Study on prevention and control measures of sandstone geothermal reinjection plugging.

In the process of geothermal tailwater reinjection of sandstone, the problem of plugging has been seriously restricting the continuous development of geothermal reinjection for many years, and the problems of plugging are complex and changeable. The plugging in the process of reinjection can be divided into physical plugging, chemical plugging, microbial plugging and gas plugging. Given these four types of blocking, according to the mechanism characteristics of the blocking caused by them, this paper puts forward corresponding blocking prevention measures and solves the current blocking problems by filtering, adding a scale inhibitor, intermittent reinjection, adding chlorine dioxide and regular lifting. In addition, the existing reinjection process and the equipment flow are relatively simple and cannot achieve the goal of efficient reinjection. Therefore, a complete set of reinjection processes is designed to ensure the efficient reinjection of sandstone geothermal tailwater.

IL2-inducible T-cell kinase inhibitor ibrutinib reduces symptoms and Th2 differentiation in mouse allergic-rhinitis model.

Th2 and Th17 immune response contribute to allergic rhinitis (AR) development. Targeting Th2 and Th17 response has been shown to ameliorate AR. Ibrutinib is an inhibitor for IL2-inducible T-cell kinase, which can promote Th2 and Th17 immune response. We sought to investigate the effect of ibrutinib on AR and the underlying mechanisms. We established house dust mite-induced AR mouse model and treated AR mice with ibrutinib. The symptoms of AR, serum level of immunoglobulin E, percentage of Th1, Th2, Th17, and Treg in nasal lymphoid tissues were monitored. We also established in vitro T cell differentiation cell culture model. The T cells were treated with ibrutinib and the expression of specific transcriptional factors and cytokines was measured. The activation of PLC-γ1/calcium/NFAT2 signaling pathway was detected. Ibrutinib treatment had no effects on the development of lymphocytes and myeloid cells, but alleviated AR symptoms and decreased Th2 cell population in nasal lymphoid tissue. Meanwhile, iburitnib suppressed Th2 and Th17 differentiation in vitro. Moreover, iburitnib prevented phosphorylation of PLC-γ1and nuclear translocation of NFAT2 in Th2 cells. Our results suggested that ibrutinib could ameliorate AR symptoms through suppression of Th2 differentiation in AR mouse model.

The calcimedin annexin A3 displays tumor-promoting effect in esophageal squamous cell carcinoma by activating NF-κB signaling.

Esophageal squamous cell carcinoma (ESCC) is one of the lethal malignancies commonly found in the eastern world, with overall five-year survival rates less than 25%. The present study aimed to investigate the biological function of annexin A3 (ANXA3) in ESCC cell proliferation. The mRNA and protein levels of ANXA3 in ESCC tissues and cell lines were determined by real-time PCR and Western blot, respectively. Lentiviral transduction was applied to overexpress or reduce ANXA3 expression in ESCC cell lines. The effect of ANXA3 on ESCC cell proliferation was evaluated by cell-counting kit-8 assay in vitro and tumor-bearing animal model in vivo. We found that ANXA3 was substantially upregulated in ESCC tissues compared to adjacent normal tissues as well as ESCC cell lines compared to normal esophageal endothelial cells. Suppression of ANXA3 significantly inhibited ESCC cell proliferation in vitro and tumor growth in vivo. We further revealed that NF-κB was involved in ANXA3-mediated ESCC cell proliferation. Our results suggest that ANXA3 acts as an oncogene in ESCC, and targeting ANXA3 or NF-κB may serve as potential therapeutic strategies for patients with ESCC.

Spleen Tyrosine Kinase Mediates Microglial Activation in Mice With Diabetic Retinopathy.

Purpose: Diabetic retinopathy (DR) is a leading cause of blindness in developed countries, in which microglial activation is involved. However, the mechanism of microglial activation in DR remains largely unknown. Methods: We used Cx3cr1CreERT2; Sykfl/fl mice to knockout microglial spleen tyrosine kinase (Syk) in the retina of mice (cKO mice) after streptozotocin injection to induce diabetes. We also isolated primary retinal microglia from wild-type and cKO mice, respectively, to explore the role of microglial Syk in DR. Results: The deletion of microglial Syk in the retina of mice or in the primary retinal microglia inhibited microglial activation and inflammatory response, eventually leading to the improvement of DR by regulating the expressions of interferon regulatory factor 8 (Irf8) and Pu.1 both in vivo and in vitro. Conclusions: The deletion of microglial Syk in the retina effectively ameliorated microglial activation-induced DR, suggesting the potential of microglial Syk as a therapeutic target for DR. Translational Relevance: Microglial spleen tyrosine kinase might serve as a potential therapeutic target for diabetic retinopathy.