Objective:To investigate the cure effect of human cytokine-induced killer (CIK) cells on the model of human hepatocellular carcinoma in nude mice. Methods:Peripheral blood mononuclear cells(PBMC)were obtained from healthy volun- teers by Ficoll gradient centrifugation and CIK cells were induced by culturing PBMC in the completed medium containing rhIFN-?,rhIL-2 and mAb against CD3.By intraperitoneal injection of CIK cells in LCI-D20, the effect of prevention and therapy to HCC in LCI-D20 were assessed. Results:The weight of tumor in the CIK cells group and negative group was (1.125?0.363)gram and(2.682?0.526)gram respectively(t=6.06,P

Objective To investigate the cerebral protective effect of intracarotid infusion of propofol in patients undergoing resection of cerebral gliomas. Methods Sixty ASA Ⅰ- Ⅲ patients with cerebral glioma aged 40-64 yr weighing 48-73 kg were enrolled in this study. Forty patients undergoing resection of glioma under general anesthesia were randomly divided into 2 groups ( n = 20 each): intracarotid propofol group (group IA ) and intravenous propofol group (group Ⅳ). Twenty patients undergoing biopsy of glioma under local infiltration anesthesia with 2% lidocaine 15-20 md served as control group (group C). In IA and Ⅳ groups anesthesia was induced with TCI of propofol and remifentanil. Tracheal intubation was facilitated with rocuronium 0.6 mg/kg. The patients were mechanically ventilated. PErCO2 was maintained at 35-45 mm Hg. Anesthesia was maintained with TCI of propofol and remifentanil and intermittent iv boluses of rocuronium. In group IA internal carotid artery was cannulated after induction of anesthesia and propofol was administered by TCI via carotid artery while remifentanil was administered by TCI via peripheral vein. BIS was maintained at 40-60 during operation. ECG, MAP, HR, SpO2, PETCO2 and BIS were continuously monitored. MAP and HR were recorded before induction of anesthesia (T1) ,during skin incision (T2 ), at the end of operation (T3), during extubation ( T4 ). The glioma specimens were obtained for microscopic examination and determination of aquaporin 1 and aquaporin 4 ( AQP1, AQP4) expression by immunohistochemistry. Results MAP and HR were significantly decreased at T2 and T3 as compared with the baseline at T1 in group Ⅳ ( P ＜ 0.05), while there was no significant change in MAP and HR after induction of anesthesia in group IA ( P ＞ 0.05). The expression of AQP1 and AQP4 was down-regulated in IA and Ⅳ groups compared with group C (P ＜0.05). The propofol consumption during anesthesia was significantly less in group IA than in group Ⅳ (P ＜0.05). There was no significant diffe-rence in AQP1 and AQP4 expression, the amount of remifentanil and recuronium consumed and duration of operation betweenIA and Ⅳ groups ( P ＞ 0.05). Concltsion Intracarotid propofol can decrease the amount of propofol needed for maintenance of anesthesia as compared with intravenous administration and attenuate brain edema,indicating cerebral protective effect.

Objective To investigate the effects of propofol on cultured primary neurons isolated from fetal Wistar rats against anoxic-reoxygenated injury and its neuro-protective mechanisms at cellular level. Methods Neuronal cells were isolated from brains of fetal Wistar rats and cultured for 12 days. The cultured neuronal cells were randomly divided into 4 groups : (Ⅰ) control group; (Ⅱ) anoxic-reoxygenated group in which neurons were exposed to 95% N2 + 5% CO2 at 37?for 3O min; (Ⅲ) propofol pretreatmenl group in which propofol was added to the culture medium (the final concentrations of propofol were 14 ?mol?L-1) 1 h before exposure to anoxia. (Ⅳ) propofol pretreatment group (the final concentrations of propofol were 56 ?mol?L-1) . Neuronal activity was detected by MTT analysis and NO output was assayed with nitrate reductase method at 1, 2, 4, 6 and 24 h after reoxygenation. The synthesis of heat shock protein (Hsp)70 mRNA was measured by in situ hybridization technique and the synthesis of Hsp70 was measured by immuno-histochemical technique at 1, 3, 8, 24, 48 h and 72 h after reoxygenation.Results (1) 30-min anoxia decreased neuronal activity, increased NO output and significantly increased the synthesis of Hsp70 mRNA and Hsp70. The expression of Hsp70 mRNA reached its peak at 24 h after reoxygenation and that of Hsp70 at 48 h after reoxygenation. (2) Propofol pretreatment significantly increased neuronal activity at 1, 2, 4, 6 and 24 h after reoxygenation and decreased NO output at 1, 2 and 4 h after reoxygenation compared with those in anoxia-reoxygenated group. (3) The synthesis of Hsp70 mRNA was significantly increased and accelerated by pretreatment with both concentrations of propofol but the synthesis of Hsp70 was significantly increased and accelerated by pretreatment with 56?mol?L-1 propofol only. Conclusion Propofol pretreatment can inhibit anoxia-reoxygenation injury to neurons by decreasing NO output and increasing expression of Hsp70 through inducing the synthesis of Hsp70 at both transcription and translation levels.

Objective To explore the role of excitatory amino acid carrier 1 (EAAC1)in dorsal root ganglion (DRG) in the mechanism of developing morphine tolerance. Methods Thirty male SD rats were implanted intrathecal catheters and randomized into 6 groups with 5 rats each. The rats of 4 groups were made into the model of adjuvant-induced arthritis in the left hind limb and were administered intrathecally, morphine 10 μg(group M_(10)), morphine 20μg(group M_(20)), morphine 20 μg plus naloxone 10 μg(group MN) ,or saline(group C) respectively. The other 2 groups without were administered intrathecally saline (group C_0) or morphine 20 μg (group M0). The drugs were administered twice daily for 7 days. Mechanical withdrawl threshold(MWT) of the left hind limb was examined to evaluate the behavior. Immunohistochemistry was used to detect the expression of EAAC1 in the left L_(3-4) and L_(4-5) DRG. Results Morphine tolerance was formmed stably in the arthritis rats of group M_(10) and group M_(20) after administering morphine for 7 days. The expression of EAAC1 in DRG was downregulated. Conclusion DRG EAAC1 may be involved in the mechanism of developing morphine tolerance in rats with inflammatory pain.

Objective To investigate the changes in the expression of glutamate-aspartste transporter in spinal dorsal horn in rats with inflammatory pain and chronic morphine tolerance. Methods Thirty healthy male SD rats in which intrathecal (IT) catheters were successfully placed without complications were randomized into 3 groups ( n = 10 each): normal saline group ( group NS), arthritis group ( group A), and arthritis + morphine group (group AM). NS 50 μl was injected into the ankle joint of the left hindlimb in group NS, while complete Freund's adjuvant was injected in the other two groups instead. After 3 days, group NS and A received IT NS 10 μl twice a day for 7 consecutive days, group AM IT morphine 10 μg (10 μl) twice a day for 7 consecutive days. Mechanical pain threshold (MPT) was measured before IT administration and at day 2, 4, 6 and 8 after IT administration (T0-4). The animals were sacrificed after the last MPT measurement. The spinal cords were isolated for determination of GLAST expression in spinal dorsal horn. Results Compared with group NS, MPT was significantly decreased in the other groups and GLAST expression was down-regulated in group AM (P ＜ 0.05). Compared with group A, no significant change was found in MPT at T3,4 (P ＞ 0.05), while GLAST expression was down-regulated in group AM ( P ＜ 0.05). Conclusion The development of chronic morphine tolerance is related to the decrease in the function of GLAST in spinal dorsal horn in rats with inflammatory pain.

[Objective] To explore the effects of mycocide and insecticide on indoor air quality in archives.[Methocls] The levels of camphor, formaldehyde and 2, 2-dichlorovinyldimethyl phosphate (DDVP) in indoor airwere determined in 17 archives. [Results] The average concentration of camphor in indoor air was 1.00mg/L inarchives applying synthetic camphor, 0.74 mg/m3 in archives applying commercialized mycocide (the main compo-nents were synthetic camphor and pyrethrin ), and 0.14 mg/m3, applying natural camphor. The concentrations offormaldehyde reached 0.297 mg/m3 at the 10th day after the co-fumigation by formaldehyde and DDVP. At thesametime, DDVP was not found in indoor air of archives.[Conclusion]The pollution of formaldehyde and camphorin indoor air of archives should be paid more attention to.

Objective: To study human peripheral blood dendritic cells(DC) inducing Th0 differentiation to Th1/Th2 at different DC/Th0 ration。 Methods: Mononuclear cells in healthy human peripheral blood were induced to DC through tradition method,4 days of culture of mixed DC/Th0 different ration( 1∶4 and 1∶300),harvesting Th,after 48 h of CD3 mAb and CD28 mAb expantion,in supernant IL-4 and IFN-? measurement were determined using ELASA。 Results:Expresse CD83(73.4%), CD86 (90.3%), HLA-DR(68.5%),CD40(73.7%).DC/Th0 ration(1∶4) produced IFN-? (34?4.3) ?g/L, a little amount of IL- 4(25?4.3) ng/L. DC/Th0 ration(1∶300) produced IFN-?(3.5?1.2) ?g/L, a large amount of IL- 4(350?120) ng/L. Conclusion:Highly mixed DC/Th0 ration induced Th0 differentiation to Th1, low mixed DC/Th0 ration induced Th0 differentiation to Th2, DC regulating immunology response type were plastic which provided the basis for clinic GVHD therapy.

Objective:To explore the impact of special rectification on antibiotics application in the patients during perioperative period with gynecologic typeⅡincision in our hospital. Methods:The antibiotics type, use frequency, expense, administration time, dosage, treatment course and combined medication were retrospectively compared between April to September in 2011(before the recti-fication) and April to September in 2013 (after the rectification). Results: After the special rectification, the total DDDs was de-creased from 1 564. 5 to 419. 3, the expense for antibiotics and all drugs was respectively decreased from (297. 5 ± 47. 1) yuan to (108. 3 ± 29. 6) yuan and (806. 4 ± 63. 1)yuan to (498. 1 ± 70. 2) yuan, the proportion of antibiotics was decreased from (36. 9 ± 9.1) % to (21.7 ±6.8) %, and the treatment course was reduced from (3.7 ±1.4)d to (1.5 ±0.6)d(P<0.05). The rational rate of administration time, dosage and combined medication was respectively increased from 67. 7% to 98. 6%, 81. 5% to 100. 0%and 41. 1% to 80. 7%(P<0. 05). Conclusion:Special rectification can effectively improve the rational antibiotics use in gynecology department of our hospital during perioperative period of type Ⅱincision.

Objective To observe apoptosis and proliferation of intestinal epithelial cells and to explore the mechanism of protective effects of rhubarb monomers on intestinal epithelial cells in septic rats.Methods Eighty male Sprague-Dawley (SD) rats (230-250 g) under anesthesia and sedation were subjected to cecal ligation and perforation (CLP).After surgical preparation,rats were randomly (ramdom number) divided into 8 groups (n =10 each):a sham group (A) [normal saline (NS) gavage];a sepsis group (B) (NS gavage);group C (ip dexamethasone 0.5 mg/kg immediately after CLP) (C);and rhubarb monomer 100 mg/kg in NS treated groups including:rhein group (D),emodin group (E),3,8-dihydroxy-1-methyl-anthraquinone-2-carboxylic acid group (F),1-O-caffeoyl-2-(4-hydroxy-O-cinnamoyl)-D-glucose group (G),and 3,8-dihydroxy-1-methyl-anthraquione group (H).Animals were sacrificed 24 hrs after treatment.Intestinal histopathology,apoptosis (TUNEL) and proliferation of intestinal epithelial cells (proliferating cell nuclear antigen,PCNA) were measured.Multiple comparisons were carried out with one-way analysis of variance (ANOVA).Results Histopathology revealed injury to the intestinal mucosal villi induced by sepsis in group B compared with group A.The injury was significantly ameliorated in groups C,D,E,F,G,and H compared with group B.The apoptosis index in group B was significantly higher than that in group A (P ＜ 0.05) and the apoptosis index in groups C,D,E,F,G,and H was significantly lower than that in group B (P ＜ 0.05).The PCNA positive index in group B was significantly lower than that in group A (P ＜ 0.05),but was significantly higher in groups C,D,E,F,G,and H than that in group B (P ＜ 0.05).Conclusion Rhubarb monomers can promote the proliferation of mucosal cells and prevent apoptosis of intestinal mucosal cells.In addition,rhubarb monomers may play a role in protecting the intestinal barrier function.

Objective To analyse a novel splice mutation in EXT1 gene of hereditary multiple osteochondroma, and study its pathogenic mechanism.Methods In April of 2013, the proband was hospitalized from the outpatient department with multiple joint deformity for more than 20 years, peripheral blood of the proband and his parents were collected and genomic DNA was extracted .Coding regions and adjacent intron sequences of EXT1/EXT2 genes in genomic DNA of the family members were amplified and sequenced.Bioinformatics was used to analyze the mutation from sequencing .cDNA from peripheral blood of the proband ,the mother and normal control was made respectively as a template for amplifying coding regions of EXT1 gene, and the product was T-A cloned and sequenced.The abnormal transcripts of each group were counted and analyzed using chi square test to study the pathogenic mechanism of the mutation .Results Sequencing results of family members revealed that there was a heterozygous deletion mutation ( c.1284 +2del) in the 5′splice site of intron 4 in EXT1 gene of the proband and his mother .Bioinformatics predicted that exon 4 of EXT1 gene was skipping or spliced aberrantly due to the mutation .T-A clone and sequencing results as well as the statistical analysis suggested that there was a significantly higher proportion of transcripts with skipping exon 4 in the proband and his mother compared with the normal control (P=0.000, P<0.01).Conclusions c.1284+2del in EXT1 gene is reported for the first time internationally , which results in a considerable number of abnormal transcripts with skipping exon 4 in EXT1 gene, thereby influences the normal transcription and translation of EXT1 gene.