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Objective:To investigate the relationship between monocyte-to-lymphocyte ratio (MLR) in serum and the all-cause mortality in patients with acute paraquat (PQ) poisoning.Methods:Patients with acute PQ poisoning in the First Affiliated Hospital of Nanchang University from December 2013 to October 2018 were retrospectively selected and followed up until July 1, 2019. The primary endpoint was all-cause mortality. Patients were classified into quartiles based on serum MLR and also dichotomized based on the optimal cutoff at a MLR of 0.61, determined from the receiver operating characteristic (ROC) curve analysis. The Kaplan-Meier curve was used for survival analysis. Multivariate Cox regression analysis was performed to identify risk factors, and ROC curve was applied to analyze the predictive efficacy of MLR in all-cause mortality of acute PQ patients.Results:Of the 117 patients included in the study, 49 (41.88%) patients were male and 68 (58.12%) were female with a mean age of 36.91±16.00 years. The total mortality was 59.8% (70/117). On the Kaplan-Meier analysis, patients in quartile 4 had worse prognosis than patients in quartiles 1, 2 and 3 (Log-rank=33.376, P<0.01), and patients with MLR≥0.61 had a significantly higher all-cause mortality than those with MLR<0.61 (Log-rank=26.451, P<0.01). Cox regression model analysis showed that MLR was an independent predictor of all-cause mortality on the quartile analysis (quartile 4 vs. quartile 1: hazard ratio 2.773, 95% confidence interval ( CI): 1.250 to 6.154, P=0.012). ROC curve showed that the optimal cut-off value of MLR was calculated to be at 0.61, the area under the curve (AUC) was 0.684 (95% CI: 0.591-0.767, P=0.0002), with a sensitivity of 47.14% and a specificity of 91.49%. Conclusions:High MLR was associated with mortality risk in patients with acute PQ poisoning, and MLR may be an effective predictor of all-cause mortality in this population.
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Objective:To investigate the relationship between caspase recruitment domain protein 9 (CARD9) level and inflammatory response in cerebral tissue of ischemic brain injury mice.Methods:Totally 24 SPF BALB/c male mice were randomly(random number) divided into 4 groups: sham operated group, ischemia 3 h group, ischemia 6 h group, and ischemia 12 h group, 6 mice in each group. The permanant middle cerebral artery occlusion (pMCAO) model in the ischemia groups was established by using line embolism to block blood flow. Mice in each group were sacrificed at the predetermined time point after operation. CARD9 and p-p65NF-κB levels were detected by Western blot, and the inflammatory factors mRNA and protein including TNF-ɑ, IL-lβ and IL-6 were detected by RT-PCR and ELISA, respectively. The data were analyzed by SPSS 21.0 software, the comparison of measurement data between each two groups was analyzed by independent sample t test, and the correlations between CARD9 and inflammatory factors were analyzed by Pearson analysis. Results:Compared with the sham operated group, the CARD9 levels in the ischemia 3 h, 6 h and 12 h groups were increased significantly [(0.325±0.011) vs. (0.462±0.019), P=0.036; (0.735±0.036), P=0.003; (0.903±0.024), P=0.001], the p-p65NF-κB levels in the ischemia 3 h, 6 h and 12 h groups were increased significantly [(0.227±0.016) vs. (0.316±0.017), P=0.041; (0.445±0.021), P=0.016; (0.671±0.039), P=0.008], the TNF-ɑ levels in the ischemia 3 h, 6 h and 12 h groups were significantly increased [(0.53±0.06) vs. (1.06±0.10), P=0.009; (1.47±0.15), P=0.004; (2.78±0.18), P=0.001], the IL-lβ levels in the ischemia 3 h, 6 h and 12 h groups were significantly increased [(0.55±0.07) vs. (1.01±0.11), P=0.009; (2.13±0.16), P=0.003; (3.09±0.18), P=0.001], and the IL-6 levels in the ischemia 3 h, 6 h and 12 h groups were significantly increased [(1.99±0.18) vs. (4.10±0.41), P=0.006; (8.54±0.84), P=0.002; (11.56±0.96), P=0.001]. Pearson analysis showed that CARD9 was positively correlated with the p-p65NF-κB and TNF-ɑ, IL-lβ, IL-6 ( r=0.894, P=0.001; r=0.747, P=0.008; r=0.810, P=0.001; r=0.773, P=0.007). Conclusions:A positive correlation exists between CARD9 and inflammatory responses in the early stage of ischemic brain injury in mice
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Objective To explore the effects of H2S on cerebral injury after cardiopulmonary resuscitation (CPR) and its mechanism.Methods Forty-five healthy Sprague-Dawley (SD) rats were randomly (random number) divided into shame-operated group ( group A,n =5 ),resuscitation group ( group B,further divided into four subgroups as per rats sacrificed 6 h,12 h,24 h,and 72 h after resuscitation,n =5),and NaHS pretreatment group ( group C,further divided into 4 subgroups as done in group B).The ratio of water content in brain tissue was calculated.The content of H2S in cerebral cortex of rats in all groups was determined by using universal microplate reader. Immunohistochemistry method was used to count the Nestin-positive cells. Results The content of H2S in hippocampus area of brain showed dramatic changes from rising up at first and then to lowering down to the minimum and finally returning to the original level in 72 h in B group.Compare to group B,brain water content was lesser ( P ＜0.05 or P ＜ 0.01 ) and the levels of Nestin in hippocampus increased in group C(P＜0.05 or P ＜0.01).The neurological deficit score (NDS) was improved (P ＜0.05 or P ＜0.01) and pathological changes in hippocampus of rat brain detected by using hemotoxylin - eosin staining were slighter in group C in comparison with group B.Conclusions Endogenous H2S may involve in the course of formation and progress of cerebral injury after CPR and small dose of NaHS (exogenous H2S) can improve NDS by decreasing cerebral edema and up-regulating Nestin level in hippocampus of brain,playing a protection role in cerebral injury after CPR.
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Objective To investigate the relationship between aquaporin-4 (AQP4) expression level inbrain and dynamic change of brain edema in rats after cardiopulmonary resuscitation (CPR), and to evaluate the in-tervention effects of Edaravone. Method Totally 72 Sprague-Dawley male rats were randomly divided into fourgroups:normal group (n = 6, group A) ,shame-operated group ( n = 6, group B), CPR group including 1 hour,6 hours, 12 hours, 24 hours, and 72 hours after ROSC (5 sub-groups, n = 6for each,group C) ,edaravone-treat-ed group with the same time points as CPR groups(5 sub-groups, n = 6for each,group D). Asphyxia cardiac ar-rest with CPR model was used in group C and group D. Edaravone at a dose of 3.0 mg/kg was given intravenouslyand the same dose of edaravone was administered subcutaneously to the rats of group D after CPR. Anaesthosia,vascular cannulation and endotracheal intubation were pedormed in rats without asphyxia and CPR in group B. Ateach interval, the brain water content was calculated. The AQP4 expression level in brain tissue was determinedusing immunohistocbemical staining. Neurodeficit scores were assessed and pathological change was observed, Re-sults The brain water content in rats of group C increased obviously along with the prolongation of time followingROSC,and reached its peak at ROSC 24h,which was much higher than that of group B (P<0.01). Meanwhile,AQP4 expression in brain had a trend towards increasing and the integral optical density(iOD) and coloratian arearatio(△S) in group C were significantly increased compared with group B ( P<0.01). The trend of changes wasnearly the same as that of the brain water content. The correlation analysis demonstrated that AQP4 expression levelsuch as iOD (r=0.858, P < 0.01 ) and △S ( r = 0.870, P < 0.01 ) were correlated with the brain watercontents apparently. Compared with group C, the brain water content was decreased obviously (P<0.05), iODand △S was down-regulated at the same lime (P<0.01) in group D. The neurodeficit scores increased (P <0.05) and pathological damage was dramatieaUy ameliorated. Conclusions AQP4 expression increased greatly inbrain after CPR and the relationship between AQP4 and brain edema was positively correlated. AQP4 may play arole in the formation of brain edema following CPR. Edaravone could attenuated brain edema after CPR in rats byway of inhibiting the expression of AQP4. It had neuroprotective effect.