Objective:To correlate serum levels of neuron specific enolase (NSE) and inflammatory factors with recovery of neurological function in patients with severe traumatic brain injury.Methods:Ninety-six patients with severe traumatic brain injury who received treatment from January 2018 to January 2020 in Taizhou Hospital were included in this study. These patients were divided into a mild-to-moderate group ( n = 51) and a severe group ( n = 45). Additional 60 healthy controls who concurrently received health examination were included in the healthy control group. Serum NSE level was detected by enzyme-linked immunosorbent assay, serum C-reactive protein (CRP) level by immunoturbidimetry, serum procalcitonin (PCT) level by chemiluminescent assay, and serum interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels by enzyme-linked immunosorbent assay. All patients were followed up for 3 months. Recovery of neurological function was evaluated by modified Rankin Scale. Results:Serum NSE level was (50.42 ± 13.25) μg/L and (36.79 ± 10.28) μg/L in the severe and mild-to-moderate groups, respectively, which was significantly higher than that in the healthy control group [(6.13 ± 1.78) μg/L, t = 25.641, 22.688, both P < 0.05). Serum NSE level in the severe group was significantly higher than that in the mild-to- moderate group ( t = 5.576, P < 0.05). Serum CRP, PCT, IL-6 and TNF-α levels were (78.95 ± 15.46) mg/L, (3.46 ± 0.75) μg/L, (432.15 ± 78.29) μg/L and (36.57 ± 8.98) μg/L] respectively in the severe group, (34.65 ± 7.48) mg/L, (1.68 ± 0.51) μg/L, (285.41 ± 36.75) μg/L and (17.54 ± 5.26) μg/L] respectively in the mild-to-moderate group and (3.25 ± 0.86) mg/L, (0.08 ± 0.02) μg/L, (73.52 ± 13.89) μg/L and (1.64 ± 0.50) μg/L, respectively in the healthy control group. Serum CRP, PCT, IL-6 and TNF-α levels in the severe and mild-to-moderate groups were significantly higher than those in the healthy control group ( t = 37.890, 34.922, 34.870, 30.099, 32.284, 24.315, 40.980, 23.312, all P < 0.05). Serum levels of these indicators in the severe group were significantly higher than those in the mild-to-moderate group ( t = 17.493, 13.414, 11.500, 12.451, all P < 0.05). In the severe group, neurological function recovered well in 34 patients and poorly in 17 patients. Serum NSE level in patients with poor neurological function recovery was significantly higher than that in patients with good recovery [(68.93 ± 14.25) μg/L vs. (34.61 ± 12.36) μg/L, t = 8.457, P < 0.05). Serum CRP [(113.24 ± 27.39) mg/L], PCT [(4.57 ± 0.87) μg/L], IL-6 [(598.90 ± 43.52) μg/L] and TNF-α [(58.78 ± 12.13) μg/L] levels in patients with poor recovery were significantly higher than those in patients with good recovery [(32.19 ± 6.90) mg/L, (2.23 ± 0.65) μg/L, (261.39 ± 26.56) μg/L and (14.53 ± 4.26) μg/L, t = 11.956, 9.788, 29.280 and 14.537, all P < 0.05). Serum NSE, CRP, PCT, IL-6 and TNF-α were positively correlated with poor prognosis ( r = 0.849, 0.743, 0.795, 0.683, 0.701, all P < 0.05). Conclusion:In patients with severe traumatic brain injury, serum NSE, CRP, PCT, IL-6 and TNF-α levels increase, which are positively correlated with poor prognosis.

Objective To analyze the protective effect of esmolol combined with early goal-directed therapy on myocardial function in patients with severe sepsis. Methods The clinical data of patients with severe sepsis who were treated in our hospital were retrospectively analyzed. According to the principles of randomization, balance and control, 30 cases receiving esmolol combined with early goal-directed therapy were selected as the observation group. The other 30 cases who were given early goal-directed therapy during the same period were selected as the control group. The effects of the two treatment regimens on the levels of hemodynamic indices, cTnT, BNP, TNF-a, IL-1β, Lac, central venous oxygen saturation(ScvO2) and other indices were compared, and 28-day survival rate was statistically analyzed. Results After treatment, Ea/Aa in the observation group was increased significantly, and HRwas decreased significantly. Only HRwas decreased significantly in the control group. There was no statistically significant difference within groups and between the two groups in other hemodynamic indices (P＞0. 05); the levels of cTnT, BNP, TNF-a, and IL-1β in both groups were significantly decreased and the observation group was lower than the control group. The differences within groups and between groups were statistically significant; the serum Lac was decreased and ScvO2 was increased in both groups. The serum Lac in the observation group was lower than that in the control group, and ScvO2 was higher than that in the control group. There were statistically significant differences within groups and between groups (P＜0. 05); the survival rate in the observation group was slightly higher than that in the control group, but the difference was not statistically significant(χ2=0. 480, P=0. 488). Conclusion Esmolol combined with early goal-directed therapy may benefit myocardial protection in patients with severe sepsis.

Objective To investigate the protective effect of NDUFA13 protein against acute liver injury and liver fibrosis in mice and explore the possible mechanisms.Methods BALB/C mice(7 to 8 weeks old)were divided into normal group,CCl4 group,CCl4+AAV-NC group and CCl4+AAV-NDU13 group(n=18).Mouse models of liver fibrosis were established by intraperitoneal injection of CCl4 twice a week for 3,5 or 7 weeks,and the recombinant virus AAV8-TBG-NC or AAV8-TBG-NDUFA13 was injected via the tail vein 7-10 days prior to CCl4 injection.After the treatments,pathological changes in the liver of the mice were observed using HE and Masson staining.Hepatic expression levels of NDUFA13 and α-SMA were detected with Western blotting,and the coexpression of NDUFA13 and NLRP3,TNF-α and IL-1β,and α-SMA and collagen Ⅲ was analyzed with immunofluorescence assay.Results HE and Masson staining showed deranged liver architecture,necrotic hepatocytes and obvious inflammatory infiltration and collagen fiber deposition in mice with CCl4 injection(P<0.001).NDUFA13 expression markedly decreased in CCl4-treated mice(P<0.001),while a significant reduction in inflammatory aggregation and fibrosis was observed in mice with AAV-mediated NDUFA13 overexpression(P<0.001).In CCl4+AAV-NDU13 group,immunofluorescence assay revealed markedly weakened activation of NLRP3 inflammasomes(P<0.001),significantly decreased TNF-α and IL-1β secretion(P<0.001),and inhibited hepatic stellate cell activation(P<0.05)and collagen formation in the liver(P<0.001).Conclusion Mitochondrial NDUFA13 overexpression in hepatocytes protects against CCl4-induced liver fibrosis in mice by inhibiting activation of NLRP3 signaling.

Objective To investigate the protective effect of NDUFA13 protein against acute liver injury and liver fibrosis in mice and explore the possible mechanisms.Methods BALB/C mice(7 to 8 weeks old)were divided into normal group,CCl4 group,CCl4+AAV-NC group and CCl4+AAV-NDU13 group(n=18).Mouse models of liver fibrosis were established by intraperitoneal injection of CCl4 twice a week for 3,5 or 7 weeks,and the recombinant virus AAV8-TBG-NC or AAV8-TBG-NDUFA13 was injected via the tail vein 7-10 days prior to CCl4 injection.After the treatments,pathological changes in the liver of the mice were observed using HE and Masson staining.Hepatic expression levels of NDUFA13 and α-SMA were detected with Western blotting,and the coexpression of NDUFA13 and NLRP3,TNF-α and IL-1β,and α-SMA and collagen Ⅲ was analyzed with immunofluorescence assay.Results HE and Masson staining showed deranged liver architecture,necrotic hepatocytes and obvious inflammatory infiltration and collagen fiber deposition in mice with CCl4 injection(P<0.001).NDUFA13 expression markedly decreased in CCl4-treated mice(P<0.001),while a significant reduction in inflammatory aggregation and fibrosis was observed in mice with AAV-mediated NDUFA13 overexpression(P<0.001).In CCl4+AAV-NDU13 group,immunofluorescence assay revealed markedly weakened activation of NLRP3 inflammasomes(P<0.001),significantly decreased TNF-α and IL-1β secretion(P<0.001),and inhibited hepatic stellate cell activation(P<0.05)and collagen formation in the liver(P<0.001).Conclusion Mitochondrial NDUFA13 overexpression in hepatocytes protects against CCl4-induced liver fibrosis in mice by inhibiting activation of NLRP3 signaling.

OBJECTIVE: To investigate the role of NDUFA13 inactivation in the pathogenesis of spontaneous hepatitis in mice and explore the possible mechanisms. METHODS: Hepatocyte-specific NDUFA13 knockout (NDUFA13 RESULTS: Liver-specific NDUFA13 heterozygous knockout mice were successfully constructed as verified by PCR results. HE staining revealed severe liver damage in both 4- week-old and 2-year-old NDUFA13 CONCLUSIONS Hepatocytes-specific NDUFA13 ablation can trigger spontaneous hepatitis in mice possibly mediated by the activation of ROS/NF-κB/NLRP3 signaling.
Animals ; Hepatitis ; Inflammasomes ; Mice ; NF-kappa B/metabolism* ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics* ; Signal Transduction