Objective To investigate the effect of ambroxol pretreatment on the inflammatory response and lipid peroxidation during one-lung ventilation (OLV) .Methods Forty-five ASA I or II patients aged 37-64 yr weighing 53-65 kg undergoing thoracotomy under general anesthesia were randomly divided into 3 groups ( n = 15 each): group A two-lung ventilation (TLV); group B OLV and group C ambroxol 1 mg/kg + OLV. Anesthesia was induced with midazolam, fentanyl, propofol and atracurium and maintained with propofol infusion and intermittent iv boluses of fentanyl and atracurium. The patients were mechanically ventilated (VT8-10 ml/kg, RR 12 bpm during TLV, VT 6-7 ml/kg, RR 16 bpm during OLV, I: E 1:2, FiO2 100% ). In group C ambroxol 1 mg/kg in normal saline ( NS) 100 ml was infused at 25 min before OLV (infusion rate 4 ml/min) , while in group A and B equal volume of NS was infused instead of ambroxol. Blood samples were obtained from radial artery before induction of anesthesia and OLV (T0.1 ) and at 0.5, 1, 2 h of OLV (T2-4 ) and 1, 2 h of TLV (T5,6 ) and at 24 h after operation (T7) in group B and C for determination of serum SOD activity and TNF-α, IL-6 and IL-8 concentrations and WBC and neutrophil granulocyte counts. The same indexes were detected in group A at the corresponding time points.Results Serum SOD activity was significantly lower and serum TNF-α, IL-6 and IL-8 concentrations and WBC and neutrophil granulocyte counts were significantly higher in group B than in group A. Serum SOD activity was significantly higher and serum TNF-a, IL-6 and IL-8 concentrations and WBC and neutrophil granulocyte counts were significantly lower in group C than in group B. Conclusion Pretreatment with ambroxol 1 mg/kg can inhibit inflammatory response and lipid peroxidation during OLV.

To investigate the associations between gene polymorphisms of signal transducer and activator of transcription 3 (STAT3) and liver cirrhosis (LC) after hepatitis B virus (HBV) infection. A case-control study was conducted in 243 patients with hepatitis B cirrhosis (HBV-LC, case group) and 486 HBV-infected subjects without LC (non-LC, control group) collected from January 2018 to September 2020 at the Changsha Central Hospital Affiliated to Nanhua University. Three single nucleotide polymorphisms (SNPs) of STAT3 gene, including rs4796793C>G, rs2293152C>G, and rs1053004T>C were selected through literature and biological information database, and the genotypes were detected by real-time fluorescent quantitative PCR (RFQ-PCR). The distribution differences of STAT3 SNPs genotypes between the two groups were compared using Chi-square test and haplotype analysis was conducted by Shesis online. The proportion of HBV C genotype in HBV-LC patients was significantly higher than that in the control group (80.91% vs. 70.79%, χ²=7.109, P=0.008), while the logarithm of ALT was significantly lower than that of the control group (1.78±0.43 vs. 1.95±0.54, t=3.801, P=0.000). The genotypes distributions of rs4796793, rs2293152, and rs1053004 were not significantly different between HBV-LC and non-LC in overall analysis and stratified analysis by gender (χ²=2.610, 1.505, 0.586, 2.653, 2.685, 1.583, 0.351, 5.388, 0.339, respectively, P>0.05 for each). Among the subjects infected with HBV genotype C, rs1053004 CC (vs. TT) significantly increased the risk of HBV-LC [odds ratio (OR) = 1.40, 95% confidence interval (CI): 1.03-1.91]. Among the HBV-infected subjects with HBeAg negative, rs4796793 GG genotype (vs. CC) and G allele (vs. C) significantly increased the risks of HBV-LC (OR = 2.17, 95%CI: 1.11-4.23; OR = 1.45, 95%CI: 1.06-1.97, respectively). Haplotypes analysis showed that the frequency of haplotype C-G-T composed of rs4796793, rs2293152, and rs1053004 was significantly lower in HBV-LC than that in the control group (non-LC) (27.3% vs. 35.6%, χ²=9.949, P = 0.001). The correlation between STAT3 and HBV-LC is different in HBV-infected subjects with different infection status. The HBV-infected subjects carrying haplotype rs4796793C-rs2293152G-rs1053004T of STAT3 gene have significantly decreased risk of LC.
Carcinoma, Hepatocellular/genetics* ; Case-Control Studies ; Genetic Predisposition to Disease ; Genotype ; Hepatitis B virus/genetics* ; Hepatitis B, Chronic/genetics* ; Humans ; Liver Cirrhosis/genetics* ; Liver Neoplasms/genetics* ; Polymorphism, Single Nucleotide ; STAT3 Transcription Factor/genetics*

Objectives To establish a new transgenic mouse model for determining the function and role of human scavenger receptor A (SR-A) in atherosclerosis in vivo. Methods Human scavenger receptor minigene-driven mouse tie-1 promoter was constructed and confirmed by endonuclease digestion and sequence analysis. Transgenic mice were generated via the microinjection method. PCR and Southern blot were used to screen the positive transgenic mice. RT-PCR and immunohistochemical analysis were used to detect the level and location of human SR-A Ⅰ expression in transgenic mice. The activity of human SR-A Ⅰ was determined by morphologic observation of aortic endothelial cells of transgenic mice under transmission electron microscopy. Results The electrophoresis assay showed the expected 4 fragments of 0.9 kb, 1.1 kb, 1.2 kb and 4.2 kb in the Sma Ⅰ digest and 2 fragments of 0.8 kb and 6.7 kb in Bgl Ⅱ digest of plasmids pTie-1/hSR-A. The fragment sequence of tie-1 promoter and human SR-A cDNA in plasmids pTie-1/hSR-A was correct and no ATG before the translation initiation sites of human SR-A was found by sequence analysis. 561 injected and surviving embryos with the purified human SR-A minigene were implanted into the oviducts of 19 ICR pseudopregnant mice. Among the 54 surviving pups from 13 foster mothers, 7 were identified by PCR and Southern blot analysis. The results of RT-PCR and imrnunohistochemical analysis showed human SR-A was specifically expressed on vascular endothelial cells of the aorta and renal artery, as well as hepatic sinusoidal endothelial cells in transgenic mice. Transmmion electron microscope (TEM) of aorta of transgenic mice showed that a large number of vesicles, multivesicle bodies and swollen mitochondria filled the plasma of endothelial cells. Conclusions A transgenic mouse model with overexpression of human SR-A in endothelial cells was successfully established. The transgene was integrated and transmitted into the chromosome of transgenic mice. Tie-1 promoter controlled the transgene to express in endothelial cells in mice. Pinocytic activity of aortic endothelial cells in transgenic mice was higher than that of C57BL/6J mice. Our studies will provide a new transcgenic model for investigation of atherosclerosis and functions of human SR-A.