Objective To determine the effect of activating parvalbumin (PV) positive inhibitory neurons on memory impairment caused by frontal cortex ischemia and analyze the related mechanism. Methods Adult PV-Cre mice were randomly divided into control group [frontal cortex injection of 0.9% NaCl+ intraperitoneal injection of clozapine N-oxide hydrochloride (CNO)], model group (frontal cortex injection of endothelin+intraperitoneal injection of 0.9% NaCl) and intervention group (prefrontal cortex injection of endothelin+intraperitoneal injection of CNO). Among them, virus microinjection technology was adopted to specifically express mCherry in the PV neurons in the frontal cortex of mice from the control group, while specifically express hM3d-mCherry in the PV neurons from the model group and the intervention group. Injection of CNO was performed in the intervention group to specifically activate PV positive neurons through hM3d. The memory and motor functions of mice were detected by T-maze and object location and recognition tasks. The changes of dendritic spine density of pyramidal neurons in frontal cortex were analyzed by Golgi staining. Results The administration of endothelin in frontal cortex caused local ischemia. Compared with the normal control group, the density of dendritic spines on pyramidal neurons was decreased after frontal cortex ischemia, resulting in the decrease of selection accuracy in T-maze and exploration scores in object location and recognition tasks (P < 0.01). On the contrary, activation of PV positive neurons significantly increased the density of dendritic spines in frontal cortex, and significantly improved the selection accuracy of mice in T-maze test (P < 0.05) and the exploration score in object location and recognition tasks (P < 0.05). Conclusion Activation of PV positive neurons can improve memory impairment caused by frontal cortex ischemia, which may be related to increasing the density of dendritic spines in frontal cortex.

生长停滞特异性蛋白6(growth arrest specific protein 6,GAS6)在肿瘤发生发展中发挥重要作用,其信号转导参与细胞增殖、黏附与迁移,但它在子宫内膜异位症(endometriosis,EMs)的相关功能及分子机制尚不明确.本研究从GEO数据库检索并下载子宫内膜异位症相关转录物组数据集,并对其进行GEO在线分析,筛选差异表达基因并进行GO聚类和KEGG通路富集分析.利用10例无内异症且无明确疾病妇女的在位子宫内膜,以及11例卵巢巧克力囊肿病人异位子宫内膜,对3个以上数据集共有的差异基因的mRNA水平进行实时荧光定量PCR验证.在子宫内膜异位症临床样本中,采用免疫组化、实时荧光定量PCR验证关键调控因子GAS6及上皮间充质转化(epi-thelial mesenchymal transition,EMT)标记基因的表达水平,并利用免疫荧光对GAS6和E-钙黏着蛋白(E-cadherin)进行共标.研究发现:从4个转录物组数据集中共筛选出47个差异表达基因,其主要富集于细胞迁移等过程以及MAPK、PI3K-AKT、紧密连接等相关信号通路.3个以上数据集所共有的9个差异基因在子宫内膜异位症病人中的mRNA水平均符合生物信息学分析的结果.GAS6在子宫内膜异位症病人异位内膜中的表达水平高于对照组(P＜0.05),并且子宫内膜异位症病人的内膜组织中存在EMT现象,EMT的标志物E-钙黏着蛋白表达水平下调(P＜0.05)、波形蛋白(vimentin)表达水平上调(P＜0.01).在GAS6高表达的子宫内膜异位症患者异位子宫内膜腺上皮细胞中,E-cadherin显示低表达,提示GAS6可能在子宫内膜异位症中介导EMT过程.综上所述,本研究初步揭示GAS6在子宫内膜异位症病人中高表达,及其可能介导EMT过程参与子宫内膜异位症的发生与发展,为子宫内膜异位症的临床治疗提供潜在靶标.

Objective To determine the expression of S100A6 in liver tissues and investigate its role in the activation of hepatic stellate cells (HSCs). Methods Twelve C57BL/6 mice were randomly assigned to control group and liver fibrosis group. The mice in the latter group was administrated with carbon tetrachloride for 6 weeks to induce liver fibrosis. The liver tissue was harvested for Masson staining and S100A6 detection by immunohistochemistry. The expression of S100A6 at mRNA and protein levels was detected by RT-qPCR and Western blotting. After primary HSCs were isolated and cultured, their morphological changes in quiescence and activation were observed, and the mRNA and protein levels of S100A6 were detected after cultured for different time periods. Additionally, siRNA was utilized to interfere S100A6 expression in HSCs, and the mRNA and protein levels of S100A6, Collagen Ⅰ and α-SMA were tested by RT-qPCR and Western blotting. Results Masson staining displayed fibrosis in liver tissue in the mice of the liver fibrosis group, and S100A6 was also significantly expressed in the corresponding fibrous cord area of liver tissue in liver fibrosis group, and its mRNA and protein levels were obviously enhanced in the liver tissue when compared to the control group (P < 0.05). In vitro, HSCs auto-activated with the process of culture, and the mRNA and protein expression levels of S100A6 were gradually increased in a time depended manner in the HSCs (P < 0.05 or P < 0.001). Undoubtedly, the interference of S100A6 by siRNA efficiency dramatically inhibited the mRNA and protein expression of S100A6, Collagen Ⅰ, α-SMA (P < 0.05 or P < 0.001). Conclusion S100A6 is specifically expressed in hepatic fibrosis and activated HSCs, and is an important protein regulating the activation of HSCs. Thus, S100A6 might play important role in the pathogenesis of liver fibrosis.

目的 探究C-13呼气试验检测系统(13C)检测幽门螺杆菌(Hp)阳性患者中实施品管圈活动对提高复诊率的促进作用.方法 成立品管圈小组,选定主题后进行现状把握、原因分析、目标设定、制定对策并组织实施,分别比较实施前后的有形成果和无形成果.结果 实施品管圈活动后,100例13C阳性患者复诊90人,幽门螺杆菌(Hp)阳性患者复诊率明显提高;圈员在绘制柏拉图、用鱼骨图解析问题等方面的品管手法、团队精神、工作积极性、工作责任心、沟通协作能力、解决问题能力均显著提高,与实施前对比,差异有统计学意义(P<0.05).结论 在13C检测Hp阳性患者中实施品管圈活动,复诊率及患者满意度均显著提高,能够有效促进幽门螺杆菌(Hp)阳性患者复诊工作的持续改进,保障医患双方利益、优化医患关系,为医院长期发展奠定良好基础.

Objective To determine the effect of progesterone on axon regeneration of cerebral ganglia neurons after intracerebral hemorrhage (ICH), and explore the underlying mechanism. Methods SD rats were randomly divided into ICH group, low- (8 mg/kg) and high-dose progesterone (16 mg/kg) groups, and sham operation group. Combined treatment of high-dose progesterone and PI3K/Akt pathway inhibitor LY294002 was given to the rats from the inhibitor group. The neurological deficits, brain water content and pathological changes and expression of axon growth-related proteins were observed at 1, 3, 7 and 14 d after operation. And the cerebral hematoma volume and oxidative stress related indexes were analyzed at 3 d after operation. The expression levels of axonal-associated proteins and pathway proteins p-Akt and RhoA were detected at 3 d after operation, and the locations of GAP43 and p-Akt/RhoA were identified with immunofluorescence staining. Results The ICH group had severest neurological dysfunction and cerebral edema at each time point, and largest volume of cerebral hematoma and highest levels of oxidative stress products. After progesterone intervention, the damage was relieved at each time point, with the efficacy of high-dose more obvious than low-dose (P < 0.05). Western blot Results showed that the high-dose progesterone intervention increased the expression levels of GAP43 and NF200 and decreased those of MAG and Nogo-A when compared to the low-dose progesterone and ICH groups (P < 0.05). Western blot analysis indicated that the expression of GAP43, NF200 and p-Akt was down-regulated while that of MAG, Nogo-A and RhoA was increased in the inhibitor group compared with the high- and low-dose progesterone groups (P < 0.05). The Results of double-labeled fluorescence staining showed that the expression of p-Akt was increased and that expression of RhoA was decreased in neuronal cells of the high-dose progesterone group compared with ICH group (P < 0.05). Conclusion Progesterone improves neurological dysfunction after cerebral hemorrhage and promotes regeneration and repair of damaged axons, which may be related to activation of PI3K/Akt pathway and inhibition of RhoA expression.

Objective To investigate the mechanism by which resveratrol (RES) promotes axonal regeneration in rats after intracerebral hemorrhage (ICH) and explore the role of the PI3K/Akt pathway that regulates the AMPKα pathway. Methods A total of 126 male adult SD rats were randomized into sham- operated group (n=30), ICH group (n=30), low-dose (20 mg/kg) RES group (n=30), high-dose (40 mg/kg) RES group and PI3K/Akt inhibitor (LY294002) group (n=6). Rat models of ICH were established by stereotaxic injection of autologous blood into the basal ganglia with subsequent treatments as indicated. The neurological deficits of the rats were evaluated, and the pathological changes in the brain tissues were observed with HE staining. The parameters of oxidative stress in each group were detected using ELISA. Western blotting, immunohistochemistry and immunofluorescence assay were performed to detect the expressions of neurofilament 200 (NF200), microtubule-associated protein-2 (MAP-2), myelin basic protein (MBP), growth-associated protein 43 (GAP43), protein kinase B (PKB or Akt), AMP-activated protein kinase alpha (AMPKα) and glycogen synthase kinase 3 beta (GSK-3β) in the brain tissue. Results The rats exhibited significant neurological deficits, obvious brain pathologies, and elevated oxidative stress level following ICH. Intervention with RES, especially at the high dose, obviously alleviated the injuries of the brain tissue. Western blotting and immunohistochemistry showed that compared with those in ICH group, the expression of NF200 and MAP-2 increased significantly in the hemorrhagic region in rats receiving RES treatment, and the effect was more obvious in the high-dose group than in the low-dose group (P < 0.05). Immunofluorescence assay showed that RES treatment of the rats, especially at the high dose, obviously enhanced MBP expression in the brain tissue as compared with that in ICH group (P < 0.05), and AMPK was found to mediate the effect of RES on the axons. The results of Western blotting further confirmed that RES treatment significantly decreased the expressions of p-AMPKα and p-GSK-3β and increased the expressions of NF200, MAP-2, MBP, GAP43 and p-Akt in the hemorrhagic brain tissues of the rats, as compared with those in ICH group, and high-dose RES produced significantly stronger effects on these proteins (P < 0.05). These effects of RES were obviously reversed by the application of PI3K/Akt inhibitor in the rat models of ICH. Conclusion RES can promote axonal regeneration and neurological function recovery in rats after ICH possibly by down-regulating the AMPK pathway through the PI3K/Akt pathway.

Objective:To investigate the role of pre-B-cell colony enhancing factor（PBEF）in the pathogenesis of acute respiratory distress syndrome（ARDS）. Methods:Human pulmonary microvascular endothelial cell line（HPMEC） and human type Ⅱ alveolar epithelial cell line（A549）were constructed by increasing human recombinant PBEF（r PBEF）concentrations（0,50,100,500,1 000,2 000 ng/mL）in a stepwise manner. The cell viabilities to r PBEF were tested by MTT assay. And then the cells were stimulated with 100 and 1 000 ng/mL r PBEF while the blank control group was set up. The cell cycle and cell apoptosis were analyzed using flow cytometry（FCM）. Morphological changes of apoptosis were observed by transmission electron microscopy. The expres-sions of caspase-3,B-cell lymphoma/leukemia-2 gene were detected by Western blot. The expressions of aquaporin 1,interleukin-8 and interleukin-1β were detected using RT-PCR and Western blot. Results:The cell viabilities were significantly inhibited in the r PBEF group with 100,500,1 000,2 000 ng/mL r PBEF compared with those in blank control group（P<0.05）. FCM showed that the percentage of S phase in 100 and 1 000 ng/mL r PBEF groups[HPMEC:（43.847±1.272）%,（63.300±2.102）%;A549:（36.247±2.045）%,（46.400±1.346）%)] were significantly higher than those in the blank control group[HPMEC:（19.347±2.052）%;A549:（17.297±0.800）%]（all P=0.000）and the apoptic rate in 100 and 1 000 ng/mL r PBEF groups[HPMEC:（11.317±0.533）%,（15.227±0.637）%;A549:（6.120±0.439）%,（8.633±0.497）%] were significantly higher than those in the control group[HPMEC:（8.433±0.600）%;A549:（3.877±0.666）%)](PHPMEC= 0. 001,PHPMEC= 0. 000;P;= 0. 002,P;=0.000). Transmission electron microscopy showed typical apoptosis,such as heterochromatin concentrated which was set in the nuclear membrane and visible apoptotic bodies in 1 000 ng/mL r PBEF group. The expressions of Bcl-2 protein in 100 and 1 000 ng/mL r PBEF groups [HPMEC :（0.418±0.043）,（0.190±0.012）;A549:（1.276±0.212）,（0.601±0.164）] were significantly decreased（all P=0.000）and the expressions of caspase-3 protein were significantly increased in 100 and 1 000 ng/mL r PBEF groups [HPMEC :（0.763 ±0.030）,（1.170±0.056）;A549:（0.217±0.010）,（0.375±0.032）],respectively,compared with those of blank control group(PHPMEC=0.000,PHPMEC=0.000;P;=0.001,P;=0.000). The expressions of AQP1 gene and protein in 100 and 1 000 ng/mL r PBEF groups were statistically lower than blank control group[mRNA:HPMEC（0.543±0.113）,（0.287±0.093）vs.（1.050±0.155）（P=0.002,P=0.000）,A549（0.823±0.104）,（0.463±0.184）vs.（1.317±0.215）（P=0.013,P=0.001）;protein:HPMEC（0.494±0.038）,（0.233±0.030）vs.（0.824±0.067）（all P=0.000）,A549（0.850±0.157）,（0.484±0.118）vs.（1.344±0.136）（P=0.005,P=0.000）] while the expressions of IL-8 and IL-1βgene and protein were statistically higher than blank control group in 100 and 1 000 ng/mL r PBEF groups（P<0.05）.Conclusion:PBEF may induce the apoptosis of HPMEC and A549 by down-regulating the expression of Bcl-2 and up-regulating the expression of caspase-3 and PBEF could induce low expression of AQP1 which suggests that PBEF may play an critical role in the development of ARDS.

Objective To investigate the clinical efficacy and life quality of patients with advanced colon cancer by tra-ditional Chinese and Western Medicine. Methods 73 cases of advanced colon cancer patients diagnosed by pathological exam-ination in our hospital were selected, which were randomly divided into Chinese and Western medicine (CW) group and West-ern medicine group. The CM group was received Fuzheng Xiaoji decoction combined with XELOX regimen (capecitabine plus oxaliplatin) treatment, and the Western medicine group was only given XELOX plan treatment. The short-term curative effect, TCM symptom score, tumor markers, immune cell level and quality of life before and after treatment between two groups were compared. Results TCM symptom score in CW group was higher than that in Western medicine group (P<0.05). Carcinoem-bryonic antigen (CEA) in CM group was lower than those in Western medicine group and before treatment (P<0.05). The CD4+and CD8+ in CW group was higher than those in Western medicine group (P<0.05), there was no difference than before treat-ment (P>0.05). Conclusion Combination of traditional Chinese and Western medicine show better effect than western medicine alon on treatment of advanced colon cancer, which could reduce the TCM symptom score, improve the quality of life, and have little affect on the immune system.

目的 炎症通过其对肿瘤微环境的影响在癌症的发展过程中起着重要作用.然而炎症与肿瘤之间的关系仍然需要进一步阐明.本研究主要观察IL-21R在舌鳞状细胞癌的表达和分布情况.方法 使用逆转录酶聚合酶链反应(RT-PCR)、Western blot免疫印迹方法检测来自54个舌鳞状细胞癌患者手术标本IL-21R的基因和蛋白表达,并且观察IL-21R表达与临床病理特征的关系.同时,进一步通过免疫组织化学和免疫荧光技术观察IL-21R表达与分布规律.结果 RT-PCR和Western印迹分析的结果表明,与癌旁组织相比,舌鳞状细胞癌标本中IL-21R基因和蛋白表达显著降低(P＜0.05).IL-21R低表达与性别、年龄、分化程度、肿瘤大小均无密切关系.这种表达特点主要与临床分期呈正相关.免疫组织化学结果显示,IL-21R主要表达于舌癌旁组织鳞状细胞和上皮细胞,而鳞状细胞癌组织中表达较弱或散在的表达.IL-21R与IL-10的双染荧光结果显示,IL-21R阳性的细胞中可见IL-10的阳性染色.结论 这些数据表明IL-21R在舌癌肿瘤发生与侵袭性过程中可能起着重要作用.

Objective:To preliminarily investigate the effects of tetramethylpyrazine(TMP)on expressions of aquaporin1,5 in lipopolysaccharide(LPS)-induced lung injury in rats. Methods:Thirty-two healthy male SPF grade SD rats were randomly divided into the normal control group(group C),the TMP intervention group(group T),the LPS stimulation group(group L) and the TMP treatment group(LT group),with eight rats in each group. Rats in the group L were given LPS(6 mg/kg)through tail vein injection,rats in group T were given TMP(100 mg/kg)through intraperitoneal injection,and rats in group LT were given LPS for 1 h followed by TMP(100mg/kg)through intraperitoneal injection immediately. After 8 hours,all rats were anesthetized and sacrificed,with lung tissue specimens harvested. Wet/dry ratio(W/D)of the lung tissue was detected. In addition,hematoxylin-eosin(HE) staining was performed to observe the lung tissue morphology;Quantitative real-time PCR(q RT-PCR)was used to detect the AQP1 m RNA and AQP5 m RNA levels of the lung tissue homogenate. In addition,immunohistochemistry and Western blot were used to detect the protein expression of AQP1 and AQP5 in the lung tissue. Results:After HE staining of the lung tissue sections,the lung tissue was integral and clear in its structure in group C and T under light microscope. Alveoli were disorderly in structures,the diffuse alveolar septa were thickened,and alveolar inflammatory cell infiltration,hemorrhage and edema were observed in group L. While the LT group had milder pathological manifestations than group L. The average W/D ratio of the lung tissue in group L(5.577±0.243)was higher than that of each of the other three groups significantly(P<0.01). Compared with group C and T(3.430±0.251、3.251±0.142),the W/D ratio in the group LT(4.384±0.236)was increased,and the difference was significant(P<0.01). The results of q RT-PCR showed that the levels of AQP1 RNA and AQP5 RNA in group T(1.462±0.080,1.267±0.063)were higher than those in group C(1.160±0.229,0.940±0.087)and the levels in group L(0.607±0.203,0.139±0.046)were down-regulated. Meanwhile,the levels in group LT(0.848±0.071,0.314±0.134)were higher than those in group L(P<0.05). The results of immunohistochemistry(C group:2.096±0.114,2.285±0.266;T group:3.253±0.149,3.790±0.308;L group:1.133±0.202,1.068 ±0.221;LT group:1.562 ±0.085,1.647±0.239)and Western blot(C group:1.443±0.103,1.278±0.061;T group:1.667±0.087,1.644±0.102;L group:0.974±0.090,0.529±0.100;LT group:1.179±0.051,0.805±0.082)were consistent with those of q RT-PCR(P<0.05). Conclusion:TMP can exhibit positive protective effects by mitigating LPS-induced pulmonary edema in ARDS effectively,and the mechanism may be associated with the upregulation of the expressions of AQP1 and AQP5.

目的 研究人第10号染色体缺失的磷酸酶及张力蛋白同源基因(phosphatase and tensin homolog deleted on chromosome 10,PTEN)在小鼠动脉血管钙化形成过程中的作用.方法 ①构建血管特异性PTEN敲除小鼠(PTEN△/△),对照组小鼠为PTENf/f;②免疫组化检测ApoE全敲除小鼠钙化血管中PTEN的表达水平;③体外通过钙化培养基诱导血管钙化;④Alizarin Red染色和Von Kossa染色评估PTEN敲除后小鼠血管钙化程度;⑤实时荧光定量PCR检测血管钙化标志物Runx2、骨钙蛋白和BMP2的表达水平.结果 ①与普通饮食组相比,高脂饮食诱导的ApoE基因敲除小鼠血管钙化明显,而钙化后的血管中PTEN的表达水平显著下降(P＜0.01);②经体外诱导后,PTEN△/△小鼠血管明显钙化,而PTENf/f小鼠血管几乎无钙化;③与PTENf/f组相比,PTENⅣ△小鼠血管钙化标志物Runx2、骨钙蛋白和BMP2的表达均明显升高(P＜0.05).结论 血管特异性PTEN基因敲除促进小鼠血管钙化的形成.

Objective To investigate the effect of dopamine on lipopolysaccharide (LPS)-induced inflammatory response in mouse peritoneal macrophages (MPMs).Methods MPMs were isolated after injection of thioglycolate broth into the peritoneal cavity.MPMs from wild type C57 mice were distributed into control group,LPS group,dopamine pretreatment group,dopamine D1-like and and D2-like receptor antagonist groups (D1 and D2 antagonist groups).In the latter two groups,MPMs were pretreated with Dl-like and D2-like receptor antagonist respectively for 30 min,and then stimulated with dopamine and LPS.MPMs from wild type (TLR4 +/+) and TLR4 knock-out (TLR4-/-) mice were only divided into LPS group and dopamine pretreatment group.In LPS group,MPMs were stimulated with 1 μg/ml LPS for 6 h.In dopamine pretreatment group,MPMs were pretreated with 10-4 mol/L dopamine for 2 h,and then stimulated with 1μg/ml LPS for 6 h.Expressions of TLR4 and pro-IL-1βwere detected by Western blot and tumor necrosis factor-α (TNF-α) in cell culture supernatant by ELISA method.Results (1) Expressions of TLR4,pro-IL-1β and TNF-α in control group were (0.56 ± 0.07),(0.65 ± 0.11) and (1,770.6 ±448.8) pg/ml;in LPS group were (1.12 ± 0.15),(1.24 ± 0.20) and (15,569.5 ± 822.7) pg/ml;in dopamine pretreatment group were (0.28 ± 0.11),(0.22 ± 0.08) and (7,800.7 ±862.6)pg/ml;in D1 antagonist group were (0.25 ±0.12),(0.18 ±0.09) and (7,065.0 ± 1016.8)pg/ml;in D2 antagonist group were (0.80 ±0.09),(0.44 ±0.08) and (14,299.6 ± 1430.9)pg/ml.The three indicators in LPS group were increased compared to control group and dopamine pretreatment group (P ＜ 0.05),and in D2 antagonist group were increased compared to dopamine pretreatment group (P ＜ 0.05).There were no obvious differences between D1 antagonist group and dopamine pretreatment group(P ＞0.05).(2) After LPS stimulation,expressions of pro-IL-1 β and TNF-α in TLR4+/+ mice were (0.94 ±0.17) and (15,109.0 ± 1,903.4)pg/ml,and were (0.08 ±0.04) and (5,063.6 ± 512.8) pg/ml in TLR4-/-mice (P ＜0.05).After dopamine pretreatment,expressions of proIL-1β and TNF-α were (0.45 ±0.12) and (6,383.9 ± 1,287.3) pg/ml in TLR4+/+ mice,and were (0.05 ± 0.02) and (4,863.0 ± 824.7) pg/ml in TLR4-/-mice.Expressions of pro-IL-1β and TNF-o were higher in TLR4 +/+ mice than in TLR4-/-mice after LPS stimulation (P ＜ 0.05).Expressions of pro-IL-1β and TNF-αin TLR4 +/+ mice were reduced after dopamine pretreatment compared to LPS stimulation (P ＜ 0.05),while were similar in TLR4-/-mice (P ＞ 0.05).Conclusion Dopamine can inhibit LPS-induced inflammatory response in MPMs,and the inhibition is strongly related to dopamine D2-1ike receptor and TLR4.

Objective To assess diagnosis value of detecting ANCA and ASCA on adult IBO subgroups. Methods Through searching literatures involving in correlations between ANCA,ASCA and adult colitis gravis and Crohn′s disease(CD) in and aboard,adopting the QUADAS—2 scale to assess the quality of the literatures included and metadisc heterogeneous computing , The combined sensitivity,specificity,positive likelihood ratio,negative likelihood ratio as well as the diagnostic odds ratio,the curve of the testees was drawn. Results In line with the inclusion and exclusion standards ,13 independent studies were considered. The pooled sensitivity,specificity,positive and negative likehood ratio,diagnostic odds ratio and area under curve (AUC) in diagnosis of colitis gravis by ANCA with meta—disc1.4 software were 0.51,0.92,6.06,0.53,12.56,0.79,0.56,0.92,5.13, 0.57,10.33,0.8169 accordingly and those of and CD by ASCA being 0.56,0.92,5.13,0.57,10.33,0.82 successively. Conclusion ANCA and ASCA are beneficial to the diagnosis of IBD subgroups. The suspected patients in clinic may select this examina—tions. Those whose serum markers are positive may treated as early as possible ,the others who are negative may choose the colonoscopy examination. The thought is subject to major significance i improving the compliance and prognosis. More prospec—tive,double—blind,large—size samples were required to verify its clinical value further.

目的：探讨肾脏去神经（ renal denervation， RDN）对动脉粥样硬化（ atherosclerosis，AS）家兔肿瘤坏死因子α（TNF－α）、白细胞介素1α（IL－1α）和白细胞介素6（IL－6）的影响。方法：28只雄性新西兰白兔随机分为对照组、RDN后高脂饲养（ high－fat diet， HFD）组（ RDN组）、假手术后HFD组（假手术组）和单纯HFD组（ HFD组），每组7只。测量各组血浆去甲肾上腺素（ norepinephrine，NE）、炎症因子及血脂水平；免疫组化检测血管紧张素II （Ang II）的表达，Western blot检测核因子κB（NF－κB）和血管紧张素II 1型受体（AT1R）的表达；real－time PCR检测TNF－α、IL－1α和IL－6 mRNA的表达；光镜下观察肾动脉结构改变和主动脉病理变化。结果：8周后RDN组NE水平明显低于假手术组和HFD组（P＜0．05）；RDN组血浆甘油三酯（TG）水平低于HFD组（P＜0．05）；RDN组的Ang II蛋白表达低于假手术组和HFD组（P＜0．01）；RDN组NF－κB蛋白表达低于假手术组（P＜0．05）；RDN组TNF－α和IL－1α的血浆水平低于假手术组和HFD组（P＜0．05），RDN组IL－6 mRNA的表达低于假手术组（P＜0．01）。结论：RDN能有效抑制全身交感神经活性，降低血浆TG水平，减轻血管炎症反应，延缓动脉粥样硬化的发展。

目的:观察前B细胞克隆增强因子(pre-B cell colony enhancing factor,PBEF)在急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)大鼠中肺组织的表达,以及对ARDS大鼠肺组织炎症因子肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-1β(interleukin-1β,IL-1β)mRNA以及核因子-κB (nuclear factor-κB,NF-κB)p65蛋白表达的影响,通过以上指标的变化,结合已有体外实验所观察到的现象试图证实前B细胞克隆增强因子在ARDS中的促炎作用.方法:将40只成年SD大鼠随机分为空白对照组(C组)、模型组(OA组)、药物干预组(D组)、溶媒对照组(S组),OA组、D组及S组大鼠用油酸尾静脉注射复制ARDS模型,D组造模前腹腔内注射PBEF抑制剂FK866,S组造模前注射等体积FK866溶媒二甲基亚砜.造模成功6h后取材,比较各组大鼠肺组织PBEF、TNF-α、IL-1β mRNA以及NF-κB p65蛋白表达情况.结果:C组大鼠肺组织中几乎见不到PBEF表达,而在其他各组大鼠肺组织肺泡壁及肺泡水肿液中、支气管黏膜上皮及血管内皮均可发现PBEF蛋白分布;OA组、D组和S组大鼠PBEF及炎症因子mRNA和NF-κB p65蛋白表达增加(PBEF:P=0.000,P=0.000,P=0.000;TNF-α:P=0.035,P=0.000,P=0.000; IL-1β:P=0.000,P=0.000,P=0.000;NF-κB p65:P=0.000,P=0.000,P=0.000),D组大鼠肺组织PBEF、炎症因子mRNA和NF-κB p65蛋白表达较OA组和S组低(PBEF:P=0.002,P=0.006; TNF-α:P=0.004,P=0.001;IL-1β:P=0.001,P=-0.015; NF-κB p65:P=-0.001,P=0.000).结论:PBEF可能通过激活炎症反应、促进炎症因子表达等途径造成肺组织的炎性损伤,进而在ARDS发生发展中起重要作用.

Objective To evaluating the effect of metformin to biochemical outcomes of non-alcoholic fatty liver disease patients . Methods By computer search ,the data of thirteen randomized controlled clinical trials were searched .Meta-analyses were per-formed ,by Review manager5 .0 statistical software with assessment for heterogeneity .Results Comparing with diet/exercise thera-py/placebo/hepatoprotectants ,metformin could improve the level of ALT and AST ,the weighted mean differences (WMDs) were-22 .72 U/L(95% CI:-31 .66 - -13 .79 ,P<0 .000 01) ,-10 .99 U/L(95% CI:-16 .04 - -5 .95 ,P<0 .000 1) .At the same time ,meformin also could improve the level of TC and TG ,the weighted mean differences(WMDs) were -0 .59 mmol/L(95% CI:-1 .08- -0 .10 ,P=0 .02) ,-0 .48 mmol/L(95% CI:-0 .70 - -0 .26 ,P<0 .000 1) .The data showed that metformin can im-prove the level of HOMA-IR obviously ,the weighted mean difference(WMD) was -0 .62(95% CI:-0 .94- -0 .30 ,P=0 .000 2) . But through the study data ,metformin could not improve the level of BMI ,the weighted mean difference(WMD) was -1 .54 kg/m2 (95% CI:-3 .22-0 .15 ,P=0 .07) .Conclusion Metformin can improve the level of ALT ,AST ,TC ,TG and obviously improve the insulin resistance of non-alcoholic fatty liver disease patients .the study data suggests that metformin has therapeutic effect to non-alcoholic fatty liver disease patients .

Objective:To investigate the correlation between polymorphisms of serine hydroxymethyltransferase1 gene and the adverse reactions of high-dose methotrexate (HD-MTX) in children with acute lymphoblastic leukemia (ALL). Methods:A total of 51 patients with ALL were treated with HD-MTX, and clinical manifestations after HD-MTX treatment were evaluated retrospectively. cD-NA was obtained from mRNA. The polymorphisms of SHMT1 gene containing rs1979277, rs3783, rs1979276, and rs12952556 sites were tested by denaturing gradient gel electrophoresis and direct sequencing. Effects of SHMT1 gene polymorphisms on HD-MTX ad-verse reactions were evaluated. Results:Severe adverse reactions in ALL patients treated with HD-MTX appeared to be mainly neutro-penia and hepatoadverse reactions. The frequency distributions of rs3783 (C>G), rs1979276 (C>T), rs12952556 (A>G), and rs1979277 (C>T) were the same. The polymorphisms of rs1979277 showed no correlation with neutropenia (P>0.05) but rs1979277 CT and TT genotypes were correlated with hepatoadverse reactions (CT: OR=0.129, 95% CI: 0.020 to 0.817, P=0.03; TT: OR=0.103, 95% CI:0.017 to 0.620, P=0.013). Conclusion: No correlation was found between the combination of rs1979277, rs3783, rs1979276, rs12952556, and neutropenia, but one or more of these loci may reduce the risk of hepatoadverse reactions.

目的:探讨肿瘤坏死因子(tumor necrosis factor,TNF)-β基因+252MG多态性与胃癌的发病相关性.方法:检索Pubmed、Ovid、Springer、CBM、CNKI、万方数据库,时间从建库至2013年6月期间关于TNF-β基因+252 A/G多态性与胃癌发病相关性的病例-对照研究.根据纳入排出标准选择文献,提取资料,评价纳入研究质量,采用Review Manager 5.2及Stata 12.0软件进行Meta分析,亚组分型及敏感性分析评估其结果稳定性,并用Begg's漏斗图和Egger's回归图来评估发表偏倚.结果:共纳入了16篇病例对照研究,共计病例组2 538人,对照组3 908人.Meta分析结果显示:在各组遗传模型中,TNF-β基因+252A/G多态性与胃癌发病无统计学意义:共显性遗传模型(G/G vs.A/A):OR及95％CI:0.95 (0.76,1.20);显性遗传模型[(A/G+G/G)vs.A/A]:OR及95％CI:1.09(0.91,1.32);隐性遗传模型[G/G vs.(A/G+A/A)]:OR及95％CI:0.88(0.72,1.07);等位基因遗传模型(G vs.A):OR及95％CI:1.00(0.90,1.11)(G/G、A/G、A/A分别代表基因型).针对人种的亚组分析也无统计学意义.结论:TNF-β+252A/G基因多态性与胃癌发病无明显相关性.本次结果受纳入研究质量及数量的限制,结论仍需进一步大规模研究验证.

<正>急性肺损伤(acute lung injury,ALI)是重症监护病房(intensive care unit,ICU)中的常见病和多发病,各种因素如肺部感染、脓毒血症、重症急性胰腺炎、创伤、输血[1]等均可导致急性肺损伤/急性呼吸窘迫综合征(ALI/acute respiratory distress syndrome,ARDS)的发生。随着社会进步、医疗条件不断改善以及医疗方法的不断发展,急性肺损伤的病死率较以前明

OBJECTIVE To synthesize emodin derivatives and evaluate its anti-tumor activities in vitro.METHODS A new emodin trimethoxy derivatives were synthesized from emodin with (Me)2SO4. The physicochemical property of the new derivatives was identified with routine methods. And its structure was characterized by HPLC and ESI-MS spectra. The effect of the new derivatives on K562 cell proliferation was detected by MTT, as well as the cell cycle by flow cytometry.RESULTS Emodin derivatives were slight yellow powder with mp:226-227 ℃, And its structure was confirmed by ESI-MS spectra and HPLC. The new derivatives could inhibit K562 cell proliferation in dose-dependent manner and arrest cell cycle in G0/G1.CONCLUSION The new derivatives were synthesized from emodin successfully. The emodin derivatives had anti-tumor activities of K562 cell proliferation inhibition and cell cycle arresting from G0/G1 to S phase.