OBJECTIVE To explore the improvement effect and mechanism of acacetin on juvenile asthma rats based on the silence information regulator 1 （SIRT1）/AMP-activated protein kinase （AMPK） signaling pathway. METHODS Juvenile SD rats were randomly divided into control group， asthma group， acacetin group （13.33 mg/kg， gavage）， SIRT inhibitor EX-527 group （1 mg/kg， intraperitoneal injection） and acacetin+EX-527 group （13.33 mg/kg acacetin， gavage+1 mg/kg EX-527， intraperitoneal injection）， with 12 rats in each group （half male and half female）. Except for the control group， the other groups were sensitized by intraperitoneal injection of ovalbumin and nebulized inhalation of ovalbumin to induce the asthma model. After modeling， rats in each drug group were orally administered or （and） intraperitoneally injected with the corresponding medication once a day for 2 weeks. After the last administration， the total number of cells， the proportion of eosinophils， and the levels of interleukin-5 （IL-5）， IL-4 and tumor necrosis factor-α （TNF-α） in the bronchoalveolar lavage fluid （BALF） were measured. The pathological changes and abnormal proliferation of goblet cells in lung tissue were observed， the levels of malondialdehyde （MDA） and superoxide dismutase （SOD） in lung tissue and the protein expressions of SIRT1, AMPK and peroxisome proliferator activated receptor-gamma co-activator factor-1α（PGC-1α） were detected. RESULTS Compared with control group， there was a large number of inflammatory cell infiltration and obvious goblet cell dysplasia in the lung tissue of rats in asthma group； the total number of cells in BALF， the proportion of eosinophils， the levels of IL-5， IL-4 and TNF-α in BALF， PAS score and MDA level in the lung tissue were significantly increased （P＜0.05）； the SOD level， protein expressions of SIRT1 and PGC-1α and protein phosphorylation level of AMPK in lung tissue were significantly decreased in asthma group （P＜0.05）. Compared with the asthma group， the pathological changes of lung tissue and goblet cell dysplasia of rats were reduced， and all quantitative indexes were significantly improved in acacetin group （P＜0.05）， while the pathological changes of lung tissue and goblet cell dysplasia of rats were increased， and all quantitative indexes were significantly worsened in EX-527 group （P＜ 0.05）. The combination of EX-527 could significantly reverse the effects of acacetin on oxidative stress and airway inflammation in juvenile asthma rats. CONCLUSIONS Acacetin can inhibit oxidative stress and airway inflammation in juvenile asthma rats，which may be related to the activation of the SIRT1/AMPK jinanlvshishen@163.com signaling pathway.

OBJECTIVE To investigate the effects of polydatin （PD） on cell proliferation， migration， invasion and tumor growth of acute myeloid leukemia （AML）. METHODS Human AML cell KG-1 were divided into normal group， PD low-， medium- and high-concentration groups （10， 30， 60 μmol/L PD）， SQ22536 group [cyclic adenosine monophosphate （cAMP） inhibitor， 100 μmol/L]， high concentration of PD+SQ22536 group （60 μmol/L PD+100 μmol/L SQ22536）. The effects of PD on cell activity， apoptotic rate， invasion and migration ability， cAMP level， the expression of epithelial-mesenchymal transition （EMT） related proteins and protein kinase A （PKA） were investigated. Using BALB/c nude mice as subjects， a transplanted tumor model of AML nude mice was induced by subcutaneous inoculation of KG-1 cell suspension and then divided into control group， PD group， SQ22536 group and PD+SQ22536 group （with 6 mice in each group）. The effects of PD on tumor volume and mass were measured. RESULTS Compared with the normal group or control group， the cell viabilities， the number of migrating cells， the number of invasive cells， the relative expressions of vimentin and Snail as well as the tumor volume and mass were decreased significantly in PD groups， while the apoptotic rates， cAMP levels， the relative expressions of E-cadherin and PKA were significantly increased， with a dose-dependent manner （P＜0.05）. SQ22536 had opposite effects on cells and nude mice compared to PD， and could significantly reverse the anti-tumor activity of PD （P＜0.05）. CONCLUSIONS PD may inhibit the proliferation， migration， invasion and EMT process of KG-1 cells， induce apoptosis， and inhibit tumor growth， by activating the cAMP/PKA signaling pathway， thereby exerting anti-AML effects.

Objective: To detect the expression and the differential significance of CK5/6, DSG3, P40, TTF-1, CK7, NapsinA in small biopsy specimens of non-small cell lung cancer (NSCLC), squamous cell carcinoma (SCC) and adenocarcinoma (AC). Methods: Immunohistochemical SP method was used to detect the expressions of CK5/6, DSG3, P40, TTF-1, CK7 and NapsinA in 120 small biopsy specimens of NSCLC hospitalized in the Central People's Hospital of Tengzhou from January 2016 to December 2017, and the results were analyzed combined with the clinical characteristics of NSCLC. Results: The positive expression rates of CK5/6, DSG3 and P40 in lung SCC were 100.0%(56/56), 89.3%(50/56) and 96.4%(54/56), respectively, with specificity of 90.6%, 100.0% and 100.0%, respectively.The positive expression rates of NapsinA, TTF-1 and CK7 in lung AC were 81.3%(52/64), 90.6%(58/64) and 93.8%(60/64), respectively, with specificity of 100.0%, 92.9% and 96.4%, respectively.The positive expression rates of CK5/6, DSG3, P40 in SCC had statistically significant differences compared with those in AC (all P<0.05), and the expression of TTF-1, CK7 and NapsinA in AC had statistically significant differences compared with those in SCC (all P<0.05). Conclusion CK5/6, DSG3, P40, TTF-1, CK7 and NapsinA are of great significance in the differential diagnosis of SCC and AC in small biopsy specimens of NSCLC.

[摘 要] 目的：探讨中药地黄提取物梓醇（Cat）对乳腺癌MCF-7细胞增殖与凋亡，以及裸鼠移植瘤生长的影响及其机制。方法：以不同质量浓度（0、5、25、50、100、200 μg/mL）Cat处理人乳腺癌MCF-7细胞，用MTT法筛选Cat给药浓度。将MCF-7细胞分为空白对照组、Cat低剂量组、Cat中剂量组、Cat高剂量组、Cat+sh-NC组和Cat+sh-FOXO3组，采用Edu细胞增殖实验、平板克隆实验、流式细胞术分别检测各组细胞的增殖与克隆形成能力、凋亡率和细胞周期，WB法检测各组细胞中FOXO3、FOXM1、caspase-3和caspase-8蛋白表达。构建乳腺癌MCF-7细胞裸鼠移植瘤模型，观察Cat对移植瘤生长的影响，WB法检测移植瘤组织中FOXO3和FOXM1蛋白表达。结果：Cat低（50 μg/mL）、中（100 μg/mL）、高（200 μg/mL）剂量处理的MCF-7细胞的增殖能力均显著下降（均P<0.05）。与空白对照组比较，Cat低、中、高剂量组Edu阳性细胞率、克隆形成数、S期与G2/M期细胞比例及FOXO3蛋白表达均显著降低（均P<0.05），细胞凋亡率、G0/G1期细胞比例及FOXM1、caspase-3、caspase-8蛋白表达均显著升高（均P<0.05）；与Cat+sh-NC组比较，Cat+sh-FOXO3组Edu阳性细胞率、克隆形成数、S期与G2/M期细胞比例及FOXO3蛋白表达均显著升高（均P<0.05），细胞凋亡率、G0/G1期细胞比例及FOXM1、caspase-3和caspase-8蛋白表达均显著下降（均P<0.05）。Cat组MCF-7细胞裸鼠移植瘤体积、质量和FOXO3蛋白表达均显著降低（均P<0.05），FOXM1的蛋白表达显著升高（P<0.05）。结论：Cat抑制乳腺癌MCF-7细胞增殖并促进凋亡，在体内抑制裸鼠移植瘤的生长，其机制可能与上调FOXO3、下调FOXM1的表达有关。

OBJECTIVE: To investigate the effect of miR-22 targeting formin-like protein 2 (FMNL2) on the migration and apoptosis of childhood acute myeloid leukemia (AML) cells. METHOD: Peripheral blood samples from 11 children with AML, 10 children with immune thrombocytopenia, human AML cell lines TF-1a, HL-60, THP-1 and human bone marrow stromal cells HS-5 were used as the research objects. UniCel DxH 800 automatic hematology analyzer detected platelet count, hemoglobin, and white blood cell count in peripheral blood samples, and RT-qPCR detected miR-22 expression in peripheral blood samples and AML cells. HL-60 cells were transfected with Lipofectamine^TM 2000 kit, the experiments were divided into seven groups: blank (no cells transfected), miR-NC, miR-22 mimics, si-NC, si-FMNL2 , miR-22 mimics+OE-NC and miR-22 mimics+OE-FMNL2 . RT-qPCR was used to detect the expression of miR-22 in each group. Transwell was used to detect cell migration. Flow cytometry was used to detect cell apoptosis. Dual-luciferase reporter gene detection experiments verified the targeting relationship between miR-22 and FMNL2 . Western blot was used to detect the expression of FMNL2 protein. RESULTS: Compared with the control group, the number of leukocytes in the peripheral blood of children with AML was significantly increased (P <0.001), while the concentration of hemoglobin and the number of platelets were significantly decreased P <0.001). The expression level of miR-22 in peripheral blood of children with AML was significantly lower than that in control group (P <0.001). Compared with HS-5 cells, the expression levels of miR-22 in TF-1a, HL-60, and THP-1 cells were significantly decreased (P <0.05), and in HL-60 cells was the lowest. Therefore, HL-60 cells were selected for subsequent experiments. Up-regulation of miR-22 or silencing of FMNL2 could reduce the number of migrating cells and increase apoptosis rate (P <0.05). MiR-22 targeted and negatively regulated the expression of FMNL2 . FMNL2 overexpression reversed the effects of up-regulated miR-22 on migration and apoptosis of HL-60 cells. CONCLUSION MiR-22 can inhibit the migration and promote apoptosis of HL-60 cells by down regulating the expression of FMNL2 .
Humans ; Child ; MicroRNAs/metabolism* ; Leukemia, Myeloid, Acute/metabolism* ; Cell Proliferation ; Apoptosis ; Myeloproliferative Disorders ; Cell Movement ; Hemoglobins ; Cell Line, Tumor ; Formins

[摘 要] 目的：探讨布托啡诺（BPH）对骨肉瘤（OS）细胞增殖、迁移和侵袭的影响及其相关的作用机制。方法：将MG-63细胞分为对照组、YAP抑制剂组（维替泊芬组）和BPH低、中、高浓度组，MTT法、克隆形成实验、FCM术、划痕愈合实验、Transwell实验、qPCR法、WB法和移植瘤实验分别检测处理后各组细胞的增殖活性、克隆形成数、细胞凋亡率、划痕愈合率，以及上皮钙黏蛋白（E-cadherin）、神经钙黏蛋白（N-cadherin）、波形蛋白（vimentin）mRNA的表达和YAP、TAZ蛋白的表达，同时观察BPH和维替泊芬对移植瘤生长的影响。结果：与对照组相比，维替泊芬组和BPH低、中、高浓度组细胞增殖活性、克隆数、划痕愈合率、侵袭细胞数，以及N-cadherin和vimentin mRNA水平、YAP和TAZ蛋白表达及移植瘤体积均显著降低（均P<0.05），细胞凋亡率、E-cadherin mRNA水平及对移植瘤的抑瘤率均升高（均P<0.05），且BPH高浓度组与维替泊芬组之间各项指标均无明显差异（均P>0.05）。结论：BPH可能通过抑制Hippo/YAP信号通路来抑制OS细胞MG-63增殖、迁移和侵袭。

Objective: To investigate the risk factors of postoperative complications after laparoscopic transabdominal preperitoneal hernia repair. Methods: The clinical data of 481 cases of laparoscopic preperitoneal hernia repair in the Central People's Hospital of Tengzhou from March 2014 to February 2018 were retrospectively analyzed.The patients were divided into complications group and control group according to whether complications occurred.The clinical data of the two groups were compared and the risk factors of complications were summarized. Results: Postoperative complications occurred in 78 cases of 481 patients(16.22%). The proportions of age, operation time, diameter of hernia sac, intraoperative bleeding volume, incarcerated hernia and recurrent hernia in the complications group were 65.3%, 32.0%, 29.5%, 85.9%, 20.5% and 5.1%, respectively, which in the control group were 46.6%, 2.4%, 53.8%, 30.7%, 3.4% and 1.4%, respectively, the differences were statistically significant(χ²=9.175, 17.354, 84.692, 82.959, 32.444, 4.252, all P<0.05). The results showed that age>60 years, operation time>100 minutes, intraoperative bleeding>15 mL, hernia sac diameter>4 cm, incarcerated hernia were the risk factors of postoperative complications after laparoscopic transabdominal preperitoneal hernia repair. Conclusion Age>60 years old, operation time>100 minutes, intraoperative bleeding>15 mL, hernia sac diameter>4 cm, incarcerated hernia are the independent risk factors of postoperative complications after laparoscopic transperitoneal hernia repair.The patients combined with characteristics above should be given early intervention.

This paper reports a female patient with Gongylonema pulchrum parasitizing in the esophagus, with aims to call for the attention to the role of parasite detection in the diagnosis of human diseases.

[摘 要] 目的： 基于Hedgehog信号通路探讨石斛提取物毛兰素（erianin，ER）抑制结直肠癌HT29细胞上皮间质转化（EMT）和血管生成的作用机制。方法: 将HT29细胞分为空白对照组、ER-L（25 μg/mL）组、ER-M（50 μg/mL）组、ER-H（75 μg/mL）组、ER-H（75 μg/mL）+PM（Hedgehog通路激活剂，1.5 μmol/L）组。MTT法检测细胞增殖活力，克隆形成实验检测细胞克隆形成能力，划痕实验和Transwell实验检测细胞迁移与侵袭能力，血管拟态形成实验检测血管生成能力，WB法检测与EMT进程、Hedgehog信号通路和拟态血管生成相关蛋白质的表达。结果: HT29细胞增殖活性随着ER质量浓度的升高而逐渐降低（P<0.05）；与空白对照组比较，ER各组细胞克隆形成率、迁移与侵袭能力、血管形成能力、间质标志蛋白（N-cadherin、vimentin）、血管生成相关蛋白（VEGF、VE-cadherin）及Hedgehog通路相关蛋白（SHH、GLI1、SMO、c-Myc）表达均显著下降（均P<0.05），上皮标志蛋白（E-cadherin）、Hedgehog通路中融合蛋白抑制剂（SUFU）蛋白表达均显著上升（均P<0.05）；PM处理在一定程度上逆转了ER对于HT29细胞增殖、EMT和血管生成的抑制作用（均P<0.05）。结论: ER可以抑制结直肠癌HT29细胞的增殖、迁移与侵袭、EMT和血管生成，其机制可能与抑制Hedgehog信号通路激活有关。

Objective To study the expression of Stathmin gene in ovarian cancer tissue and its valuation value on effect of Paclitaxel combined with cisplatin chemotherapy.Methods 92 cases of ovarian cancerpatients underwent surgical and postoperative chemotherapy treatment in our hospital during July 2012 to February 2016 were selected with research subject.The expression of Stathmin gene in ovarian cancer tissues and adjacent tissues was measured by fluorescence quantitative PCR.All ovarian cancer patients were divided into high Stathmin group and low Stathmin group with 46 cases according to the expression of Stathmin gene in ovarian cancer tissues.Comparison the chemotherapy effectin ovarian cancerpatients with different Stathmin gene expression.Results The expression of Stathmin mRNA in ovarian cancer tissues was significantly higher than that in adjacent tissues(P<0.05).After chemotherapy, serum tumor markers such as HE4, CA199, CA153, β-HCG in high Stathmin group were higher than those in low Stathmin group, angiogenesis indexes such as CXCR4, SDF-1, VEGF, Ang2 were lower than those in low Stathmin group, apoptotic indexes such as Fas/Apo-1 and Bcl-2 were higher than those in low Stathmin group(P<0.05).Conclusion Stathmin gene is highly expressed in ovarian cancer tissues, and the expression of Stathmin is negatively correlated with chemotherapy.