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.

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.

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 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 analyze the clinical features, recurrent characters in patients with recurrent Tolosa-Hunt syndrome (THS). Methods The clinical data of 24 hospitalized patients with recurrent THS from January 2006 to May 2016 were collected The general features, clinical manifestations, disease courses, recurrent features, lab and imaging studies, treatment measures and outcoming of recurrent THS patients was investigated , and compared with 69 patients with first attack THS in corresponding period. Results Recurrent THS patients were 25.8%(24/93) of total THS. The male rate in recurrent group was significantly higher than that in first attack group: 66.7%(16/24) vs. 42.0%(29/69), P<0.05. The involved rate of trigeminal nerves in recurrent group was significantly lower than that in first attack group:16.7%(4/24) vs. 33.0%(23/69), P<0.05. The disease courses were from 3 months to 20 years. The total recurrent frequencies were from 2 to 10 times. The recurrence occurred in the same side in 18 patients, and in contralateral in other 6 patients. The intervals were from 3 months to 6 years, and average intervals were 1.9 years. Two patients recurred in hormone reduction, and 22 patients recurred in hormone withdrawal. All cases received MRI examination. Nineteen patients (79.2%) of them had lesions in cavernous sinus. 16 patients had one side lesions and 3 patients had bilateral lesions. The recurrent patients still had good responds to corticosteroids treatment. Conclusions Recurrences in THS are common, taking place in about 26%total patients, and usually at an interval of months or years from the initial attack. These recurrences may be ipsilateral, contralateral, or rarely, bilateral. Corticosteroids are still effective to recurrent cases.

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 investigate the effect of SOCS1 and SOCS3 hypomethylation on homeostasis of Th1/Th2 in Kawasaki disease(KD). Methods Thirty-six children with KD and sixteen age-matched healthy children consented to participate in this study. Protein concentration of IL-6 in plasma was measured by ELISA. Transcriptional levels of SOCS1, SOCS3, T-bet, IFN-γ, GATA3 and IL-4 were assessed by realtime PCR. The proportion of Th1 and Th2 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 SOCSl exon2, and three potential binding sites for STAT3 in 5'-untraslated region(5'-UTR)of SOCS3 in CD4+T cells. Comparisons between groups were performed with t-test. Results ①Compared with healthy volunteers, plasma IL-6 concentration[(51.8±16.3)pg/ml vs(8.6±2.0)pg/ml, respectively]and MFI for pSTAT3[(52±14)vs(10±4), respectively]in CD4+ T cells were elevated significantly during acute phase of KD(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:(87.2±27.4)pg/ml vs(36.2±12.8)pg/ml, P＜0.05; pSTAT3 MFI:(75±15)vs(42±11), P＜0.05]. ② The proportions of Th1 and Th2 cells and transcription levels of Th-associating factors(T-bet, IFN-γ, GATA3 and IL-4)in CD4+ T cells increased significantly in acute KD(P＜0.05), while the rate of Thl div Th2 in KD patients was found to be lower than that in normal controls(P＜0.05). In addition, the proportions of Th1 and Th2 cells and expressions levels of Th-associating factors in KD-CAL+ group were higher than those in KD-CAL-group, as well as the rate of Thl div Th2 cells in KD -CAL+ group were lower than that in KD-CAL- group(P＜0.05). ③ The mRNA levels of SOCSl and SOCS3 in CD4+ T cells increased significantly during acute phase of KD(P＜0.05), while the two items in KDCAL+ group were lower than those in KD-CAL- group(P＜0.05). Furthermore, CpG islands in SOCSl exon2 and the third potential binding site for STAT3 in SOCS3 5'-UTR were hypomethylated in acute KD, while those in healthy volunteers were fully demethylated(P＜0.05). Demethylation levels of the two items mentioned above in the KD-CAL+ group were lower than those in the KD-CAL-group(P＜0.05). CpG islands in the other two binding sites for STAT3 in SOCS3 5'-UTR were fully demethylated among all the groups(P＞0.05).Conclusion Relative insufficiency of SOCS1 and SOCS3 expression caused by hypomethylation may be one contributing factor for the imbalance of Th1/Th2 in KD.