目的 研究TLR2(Toll-like receptor 2,TLR2)基因对非小细胞肺癌(non-small cell lung cancer,NSCLC)细胞增殖能力的影响及其对ERK信号通路的调节作用.方法 将人非小细胞肺癌细胞株A549细胞分为空白组、空载体组、TLR2基因过表达组,MTT法检测细胞增殖能力,Western blot法检测ERK1/2和p-ERK1/2蛋白表达水平.结果 在A549细胞中,过表达TLR2基因可促进非小细胞肺癌细胞增殖并上调ERK1/2磷酸化水平;U0126能抑制过表达TLR2基因对非小细胞肺癌细胞增殖的促进作用.结论 TLR2基因可通过调控ERK信号通路促进体外非小细胞肺癌细胞增殖.

Invariant natural killer T cells (iNKTs) are important innate immune cells which get involved in various immune responses in both mice and humans. These immune reactions range from self-tolerance to development of autoimmunity and responses to pathogens and tumor development. In this study, we aimed to explore the effects of the novel immunostimulators (CH1b and CH2b) containing thiazolidin-4-one on the functions of human invariant natural killer T cells (iNKTs). First of all, iNKTs in peripheral blood mononuclear cells were expanded with α-Galactosylceramide (α-Galcer) in vitro. Then, the highly purified iNKTs were isolated from PBMCs using magnetic cells sorting (MACS). Next, we investigated the impacts of CH1b and CH2b on proliferation, cytokines production, cytotoxicity, and the associated signaling pathways in iNKT cells. Finally, we found that CH2b could significantly promote the activated iNKTs proliferation, increase the production of Th2 cytokines, and induce Th0 differentiation into Th2 subset via GATA 3 signaling pathway. Besides, CH2b could markedly enhance the cytotoxic ability of the activated iNKTs. Therefore, we concluded that CH2b, a promising candidate immunostimulator, might be used for the treatment of infections, tumors, autoimmune and allergic diseases, and for the correction of Th1/Th2 balance disorders in future.

Objective To observe expressions of γ-tubulin, HER-2 and k-ras in breast cancer tissues, and to study its clinical significance. Methods Samples of 60 cases of ductal carcinoma in situ ( DCIS) tissues by surgical ab-lation were collected. The expression of K-ras, HER-2 andγ-tubulinin was observed in 60 cases of infiltrating duct carci-noma ( IDC) tissues and 60 cases of normal breast tissues during January 2010 and December 2014 were recruited in this study. Expressions ofγ-tubulin, HER-2 and k-ras were observed. Results Light microscope observation showed thatγ-tubulin was positively expressed in epithelial cytoplasm, HER-2 and K-ras were positively expressed in cell membrane. Positive expression rates of γ-tubulin, HER-2 and K-ras in breast cancer tissues were significantly higher than those in normal breast tissues, and positive expression rates of HER-2 and K-ras in IDC tissues were higher than those in DCIS tis-sues (P<0. 05). Conclusion High expressions ofγ-tubulin, HER-2 and K-ras in breast tissued indicates that it is in-volved in pathogenesy and development of breast cancer.

Aim of study: To evaluate the effect of fibroblast growth factor receptor.2. (FGFR2) on genetic susceptibility for breast cancer. (BC) in Chinese populations. Materials and Methods: A computerized literature search was carried out in PubMed, Chinese Biomedical Database. (CBM), and Chinese National Knowledge Infrastructure. (CNKI) to collect relevant articles. Pooled odds ratio. (OR) and 95% confidence interval. (CI) were used to assess the strength of the associations. Results: A total of 21 articles involving a total of 15 polymorphisms of the FGFR2 gene were included in the meta-analysis. Due to the limited studies for rs17102287, rs2981578, rs3135718, rs3803662, rs3750817, rsl0510097, rsl7542768, rs13387042, and rs1982073; we only pooled the six polymorphisms. (rs11200014, rs1219648, rs2420946, rs2912778, rs2981579, and rs2981582) into this meta.analysis. Overall, significantly increased BC risk was associated with five polymorphisms. (rs2981579, rs2981582, rs1219648, rs2420946, and rs2912778) when all studies were pooled into the meta.analysis. When stratified by ethnicity and source of controls, similar results were also detected. However, for rs2981579 no significant association was found among Chinese Han in all genetic models. Conclusion: Our meta-analysis suggests that FGFR2 is likely an important genetic marker contributing to susceptibility of BC. We recommend that these single nucleotide polymorphisms to be included in future association studies and functional assays.

Cajal间质细胞(interstitial cells of Cajal,ICC)是一类主要分布于胃肠道的间质细胞,与平滑肌细胞以及肠神经细胞有着紧密的关系.ICC分布于整个胃肠道,是胃肠道起搏细胞,具有产生和传播慢波的功能,参与神经递质调节,在一些胃肠动力性疾病中表现为异常状态.近期,关于ICC的生理功能、损伤和恢复机制的研究取得了显著的进展.ICC网络存在动态平衡,为了维持ICC网络功能,ICC周期代谢需要被紧密的控制调节平衡ICC死亡和更替.研究表明,ICC具有高度的可塑性,在一些缺失ICC的疾病中ICC并不一定死亡,转分化、去分化和细胞凋亡可能是ICC丢失的机制..本文主要对Cajal间质细胞及其可塑性的研究进展进行了综述.

Purpose: The purpose of this study is to examine the expression and clinical significance microRNA-383 (miR-383) in non-small cell lung cancer (NSCLC) both in vitro and in vivo.Methods: Tumorous miR-383 expressions were compared between NSCLC cell lines and normal lung cells. MiR-383 was upregulated in A549 and H596 cells to evaluate its tumor suppressive effect on NSCLC proliferation, invasion and migration in vitro. MiR-383 expression was also compared between 139paired clinical NSCLC tissues and their adjacent non-carcinoma lung tissues, as well as between earlystage NSCLC tissues and advanced-stage NSCLC tissues. Correlation between tumorous miR-383 expression and NSCLC patients' clinicopathological features and overall survival (OS) were also statistically analyzed.Results: MiR-383 was significantly downregulated in NSCLC cell lines. MiR-383 overexpression reduced proliferation, invasion and migration of A549 and H596 cells. In clinical samples, miR-383 was also found to be markedly downregulated in NSCLC carcinomas than in non-carcinoma lung tissues, and in advanced-stage carcinomas than in early-stage carcinomas. It was also found low tumorous miR-383 expression was significantly associated with NSCLC patients' poor prognosis, including advanced TNM stages, positive lymph node metastasis, and shorter OS.Conclusion: Endogenous miR-383 is a functional tumor suppressor in NSCLC. It may also serve as an independent prognostic factor for patients with NSCLC. (C) 2016 Elsevier Masson SAS. All rights reserved.

Background and AimHepatic cirrhosis is the final stage of liver dysfunction, characterized by diffuse fibrosis, which is the main response to the liver injury. This study is to investigate the effects of ursolic acid (UA) on liver functions and fibrosis in bile duct ligation (BDL) mice and to determine the underlying mechanisms.MethodsCultured hepatocytes were treated with lipopolysaccharide (LPS) in the presence or absence of UA. The reactive oxygen species (ROS) level, protein levels of IB, iNOS and Cox-2, and NF-B activation were detected, respectively. C57/BL6 and AMP-activated protein kinase (AMPK)2(-/-) mice were subjected to BDL for 14 days. UA was administered by gavage. The markers of liver function and oxidative stress, and liver histopathology were analyzed after treatment.ResultsTreatment of hepatocytes with UA dose-dependently activates AMPK, which is abolished by silence of liver kinase B1 (LKB1). LPS significantly increased ROS productions, apoptosis, NF-B activation, and expressions of iNOS and Cox-2 in cultured hepatocytes. All these effects were blocked by co-incubation with UA. Importantly, silence of LKB1, AMPK, or iNOS/Cox-2 by small interference RNA transfection reversed UA-induced effects in cultured cells. In an animal study, 14-day BDL induced liver fibrosis and liver injury, accompanied with increased oxidative stress and protein expressions of iNOS and Cox-2 in liver. Treatment of UA significantly attenuated the BDL-induced detrimental effects in wild-type mice but not in AMPK2(-/-) mice.ConclusionUA via LKB1-AMPK signaling offers protective effects on BDL-induced liver injury in mice, which may be related to inhibition of oxidative stress.

目的 观察促胰液素(secretin)对小脑中间神经元—浦肯野细胞抑制性突触的影响.方法 采用小脑脑片膜片钳技术,脑片灌流液中给予secretin,观察其对浦肯野细胞上抑制性突触后电流的影响.结果 Secretin应用后,浦肯野细胞诱发性抑制性突触后电流增强;自发性抑制性突触后电流也增强.结论 Secretin可能参与调节浦肯野细胞的功能及其信号传递,从而参与小脑功能的调节.

The TES gene was frequently lost in breast cancer, which could inhibit tumor invasion and the formation of distant metastasis. However, the underlying mechanisms remain unknown yet. In the present study, we aimed to investigate how TES was silenced and its roles in EMT—the key step for tumor metastasis. Real-time polymerase chain reaction (PCR) and Western blot were used to detect the mRNA and protein expression of target genes; the status of TES promoter was determined by methylation-specific PCR and subsequently, DNA sequencing. Overexpression or downregulation of TES was achieved by pcDNA3.1-TES or shRNA-TES transfection. Cellular adhesion and migration were investigated by the adhesion and Transwell assays. Morphological changes of breast cancer cells were observed under the optical microscope. The Rho A activity was measured using a commercial kit, and its roles in TES-manipulated EMT were determined by real-time PCR and Western blot. The 42.3 % (33/78) breast cancer tissues presented hypermethylation of the TES gene, whereas only 2 (2.6 %) non-malignant cases were hypermethylated (P < 0.001). Moreover, TES hypermethylation was significantly correlated with larger tumor diameter (P = 0.03) and lympho node metastasis (P = 0.024). In primary cultured breast cancer cells, the demethylation treatment using 5-aza-dC notably restored the expression of TES. In vitro, overexpression of TES enhanced cellular adhesion inhibited migration and suppressed EMT, while downregulation of TES impaired cellular adhesion, promoted migration, and enhanced EMT. TES overexpression also activated the Rho A signal, which is a critical factor for the effects of TES on the EMT procedure. We firstly proved that frequent loss of TES in breast cancer was caused by promoter hypermethylation, which was correlated with poor prognosis. In vitro, TES enhanced cellular adhesion, suppressed tumor migration, and inhibited EMT. Moreover, the Rho A pathway was critical for the effects of TES on EMT, which can be blocked by the Rho A inhibitor. Therefore, we propose restoration of TES as a potent strategy for breast cancer therapy.

Although many epidemiologic studies investigated the methylenetetrahydrofolate reductase (MTHFR) polymorphisms and their associations with esophageal cancer, definite conclusions could not be drawn. To clarify the effects of MTHFR polymorphisms on the risk of esophageal cancer, a meta-analysis was here performed in Chinese populations. A total of 16 studies including 3,040 cases and 4,127 controls were involved in this meta-analysis. Overall, significant associations were found between the MTHFR C677T polymorphism and esophageal cancer risk when all studies in Chinese populations were pooled into the meta-analysis (T vs. C, OR = 1.19, 95% CI = 1.06-1.34; TT vs. CC, OR = 1.35, 95% CI = 1.07-1.70; TT + CT vs. CC, OR = 1.29, 95% CI = 1.08-1.54; TT vs. CC + CT, OR = 1.19, 95% CI = 1.03-1.37). In subgroup analyses stratified by ethnicity and source of controls, the same results were found in Kazakh (TT vs. CC, OR = 1.38, 95% CI = 1.02-1.87; TT + CT vs. CC, OR = 1.50, 95% CI = 1.03-2.18), in not stated populations (T vs. C, OR = 1.24, 95% CI = 1.08-1.42; TT vs. CC, OR = 1.47, 95% CI = 1.10-1.96; TT + CT vs. CC, OR = 1.30, 95% CI = 1.05-1.60; TT vs. CC + CT, OR = 1.32, 95% CI = 1.12-1.56), and in hospital-based studies (T vs. C, OR = 1.34, 95% CI = 1.19-1.51; TT vs. CC, OR = 1.81, 95% CI = 1.37-2.39; TT + CT vs. CC, OR = 1.51, 95% CI = 1.26-1.83; and TT vs. CC + CT, OR = 1.39, 95% CI = 1.13-1.70). In conclusion, this meta-analysis provides evidence that the MTHFR C677T polymorphism contributes to esophageal cancer development in Chinese populations.

Objective To investigate the treating mechanism of Fuzhenghuoxueqingrefang on acute radiation enteritis(ARE)in rats.Methods Thirty two Wistar male rats were randomly divided into 4 groups(8 rats each group),which were composed of blank control,model,dexamethasone,and Fuzhenghuoxueqingrefang groups.The physiological saline,dexamethasone and Fuzhenghuoxueqingrefang were administrated separately at the first day after abdominal irradiation by daily rectal clysma for 5 days.All the rats were anesthetized and the serum activity of peroxidase(CAT) and contents of malonic aldehyde(MDA) were detected at the seventh day after abdominal irradiation separately.Results The activity of serum CAT in the blank control,dexamethasone and Fuzhenghuoxueqingrefang groups were obviously higher than that of the model group(F=23.79,P<0.01).The content of serum MDA in the blank control,dexamethasone and Fuzhenghuoxueqingrefang groups were significantly lower than that of the model groups(F=36.41,P<0.01).Conclusion Fuzhenghuoxueqingrefang could treat ARE in rats by down-regulating the lipid peroxidation in the damaged tissue.

Objective To evaluate the possible role of qingre zhixiefang in treating acute radiation enteritis(ARE)in rats.Methods Forty eight Wistar male rats were randomly divided into 6 groups(8 rats in each group),including the blank control,model control(normal saline),positive control(dexamethasone 1.425 mg·kg-1),qingre zhixiefang at high(16.0 g·kg-1),medium(12.0 g·kg-1) and low dose(8.0 g·kg-1) groups.One day after abdominal irradiation,the rats were administrated rectally with placebo or drugs every other day for one week.The morphologic changes(HE stain) and the serum activity of malonaldehyde(MDA) and superoxide dismutase(SOD) were evaluated on the third day after abdominal irradiation.The tissue within the radiation area was taken out for histological test.Results It was shown that the positive control and qingre zhixiefang at high and middle doses were effective on ARE from the histopathologic evaluation(HE stain).The activity of serum MDA in the positive control and the middle dose groups was significantly lower than that in the model control and the low dose group(P<0.01),but higher than the blank control group(P>0.05).The activity of serum SOD was significantly higher than the model group and the low dose group(P<0.01),but lower than the blank control group(P>0.05).Conclusion Reduction of MDA level and sustaining serum SOD activity may provide explanations to the therapeutic effect of qingre zhixiefang on ARE.

目的 通过观察血府逐瘀汤对动脉粥样硬化大鼠( atherosclerosis,AS)血脂及血浆内前列环素及血栓素A2的影响,探讨血府逐瘀汤抗动脉粥样硬化的机制.方法 将40只SD大鼠随机分为对照组、模型组、治疗组(血脂康组、血府逐瘀汤高剂量组、血府逐瘀汤低剂量组).对照组给予正常饮食；模型组给予高脂饮食；治疗组在高脂饮食基础上分别给予血府逐瘀汤高、低剂量或血脂康.12周后光镜观察主动脉粥样斑块形成情况并检测血脂及测定血栓素B2(TXB2)和6-酮-前列腺素(6- Keto -PGF1α)的含量.结果 与模型组相比血府逐瘀汤高、低剂量组、血脂康组均能降低血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL -c)和TXB2,升高高密度脂蛋白(HDL -c)和6- Keto - PGF1α(P＜0.05).结论 血府逐瘀汤能调节AS大鼠血脂紊乱和维持前列环素(PGI2)和血栓素(TXA2)的平衡,这可能是其有效防治AS的机制之一.

Due to the important position and the role of pathology in the educational system of the medical sciences and the process of training medical students' inherent driving forces of learning,the paper proposes the remarkable teaching application value of the excellent teaching PPT of pathology(ETPP) in routine teaching and the principles and the useful skills of making ETPP which includes the emphasis of the keypoints,and the requirements of selecting figures and tables,and the plans of the color matching between the words and the backgrouds,and the moderate design of the multimedia effects in the pages.

目的 观察乳腺癌组织中表皮生长因子受体三型突变体( EGFRvⅢ)、中心体相关微管蛋白α(Tubulinα)的表达变化,并探讨其意义.方法 采用免疫组化SP法检测30例正常乳腺组织(NB组)、50例导管原位癌(DCIS组)和50例乳腺浸润性导管癌(IDC组)组织中的EGFRvⅢ、Tubulin-α.结果 IDC组EGFRvⅢ、Tubulin-α阳性表达率分别为70％( 35/50)、74％ (37/50),DCIS分别为38％ (19/50)、64％ (32/50),NB组分别为0、3％(1/30)；各组间EGFRvⅢ阳性表达率两两比较,P均＜0.05；IDC组、DCIS组Tubulin-α阳性表达率高于NB组(P均＜0.05),但IDC组与DCIS组比较,P＞0.05.乳腺癌组织中,EGFRvⅢ、Tubulin-α的表达呈正相关(r=0.909,P＜0.01).结论 乳腺癌组织中EGFRvⅢ、Tubulin-α高表达,二者在乳腺癌的发生发展过程中发挥作用.

高尿酸血症是目前公认的痛风发作的重要危险因素,控制高尿酸血症能够有效避免痛风发作[1-2].在临床工作中,高尿酸血症和痛风患者可能常需要服用中药.本实验选取了8种常用的动物性中药,以紫外分光光度计法测定其腺嘌呤含量,为指导临床用药提供依据.

Objective To discuss the relationship between the expression of Her2/Neu and EGFRvⅢ and the pathogenesis of the occurring and the invasion in the breast carcinoma.Methods The expressions of Her2/Neu and EGFRvⅢ were studied by S-P immunohistochemical staining in the paraffin embedded specimens,30 cases of the normal breast(NB),50 cases of ductal carcinoma in situ(DCIS)and 50 cases of invasive ductal carcinoma,no otherwise specified(IDCNOS).Results The significant increasing trend of the positive expression was observed in both Her2/Neu and EGFRvⅢ among the group of NB,DCIS,and IDCNOS(p<0.01).The higher expression of EGFRvⅢ was observed in IDCNOS than DCIS(p<0.01).The postive correlation was found between the expression of Her2/Neu and EGFRvIII in the groups of NB,DCIS and IDCNOS(r = 0.597,P< 0.001).Conclusion It seems that both Her2/Neu and EGFRvⅢ are related to the occurring of the breast carcinoma,and EGFRvⅢ might play an important role in the pathogenesis of the invasion.

目的 观察乳腺癌组织中表皮生长因子受体(EGFR)、细胞信号转导通路相关基因ras(K-ras)蛋白、中心体相关微管蛋白γ(Tubulin-γ)的表达变化,并探讨其意义.方法 采用免疫组化SP法检测30例正常乳腺(NB)组织、50例导管原位癌(DCIS)组织和50例乳腺浸润性导管癌(IDCNOS)组织中的EGFR、K-ras、Tubulin-γ.结果NB、DCIS、IDCNOS组织中EGFR的阳性表达率分别为3％、60％、74％,K-ras的阳性表达率分别为0、62％、74％,Tubulin-γ的阳性表达率分别为13％、84％、88％,三种组织中各指标的阳性表达率相比,P均＜0.01；三个指标的阳性表达呈正相关(r分别为0.929、0.843、0.828,P均＜0.01).结论 乳腺癌组织中EGFR、K-ras、Tubulin-γ的阳性表达率明显升高,三者同时高表达可能与乳腺癌的发生有关.

To study the effect of Xuefu Zhuyu decoction on attenuation of the atherosclerosis in the rats with atherosclerosis.Forty Sprague Dawley rats were divided randomly into groups of 8 rats each,control group,model group,and three treatment groups(Xue Zhi Kang group,high dose Xuefu Zhuyu decoction group,and low dose Xuefu Zhuyu decoction group).The control group was fed with normal diet,model group a high-fat diet,treatment groups the high fat diet mixed with Xue Zhi Kang,High dose and low dose Xuefu Zhuyu decoction respectively.After 12 weeks,treatment,the morphological characteristics(HE stain and ultrastructure) of the aorta were observsed,the blood were taken from the abdominal aorta,and the blood levels of cholesterol(TC),triglycerides(TG),low-density lipoprotein(LDL-c),and high-density lipoprotein(HDL-c) were detected later.It was found that the aortic morphological changes of both the high and dose Xuefu Zhuyu decoction group are lighter than that of model group.The Xuefu Zhuyu decoction groups could significantly decrease the blood level of TC,TG,and LDL-c,increasing that of HDL-c(P<0.01).So Xuefu Zhuyu decoction can attenuate the atherosclerosis effectively,whose pathogenesis might be related with its adjusting role on the blood level of lipid.

目的研究老年心源性猝死(SCD)的特点,探讨预防SCD的对策。方法对1例老年SCD者的尸检资料进行回顾性分析并复习相关文献。结果饮酒、情绪激动及劳累为SCD的主要诱因,胸闷为本例死者猝死前临床先兆症状,尸检示冠状动脉粥样硬化并急性心肌缺血。结论避免诱因是预防猝死的关键,应高度重视猝死的先兆症状,尽快、有效地进行抢救,以降低猝死的发生率;尸检有助于明确死亡原因。