AIM To investigate the protective effect of sodium gamma-hydroxybutyrate (?-OH) against cerebral ischemia-reperfusion injury in gerbils and the neuroprotective mechanism of ?-OH. METHODS The occlusion of bilateral carotid arteries of gerbil was used to make the cerebral ischemia-reperfusion models. Different doses of ?-OH were administered intraperitoneally 40 min prior to the onset of ischemia. After 10 min ischemia and 1 h reperfusion, bilateral hippocampus, cortex and striatum were taken out to measure ATPase, SOD and MDA. RESULTS The contents of MDA markedly elevated while Na +,K +-ATPase, Ca 2+ -ATPase and SOD activities decreased in hippocampus, cortex and striatum 1 h after ischemia-reperfusion. ?-OH administered prior to ischemia can partly reverse the elevation of MDA contents and the reduction of SOD activities. ?-OH given after ischemia can still provide partly protective effect. CONCLUSION ?-OH provides significant protective effect against cerebral ischemia-reperfusion injury by protecting ATPase and SOD activities, deleting free radicals and reducing the lipid peroxidation.

AIM To investigate the effects of melatonin (MT) on glutathione peroxidase(GPx), superoxide dismutase(SOD) activities and malondialdehyde(MDA) contents in the cerebrum of cerebral ischemia-reperfusion gerbils, so as to explore the protective mechanisms of MT. METHODS Cerebral ischemia-reperfusion model was made by 10 min occlusion of bilateral carotid arteries of gerbil. MT was administered intraperitoneally 30 min prior to the onset of ischemia. After 1 h reperfusion, bilateral cortex and striatum were taken out for measurement of GPx, SOD and MDA. RESULTS Ischemia-reperfusion lowered the activities of GPx and SOD in cerebral cortex and striatum. Conversely, it elevated the contents of MDA in both areas. Treatment with MT at 5, 10, or 20 mg?kg -1 partly reversed these effects. CONCLUSION MT provides protective effect against cerebral ischemia-reperfusion injury by protecting GPx and SOD activities and reducing the lipid peroxidation.

Aim To study the effect of gamma-hydroxybutyric acid receptor(GHBR ) on neuronal apoptosis suffering from focal cerebral ischemia-reperfusion injury in rats. Methods The male Sprague-Dawley rats weighing 240～280 g were randomly divided into seven groups: sham operation group(sham), ischemia-reperfusion group(Isc/R) ,NCS-356 160、320、640 ?g?kg-1 group(N1、N2、N3),NCS-382 640+NCS-356 640 ?g?kg-1 group(NCS-382+N3),and nimodipine 600 ?g?kg-1 group(Nim).The middle cerebral artery occlusion(MCAO) model invented by Zea Longa with modifications was adopted. The experiment was divided into two parts after ischemia reperfusion for 24h:In the first part,we measured the cerebral expression of Bax, Bcl-2, Caspase-3 by immuneohistochemical method. In the second part,we measured neuronal apoptotic rate by flow cytometry in the ischemic cortex region. Results The expression rate of Bcl-2 and Bcl-2/Bax ratio of N1,N2,N3 and Nim groups were all higher than that of Isc/R group(P

AIM: To investigate the relationship between the protective effect of sodium oxybate on neuronal damage induced by hypoxia reoxygenation and GABA A receptor in primary cultured rat cortical neurons. METHODS: The primary cultured rat cortical neurons were used to make the hypoxia reoxygenation damage model. The morphology of cell was observed. The lactate dehydrogenase (LDH) effluxed into the media as an indicator of neuronal injury was detected after 6 h of the reoxygenation injuries. The malonyldialdehyde (MDA) contents, superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities were determined at the same time. RESULTS: The hypoxia reoxygenation caused neuronal swelling and widespread neuronal degeneration, increased LDH efflux and MDA contents, and decreased SOD and GPX activities. Sodium oxybate assuaged neuron damage, decreased LDH efflux and MDA contents (P

Objective:To investigate the value of neutrophil-to-lymphocyte ratio (NLR) in predicting the prognosis of patients with severe heat stroke.Methods:A retrospective analysis was performed on patients with severe heat stroke hospitalized in the ICU of Changzhou No. 2 People's Hospital from June 2013 to September 2019. The patients were divided into the survival group and death group according to their 30-day survival. The basic data of the patients were recorded. Blood routine, liver and kidney function parameters, troponin, brain natriuretic peptide, myocardial enzyme spectrum, blood coagulation routine, and acute physiology and chronic health evaluation (APACHE)Ⅱ were analyzed within 24 h after admission. Multivariate COX regression analysis was used to screen the risk factors of 30-day death. Spearman correlation test was used to analyze the correlation between NLR and APACHEII score. Receiver operating characteristic (ROC) curves were drawn to assess the predictive value of NLR for the 30-day death in patients with severe heat stroke. Kaplan-Meier survival curve was used to analyze 30-day cumulative survival of high-risk patients.Results:A total of 115 patients with severe heat stroke were included in this study, and they were divided into the survival group ( n=92) and the death group ( n=23) according to the prognosis. NLR in the death group was significantly higher than that in the survival group ( P<0.05). Multivariate COX regression analysis showed that NLR was an independent risk factor for death after adjusting confounders ( HR=1.091, 95% CI: 1.049-1.136, P<0.001). Spearman correlation test showed a correlation between NLR and APACHEII score ( r=0.655, P<0.001). ROC curve analysis showed that NLR had the greatest predictive value for 30-day death, with an area under ROC curve (AUC) of 0.787, a sensitivity of 82.6%, a specificity of 67.4%, and the cut-off value of 7.35. Kaplan-Meier survival analysis curve shows that patients in the below NLR cut-off value group had a significantly higher 30-day survival rate than those in the above NLR cut-off value group ( P<0.001). Conclusions:The increased NLR is a high risk factor for death in patients with severe heat stroke, and helps predict the prognosis of patients with severe heat stroke.

OBJECTIVE: To investigate the clinical significance of early troponin I (TnI) level in the prognosis of severe heat stroke. METHODS: Clinical data of 131 patients with severe heat stroke in the intensive care unit (ICU) of the Affiliated Changzhou NO.2 People's Hospital of Nanjing Medical University (study dataset) and ICU 67 patients with severe heat stroke in Jintan First People's Hospital of Changzhou (validation dataset) were retrospectively analyzed from June 2013 to September 2022. The patients were divided into survival group and death group according to 30-day outcomes. TnI was collected within 24 hours after admission to the emergency department. Cox regression analysis was performed to analyze the risk factors of severe heat stroke death. Spearman correlation test was used to analyze the correlation between TnI and heart rate, and peripheral systolic blood pressure. The receiver operator characteristic curve (ROC curve) was drawn to evaluate the predictive value of TnI for death in patients with severe heat stroke. Decision curve analysis (DCA) was conducted to assess the clinical net benefit rate of TnI prediction. Grouping by TnI cut-off value, Kaplan-Meier survival curve was used to analyze 30-day cumulative survival. Sensitivity analysis included modified Possion regression, E-value, and subgroup forest map was used to evaluate the mortality risk of TnI in different populations. External dataset was used to verify the predictive value of TnI. RESULTS: The death group had significantly higher TnI compared to the survival group [μg/L: 0.623 (0.196, 1.510) vs. 0.084 (0.019, 0.285), P < 0.01]. Multivariate Cox regression analysis after adjusting for confounding factors showed that TnI was an independent risk factor for death [hazard ratio (HR) = 1.885, 95% confidence interval (95%CI) was 1.528-2.325,P < 0.001]. Spearman correlation test showed that TnI was positively correlated with heart rate (r = 0.537, P < 0.001) and negatively correlated with peripheral systolic blood pressure (r = -0.611, P < 0.001). ROC curve showed that the area under the curve (AUC) of the TnI (0.817) was better than that of the acute physiology and chronic health evaluation II (APACHE II, 0.756). The DCA curve showed that the range of clinical net benefit rate of TnI (6.21%-20.00%) was higher than that of APACHE II score (5.14%-20.00%). Kaplan-Meier survival curve showed that patients in the low-risk group (TnI ≤ 0.106) had a significantly higher 30-day survival rate than that in the high-risk group (TnI > 0.106) group (Log-Rank test: χ² = 17.350, P < 0.001). Modified Possion regression with adjustment for confounding factors showed that TnI was still an independent risk factor for death in patients with severe heat stroke [relative risk (RR) = 1.425, 95%CI was 1.284-1.583, P < 0.001]. The E-value was 2.215. The subgroup forest plot showed that the risk factors of TnI were obvious in male patients and patients ≤ 60 years old (male: HR = 1.731, 95%CI was 1.402-2.138, P < 0.001; ≤ 60 years old: HR = 1.651, 95%CI was 1.362-2.012, P < 0.001). In the validation dataset, ROC curve analysis showed that the AUC (0.836) of TnI predicting the prognosis of severe heat stroke was still higher than the APACHE II score (0.763). CONCLUSIONS Early elevation of TnI is a high-risk factor for death in patients with severe heat stroke, and it has a good predictive value for death.
Humans ; Male ; Middle Aged ; Troponin I ; Retrospective Studies ; Clinical Relevance ; ROC Curve ; Prognosis ; Intensive Care Units ; Heat Stroke/diagnosis* ; Sepsis