Objective To determine the relationship between polymorphism of apolipoprotein E gene (APOE) and electroencephlogram in patients with mild/moderate traumatic brain injury. Methods (1) Venous blood for 2 ml was collected from 81 patients with mild/moderate traumatic brain injury on admission. APOE genotype was identified by PCR restriction fragment length polymorphism ( PCRRFLP). (2) All the patients were monitored by electroencephalogram for 2-3 times within a week after injury. X2 test and logistic regression analysis via SAS version 8.2 were performed to analyze the results of genotype and electroencephalogram and clinical data. Results The distributions of genetypes and alleles among 81 patients matched with Haldy-Weinberg Law. The findings of electroencephalogram were significantly different between patients with and without APOEε4 (P<0.05). Ten (63%) out of 16 patients with APOEε4 showed an aggravated electroencephalogram,while only 16 (25%) out of 65 patients without APOEε4 showed the same results of electroencephalogram. Logistic regression analyses showed that APOEε4 was a risk factor for electroencephalogram aggravation after traumatic brain injury. Conclusion APOEε4 is a risk factor for electroencephalogram aggravation during acute stage after mild/moderate traumatic brain injury.

Objective To study the influence of ANGPTL8 in lipopolysaccharide(LPS)-induced hepatic lipid deposition.Methods Male wild-type(WT)and ANGPTL8 knockout mice at 6-8 weeks were used to induce sepsis models by intrabitoneal injection of LPS(10 mg/kg).qPCR and immunofluorescence were used to detected the mRNA and protein expression of ANGPTL8 in liver tissue and HepG2 cells respectively;The contents of alanine aminotransferase(ALT),aspartate aminotransferase(AST)in serum and the triglyceride(TG)and malondialdehyde(MDA)in liver homogenate were detected by kits;the histopathological changes of liver tissue were analyzed through HE staining.Lipids accumulation in liver were detected by oil red O staining.The apoptosis of liver was determinated by TUNEL staining.RNA-seq was used to analyzing the differentially expressed genes in the liver tissue of WT and ANGPTL8 KO mice,and the qPCR and Western Blot were used to verify the differential expressed genes.Results The expression of ANGPTL8 in the liver was significantly upregulated at 48 hours after LPS stimulation.Compared with WT mice,the hepatic lipid deposition,steatosis,and apoptosis were significantly alleviated in liver of ANGPTL8 KO mice,the ALT and AST levels in serum and the TG and MDA content in liver homogenate of ANGPTL8 KO mice were also reduced significantly.The expression of caveolin-1(CAV1)in liver of ANGPTL8 KO mice was significantly higher than that of WT mice.Conclusions LPS promoted the expression and secretion of ANGPTL8 in liver tissue,and ANGPTL8 increased hepatic lipid deposition and peroxidation by inhibiting the expression of CAV1.