Effects of Water–Rock Interaction on the Permeability of the Near-Well Reservoir in an Enhanced Geothermal System

During the operation of an enhanced geothermal system (EGS), the non-equilibrium temperature, pressure, and hydrochemistry caused by fluid injection intensify water–rock interactions, induce the mineral dissolution and precipitation in the reservoir near an injection well (also referred to as the near-well reservoir), and change reservoir permeability, thus affecting continuous and efficient geothermal exploitation. Based on the investigation of the M-1 injection well of the EGS in the Matouying uplift of Hebei Province, China, a THC reactive solute transport model using the TOUGHREACT program was established in this study to explore the mineral dissolution and precipitation laws of the near-well reservoir and their influencing mechanisms on the reservoir porosity and permeability in the long-term fluid injection of this well. As indicated by the results, the dissolution of primary feldspar and chlorite and the precipitation of secondary minerals (mainly dolomite and illite) occurred and water–rock interaction significantly reduced the porosity and permeability of the near-well reservoir in the long-term continuous injection process. Appropriate reduction in the injection flow rate, injection temperature, and the Mg2+ and K+ contents in the injected water can help inhibit the formation of secondary minerals and delay the plugging process of the near-well reservoir

Intraportal Infusion of Ghrelin Could Inhibit Glucose-Stimulated GLP-1 Secretion by Enteric Neural Net in Wistar Rat

As a regulator of food intake and energy metabolism, the role of ghrelin in glucose metabolism is still not fully understood. In this study, we determined the in vivo effect of ghrelin on incretin effect. We demonstrated that ghrelin inhibited the glucose-stimulated release of glucagon-like peptide-1 (GLP-1) when infused into the portal vein of Wistar rat. Hepatic vagotomy diminished the inhibitory effect of ghrelin on glucose-stimulated GLP-1 secretion. In addition, phentolamine, a nonselective α receptor antagonist, could recover the decrease of GLP-1 release induced by ghrelin infusion. Pralmorelin (an artificial growth hormone release peptide) infusion into the portal vein could also inhibit the glucose-stimulated release of GLP-1. And growth hormone secretagogue receptor antagonist, [D-lys3]-GHRP-6, infusion showed comparable increases of glucose stimulated GLP-1 release compared to ghrelin infusion into the portal vein. The data showed that intraportal infusion of ghrelin exerted an inhibitory effect on GLP-1 secretion through growth hormone secretagogue receptor 1α (GHS1α receptor), which indicated that the downregulation of ghrelin secretion after food intake was necessary for incretin effect. Furthermore, our results suggested that the enteric neural net involved hepatic vagal nerve and sympathetic nerve mediated inhibition effect of ghrelin on incretin effect

Musashi-1 and miR-147 Precursor Interaction Mediates Synergistic Oncogenicity Induced by Co-Infection of Two Avian Retroviruses

Synergism between avian leukosis virus subgroup J (ALV-J) and reticuloendotheliosis virus (REV) has been reported frequently in co-infected chicken flocks. Although significant progress has been made in understanding the tumorigenesis mechanisms of ALV and REV, how these two simple oncogenic retroviruses induce synergistic oncogenicity remains unclear. In this study, we found that ALV-J and REV synergistically promoted mutual replication, suppressed cellular senescence, and activated epithelial-mesenchymal transition (EMT) in vitro. Mechanistically, structural proteins from ALV-J and REV synergistically activated the expression of Musashi-1(MSI1), which directly targeted pri-miR-147 through its RNA binding site. This inhibited the maturation of miR-147, which relieved the inhibition of NF-κB/KIAA1199/EGFR signaling, thereby suppressing cellular senescence and activating EMT. We revealed a synergistic oncogenicity mechanism induced by ALV-J and REV in vitro. The elucidation of the synergistic oncogenicity of these two simple retroviruses could help in understanding the mechanism of tumorigenesis in ALV-J and REV co-infection and help identify promising molecular targets and key obstacles for the joint control of ALV-J and REV and the development of clinical technologies