are applicable to biomonitoring of atmospheric element deposition and, in most cases, yield comparable results.

The voltage-gated sodium channel (VGSC) interacting peptide is of special interest for both basic research and pharmaceutical purposes. In this study, we established a yeast-two-hybrid based strategy to detect the interaction(s) between neurotoxic peptide and the extracellular region of VGSC. Using a previously reported neurotoxin JZTX-III as a model molecule, we demonstrated that the interactions between JZTX-III and the extracellular regions of its target hNav1.5 are detectable and the detected interactions are directly related to its activity. We further applied this strategy to the screening of VGSC interacting peptides. Using the extracellular region of hNav1.5 as the bait, we identified a novel sodium channel inhibitor SSCM-1 from a random peptide library. This peptide selectively inhibits hNav1.5 currents in the whole-cell patch clamp assays. This strategy might be used for the large scale screening for target-specific interacting peptides of VGSCs or other ion channels. [ABSTRACT FROM AUTHOR]