Objective To explore the relationship between life events,efficacy of self learning and learning burnout of Left-behind middle school Students.Methods 526 left-behind middle school students and 860 non -left-behind students were tested by means of scales of life events,academic self-efficacy and learning burnout.Results The degree of interpersonal relationship,learning pressure,health adaptation,life events,self-efficacy of learning ability,learning behaviors,and learning,sense of alienation between teacher and students,physiological depletion,and learning burnout of left-behind middle school students were lower than non left-behind students,and were statistically significant.The interpersonal relationship(r=0.270,P＜0.001),learning pressure(r=0.289,P＜ 0.001),being punished(r=0.242,P＜0.001),health adaptation(r=0.301,P＜0.001) and others (r=0.322,P＜ 0.001) were positively related to learning burnout.Self-efficacy of learning ability(r=-0.334,P＜0.01) and learning behaviors(r=-0.157,P＜0.001) were significantly and negatively related.Interpersonal relationship (r=-0.092,P＜0.05),learning pressure (r=-0.123,P＜0.01),being punished (r=-0.178,P＜0.001) and others (r=-0.254,P＜ 0.001) were negatively related to self-efficacy of learning ability.Being punished (r=-0.109,P＜ 0.05)and others(r=-0.209,P＜0.001) were significantly and negatively related to self-efficacy of learning behaviors.Self-efficacy,health adaptation,learning pressure,self-efficacy of learning behavior and others all entered the regression equation.Path analysis showed that there were five paths that have significant influences on learning burnout.Conclusion The levels of response to emergency of life events and enhance the academic self-efficacy of leftbehind students can be improved to reduce and prevent learning burnout.

0 35 The patients had no endocrine or immune disease and received neither radio , chemo nor hormone therapy Anesthesia was induced with propofol, midazolam, fentanyl and succinylcholine After tracheal intubation the patients were mechanically ventilated Anesthesia was maintained with enflurane inhalation and intermittent intravenous boluses of midazolam, fentanyl and vecuronium After operation the patients were transferred to recovery room and PCA was started when the patients were wide awake VAS was maintained at 2 4 Venous blood samples were taken before surgery, before blood transfusion and on the 1st and 5th postoperative day for determination of T lymphocyte subsets and natural kill cell counts by flow cytometry (EPICS Elite USA) Results The two groups were comparable regard to sex, types of operation, intraoperative blood loss and volume of fluid infused The mean duration of operation of the two groups was (196?42) min The NK cell and CD + 3 and CD + 4 counts and CD + 4/CD + 8 ratio before transfusion were not significantly different from those before operation in both groups The NK cell, CD + 3 and CD + 4 counts and CD + 4/CD + 8 ratio decreased significantly on the 1st postoperative day in both groups but the decrease was more pronounced in group H On the 5th postoperative day the NK cell, CD + 3, CD + 4 counts and CD + 4/CD + 8 ratio returned to preoperative level in group A but remained low in group H Couclusions Perioperative homologous blood transfusion has serious and prolonged inhibitory effects on patient′s immune function In autologous blood transfusion group the changes are milder and the recovery is more rapid as compared with those in group H

AIM: To study the effects of droperidol on the enhancement of persistent sodium currents induced by in vitro ischemia-like condition in isolated rat CA1 paramidal neurons. METHODS: Whole-cell patch-clamp recordings were made from enzymatically isolated rat CA1 hippocampal paramidal neurons. Ischemia was induced by oxygen and glucose deprivation. RESULTS: All of 3, 10 ,and 30 ?mol?L -1 of droperidol significantly inhibited the enhancement of persistent sodium currents induced by ischemia, but the different concentrations did not show significant difference. CONCLUSION: Droperidol in clinical concentration can inhibit the enhancement of persistent sodium current induced by ischemia.

微小RNA（microRNA，miRNA）是一种内源性的长度为18~25个核苷酸的非编码RNA，通过与蛋白质编码基因的 mRNA结合来发挥重要的基因调控作用，与恶性肿瘤的发生发展密切相关。miR-32作为miRNA家族的重要成员，在不同肿瘤中 表达水平存在明显差异，因其与恶性肿瘤的相关性及本身表达的正反作用双向性， 在miRNA领域受到了更多的关注。近年来研 究发现，miR-32对恶性肿瘤细胞的增殖、迁移与侵袭、自噬和凋亡均有影响。此外，miR-32与其上游靶基因、肿瘤代谢及临床诊 断和治疗也有密切的关系。本文就miR-32在恶性肿瘤发生发展中的作用及其机制、临床诊治中应用等最新研究进展作一综述。

Objective To evaluate the effect of intrathecal IL-10 gene on neuropathic pain induced by chronic constriction injury (CCI) to the sciatic nerve. Methods Sixty female SD rats weighing 230-250 g were anesthetized with pentobarfaital. Right sciatic nerve was exposed at the midthigh level and 4 ligatures were placed on the sciatic nerve with 4.0 catgut at 1mm interval. Intrathecal catheter (PE-10 tubing) were inserted at L5,6 interspace and correct placement was confirmed by outflow of CSF. The animals were randomized into 5 groups ( n = 12): group Ⅰ sham operation; group Ⅱ CCI; group Ⅲ,Ⅳ and Ⅴ received intrathecal (IT) normal saline (NS) (Ⅲ) or pcDNA 3.1 (Ⅳ) or pcDNA 3.1-IL-10 (Ⅴ) 3 days after CCI when the animals developed thermal hyperalgesia. Threshold to noxious thermal stimuli was measured before CCI (baseline), before and 2, 4, 7, 10 and 14 days after IT injection. CSF was collected on 1, 3, 7 and 10 days after IT injection for determination of CSF IL-10 concentration. Six animals were killed on 3rd and 14th days after IT injection respectively in each group and the sciatic nerve, lumbar segment of spinal cord ( L3-6) and hippocampus were isolated and blood was collected for determination of IL-10 mRNA expression (by RT-PCR) (on 3rd day after IT) and TNF-? content (on 14th day after IT) .Results Paw removal latencies were significantly longer 2-14 days after IT injection in group Ⅴ(CCI + pcDNA 3.1-IL-10) than in group Ⅲ (CCI + NS) and Ⅳ (CCI + pcDNA 3.1). The IL-10 mRNA expression in sciatic nerve, lumbar segment of spinal cord and hippocampus was significantly higher 3 days after IT injection while their TNF-? contents were significantly lower 14 days after IT injection in group Ⅴ than in the other 4 groups. The CNS IL-10 concentration on day 1-7 after IT injection was significantly higher in group Ⅴ than in the other 4 groups. Conclusion Intrathecal IL-10 gene injection can ease pain induced by CCI of the sciatic nerve through inhibition of inflammatory response.

Objective To study the effects of propofol on enhancement of persistent sodium currents in isolated rat hippocampal CA1 pyramidal neurons induced by ischemia. Methods Whole-cell patch clamp recordings were made from enzymatically isolated SD rat hippocampal CA1 pyramidal neurons. Ischemia was induced by anoxia and glucose deprivation. Results Both propofol 10 umol.L-1 and 100umol . L-1 significantly inhibited the enhancement of persistent sodium currents induced by ischemia and the effect of propofol 100 umol. L-1 was significantly greater than that of propofol 10umol.L-1 . Propofol 1 umol.L-1 didn't have any significant eflect on the enhanced persistent sodium currents induced by ischemia.Conclusion Propofol can inhibit the enhancement of persistent sodium currents induced by ischemia. It may explain the cerebral protective effect of propofol.

BACKGROUND: Both abnormal permeability of ionic channel and disturbance of ionic balance between inside and outside nerve cell are key factors for ischemic brain injury after ischemia. Depolarization induced by activation of sodium channel is starting link for cerebral ischemic injury.OBJECTIVE: To study the effects of droperidol on persistent sodium channel currents of pyramidal cell in hippocampal CA1 area of rats with cerebral ischemia with patch clamp technique so as to analyze whether droperidol can protect cerebral ischemic injury.DESIGN: Randomized controlled animal study.SETTING: Department of Anesthesiology of the Sixth People's Hospital Affiliated to Shanghai Jiaotong University and Department of Anesthesiology of the First People's Hospital Affiliated to Shanghai Jiaotong University.MATERIALS: The experiment was carried out at the Department of Anesthesiology of the First People's Hospital Affiliated to Shanghai Jiaotong University from April 2002 to April 2003. Totally 14 SD rats, aging 10-14days, without ablactation, were selected. Two cells in hippocampal CA1area of each rat were collected, totally 28 cells were divided into 4 groups:ischemic control group, 3 μmol/L droperidol group, 10 μmol/L droperidol group and 30 μmol/L droperidol group, with 7 cells in each group.METHODS: Pyramidal cells in hippocampal CA1 area were separated with digested enzyme method, and ischemic model of neuron was established through hypoxia and no sugar method. Cells were selected with the following conclusion criteria: well adherent wall, triangle or starry shape,bright soma, well refraction, obvious apophysis, steady plasma, and transparent nucleolus. Y-tube system was used for rapid medication. 3, 10 and 30 μmol/L droperidol were given to rats in 3, 10 and 30 μmol/L droperidols respectively, but rats in ischemic control group were not given any medicine. Whole-cell patch-clamp was used to recorded basic value of persistent sodium currents and changes of sodium channel currents during 3-minute and 5-minute ischemia.MAIN OUTCOME MEASURES: ① Record of normal persistent sodium current of neuron in cerebral hippocampal CA1 area; ② Record of persistent sodium current of neuron in cerebral hippocampal CA1 area during cerebral ischemia; ③ Effect of droperidol in various concentrations on persistent sodium current of neuron in cerebral hippocampal CA1 area during cerebral ischemia.RESULTS: Totally 28 cells in cerebral hippocampal CA1 area of 14 rats were entered the final analysis. ① Record of normal persistent sodium current of neuron in cerebral hippocampal CA1 area: 0.5 mmol/L CdCl2 calcium channel blocking agent and 20 mmol/L TEA kalium channel blocking agent were used to perform 400 ms square-wave stimulation under -105 mV claw voltage and -30 mV stimulated voltage. Introversion current,slight, late activation and lasting for a long time, was recorded and deter mined as persistent sodium currents by blocking toxin of puffer fish. ② Record of persistent sodium current of neuron in cerebral hippocampal CA1 area during cerebral ischemia: After 3-minute ischemia, persistent sodium currents in ischemic control group was increased as (1.60±0.21) times as that in normal group, and was (2.87 ±0.45) times after 5-minute ischemia. The difference was significant (P ＜ 0.05). ③ Effect of droperidol at various concentrations on persistent sodium current of neuron in cerebral hippocampal CA1 area during cerebral ischemia: Basic values of persistent sodium currents were (77.42±15.17) pA, (87.44±21.56) pA, (84.13±20.06) pA and (80.22±19.30) pA in ischemic control, 3, 10 and 30 μmol/L droperidol groups respectively, and the differences among groups were not significant. After 5-minute ischemia, values of persistent sodium currents were (105.36±17.16) pA, (94.74±18.88) pA and (84.88±13.94) pA in 3, 10 and 30 μmol/L droperidol groups respectively, which were obviously lower than that in the ischemic control group (218.31±29.34) pA.CONCLUSION: Persistent sodium currents increase under -105 mV claw voltage and -30 mV stimulated voltage during cerebral ischemic injury. Droperi dol can protect neuron by inhibiting the increase of persistent sodium current.

Objective To investigate the role of IL-6/STAT3 signaling in Th17/Tr imbalance of Kawasaki disease(KD). Methods Forty-eight children with KD and eighteen age-matched healthy children were consented to participate in this study. Protein concentration of IL-6 in plasma was measured by ELISA. Transcriptional levels of IL-17A, IL-17F, RORγt, Foxp3, SOCS1 and SOCS3 were assessed by real-time PCR. The proportion of CD4+CD25+Foxp3+ regulatory T(Tr) cells and mean fluorescence intensity(MFI) for phosphorylated-STAT3(pSTAT3) protein in CD4+ T cells was analyzed by flow cytometry. A quantitative methylation specific PCR based on SYBR Green was used to evaluate methylation status of CpG islands in SOCS1 exon2, three potential bind sites for STAT3 in 5'-untraslated region(5'-UTR) of SOCS3 in CD4+ T cells. Results (1)Compared with healthy volunteers, plasma IL-6 concentration and MFI for pSTAT3 in CD4+ T cells were elevated significantly during acute phase of KD[IL-6:(54.02±20.58) pg/ml vs (8.72±2.06) pg/ml, P<0.05;pSTAT3 MFI:(55.41±15.08) vs (9.35±3.76), P<0.05], and the two items in KD patients with coronary artery lesion (KD-CAL+) were found to be higher than those in KD patients without coronary artery lesion (KD-CAL-)[IL-6:(84.76±29.35) pg/ml vs (38.65±13.76) pg/ml, P<0.05;pSTAT3 MFI:(72.36±16.81) vs (46.93±13.57), P<0.05]. (2)Transcription levels of IL-17A, IL-17F and RORγt in patients with KD were significantly elevated (P<0.05) while the proportion of CD4+CD25+Foxp3+ Treg and expression levels of Foxp3 were detected to be lower than those in normal controls (P<0.05). The mRNA levels of IL-17A, IL-17F and RORγt in KD-CAL+ group were higher than those in KD-CAL- group(P<0.05), as well as expression level of Foxp3 were found to be lower in KD-CAL+ group(P<0.05). (3)The mRNA levels of SOCS1 and SOCS3 in CD4+ T cells increased significantly during acute phase of KD(P<0.05), while the two items in KD-CAL+ group were lower than those in KD-CAL- group(P<0.05). Furthermore, CpG islands in SOCS1 exon2 and the third potential bind site for STAT3 in SOCS3 5'-UTR were hypomethylated in acute KD, while those in healthy controls were fully demethylated(P<0.05). Demethylation levels of SOCS1 exon2 and the third potential bind site for STAT3 in SOCS3 5'-UTR in KD-CAL+ group were lower than those in KD-CAL- group(P<0.05). CpG islands in the other two bind sites for STAT3 in SOCS3 5'-UTR were fully demethylated among all the groups(P>0.05). ConclusionAberrant activation of IL-6/STAT3 signaling caused by hypomethylation of SOCS1 and SOCS3 might be one contributing factor to unbalance of Th17/Tr in KD.

Objective To investigate the methylation status of Foxp3 gene and its roles in immunological pathogenesis of Kawasaki disease(KD). Methods Thirty children with KD and eighteen agematched healthy children consented to participate in this study. Quantitative methylation specific polymerase chain reaction(MSQP) was used to assess the methylation status of Foxp3 promoter and regulatory T cells specific demethylated region(TSDR) in CD4+ T cells. The proportion of CD4+ CD25 + Foxp3 + regulatory T (Tr) cells was analyzed by flow cytometry. Transcriptional levels of CD4+ CD25 + Foxp3 + Tr associating genes (Foxp3, CTLA4, GITR, LAG3 and CCR8 ) and Foxp3-dependent molecules (UBD and LGAIS3)were measured by real-time PCR. Results ( 1 ) Demethylation level of Foxp3 promoter in CD4 + T cells from patients with KD was lower significantly than that of health subjects( P ＜ 0.01 ), and increased significantly after treated with intravenous gamma globulin therapy(IVIG) (P ＜ 0.01 ). No difference of demethylation level of TSDR region was observed among all groups ( P ＞ 0. 05 ). ( 2 ) The proportion of CD4 + CD25 + Foxp3 + Tr in peripheral blood from patients with KD , as well as mRNA levels of Foxp3 gene in CD4+ T cells, was significantly lower than those of health subjects ( P ＜0. 01 ), and increases significantly after IVIG therapy (P ＜0.01 ). Significant positive correlations between demethylation level of Foxp3 promoter and the proportion of CD4 + CD25 + Foxp3 + Tr , or expression levels of Foxp3 in CD4 + T cells, were observed during acute phase of KD (CD4+CD25+ Foxp3+ Tr: r=0.76, P＜0. 01; Foxp3: r=0.89, P＜0. 01). (3)Transcription level of CD4+ CD25+ Foxp3+ Tr associating factors, such as CTLA4, GITR, LAG3 and CCR8, was significantly down-regulated in acute phase of KD(P＜0. 01 ), and up-regulated to some extent after treated with IVIG(P ＜0. 01 ). Expression levels of Foxp3-dependent molecules UBD and LGALS3 in CD4 + T cells decreased significantly during acute phase of KD (P ＜ 0.01 ), and basically recovered to the levels of health subjects( P ＜ 0.01 ). Conclusion Decrease of demethylation level of Fopx3 promoter is correlated with immune dysfunction in Kawasaki disease.

Objective To explore whether Cdc42 is an independent influence factor in regulating the migration of A549 cells by using quantitative measurement method,and to verify the effectiveness of an automatic measurement and calculation method for in vitro cell migration assay.Methods Cdc42 was overexpressed in human lung adenocarcinoma A549 cell line,and then in vitro scratch assay was applied to evaluate the migration of the cells.Different methods were used to measure the images acquired at different time points for quantitative analysis.Accuracy and repeatability of different measurement methods were analyzed.Results The results showed that overexpression of Cdc42 alone significantly advanced the migration of A549 cells (P＜0.05).The new method is efficient,accurate and reproducible as compared to manual measurement,and has significant advantages in target recognition and noise removal as compared to the existing measurement method in Image Pro Plus 6.0.Conclusions Over expression of Cdc42 significantly increased A549 cell migration ability in vitro.The new method can realize the automatic quantitative analysis of cell migration in vitro.