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Objective To improve the understanding of perioperative anesthesia management in patients with anti-N-methyl-D-aspartate receptor encephalitis combined with a history of ovarian teratoma.Methods Case information of 10 patients with anti-N-methyl-D-aspartate receptor encephalitis with a history of ovarian teratoma admitted to the Third Affiliated hospital of Sun yat-sen University from July 2014 to November 2018 were retrospectively analyzed.Results A total of 10 patients received treatment,8 improved after treatment,2 had poor prognosis,and their families required discharge.All patients received endotracheal intubation under general anesthesia.Conclusions Anesthesiologists should pay attention to perioperative anesthesia management of patients with anti-N-methyl-D-aspartate receptor encephalitis complicated with ovarian teratoma,including preoperative evaluation,anesthesia methods and drug selection,intraoperative and postoperative management.
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Objective This study aims to investigate the effect of Lipoxin A4 receptor on acute lung injury (ALI) induced by intestine ischemia-reperfusion (IIR). Methods Thirty-two 8-week old SD rats were randomly divided into four groups: sham, intestine ischemia-reperfusion (IIR), IIR + BML111 (BML-111), Boc-2 + IIR +BML111 (Boc-2). BML-111 (1 mg/kg) was given intraperitoneally at the onset of reperfusion in the BML-111 and the Boc-2 group. Boc-2 (50 μg/kg) was given intraperitoneally after anesthesia in the Boc-2 group. Rats were subjected to superior mesenteric artery occlusion consisting of 45-min ischemia and 6-h reperfusion, and the sham laparotomy was served as controls. The lung pathology was assayed by the H&E staining. Lung water content was detected using dry/wet ratio. Concentrations of TNF-α, IL-1β, and IL-6 in lung tissue were determined by ELISA. The protein expression of p38 MAPK and NF-κB of lung was assayed by western blot. Results IIR induced serious ALI, with poor lung pathology and increased lung water content, elevation of TNF-α, IL-1β, and IL-6 levels in lung, accompanied with activation of p38 MAPK/NF-κB pathway. However, BML-111 could inhibit the activation of p38 MAPK/NF-κB pathway, leading to the reductions of TNF-α, IL-1β, and IL-6 in lung and attenuation of IIR-induced ALI. Conclusion BML-111 treatment could attenuate inflammation in lung after IIR injury via inactivating the p38 MAPK/NF-κB signaling pathway.
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AIM: To investigate the effect of rosiglitazone , a peroxisome proliferators-activated receptor γ(PPARγ) agonist, on the expression of PPARγ, the activation of NF-κB and intestine injury in the rats undergoing ortho-topic autologous liver transplantation ( OALT ) .METHODS: Sprague-Dawley male rats were randomly divided into 4 groups:control group, sham group, OALT group and rosiglitazone (0.3 mg/kg, iv) pretreatment (ROS+OALT) group. The OALT model was established , and the intestinal tissues were collected 8 h after the liver reperfusion .The intestinal tis-sue sections were stained to visualize the damage .The expression of PPARγand NF-κB in the tissues, the concentrations of diamine oxidase (DAO) and fatty acid-binding protein 2 (FABP2) in the serum and the concentration of TNF-αand IL-6 in the tissues were measured .RESULTS:Compared with sham group , the intestinal mucosa of the rats showed obvious pathological injury after liver reperfusion in OALT group and ROS group , the Chiu’s scores of intestinal mucosa was signifi-cantly higher , and the serum concentrations of DAO and FABP 2 increased ( P<0.05 ) .After rosiglitazone pretreatment , the injury of intestinal mucosa of the rats was alleviated , the Chiu’s scores was lower and the serum concentrations of DAO and FABP2 decreased (P<0.05), the PPARγexpression was obviously up-regulated in the intestinal tissues, the nuclear translocation of NF-κB was reduced and the concentrations of IL-6 and TNF-αwere decreased .CONCLUSION: During perioperative period of OALT in rats , the inflammatory responses are obvious .Furthermore, obvious intestinal injury oc-curs .PPARγagonist rosiglitazone obviously up-regulates PPARγexpression and inhibits the inflammation in the intestines , thus protecting against intestinal injury in rats undergoing OALT .
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[ ABSTRACT] AIM:To investigate the role of protease activated receptor-2 ( PAR-2 ) in the process of tryptase mediated IEC-6 cell injury.METHODS:The rat intestinal epithelial cell line IEC-6 was treated with tryptase at different concentrations (1 μg/L, 10 μg/L, 100μg/L and 1 000μg/L) in the presence or absence of PAR-2 antagonist FSLLRY-NH2 for 12 h respectively.The cell survival rate was detected by MTT assay.The protein levels of PAR-2 and cleaved-caspase 3 were determined by Western blotting.The LDH activity was also measured.RESULTS:Compared with control group, the cell survival rates were significantly decreased in 100 μg/L and 1 000 μg/L tryptase treated groups, the LDH activities were significantly increased in 10 μg/L to 1 000 μg/L tryptase treated groups, and the protein levels of PAR-2 and cleaved caspase 3 were significantly increased in 100μg/L and 1 000μg/L tryptase treated groups (P<0.05).Com-pared with 1 000 μg/L tryptase treated group, the LDH activity and cleaved caspase 3 protein level were dramatically de-creased while the survival rate was significantly increased in the presence of PAR-2 antagonist FSLLRY-NH2 (P<0.05). CONCLUSION:Tryptase induces IEC-6 cell injury in a dose-dependent manner by activating PAR-2.
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Objective To evaluate the changes in the expression of small intestinal thioredoxin 2 (Trx2) during different periods after orthotopic liver autotransplantation (OLAT) in rats.Methods Forty Sprague-Dawley rats,aged 8-10 weeks,weighing 210-260 g,were randomly divided into 2 groups using a random number table:sham operation group (group S,n =8) and OLAT group (n =32).Intestinal tissues were removed at 4,8,16 and 24 h after OLAT for microscopic examination and for determination of the levels of superoxide anion (O2--),hydrogen peroxide (H2 O2),glutathione peroxidase (GSH-Px),reduced glutathione (GSH) and Trx2.Intestinal damage was assessed and scored according to Chiu.Results Compared with S group,the Chiu's score and O2--activity at 4,8 and 16 h after OLAT and H2O2 content at 4 and 8 h after OLAT were significantly increased,and the levels of GSH-Px and GSH and expression of Trx2 at 4 and 8 h after OLAT were decreased in OLAT group (P ＜ 0.05).Chiu' s score at 4,16 and 24 h after OLAT and H2O2 content at 16 and 24 h after OLAT were significantly lower than those at 8 h in OLAT group (P ＜ 0.05).Conclusion The rats undergo decreased antioxidant capacity in the early phase and recovery in the late phase mediated by small intestinal Trx2 after OLAT.
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<p><b>OBJECTIVE</b>To observe the changes in systemic hemodynamics and their relations to the concentrations of nitric oxide, endothelin, prostacyclin, and thromboxane A2 after portal cavity clamping and opening in portal hypertensive canines.</p><p><b>METHODS</b>Twelve canines were randomly divided into control group and model group, and partial ligation of the portal vein was performed in the model group. Portal cavity clamping and opening was performed 12 weeks later in the two groups. The hemodynamic parameters including cardiac output index (CI), heart rate (HR), mean artery blood pressure (MABP), central venous pressure (CVP), pulmonary arteriole wedge pressure (PAWP), and systemic vascular resistance index (SVRI) were measured during the operation. Samples were obtained from the central vein at 3 time points during the operation for measuring NO, ET, PGI2, and TXA2.</p><p><b>RESULTS</b>Portal vein ligation and portal cavity clamping produced obvious changes in the systemic circulation of the dogs, and the alteration was milder in the control group. After obstruction of the portal vein, the NO levels in systemic circulation in portal hypertensive dogs declined obviously, but gradually recovered the normal level after reperfusion.</p><p><b>CONCLUSION</b>Systemic circulation undergoes significant alterations after portal vein obstruction, but its changes in portal hypertensive dogs are milder than those in the control group, the mechanism of which needs further investigation.</p>