A graphene-enhanced high-barrier and fast-curing film for deep in situ condition preserved coring in coal seams

Scientific research on deep in situ resources is highly important to the theory and technology system construction for deep in-situ resource exploitation.To obtain high-condition preserved core samples,it is vital to maintain the original material,humidity and luminous flux information inside the core.Therefore,this study proposes a research and development strategy for a high-toughness and highbarrier sealing film based on the molecular structure design and filler synergistic enhancement via a deep solid-state sealing film using in situ substance preservation(ISP),in situ moisture preservation(IMP)and in situ light preservation(ILP)coring principles.A graphene/epoxy composite sealing film with a high barrier,high strength and high toughness was developed.The oxygen permeability of the film was 0.23 cm^(3)/(m^(2)·d),the water vapor permeability was 1.26 g/(m^(2)·d),and the light transmittance was 0.The tensile strength reached 15.4 MPa,and the toughness was 5242.9 kJ/m^(3).The results from the film substance and moisture preservation performance verification experiments showed that the sealing film had an excellent sealing effect on small molecules,such as water,alkanes and even ions,which further verified that the sealing film greatly contributed to the maintenance and preservation of deep in-situ resource reserves and abundance.

IL-33 Downregulates Hepatic Carboxylesterase 1 in Acute Liver Injury via Macrophage-derived Exosomal miR-27b-3p

Background and Aims:We previously reported that carboxylesterase 1(CES1)expression was suppressed following liver injury.The study aimed to explore the role of interleukin(IL)-33 in liver injury and examine the mechanism by which IL-33 regulates CES1.Methods:IL-33 and CES1 levels were determined in the livers of patients and lipopolysaccharide(LPS)-,acetaminophen(APAP)-treated mice.We constructed IL-33 and ST2 knockout(KO)mice.ST2-enriched immune cells in livers were screened to identify the responsible cells.Macrophage-derived exosome(MDE)activity was tested by adding exosome inhibitors.Micro-RNAs(miRs)were extracted from control and IL-33-stimulated MDEs(IL-33-MDEs)and subjected miR sequencing(miR-Seq).Candidate miR was tested in vitro and in vivo and its binding of a target gene was assessed by luciferase reporter assays.Lentivirus-vector cellular transfection and transcript silencing were used to examine pathways mediating IL-33 suppression of miR-27b-3p.Results:Patient liver IL-33 and CES1 expression levels were inversely correlated.CES1 downregulation in liver injury was rescued in both IL-33–deficient and ST2 KO mice.Macrophages were shown to be responsible for IL-33 effects.IL-33-MDEs reduced CES1 levels in hepatocytes.Exosomal miR-Seq and qRT-PCR demonstrated increased miR-27b-3p levels in IL-33-MDEs;miR-27b-3p was implicated in Nrf2 targeting.IL-33 inhibition of miR-27b-3p was found to be GATA3-dependent.Conclusions:IL-33–ST2–GATA3 pathway signaling increases miR-27b-3p content in MDEs,which upon being internalized by hepatocytes reduce CES1 expression by inhibiting Nrf2.The elucidation of this mechanism in this study contributes to a better understanding of CES1 dysregulation in liver injury.