ENO1, a potential prognostic head and neck cancer marker,promotes transformation partly via chemokine CCL20 induction

The success of using glycolytic inhibitors for cancer treatment depends on studying the individual role of frequently deregulated glycolytic genes in cancer. This report aims to study the prognostic implication, and determine the cellular role and action mechanism of glycolytic ENO1 overexpression in head and neck cancer. The relationship of ENO1 mRNA expression in 44-pair clinical specimens with patient clinicopathologic characteristics was analysed by semi-quantitative RT-PCR, Kaplan–Meier survival curve and Cox model analyses. Following ectopic ENO1 expression or knockdown, we studied the proliferative, migratory, invasive, colony-forming and tumourigenic abilities of ENO1-genetically altered cells. DNA microarray analysis was used to identify downstream targets responsible for the ENO1 action in the cells. The expression of ENO1 mRNA was increased in 68% of tumour (T) specimens when compared to their normal (N) counterparts, and positively associated with clinical progression (p < 0.05). High ENO1 expression (T/N ? 2) was frequently observed in the patients with large primary tumours, late clinical stages or advanced neck metastasis. Moreover, high ENO1 patients had significantly poorer clinical outcomes than low expressers (T/N < 2). Ectopic ENO1 expression stimulated cell transformation, invasion and tongue tumour formation. ENO1 knockdown abrogated the stimulation. Suppression of ENO1-induced proinflammatory CCL20 chemokine expression significantly attenuated its stimulatory effects on cell transformation and invasion. A concordant expression of ENO1 and CCL20 was validated both in ENO1-expresing cells and in clinical specimens. Together, we demonstrate a prognostic role of ENO1 overexpression in head and neck cancer and ENO1-mediated promotion of cell transformation and invasion partly via induced CCL20 expression.     

尼古丁调控人牙周膜细胞自噬水平的实验研究

目的 探讨尼古丁对人牙周膜细胞（hPDLCs）自噬水平的影响。方法 选取因正畸治疗而拔除的前磨牙,采用组织块法分离培养hPDLCs。通过Western blot法筛选尼古丁影响hPDLCs自噬的最佳作用时间及浓度,使用透射电子显微镜（TEM）和免疫荧光染色法检测该作用时间及浓度下hPDLCs自噬体形成情况和自噬标志蛋白LC3的表达情况。结果 LC3Ⅱ蛋白表达在尼古丁作用的12 h内持续升高,从而确定12 h为最佳作用时间;LC3Ⅱ蛋白表达上调具有尼古丁浓度依赖性,1×10^-5 mol·L^-1为尼古丁最佳作用浓度。TEM和免疫荧光染色证实尼古丁在此浓度及作用时间下hPDLCs细胞质内自噬体的数量增加,自噬标志蛋白LC3表达升高。结论 在一定条件下,尼古丁能够上调hPDLCs自噬水平,为进一步研究细胞自噬与吸烟相关牙周炎的关系奠定了基础。     

肾移植术后肺部感染时间、病原菌分布及耐药性分析

目的 了解肾移植术后肺部感染的发病时间、病原菌分布及耐药性特点,为临床治疗提供依据。方法 收集2012年1月～2015年12月共73例肾移植术后肺部感染患者的临床资料,回顾性分析感染发生的时间、标本分离的病原菌及耐药性结果,采用WHONET5.4软件对药敏结果进行分析。结果 73例肾移植术后肺部感染发生的时间在术后1年内占83.56%(61/73),其中39例发生于肾移植术后6月内,占53.42%(39/73),22例发生于术后6月～1年,占30.14%(22/73)。病原菌分离部位以痰液、血液为主,占84.93%(62/73),其余为肺泡灌洗液、胸腔引流液及咽拭子等。共分离出病原菌79株,革兰阴性杆菌39株(49.37%),革兰阳性菌31株(39.24%)及真菌9株(11.39%)。较常见的病原菌依次为:铜绿假单胞菌12株(15.19%),表皮葡萄球菌11株(13.92%),肺炎克雷伯菌10株(12.66%),金黄色葡萄球菌9株(11.39%),鲍曼不动杆菌8株(10.13%),大肠埃希菌6株(7.59%)。大肠埃希菌和肺炎克雷伯菌中产超广谱β-内酰胺酶的检出率分别为30.0%(2/6)和20.0%(2/10)。表皮葡萄球菌和金黄色葡萄球菌中的耐甲氧西林葡萄球菌检出率分别为45.45%(5/11)和22.22%(2/9)。革兰阴性杆菌对头孢吡肟、美洛培南和亚胺培南敏感。革兰阳性球菌对万古霉素、替考拉丁和利福平敏感。结论 肾移植术后肺部感染多发生在术后1年内; 革兰阴性菌为主要的病原菌; 革兰阴性菌和革兰阳性菌常多重耐药,应尽早选用敏感药物治疗。     

Association of Empirically Derived Food-Based Inflammatory Potential of the Diet and Breast Cancer: A Hospital-Based Case-Control Study

BackgroundDiet may be a modifiable factor in the prevention of breast cancer (BC) by modulating inflammation. We used a food-based empirical dietary inflammatory index (FDII) to evaluate the association between FDII and odds of breast cancer in Iranian women.MethodsThe present case-control study carried out on 150 age-matched women with newly diagnosed breast cancer and controls. Data for dietary intake and anthropometric measures were collected. FDII score was developed according to participants dietary intakes of 27 pre-defined food groups. Multivariate odds ratios (OR) with 95% confidence intervals (CI) were used to investigate the association of empirically derived food-based inflammatory potential of the diet and breast cancer.ResultsThe odds ratios of BC according to quartiles of FDII score by multivariate logistic regression models indicated the FDII score was significantly associated with BC risk (OR: 2.38; 95% CI: 1.23-4.59, P _trend = .04). After controlling confounders, multivariate logistic regressions remained significant which revealed in participants at the fourth quartile of FDII score chance of breast cancer was 2.8 times higher than participants in the first quartile.ConclusionsThe results of our study suggested that more pro-inflammatory diet (higher FDII scores) was associated with increased BC risk. These findings suggest that developing an effective dietary modification based on FDII may reduce risk of BC.     

The puzzle of eczema and its links to asthma: The raw & irritating facts

A baby's skin traditionally is thought of as smooth, silky, and soft. Not so with the roughly 26 million U.S. infants and young children affected by atopic dermatitis (AD), commonly referred to as eczema. In these children, a red, itchy rash appears most often between the ages of 2 and 18 months, and more than half of them will still have the problem as adults. (Note: Although we will use the term eczema to refer to AD in this article, be aware that it technically refers to a broader array of skin conditions.)     

Frequent concomitant epigenetic silencing of the stress‐responsive tumor suppressor gene CADM1, and its interacting partner DAL‐1 in nasal NK/T‐cell lymphoma

Nasal NK/T‐cell lymphoma (NL) is a rare but clinically important entity of lymphoma. Its preferential incidence in Orientals but not Caucasians suggests possible genetic predisposition. 11q deletion is common in NL, indicating certain tumor suppressor genes (TSGs) at this locus involved in its pathogenesis. We investigated the expression and methylation of an 11q23.2 TSG, CADM1 (or TSLC1), and its partner DAL‐1 (or EPB41L3) in NL. Methylation and silencing of CADM1 were detected in 2 NL and 4 of 8 (50%) of non‐Hodgkin lymphoma (NHL) cell lines, but not in normal NK cells and normal PBMC. Absence of CADM1 protein was also detected in NL cell lines. 5‐aza‐2′‐deoxycytidine (Aza) demethylation or genetic knockout of both DNMT1 and 3B genes restored CADM1 and DAL‐1 expression. CADM1 methylation was further detected in 36 of 45 (80%) of NL tumors. Concomitantly, DAL‐1 was epigenetically inactivated in NL cell lines and virtually all the tumors with methylated CADM1. A significant correlation between the methylation of both genes was found (p < 0.0001). Homozygous deletion of CADM1 was detected in only 3 of 18 (17%) of tumors. The stress‐response of CADM1 was abolished when its promoter becomes methylated. Our results demonstrate a frequent, predominant epigenetic silencing of CADM1 and DAL‐1 in NL, which likely play a synergic role in NL pathogenesis. © 2008 Wiley‐Liss, Inc.