Objective To investigate the regulation of Ningchang Decoction on free radical of stressed irritable bowel syndrome (IBS) rats. Methods The stressed IBS model rats were made by chronic bandaged-stress and inserting the end. The rats were randomly divided into six groups: normal control group, model control group, positive control group, high dosage of Ningchang Decoction group, middle dosage of Ningchang Decoction group, low dosage of Ningchang Decoction group. Different treatment were given to each group by ig administration for 4 weeks. The contents of SOD, MDA and T-AOC in serum of stressed IBS rats were determined and the regulation of Ningchang Decoction on them were observed. Results Stress increased the content of MDA in serum and decreased the contents of SOD and T-AOC in serum (P

Objective To evaluate the efficacy and safety of target-controlled remifentanil infusion combined with cervical plexus block for anterior cervical decompression surgery.Methods Twenty ASAⅠ or Ⅱpatients aged 30-64 yr undergoing anterior cervical decompression were studied.After a succegsful cervical plexus block,TCI of remifentanil was started at a target plasma concentration(CP)of 1.5 ng/ml 5 min before operation.The remifentanil CP was adjusted according to the patient's response to surgical stimulation and increased or decreased by 0.2 ng/ml each time until Ramsay sedation score reached 2-3 or verbal pain score(VPS)reached 0-1.TCI of remifentanil was discontinued 5 min before the end of surgery.MAP,HR,SpO2,BIS,Ramsay sedation score and VPS were monitored and recorded before cervical plexus block(To,baseline),at 10 min after cervical plexus block(T1),5 min(T2),30 min(T3)after skin incision,when the response to tracheal traction was significant during operation(T4)and at the end of operation(T5).The highest remifentanil Cp and the side effects such as respiratory depression,muscle rigidity,nausea/vomiting and pruritis that occurred were recorded.Remits MAP,SpO2 and BIS were not significantly changed during operation as compared to the baseline values at T0.HR was significantly increased at T2 as compared with the baseline.The Ramsay score reached 2-3 and the VPS reached 0-1 in the majority of patients in group R.No marked side effects were detected during TCI of remifentanil.The remifentanil CP ranged between 1.5-5 ng/ml and the mean CP during operation was(3.4±1.0)ng/ml.Conclusion TCI of remifentanil of low concentration combined with cervical plexus block can safely and effectively induce awake analgesia in patients undergoing anterior cervical decompression surgery.

The incidence of glioma has been increasing in recent years,and threatened the human health seriously.Cystine/glutamate antiporter (system xc-) is one of the important glutamate transporters in the central nervous system,both the expression of system xc and the extracellular glutamate concentration increase in the course of brain tumor's development.Hence system xc-plays an essential role in the process of brain tumor genesis,it has become an important research field in brain tumor in the past decades.Our present review expound the important role of system xc-in the process of glioma genesis and development as well as provide theoretical foundation and new strategies for the clinical treatment and the application of drugs by connecting with anaesthetics and the effects of system xc on glioma.

Objectivc To study the effects of ketamine and MK-801 on lipopolysaccharide (LPS)-inducedexpression of intercellular adhesion molecule-1 (ICAM-1 ) and the translocation of nuclear factor-kappa B (NF-?B)into nuclei of human umbilical vein endothelial cells (HUVECs). Methods The endothelial cells obtained fromhuman umbilical vein by digestion with collagenase 1 were cultured at 37℃ in a 5 % CO_2-95% room airatmosphere for 7 days. The cultured human umbilical vein endothelial cells (HUVECs) wer randomly divided into(1) control group in which nothing was added to the RPMI-1640 culture medium; (2) LPS group in which us 1?g?ml~(-1) was added to RPMI-1640; (3) ketamine group was further divided into 4 subgroups according to theconcentration of ketamine added: 12.5 (KⅠ), 25 .0 (KⅡ), 100 (KⅢ) and 300?mol?L~(-1) (KⅣ); (4) MK-801group was further divided into 4 subgroups M Ⅰ-Ⅳ, according to the different concentrations of MK-801 added(1 .25, 2.50, 10, 30?mol?L~(-1)). In one set of experiment in ketamine and MK-801 groups after addition ofketamine and MK-801 to the RPMI-1640 culture medium, the HUVECs were incubated for 30 min at 37℃, thenLPS1?g?ml~(-1) was added and incubated for 18 h in a 5 % CO_2 atmosphere at 37℃. The HUVECs were thenharvested for determination of ICAM-1 expression by flow cytometry. In another set of experiment the culturedHUVECs were stimulated with LPS 1?g?ml~(-1) for 2 h in the absence or presence of ketamine (12.5, 25 .0, 100and 300?mol?L~(-1) ) or MK-801 (1.25, 2.50, 10 and 30?mol?L~(-1)). The translocation of NF-?B p65 into nucleiwas detected by immunohistochemistry technique. Results In group K Ⅱ, KⅢ and KⅣ the upregulation ofICAM-1 and translocation of NF-?B into nuclei of HUVECs induced by LPS were significandy reduced (P0.05). Conclusion Ketamine can suppress LPS- induced HUVEC activation at the higher concentrations (≥25?mol?L~(-1)). The inhibitory effects of ketamine ismost likely not mediated through NMDA receptor interactions.

Magnetic resonance diffusion tensor imaging (DTI) has been established as the primary imaging modality for non-invasive characterization of the direction-dependent motion of water molecules in the living tissue. DTI provides each image voxel with a 3x3 tensor matrix that can be processed to probe tissue microstructure and microarchitecture. In this paper, the imaging principle and diffusion tensor calculation are introduced. Examples are given to describe image-processing techniques for DTI visualization, fiber tracking, and applications to central nervous system.

Objective To investigate effect of autologous hematopoietic stem cell transplantation on serum trace elements and lactate dehydrogenase activity in patients with malignant lymphoma.Methods 80 patients with malignant lymphoma collected in our hospital from May 2013 to May 2014,40 cases in each group, Hodgkin lymphoma ( HL) patients were treated with ABVD ( doxorubicin, bleomycin, vincristine, dacarbazine) regimen of chemotherapy; Non-Hodgkin,s lymphoma ( NHL) patients were treated with standard CHOP ( cyclophosphamide, vincristine, epirubicin, dexamethasone) regimen of chemotherapy of two group.Chemotherapy drugs combined with granulocyte colony stimulating factor ( G-CSF) was used to mobilize APBSC.Application of 10μg/(kg? d)G-CSF 5 in bone marrow suppression after chemotherapy, detected white cell increased 3.0 ×109/L , platelets rose to 50 ×109/L, collected APBSC,The frozen stock solution of cell was joined and frozen.24 h after pre-treatment, the frozen peripheral blood hematopoietic stem cells of the subclavian vein was transfused for patients in experimental group.Control group continued to receive chemotherapy. After treatment, the Cu level, Zn level and lactate dehydrogenase activity were detected in all patients.ResuIts After treatment, Zn levels of two groups increased (P<0.05), Cu and Cu/Zn levels decreased (P<0.05).Compared with control group, the level of Zn was higher in experimental group (P<0.05), and the level of Cu and Cu/Zn was lower (P<0.05).After treatment, the lactate dehydrogenase activity of two groups decreased (P<0.05), and experimental group was more lower than control groupy (P<0.05).ConcIusion Autologous hematopoietic stem cell transplantation can significantly reduce the level of Cu in patients with malignant lymphoma , elevate Zn level and decrease the activity of lactate dehydrogenase, which has guiding significance for clinical.

To investigate whether the calcium channel blocker amlodipine could inhibit macrophage matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) expression and secretion. Methods Peritoneal macrophages were isolated from BALB/C mice and incubated with low (5μg/L), middle (15μg/L) and high (305μg/L) concentrations of amlodipine, or in the medium alone (controls) for 24 hours, and the expression and secretion of MMP-2 and MM-9 of the cells were analyzed by RT-PCR and gelatin zymography. Results Compared with controls, amlodipine at low concentration had no significant effects on the expression and secretion of either MMP-2 and MMP-9 (P＞0.05);at middle concentrationit it could inhibited MMP-2 and MMP-9 expressions completely and significantly reduced the secretion of MMP-9 (P＜0.05); but it had no effect on the secretion of MMP-2. At high concentration it also inhibited MMP-2 and MMP-9 expression completely. Conclusion Amlodipine at 15 ìg/L inhibited the expression of MMP-2 and MMP-9 and reduced the secretion of MMP-9, suggesting that amlodipine may stabilize atherosclerotic plaque.

Objective To evaluate the effect of propofol post-conditioning on hippocampal neuronal K+-Cl-co-transporter 2 (KCC2) expression in the rats with cerebral ischemia/reperfusion (I/R) injury.Methods Seventy-two male Sprague-Dawley rats,aged 7-8 weeks,weighing 250-280 g,were randomly divided into 3 groups (n =24 each):sham operation group (group S),cerebral I/R (group I/R) and propofol post-conditioning group (group PP).The model of focal cerebral I/R injury was established by occlusion of the right middle cerebral artery.Propofol 20 mg· kg-1 · h-1 was infused over 2 h starting from the onset of reperfusion through the femoral vein in group PP.The equal volume of normal saline was given in S and I/R groups.Modified neurological severity score (mNSS) was used to evaluate the impairment of neurological function.The animals were then sacrificed and brains were removed for determination of the number of neurons (by Nissl' s staining) and expression of KCC2 (by immunofluorescence and Western blot) in hippocampal CA3 region.Results Compared with group S,the scores of mNSS were significantly increased,and the number of neurons and expression of KCC2 in hippocampal CA3 region were decreased in I/R group,and mNSS scores were increased,and no significant changes were found in the other parameters in group PP.Compared with group I/R,the mNSS scores were significantly decreased,and the number of neurons and expression of KCC2 in hippocampal CA3 region were increased in group PP.Conclusion The mechanism by which propofol post-conditioning reduces cerebral I/R injury is related to up-regulated expression of hippocampal KCC2 in rats.

Objective To evaluate the role of Akt-glycogen synthase kinase-3 beta (GSK3β) signaling pathway in the long-term neuroprotection induced by propofol postconditioning in a rat model of focal cerebral ischemia/reperfusion (I/R) injury.Methods Two hundred and sixteen male Sprague-Dawley rats,weighing 250-280 g,were randomly divided into 4 groups (n =54 each):sham operation group (group S),I/R group,intralipid control group (group I) and propofol postconditioning group (group P).The model of focal cerebral I/R injury was established by middle cerebral artery occlusion.Propofol 20 mg·kg-1 · h-1 was infused over 2 h starting from the onset of reperfusion in group P,the equal volume of normal saline was given in groups S and I/R and the equal volume of 10％ intralipid was given in group I.Six rats were chosen at 3,7,14 and 28 days after occlusion and sacrificed,and brains were removed for determination of the cerebral infarct size by TTC staining.Another 6 rats were chosen at 3,7,14 and 28 days after occlusion to detect the expression of Akt,GSK3β and phosphorylation of Akt and GSK3β by Western blot.The left 6 rats were chosen at 28 day after occlusion to measure the number of newly generated neurons in hippocampal dentate gyms on the ischemic side.Results Compared with group S,the cerebral infarct volume was significantly enlarged,the newly generated neurons number was increased in the other 3 groups,and the phosphorylation of Akt and GSK3β was decreased in groups I/R and I,while increased in group P (P ＜ 0.05).The cerebral infarct volume was significantly smaller,and the newly generated neurons number and phosphorylation of Akt and GSK3β were higher in group P than in group I/R (P ＜ 0.05).Conclusion The mechanism by which propofol postconditioning provides the long-term neuroprotection is related to Akt-GSK3β signaling pathway in a rat model of focal cerebral I/R injury.

Objective To evaluate the role of phosphatidyl-inositol 3 kinase (PI3K)-α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor subunit glutamate receptor 2 (GluR2) pathway in propofol postconditioning-induced reduction of cerebral ischemia-reperfusion (I/R) injury in rats.Methods One hundred and eighty male Sprague-Dawley rats,weighing 250-280 g,were randomly divided into 5 groups with 36 rats in each group:sham operation group (group S),I/R group,propofol postconditioning group (group P),intralipid postconditioning group (group Ⅰ),and PI3K inhibitor wortmannin + propofol postconditioning group (group W +P).The rats were anesthetized with intraperitoneal 10% chloral hydrate 350 mg/kg.Cerebral I/R was produced by 60 min middle cerebral artery occlusion followed by reperfusion.Propofol and 10% intralipid were infused via the femoral vein at a rate of 20 mg· kg-1· h-1 for 2 h starting from the onset of reperfusion in groups P and I,respectively,while the equal volume of normal saline was given instead in groups I/R and S.Wortmannin 0.6 mg/kg was injected intraperitoneally at 30 min before reperfusion in group W + P.The modified Neurological Severity Score (mNSS) was assessed and the cerebral infarct volume was detected at 12 and 24 h after operation.The hippocampi on the ischemic side were obtained at 4,6,12 and 24 h after operation for determination of expression of PI3KGluR2-containing AMPA receptor (by co-immunoprecipitation and Western blot) and activity of PI3K (by ELISA).Results Compared with group S,the mNSSs and infarct volume were significantly increased at 12 and 24 h after operation,and the activity of PI3K was decreased,and the expression of PI3K-GluR2-containing AMPA receptor was down-regulated at 4,6,12 and 24 h after operation in the other four groups (P ＜ 0.05).Compared with group I/R,the mNSSs and infarct volume were significantly decreased at 12 and 24 h after operation,and the activity of PI3K was increased,and the expression of PI3K-GluR2-containing AMPA receptor was up-regulated at 4,6,12 and 24 h after operation in group P (P ＜ 0.05).Compared with group W + P,no significant change was found in the parameters mentioned above in groups I/R and I (P ＞ 0.05),and the mNSSs and infarct volume were significantly decreased at 12 and 24 h after operation,and the activity of PI3K was increased,and the expression of PI3K-GluR2-containing AMPA receptor was up-regulated at 4,6,12 and 24 h after operation in group P (P ＜0.05).Conclusion PI3K-AMPA receptor subunit GluR2 pathway is involved in propofol postconditioning-induced reduction of cerebral I/R injury in rats.