ABSTRACT
Objective:To figure out variety of the plasma level of Alpha-1-Antitrypsin(α1-AT) in patients who undergo AKI following cardiopulmonary bypass(CPB), and whether this biomarker serve as a competent predictor.Methods:We recruited 75 patients undergoing cardiac surgery with CPB from January 2018 to January 2019. Patients were categorized into two groups according to the development of AKI. The relationship between plasma concentration of α1-AT and renal injury in two groups was analyzed.Results:27 patients in the AKI group were aged (54.3±12.2)years old, including 15 males and 12 females, the time of cardiopulmonary bypass was(133.5±34.7)min. In the non-AKI group, 48 cases were aged(47.7±11.3)years old, including 26 males and 22 females, and the time of cardiopulmonary bypass was(133.5±34.7)min. α1-AT was significantly decreased in AKI group at 1 h after operation[(0.53±0.53)g/L vs. (1.46±0.91)g/L, P<0.05]compared with the non-AKI group. The sensitivity and specificity of α1-antitrypsin level at 1h after operation was the highest when α1-AT was 0.675 g/L. CPB time ( OR=5.890, 95% CI: 1.078-32.173) and age ( OR=4.427, 95% CI: 1.113-17.614) were independent risk factors for AKI after surgery, and α1-AT at 1h after CPB ( OR=0.084, 95% CI: 0.021-0.333) were protective factors after operation. Conclusion:Increased concentration of α1-AT after cardiopulmonary bypass at early time is a protective factor for AKI and the concentration of α1-AT in plasma could be used as an early biomarker of AKI after CPB.
ABSTRACT
Objective To study the mechanism of RING finger protein 34 ( RNF34 ) involved in innate immunity . Methods Recombinant PCR was used and transient expression of the plasmid was achieved in HEK 293T cells.The cells were stimulated with Sendai virus ( SeV) or N-RIG-Ⅰfor the indicated time while luciferase activity was observed using the dual-luciferase reporter assay kit .Results We constructed the plasmid pcDNA 3-Flag-RNF34 and its three mutations .The study found that when stimulated by SeV , RNF34 could inhibit the activity of NF-κB and IFN-βmore significantly than RNF34-ΔFYVE, RNF34-ΔCID and RNF34-ΔRING.We also found that RNF 34 and its three mutants had similar inhibitory effect when the activation of NF-κB and IFN-βwas stimulated by the N-RIG-Ⅰ.Conclusion RNF34 negatively regulates innate immunity by acting on the RIG-Ⅰ-MAVS signaling pathway .