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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.
ABSTRACT
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.