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Objective:To investigate the effect of venous blood carbon dioxide binding capacity (CO 2-CP) on the short-term prognosis of patients with acute ischemic stroke (AIS) after thrombolytic therapy. Methods:A total of 86 AIS inpatients who received thrombolytic therapy in the emergency department of Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University from April 2019 to May 2021 were analyzed retrospectively. According to the venous blood CO 2-CP levels at admission, the patients were divided into two groups: low CO 2-CP group (CO 2-CP < 23 mmol/L, n = 52) and high CO 2-CP group (CO 2-CP ≥ 23 mmol/L, n = 34). The CO 2-CP levels and changes between the two groups before and after thrombolytic therapy were compared. The National Institutes of Health Stroke scale (NIHSS) score was used to evaluate the improvement rate of patients after thrombolytic therapy [NIHSS score at admission-NIHSS score at discharge)/NIHSS score at admission ×100%] and in-hospital death was also recorded. The correlation between CO 2-CP levels and prognosis of patients with AIS during emergency visit was analyzed, the receiver operator characteristic curve (ROC curve) was drawn and the area under the ROC curve (AUC) was calculated to evaluate the predictive value of CO 2-CP in the prognosis of AIS patients. Results:The CO 2-CP levels of low CO 2-CP group and high CO 2-CP group after thrombolytic therapy were significantly higher than those before treatment (mmol/L: 23.08±2.34 vs. 20.46±1.51, 25.24±2.16 vs. 23.94±1.07, both P < 0.05). The differences of CO 2-CP before and after treatment in low CO 2-CP group were significantly higher than those in high CO 2-CP group (mmol/L: 2.62±0.83 vs. 1.30±1.09, P < 0.05). The improvement rate of CO 2-CP levels in the high CO 2-CP group (NIHSS improvement rate > 45%) was significantly higher than that in the low CO 2-CP group [85.29% (29/34) vs. 23.08% (12/52)], while the mortality in the low CO 2-CP group was significantly higher than that in the high CO 2-CP group [11.54% (6/52) vs. 0% (0/34), P < 0.05]. The AUC of CO 2-CP for the prognosis of patients with AIS thrombolysis was 0.820, the 95% confidence interval (95% CI) was 0.727-0.924, P = 0.000 1. Conclusion:AIS patients with CO 2-CP levels less than 23 mmol/L have a poor short-term prognosis, which has certain predictive and clinical reference value for choosing thrombolytic time in emergency stroke patients.
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Objective:To investigate the short-term prognosis of patients with acute ischemic stroke after thrombolysis with alteplase and the relationship between TOAST and OCSP classification and prognosis of patients with acute ischemic stroke.Methods:A retrospective analysis was conducted in 193 patients with acute ischemic stroke in the Emergency Department of our hospital from January 2019 to June 2020, including 158 males and 85 females, aged 69.46±13.02 years. Among them, 66 patients were treated with alteplase thrombolysis and 127 patients were not treated with thrombolysis. The short-term prognosis of thrombolytic patients and non-thrombolytic patients were compared; the influence of TOAST classification and OCSP classification on the prognosis of acute ischemic stroke was analyzed.Results:There was no significant difference in the length of hospital stay between the thrombolytic group and the non-thrombolytic group ( P>0.05), while the improvement rate of NIHSS score, GCS score, and mRS score were significantly different at admission and discharge ( P<0.05). According to TOAST classification, 78 cases (40.41%) were LAA, 100 cases (51.81%) were SAO, 9 cases (4.66%) were CE, 3 cases (1.55%) were SOE, and 3 cases (1.55%) were SUE; SAO type accounted for the highest proportion (51.81%), the improvement rate of NIHSS score at admission and discharge was significantly different from that of the LAA patients ( P<0.05), and the short-term prognosis was the best. According to OCSP classification, 39 cases (20.21%) were LACI, 64 cases (33.16%) were PACI, 55 cases (28.50%) were POCI, 35 cases (18.13%) were TACI, among which the PACI patients had the highest proportion, while the improvement rate of NIHSS score in the LACI patients was significantly different at admission and discharge compared with other types of patietns ( P<0.05), and the short-term prognosis was good. Conclusions:The short-term prognosis and symptom improvement of patients with acute ischemic stroke after alteplase thrombolytic therapy are obvious. TOAST classification and OCSP classification have certain prediction effects and play clinical reference roles on the short-term prognosis of patients with acute ischemic stroke.
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Objective To explore the effect of autophagy regulator on the injury of rat hippocampal neurons induced by oxygen-glucose deprivation (OGD).Methods Rat hippocampal neurons were cultivated in primary and subjected to OGD to simulate neuronal hypoxic ischemia injury for 2 hours or 6 hours followed by reperfusion for 12 hours with or without 3-methyladenine (3-MA, 20μmol/L) or rapamycin (0.2μmol/L). The morphology of neurons was observed with optical microscope. The expression of autophagy-related protein (LC3, P62) and apoptosis-related protein (cleaved caspase-3) were assessed by Western Blot analysis. The apoptosis of neurons was detected by flow cytometry, the release rate of lactate dehydrogenase (LDH) was calculated by automatic biochemical analyzer, and the cell activity was determined by methyl thiazolyl tetrazolium (MTT) colorimetric assay.Results Compared with the control group, the expression of LC3 Ⅱ/Ⅰ (gray value: 3.091±0.160, 3.422±0.186 vs. 0.256±0.021), cleaved caspase-3 (gray value: 0.230±0.025, 0.440±0.051 vs. 0.050±0.007), neuronal apoptotic rate, LDH release rate [(38.50±4.15)%, (59.60±5.65)% vs. (12.40±1.32)%] were increased, while the expression of P62 (gray value: 0.290±0.025,0.120±0.026 vs. 0.450±0.040), neuronal activity [(71.40±7.23)%, (42.80±4.12)% vs. (100.30±2.30)%] were decreased at 2 hours or 6 hours after OGD (allP < 0.05). When the time of OGD was 2 hours and it was combined with 3-MA, the expression of LC3 Ⅱ/Ⅰ (gray value: 2.281±0.121), the neuronal activity [(51.10±5.73)%] were decreased, while the expression of P62 and cleaved caspase-3 (gray scale: 0.410±0.037, 0.330±0.027, respectively), neuronal apoptotic rate, the injury of neurons [LDH release rate: (47.30±4.43)%] were increased (allP < 0.05). When the time of OGD was 2 hours and it was combined with rapamycin, the expression of LC3 Ⅱ/Ⅰ (gray value: 3.689±0.214), the neuronal activity [(85.30±8.56)%] were increased, while the expression of P62 and cleaved caspase-3 (gray value: 0.170±0.040, 0.090±0.096, respectively), neuronal apoptotic rate, the injury of neurons [LDH release rate: (24.30±2.14)%] were decreased (allP < 0.05). On the contrary, when the time of OGD was 6 hours and it was combined with 3-MA, the expression of LC3 Ⅱ/Ⅰ and cleaved caspase-3 (gray value: 3.021±0.178, 0.240±0.017), neuronal apoptotic rate, the injury of neurons [LDH release rate: (36.60±3.45)%] were decreased, while the expression of P62 (gray value: 0.350±0.060), the neuronal activity [(59.70±6.13)%] were increased (allP < 0.05). When the time of OGD was 6 hours and it was combined with rapamycin, the expression of LC3 Ⅱ/Ⅰ and cleaved caspase-3 (gray value: 3.923±0.201, 0.590±0.062), neuronal apoptotic rate, the injury of neurons [LDH release rate:(71.20±7.81)%] were increased, while the expression of P62 (gray value: 0.070±0.008), the neuronal activity [(27.30±2.12)%] were decreased (allP < 0.05).Conclusion The enhancement of autophagy has protective effect on neurons under the condition of mild OGD, while it can aggravate the injury of neurons induced by a long-time OGD.
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Objective To investigate the optimal injury time point of cardiac arrest (CA) induced electrically, and establish a reproducible prolonged CA and cardiopulmonary resuscitation (CPR) model in pigs. Methods Forty healthy domestic male pigs were randomly divided into four groups, which were ventricular fibrillation (VF) 8, 10, 11, and 12 minutes groups, each group for 10 animals. In these groups, VF was induced by alternating current delivered to right ventricular endocardium and untreated for 8, 10, 11, and 12 minutes, respectively, followed by 6 minutes of CPR procedure. The resuscitation and survival outcomes were recorded. Hemodynamic parameters and arterial blood gases of animals after successful resuscitation were measured and recorded for 6 hours. Those successful resuscitation animals were regularly evaluated for the neurological deficit score (NDS) and survival outcomes every 24 hours till 96 hours after resuscitation. Results The shortest duration of CPR (minute: 6.9±1.3) and the highest successful ratio of the first defibrillation (7/10) were observed in group VF 8 minutes, and the ratio of successful resuscitation was 100%. The best coronary perfusion pressure (CPP) during the CPR, less neurological impairment, longer survival time, more stable hemodynamics, and shorter time for arterial pH and lactate level restoring to the original state after CPR were also observed in group VF 8 minutes, and no severe damage was found in those animals. The longest duration of CPR (minute:10.3±2.9) and the lowest successful ratio of the first defibrillation (1/10) were observed in group VF 12 minutes, and only 4 animals achieved restoration of spontaneous circulation (ROSC), and no animal survived to CPR 96 hours. The worst CPP during CPR and the highest NDS after resuscitation were also found in VF 12 minutes animals compared to those animals in the other groups. The injuries caused by ischemia and hypoxia in groups VF 10 minutes and VF 11 minutes were in between those of the groups VF 8 minutes and VF 12 minutes, and the duration of CPR were (7.0±2.1) minutes and (8.2±2.6) minutes. There were 9 and 7 animals achieved ROSC in groups VF 10 minutes and VF 11 minutes correspondingly, and 6 and 4 animals survived to 96 hours respectively. Obviously unstable hemodynamics was observed during the period of CPR 2 hours in the two groups. At CPR 1 hour, the heart rates (HR, beats/min) in groups VF 10 minutes and VF 11 minutes increased to 172 (155, 201) and 168 (136, 196) respectively, and the mean arterial pressures (MAP, mmHg, 1 mmHg = 0.133 kPa) declined to 97 (92, 100) and 81 (77, 100), the cardiac output (CO, L/min) decreased to 5.0 (4.0, 5.8), 3.7 (3.0, 5.4) correspondingly. Distinct injuries were found in the two groups [CPR 24-96 hours NDS in groups VF 10 minutes and VF 11 minutes: 180 (110, 255)-20 (0, 400) and 275 (223, 350)-240 (110, 400)], and the arterial pH of the two group decreased to 7.26±0.09 and 7.23±0.09 respectively, and the level of lactate (mmol/L) increased to 9.17±1.48 and 12.80±2.71 correspondingly at CPR 0.5 hour. Significantly lower pH was observed in group VF 11 minutes compared to group VF 8 minutes at CPR 0.5 hour (7.23±0.09 vs. 7.33±0.04, P < 0.05). The highest level of lactate (mmol/L) was also found at the same time point in group VF 11 minutes, which recovered to normal slowly, and was still significantly higher than groups VF 8, 10, 12 minutes (7.58±3.99 vs. 2.55±1.53, 2.13±2.00, 3.40±2.30, all P < 0.05) at CPR 4 hours. Conclusions The longer duration of CA was, the more severe damage would be, the longer CPR time would be required, and the harder of the animals to achieve ROSC. In this prolonged CA and CPR porcine model, 10-11 minutes for untreated VF, was an optimal time point with appropriate successful rate of resuscitation, survival outcomes, and post-resuscitation injuries. Therefore, we recommended 10-11 minutes might be the rational length of no-flow time in this model.
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Objective: The aim of the study is to validate whether the Recognition Of Stroke In the Emergency Room (ROSIER) scale can be used by general practitioners (GPs) in an emergency medical service (EMS) protocol to transfer stroke patients from primary care center to advanced hospital with acute stroke center. Methods: GPs prospectively performed the ROSIER scale and the Cincinnati Prehospital Stroke Scale (CPSS) on suspected stroke patients as a transfer protocol. All patients were immediately transferred to the Level-II hospital for further treatment. Results: 468 of the 512 suspected stroke patients met the inclusion criteria in this study. The ROSIER scale showed a diagnostic sensitivity of 83.13% (95% confidence intervals [CI] 79.74-86.52%) and specificity of 80.88% (95% CI 77.32- 84.44%). The CPSS showed a diagnostic sensitivity of 78.01% (95% CI 74.26-81.76%) and specificity of 70.59% (95% CI 66.46-74.72%). The Kappa statistic value of the ROSIER scale and the CPSS were 0.601 and 0.454, respectively. The area under the curve (AUC) of ROSIER scale was large than the CPSS (AUC 0.855 vs. 0.791). However, the difference was not significantly different. Conclusions: This study suggest that ROSIER and CPSS could be used in an EMS protocol to transfer stroke patients from a primary care center to an advanced hospital offering thrombolysis service
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OBJECTIVE: To explore the effect of 1,2-dichloroethane(1,2-DCE) induced apoptosis on the expression of related proteins in human neuroblastoma cells(SH-SY5 Y cells). METHODS: SH-SY5 Y cells were cultured in complete medium with 1,2-DCE at final concentrations of 0,10,20,30,40,50,60,70 and 80 mmol/L. After being cultured for24 hours,the apoptosis of SH-SY5 Y cells was tested by flow cytometry using annexin Ⅴ-fluorescein isothiocyanate and propidium iodide. Western blot was used to detect the protein expression of P53,B cell lymphoma/leukmia-2(BCL-2)and BCL-2 associated X protein(BAX). RESULTS: At 1,2-DCE concentrations of 0-80 mmol/L,the total apoptosis rate of SH-SY5 Y cells increased with 1,2-DCE concentrations in a dose-dependent manner(P < 0. 01). At 1,2-DCE concentrations of 30-80 mmol/L,the early apoptosis rate and total apoptosis rate of SH-SY5 Y cells increased significantly than the control group(P < 0. 05). Compared with the other groups,the protein expression of P53 was the lowest when the1,2-DCE concentration was 20 mmol/L(P < 0. 05),and the protein expression of BCL-2 and the BCL-2/BAX ratio were the lowest when the 1,2-DCE concentration was 70 mmol/L(P < 0. 05). There is no dose-response relationship in the1,2-DCE concentrations and the protein expression levels of P53,BCL-2 and BAX,and BCL-2/BAX ratio. Linear multiple regression analysis revealed that the total apoptosis rate of SH-SY5 Y cells treated with 1,2-DCE was associated with the protein expression of P53 and BCL-2,and BCL-2/BAX ratio(P < 0. 05). CONCLUSION: 1,2-DCE could inhibit the apoptosis of SH-SY5 Y cells. The mechanisms may be related to the changes of P53 and BCL-2 protein expression,and BCL-2/BAX relative amount.
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Objective To investigate the protective effects of Ulinastatin on intestinal barrier damaged after cardiopulmonary resuscitation (CPR) in rats in order to illustrate the possible mechanism.Methods Twenty-one male SD rats were divided into three groups randomly (random number) including control group (sham group, n =7), cardiopulmonary resuscitation group (CPR group, n =7) and ulinastatin group (UTI group, n =7).The rats were anesthetized with pentobarbital sodium (45-60 mg/kg) by intraperitoneal injection.The rats of sham group were only treated with endotracheal intubation.Ulinastatin (100 000 U/kg) were injected via caudal vein 2 hours prior to CPR, and cardiac arrest was made in rats and cardiopulmonary resuscitation was carried out in the UTI group, while equivalent volume of sterile saline was used instead in the CPR group.Blood and ileum samples were obtained at 48 hour after restoration of spontaneous circulation (ROSC).The levels of tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β) were assayed by ELISA (enzyme-linked immunosorbent assay), the protein levels of caspase-3 were determined by western blot, the intestinal mucosa were stained by terminaldeoxynucleoitidyl transferase mediated nick end labeling (TUNEL) and ileac mucosa were observed under transmission electron microscope.Data were processed with SPSS 17.0 software.Results The plasma levels of TNF-α and IL-1β were dramatically higher in CPR group than those in other two groups (CPR vs.sham, P < 0.01;CPR vs.UTI, P < 0.05).Moreover, the tight junctions between cells obviously broadened and loosened in the CPR group were found under electron microscope, however, this phenomenon was not obvious in the UTI group.A large number of apoptotic cells were observed by TUNEL assay in the CPR group, but a small number of apoptotic cells were observed in the UTI group.The protein levels of caspase-3 in the UTI group were higher than those in sham group, but lower than those in CPR group (both P < 0.05).Conclusions Ulinastatin has protective effects on the intestinal barrier damaged after cardiopulmonary resuscitation in rats by decreasing the proinflammatory mediators in the blood, reducing the expression of caspase-3and then reducing the numbers of apoptotic intestinal cells.
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Objective To explore the protective effects of Caspase inhibitor on in vitro hippocampal neurons of rats with oxygen glucose deprivation (OGD) injury.Methods The primary hippocampal neurons from newborn Sprague-Dawley rats were cultured for 7 days,and then,divided into control group,OGD/re-OG treatment group,Caspase inhibitor (Z-VAD-FMK) treatment group and DMSO treatment group; and OGD/re-OG was performed in the later three groups for OGD duration of 6 h.Through the experimental process,20 μmol/L Z-VAD-FMK was given to the Z-VAD-FMK treatment group,while 1‰ DMSO was added into culture medium in the DMSO group.The morphology of the neurons was observed 24 hours after re-OG under light microscopy and electron microscopy.MTT assay was used to determine the rate of survived cells and lactate dehydrogenase (LDH) content in culture medium.The neurons apoptosis rate was measured by using flow cytometry (Annexin V-FITC/PI).Caspase-3 activity of neurons was analyzed by colorimetry.The protein expression of Caspase-3 wasassessed by Western blotting.Results Cells in the OGD/re-OG treatment group showed swelled body,some having ruptured membrane,cell integrity being damaged,cell nucleus edema,mitochondrial swelling and cristae ordered chaos; cells in the Z-VAD-FMK treatment group showed decreased injury as compared with the OGD/re-OG treatment group,having cell integrity; as compared with the OGD/re-OG treatment group,Z-VAD-FMK treatment group had significantly higher absorbance value (0.204±0.019 vs.0.303±0.018) and cell survivalrate (0.481%±0.045%vs.0.704%±0.040%),obviously decreased lactate dehydrogenase (LDH) content ([406.500±21.286] U/L vs.[326.000±20.278] U/L),apoptosis rate (49.700%±3.100% vs.29.820%±2.839%),absorbance value of the Caspase-3 active area and Caspase-3 protein expression (1.070±0.077 vs.0.785±0.058),with statistically differences (P<0.05).Conclusions Caspase inhibitor may protect rat hippocampal neurons from oxygen glucose deprivation injury by inhibiting Caspase-3 activity.
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AIM: To explore the role of P2X7 receptor in inhibition of lipopolysaccharide (LPS)-stimulated BV-2 cell activation by minocycline .METHODS:BV-2 cells were divided into 5 groups:control group, LPS group, LPS+0.1 μmol/L Mino group, LPS+1 μmol/L Mino group and LPS+10 μmol/L Mino group.The expression of P2X7 re-ceptor was determined by real-time PCR and Western blotting .The levels of TNF-αand IL-1βin the microglia culture su-pernatants were measured by ELISA .The morphological changes of the cells were also observed .RESULTS: After ex-posed to LPS, the expression of P2X7 receptor increased in BV-2 cells at mRNA and protein levels .The concentrations of TNF-αand IL-1βin the microglia culture supernatants also increased .Meanwhile, 0.1~10μmol/L minocycline inhibited those changes in a dose-dependent manner .CONCLUSION:Minocycline inhibits the activation of microglia .The mecha-nism may be related to the P2X7 receptor.
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Objective To explore the effect of Ulinastatin on blood brain barrier (BBB) and apoptosis of neural cells in septic rats.Methods Fifty-two clean level male Sprague-Dawley rats were randomly (random number table) divided into six groups:Sham groups at 6 h and 24 h,each group with six rats.Sepsis groups (CLP) and Ulinastatin treated groups (UTI) at 6 h and 24 h,each group with ten rats.In CLP and UTI groups,cecal ligation and puncture (CLP) were performed to induce sepsis.Sham group was only opened and closed abdomen.Ulinastatin (50 000 U/kg) was administered via femoral vein 1 h after CLP.The same volume of saline instead of Ulinastatin was administered in Sham and CLP groups.The neurological status was assessed by Neurological Deficit Scale Scores (NDSS) at 6 h and 24 h after CLP.Then the brain was harvested for HE staining and weighing water content.The BBB permeability was assayed by Evans Blue dye extravasations.Apoptosis of neural cells were detected by TUNEL immune fluorescence.Statistical analysis was performed with SPSS version 13.0,ANOVA was used for multiple groups comparison and t-test for paired comparison.Results The Neurological Deficit Scale Scores of UTI group was lower than Sham group (P < 0.05) but higher than that of CLP group (P < 0.05).Swelling,degeneration and edema were observed in cerebral cortex and hippocampal neurons in CLP group through light microscope,and were more serious than those in UTI group.Compared with UTI 24 h group,BBB permeability of CLP 24 h group significantly rose (P < 0.05).The number of apoptosis of neural cells increased more in CLP group than it did in UTI group (P < 0.05).Conclusions Ulinastatin could protect the cerebral tissue in septic rats by alleviating the damage of BBB and reducing the apoptosis of neural cells.
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Objective To investigate the expressions and clinical significanees of suppressors of cytokine signaling-1 (SOCS-1) and SOCS-3 in myocardium of patients with sudden cardiac death (SCD). Method This study included myocardial autopsy specimens of 24 patients admitted between 2005 and 2006. Of them, 9 cases had the findings of autopsy examination consistent with coronary atberosclerosis (non-myocardial infarction) leading to SCD (non-MI group), 7 patients died of acute myocardial infarction (MI group) and 8 patients died of traffic accidents and trauma The expressions of SOCS-1 mRNA and SOCS-3 mRNA in the myocardium of non-MI and con-trol group were detected by using RT-PCR. The levels of SOCS-1 protein and SOCS-3 protein were detected by us-ing immunohistochemistry. Statistical analysis were performed by using SPSS version 13.0 software and the data were processed with ANOVA test. Results The expressions of SOCS-1 mRNA and SOCS-3 mRNA in non-MI and MI groups were were significantly higher than those in control group (0. 788±0. 101) and (0. 741±0.111) vs.(0.436±0.044) (P <0.01); (0.841±0.092) and (0.776±0.070) vs.(0.454±0.076), P <0.01, re-spectively). The antibody-positive cells of SOCS-1 protein in myocardium of non-MI group and MI group were significantly higher than those in myoeardium of control group (320.00±48.48) and (347.14±70.88) vs.(42.50±10.35) (P < 0.01), respectively. The antibody-positive cells of SOCS-3 protein in myoeardium of non-MI group and MI group were significantly higher than those in myocardium of control group (381.11±59.25) vs.(40.00±10.69), (P < 0.01)and (332.86±111.91) vs. (40.00±10.69), (P =0.001). Conclusions The expressions of SOCS rnRNA and SOCS-3 mRNA in myoeardium of patients with SCD from coronary diseases are significantly increased contributing to the pathogenesis of SCD.
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Objective To establish the oxygen glucose deprivation (OGD)/reoxygenation experimental model of hippocatnpal neurons of rat in vitro, and to try to identify the length of time for producing optimum injury in this model. Method The primary hippocampal neurons of newborn Sprague-Dawley rats were cultured for 7 days and randomly (random number) divided into a control group and OGD groups. The OGD groups were assigned into 1 h, 2 h, 4 h, 6h, 8 h and 10 h subgroups in accordance with different lengths of time for oxygen glucose deprivation. The neurons of OGD groups were placed into a tri-gas incubator containing 0.5% oxygen and the culture medium was substituted with the glucose-free Earle' s balanced salt solution, simulating cerebral ischemia injury in vivo. The morphology of neurons was observed after reoxygenation for 24 hours. The MIT assay was used to determine the rate of survived cells derived from the value of optical density (OD) of cells. The lactate dehydro-genase (LDH) content in culture medium was detected to evaluate the neuron injury. The apoptotic rate of neurons was measured by using flow cytometry. Dunnett-test and Spearman correlation analysis were used to analyze the data with SPSS version 16.0 soft ware package. Results The morphological damage of neurons in OGD groups aggravated gradually, optical density and cell survival rate decreased (rs= -0.961 and rs = -0.966, P <0.01), and the amount of LDH increased (rs = 0.990, P <0.01) with longer duration of exposure to oxygen glucose deprivation, and the rate of neuron apoptosis increased obviously which was significantly statistical difference in com-parison with the control group (P < 0.05). Under the setting of oxygen glucose deprivation for 6 hours, the apop-tosis rate of neurons approximated to 50% . Conclusions The oxygen glucose deprivation/reoxygenation model of rat's hippocampal neurons in vitro was established successfully. From the findings of morphological changes and apoptosis rate of neurons, the oxygen glucose deprivation for 6 hours may be the suitable length of time for inducing neuron injury in this model.
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Objective To investigate immunological dysfunction of intestine mucosa barrier in a rat model of sepsis. Method Sixty Sprague-Dawley rats were assigned randomly(random number) into sepsis group (n = 45)and control group (n = 15). The animals in sepsis group were subjected to cecal ligation and puncture (CLP), whereas rats of control group underwent a sham surgery. The ileac mucosa and segments were harvested 3 h, 6 h and 12 hours after CLP, and the blood samples were collected. Pathological changes, protein levels of defensin-5 (RD-5) and trefoil factor-3(TFF_3) mRNA, lymphocytes apoptosis in the intestinal mucosa were determined. In an additional experiment, the gut-origin bacterial DNA in blood was detected. Results In the septic animals, in-testinal mucosa showed marked injury with loss of ileal villi, desquamation of epithelium, detachment of the lamina propria, hemorrhage and ulceration. Compared with control, the expression of TFF_3 mRNA and level of RD-5 pro-tein were decreased and the mucosal lymphocyte apoptosis increased (P < 0.05) in sepsis group. Compared with control group, the significant differences in RD-5 and TFF_3 mRNA appeared 3 hours after CLP and those differ-ences were progressively increased in 6 hours and 12 hours after CLP in sepsis group (P < 0.05, F of RD-5 = 11. 76, F of TFF_3 = 16.86 and F of apoptosis = 122.52). In addition, the gut-origin bacterial DNA in plasma de-tected was positive in all sepsis animals. Conclusions It suggests that immunological function of intestinal mucosa is impaired in septic rats and further worsened following the course of sepsis.
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Objective To observe the effect of injecting Xuebijing via different routes, as either treatment or pretreatment, on changes in intestinal mucosal morphology in a rat model of sepsis. Method Ninety-one healthy Sprague-Dawley rats were randomly divided into five groups: 1) control group ( n = 7) , 2) sepsis group ( n = 21) , 3) intragastric pretreatment group ( n = 21) , 4) intravenous pretreatment group (n = 21) , and 5) intravenous treatment group (n = 21) . Except for the control group, the other groups were further divided into three sub-groups for assessment at 3, 6 and 12 h post-operation ( n = 7 per group) . Sepsis was induced by cecal ligation and puncture (CLP) . For the intragastric pretreatment group, Xuebijing injection (5 mL/kg) was administered via intragastric injection 2 hours before CLP. For the intravenous pretreatment group, Xuebijing injection (5 mL/kg)was administered via the caudal vein 2 hours before CLP. For the intravenous treatment group, Xuebijing injection (5 mL/kg) was intravenously infused 2 hours after CLP. The control group received no treatment. The ileum was removed from all rats for measurement. The rats were sacrificed at 3, 6 or 12 h after operation to obtain the ileum.Intestinal mucosal damage index and morphological changes in the intestinal mucosa were detected by light microscopy and electron microscopy. Analysis of variance was used to compare the groups. P -values < 0.05 were considered to indicate statistically significant differences. Results Intestinal mucosal damage was significantly reduced in and the three treatment groups compared with the untreated sepsis group (3h, F =53.35; 6h, F =74.93; 12 h, F - 171.27; P =0.000). Intestinal damage was significantly reduced in the intravenous pretreatment group compared with the intragastric pretreatment group (3 h, F = 53.35,P =0.036; 6 h, F = 74.93,P =0.039; 12 h, F = 171.27, P =0.042). Conclusions Irrespective of the route, the administration of Xuebijing protected against intestinal mucosal damage and intravenous pretreatment exerted the most effective protection against intestinal mucosal damage in this rat model of sepsis.
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Objective To investigate the effeets of ulimstatin on expression of intestinal defemin-5 mRNAin the rat model of sepsis.Method The experiment was performed in pharmaco-laboratory of medical college,Sun Yat-Sen University.sixty Sprague-Dawley rals were randomly divided into control,sepsis,pretreated andtreated groups(n=15).Semis was induced in the mts of latter three groups by cecal lifo.and puncture(CLP).The rats of pretreated group received 25 000 U/kg ulinastatin 2 hours before operation and the rats of uli-nastatin treated groups received 50 000 U/kg ulinastatin 2 hours after operation.Some pieces of ileum mucosa weretaken 12 h after CLP.Tge pathological changes were observed and the expression of RD-5 mRNA was detectedwith RT-PCR.All data were managed by SPSS 13.0 software and arIaIyzed by using One-way ANOVA and LSD-ttest.Results The expression of RD-5 mRNA in the rats of sepsis group significantly decreased compared to col-trol(P<0.05).The expression of RD-5 mRNA of pretreated and treated groups sigificantly inereased comparedto sepsis group(P<0.05);pretreated groups had more increased expression of,RD-5 mRNA compared to treatedgroups(P<0.05).Conclusions The expression of intestinal RD-5 mRNA significantly decreases in sepsis,which could be improved by the treatment of ulinadtatin leading to intestinal mucosal protection of the siqnifleant.The pretreatment may be more effective than the theTapeatic treatment in the rat model of sepsis.
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Objective To explore the strategy of emergency medical rescue of the massive crowd in general hospital during spring festival with snow disaster. Method The clinical data of 20 966 emergency cases were analyzed retrospectively from 22 Jan,2008 to 6 Feb, 2008 with snow disaster, and concerned about the ratio of different diseases, the character of pre-hospital care and the contrast between emergency medical treatment and routine work. Results The accidence of respiratory disease ( 57.3 % ) was followed by gastrointestinal ( 25.5 % ) and trauma (6.2% )during the emergency medical treatment, and surgical trauma, syncope, coma and convulsion were the most common symptoms, also in some conditions, but empties returning was 30.3% . Similar to the above situation, the extremities (56%)and head injury (24%)were most commonly in the hospital emergency department. The incidence of falling accidents was high( 35.7 % ), and two of them were dead due to trauma on died of being trampled, and on the other was electrothermal burn and falling. Conclusions The general hospital is very important in emergency medical treatment, and it should be ready to tackle the emergency disaster, in order to reduce the loss to minimum.
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Objective:To observe the therapeutic efficacy of somatostatin combined with compound salvia miltiorrhiza injection(复方丹参注射液)on patients with acute pancreatitis(AP).Methods:By using randomized controlled trail,62 patients with AP were divided into control group(31 cases) and observation group(31 cases) in a period from June,2002 to December,2006.In the control group,routine measures,such as forbidding food,decompressing stomach and intestines,were taken,and in addition,intravenous injection of somatostatin 250 ?g with subsequent intravenous drip 3 000 ?g in normal saline 500 ml at a rate of 250 ?g/h once everyday was used for 7-14 days.On the above treatment of the control group,compound salvia miltiorrhiza injection 20 ml in normal saline 250 ml,intravenous drip every day for 7-14 days,was added in the observation group.The disappearance of symptoms and abdominal signs,amylase of urine and blood,the time of recovery of hepatic function,change of calcium concentration,incidences of multiple organ dysfunction syndrome(MODS) and case fatality were observed and compared.Results:Amylase of blood after treatment in observation group was lower than that in the control group,while serum calcium concentration was higher,especially on 3 and 5 days after treatment(all P
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AIM: To determine the changes of the serum levels of tumor necrosis factor ? (TNF-?), interleukin-6 (IL-6), IL-10, C reactive protein (CRP) and D-dimer in the patients with multiple organ dysfunction syndrome (MODS) and compare the relationship between the levels of cytokines in early stage and MODS. METHODS: The serum values of TNF-?, IL-6, IL-10, CRP and D-dimer were measured in 27 patients with MODS in 1 d, 3 d and 5 d after undergoing disease, and compared with the adult peripheral blood of 15 normal controls. The levels in the first undergoing day between the lived group (n=19) and died group (n=8) were compared. RESULTS: The serum levels of TNF-?, IL-6, IL-10, CRP and D-dimer in MODS group were higher than that in control (P
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AIM: To investigate the protective effect of ulinastatin on rats with hemorrhagic shock. METHODS: A prospective, controlled animal study was designed. The model of hemorrhagic shock in rats was produced by Chaudry method. After 60 min, rats were resuscitated by transfusion of shed blood and normal saline, but a half of them were treated with ulinastatin. At different time points after reperfusion, the levels of tumor necrosis factor-alpha (TNF-?), interleukin-6 (IL-6), malondialdehyde (MDA) and superoxide dismutase (SOD) in serum were detected. RESULTS: The levels of TNF-?, IL-6 and MDA significantly increased and the activity of SOD decreased. In the ulinastatin-treated groups, the blood pressure and heart rate were obviously improved; the levels of TNF-?, IL-6 and MDA significantly decreased and the activity of SOD had little change after hemorrhagic shock and reperfusion. CONCLUSION: Ulinastatin has a protection effect on rats with hemorrhagic shock by suppressing the production of inflammatory factors and reducing oxidative damage.