Objective To determine intra-operative changes in blood coagulation and the applicability of SCA in liver transplantation. Methods Twenty-four patients with end-stage liver disease undergoing or-thotopic Liver transplantation (OLT) were studied. Arterial blood samples were drawn for determination of celite-activated TEG, glass bead-activated SCA and RCT at 6 intervals: before anesthesia induction (T0), 60 min after operation was started (T1), 30 miu in anhepatic phase (T2), 30 min in neohepatic phase (T3) ,120 min in neohepatic phase (T4) and the end of the operation (T5) ; the variables of TEG includ-ed: reaction time(R) ,coagulation time(K), alpha angles (α) and maximal amplitude (MA) ; the variables of SCA included: activated clotting time (ACT), clot rate (CR) and platelet function(PF) ;RCT included: Plt, PT, INR, APTT, Fbg. Results The Kappa values of SCA and TEG diagnosing the deficiency of blood coagulation factors, the gel formation speed of fibrin and the function of platelet were respectively 0.371 (P < 0.05) ,0. 363 (P < 0.05) ,0.438 (P < 0.05). gbACT and R, CR and α, PF and MA were positive-ly correlative (r = 0. 790, P < 0.05 ; r = 0. 766, P < 0. 05 ; r = 0. 502, P < 0.05 ; respectively) ; CR and K were negatively correlative(r = -0. 588,P <0.05). Compared with T0, PT, INR, gbACT and R were pro-longed, FBG, CR, α and MA were decreased at T3-5 (P < 0.05). APTT was prolonged at T1 ～ T5 (P < 0.05). K was prolonged at T3 (P < 0.05) and PF was decreased at T2 ～ T4. Conclusion SCA can exactly monitor changes of blood coagulation in liver transplantation.

Objective To compare the laryngeal mask insertion conditions at different plasma target concentrations (Cp) during the induction of anesthesia with target-controlled infusion (TCI) of propofol.Methods Forty-five ASA I - II patients of both sexes aged 18-60 yr, weighing 50-80 kg undergoing minor surgery in which the use of laryngeal mask (LM) was indicated were randomly divided into 3 groups ( n = 15) according to Cp of propofol set during induction of anesthesia: 4, 6 and 8 ?g ? ml-1 . The patients were premedicated with intramuscular scopolamine 0.3 mg. Fentanyl 3 ?g?kg-1 was given i.v. . TCI of propofol was started 3 min later with Diprifusor (Graseby 3500 infusion pump). LM was inserted when the effect-site concentration (EC) of propofol reached 2.5 ?g ? ml -1 as displayed on the infusion pump. LM insertion conditions (mouth opening, gagling, coughing, head and limb movement, overall ease of insertion) were assessed. The total dose of propofol, insertion time, the time needed to reach EC 2.5 ?g?ml-1 were recorded. SP, DP, HR and BIS value were recorded at 6 time points: baseline before induction (T1 ) , at the loss of consciousness (T2), at EC 2.5 ?g ? ml-1 (T3), immediately (T4), 3 min (T5) after insertion of LM. Results The SP, DP, HR and BIS value were decreasing with increasing depth of anesthesia in the 3 groups. The decrease in BP and BIS value after insertion of LM was significantly larger in group 3 (8 ?g ?ml-1) than in group 1 and 2 (P

Adenosine ; metabolism ; Adenosine Kinase ; metabolism ; Adenosine Triphosphate ; metabolism ; Animals ; Brain ; drug effects ; metabolism ; Diet, Carbohydrate-Restricted ; methods ; Diet, Ketogenic ; Energy Metabolism ; Epilepsy ; diet therapy ; metabolism ; Humans

Yinchenzhufu decoction (YCZFD) is a classic formula for treating Yin Huang syndrome, which can improve liver injury caused by cholestasis. However, the mechanism of action of YCZFD still remains unclear. This article used network pharmacology, molecular docking, animal experiments, and molecular biology methods to explore the mechanism of YCZFD in treating liver injury caused by cholestasis. A mouse model of acute cholestasis induced by lithocholic acid was used to investigate the effects of YCZFD on liver injury. The experimental procedures described in this paper were reviewed and approved by the Ethical Committee at the Shanghai University of Traditional Chinese Medicine (approval NO. PZSHUTCM190823002). The results showed that YCZFD could reduce the levels of blood biochemical indicators and improve hepatocyte damage of cholestatic mice. Then, multiple databases were used to predict the corresponding targets of YCZFD active components on cholestatic liver injury. An intersection target protein-protein interaction (PPI) networks based on String database and Cytoscape software was used to demonstrate the possible core targets of YCZFD against cholestatic liver injury. The results indicated that core targets of YCZFD include tumor necrosis factor, interleukin-1β, non-receptor tyrosine kinase Src, interleukin-6, etc. GO (gene ontology) and KEGG (kyoto encyclopedia of genes and genomes) enrichment analysis indicated that YCZFD may regulate the tumor necrosis factor signaling pathway, nuclear factor-κB signaling pathway, bile secretion, and other related factors to ameliorate the cholestatic liver injury. AutoDockTools software was used to perform molecular docking verification on the core targets and components of YCZFD. To verify the results of network pharmacology, UPLC-MS/MS method was used to determine the effect of YCZFD on levels of bile acid profiles in mouse liver tissues. It was found that treatment with YCZFD significantly reduced the content of free bile acids, taurine bound bile acids, and total bile acids in the liver tissues of cholestatic mice. Then, results from real time PCR and Western blot also found that YCZFD can upregulate the expression of hepatic nuclear receptor farnesoid X receptor, metabolizing enzyme (UDP glucuronidase transferase 1a1), and efflux transporters (bile salt export pump, multidrug resistance-associated protein 2, multidrug resistance-associated protein 3, etc) in cholestasis mice, promote bile acid metabolism and excretion, and improve bile acid homeostasis. Moreover, YCZFD can also inhibit pyroptosis and inflammation by regulating NOD-like receptors 3 pathway, thereby inhibiting cholestatic liver injury.

Objective To observe the effect of momordicin on tumor necrosis factor-?(TNF-?) level,mRNA transcription,and protein expression in myocardium of viral myocarditis caused by coxsackievirus B3(CVB3),and explore its therapeutic mechanism on viral myocarditis in Balb/c mice.Methods Fifty Balb/c mice were randomly divided into 3 groups as follows:momordicin treatment group(20 cases),vehicle control group(20 cases) and normal control group(n=10).Mice in the vehicle control group and the momordicin treatment group were intraperitoneally inoculated with CVB3,as for the nomal control group,equal amount of culture fluid was given instead.Momordicin[25 mg/(kg?d)] was administered intraperitoneally daily from day 0 to 6.Myocardial histopathology,cardiac TNF-? antigen,protein and mRNA expression were detected on day 15 after CVB3 inoculation,respectively.Results As compared with model group,in mice treated with momordicin,the histological myocardial lesion was significantly reduced [(3.26 ?0.84) vs(1.56?0.48),t=3.90 P

Objective To observe the therapeutic effect of astragaloside on chronic coxsackievirus B3(CVB3)myocarditis in Balb/c mice.Methods Eighty Balb/c mice were randomly divided into 3 groups:astragaloside treatment group(n=30),model of viral myocarditis group(model group)(n=30),and control group(n=20).Mice in the model group and the astragaloside treatment group were monthly intraperitoneally inoculated with CVB3,but equal amount of culture fluid was given instead in control group.The model group and control group were fed with drinking water,astragaloside treatment group were fed with drinking water containing astragaloside at concentration of 300 mg/L for 3 months.Survival rates were determined,myocardial histopathology,collagen volume fraction(CVF) and apoptosis of heart tissue,and CVB3 RNA levels were detected on 3 months later respectively by semiquantitative RT-PCR.Results Compared with model group,in astragaloside treated group,the survival rate on 3 months was significantly improved(59.7% vs 76.7%,?2=4.26 P

Objective To investigate the mechanism of acute lung injury after hepatic ischemia / reperfusion and the protective effect of propofol.Method s Forty-eight male SD rats were randomly divided into Sham2 group,Sham6 group; IR2 group (IR2),IR6 group (IR6); P2 group (P2),P6 group (P6).The 1 mg·kg-1·min-1 propofol was infused from 30min before ischemia in P groups,and the same volume sodium lactate Ringer's solution was infused in Sham and IR groups.The concentration of TNF-α,superoxidedimutase(SOD),malondialdehyde(MDA),myeloperosidase(MPO),lung wet/dry weight ratio and lung histological scores were measured at the points of 2 and 6 hour after reperfusion.Results TNF-α levels were higher in IR and P groups than those in sham groups but the values in P groups were lower than those in IR groups.SOD levels decreased greatly in IR groups,there were great difference between P and IR groups.MDA levels increased greatly in IR groups and reached the peak value at 6 hour after reperfusion.MDA levels in P groups were lower than those in IR groups and there were no difference between P and sham groups.The ratio of Wet/dry levels,MPO and lung histological scores were increased greatly after reperfusion in IR and P groups.But the value in P groups was lower than those in IR groups.Conclusions Acute lung injury after hepatic ischemia / reperfusion is mainly induced by the oxidant stress and neutrophil infiltration in lung tissues.Propofol may have effects of antioxidation and decrease neutrophil infiltration which attenuate lung injury induced by hepatic ischemia/reperfusion.

Objective To explore the influence of electrical stimulation on prefrontal cortical neurons and synaptic ultramicrostructure of hypoxic-ischemic brain damage(HIBD)in neonatal rats.Methods The sixty 7-day-old newborn healthy SD rats were randomly divided into hypoxic-ischemic group(model group),electrical stimulation(intervention)group and sham operation group(control group),which 20 for each group.The models of perinatal HIBD rats were prepared by ligation of left common carotid artery with a temporary systemic hypoxia for 2 hours.Intervention group was subject to electric stimulation for 30 minutes,once everyday after surgery.Control group and model group were not subject to electric stimulation but caught to fix in corresponding period.Fastigial nucleus electric stimulations were performed for 3 d,14 d and 21 d.Five rats were killed in each group after the application of electron microscope to observe the brain cortex neurons and synaptic ultrastructure changes.Results In model group,the neuronal shrinkage,the amount of organelles dacrease,ob-vious edema of cytoplasm,obvious swellen mitochondria,and synapse quantity decrease,synaptic space fusion,obvious synaptic vesicle were observed.Intervention group different times,mitochondria hydrops gradually alleviated,synaptic space gradually cleared,synaptic vesicle increased,pathological changes obviously lessened compared to model group at the same time,and there was no apparent abnormality compared with control group on the 21st d.Conclusion Electric stimulation can promote the ultramicrostructures recovery of HIBD rats.

Objective To investigate the effects of electrical stimulation on vascular endothelial growth factor(VEGF) and its receptor expressions of neonatal rat brain with hypoxic-ischemic brain damage(HIBD).Methods Seventy-five 7-day-old newborn health SD rats were randomly divided into sham operation group(control group,n=25),hypoxia-ischemia group(model group,n=25) and the electrical sti-mulation group(intervention group,n=25).To bulid HIBD animal model of neonatal rats,the left common carotid artery was ligated and nitrogen-oxygen gas mixture was inhaled 2 hours.Fastigial nucleus stimulation was given 12 hours after the operation in intervention group,30 min?time-1,1 time?d-1,the time length was 1 d,3 d,7 d,14 d or 21 d,respectively.There was no electrical stimulation in model group and control group.The rats in these groups were captured at the corresponding time.Five rats in each group were killed at the corresponding pe-riods after electrical stimulation,the expression of VEGF and its receptor fam-like tyrosine kinase receptor(flt-1 / VEGFR1),fetal liver kinase receptor(flk-1/KDR/VEGFR2) in hippocampus were observed by immunohistochemistry.SPSS 15.0 software was used to analyze the data.Results The expression of VEGF,VEGFR1,VEGFR2 at every time point in electrical stimulation group were higher significantly than those in model group and control group(Pa0.05).Conclusion Electrical stimulation can promote the expression of VEGF and its receptors VEGFR1,VEGFR2.

Objective To evaluate the feasibility and clinical significance of radical nephrectomy with en bloc resection of involved adjacent organs.Methods Totally,24 cases of renal cancer invading adjacent structures underwent radical nephrectomy with en bloc resection of involved adjacent organs.Among the 24 cases,left radical nephrectomy with en bloc resection of splenic flexure and descending colon was performed in 7,partial resection of corpus and cauda pancreatis and spleen in 5,solitary splenectomy in 3;right radical nephrectomy with en bloc resection of hepatic flexure of the colon in 4,partial hepatectomy of right lobe and end-piece in 4,duodenectomy of pars descendens in 1.Of these cases,partial resection of the psoas muscle was performed in 5,and partial resection of mesocolon in 7.Postoperatively,9 cases received immunotherapy.Results There was no intraoperative mortality or severe posuoperative complication.Follow-up of 3-240 months was available in 21 cases.The follow-up showed that 1-,3-,5-and 8-year survival rates were 90.5%(19/21),42.9%(9/21),33.3%(7/21) and 19.0%(4/21),respectively.Conclusions Radical nephrectomy remains the treatment of choice in organ-confined stage of renal carcinoma.With careful selection,radical nephrectomy with en bloc resection of adjacent structures is technically feasible.It can obtain the radical excisional effect.Based on our experience,the operation is relatively safe.Complete surgical extirpation can lead to prolonged disease-free survival.It may also offer beneficial foundation for the subsequent systematic therapy.