Bisphenol A induce ovarian cancer cell migration via the MAPK and PI3K/Akt signalling pathways

Bisphenol A (BPA), is present in a multitude of products, including food and water containers, food can linings, dentistry sealants, and thermal paper. BPA can induce the growth of human ovarian cancer cell lines. Reduction of adhesion and the initiation of metastasis are important events in cancer progression; therefore, this study investigated the effects of BPA (0.1–100 nM) on the migration of OVCAR-3 ovarian cancer cells and the expression levels of metalloproteinases (MMPs) and cadherins. The oestrogenic compound 17β-estradiol (40 nM) was used as a positive control for estrogenic properties of bisphenol A. BPA stimulated cell migration, and the effect of BPA was similar to that of 17β-estradiol. BPA-induced cell migration was accompanied by up-regulation of the migration-related factors MMP-2, MMP-9 and N-cadherin, but E-cadherin expression and activity was unaffected. The stimulatory effects of BPA on cell migration were abolished by pre-treatment of the cells with inhibitors of the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase pathways (PI3K). In conclusion, the results presented here show that BPA induces OVCAR-3 cells migration by activating MAPK and PI3K/Akt signalling pathways.     

2-Methoxy-1,4-Naphthoquinone (MNQ) suppresses the invasion and migration of a human metastatic breast cancer cell line (MDA-MB-231)

Metastasis contributes to the escalating mortality rate among cancer patients worldwide. The search for novel and more effective anti-metastatic agent is crucial owing to the lack of anticancer drugs that can successfully combat metastasis. Hence, this study aims to examine the effects of 2-Methoxy-1,4-Naphthoquinone (MNQ) towards the metastasis of MDA-MB-231 cells. In invasion assays, the number of cells permeating across a Matrigel barrier was found to be decreased in a dose-dependent manner upon treatment with MNQ (0–7.5 μM). In wound-healing migration assays, MNQ exhibited dose-dependent inhibition of cell migration in which significant reduction in the zone of closure was observed as compared to untreated controls. Furthermore, the proteolytic activity of a pivotal metastatic mediator, matrix metalloproteinase-9 (MMP-9) was also downregulated by MNQ as determined by gelatin zymography. This study reports for the first time, the ability of MNQ to inhibit the invasion and migration characteristics of a highly metastatic MDA-MB-231 cancer cell line.     

miR-127-3p在动脉粥硬化中的表达及干扰miR-127-3p对PDGF-BB处理的HAoSMC增殖迁移的影响

目的探讨miR-127-3p对血小板衍生生长因子-BB(PDGF-BB)诱导的人主动脉平滑肌细胞(HAoSMC)增殖、迁移的影响。方法收集动脉粥硬化患者及正常者血清,将HAoSMC分为对照组(未作任何处理)、模型组(25μg/L PDGF-BB)、anti-miR-NC组(转染miR-127-3p抑制剂对照+25μg/L PDGF-BB)、anti-miR-127-3p组(转染miR-127-3p抑制剂+25μg/L PDGF-BB)。实时荧光定量PCR(RT-qPCR)检测miR-127-3p和NF-κB mRNA表达水平;流式细胞仪检测细胞周期;四甲基偶氮唑盐比色法(MTT)检测细胞增殖活力;Transwell检测细胞迁移;蛋白质印迹(Western blot)法检测细胞增殖核抗原Ki67(Ki67)、神经钙粘蛋白(N-cadherin)、上皮钙粘蛋白(E-cadherin)的表达。结果与正常对照组相比,动脉粥硬化患者血清中miR-127-3p表达水平升高(P<0.05)。与对照组相比,模型组miR-127-3p表达水平升高,G0-G1期细胞所占比例降低,S期细胞所占比例升高,细胞OD值升高,迁移细胞数增加,Ki67、N-cadherin表达水平升高,E-cadherin表达水平降低(P<0.05)。与antimiR-NC组相比,anti-miR-127-3p组miR-127-3p表达水平降低,G0-G1期细胞所占比例升高,S期细胞所占比例降低,细胞OD值降低,迁移细胞数减少,Ki67、N-cadherin表达水平降低,E-cadherin表达水平升高,NF-κB mRNA表达水平降低(P<0.05)。结论干扰miR-127-3p表达可抑制PDGF-BB处理的HAoSMC增殖、迁移,其机制可能与NF-κB信号通路有关。     

Complexities of Short-Term Mobility for Sex Work and Migration among Sex Workers: Violence and Sexual Risks,Barriers to Care,and Enhanced Social and Economic Opportunities

Despite research on the health and safety of mobile and migrant populations in the formal and informal sectors globally, limited information is available regarding the working conditions, health, and safety of sex workers who engage in short-term mobility and migration. The objective of this study was to longitudinally examine work environment, health, and safety experiences linked to short-term mobility/migration (i.e., worked or lived in another city, province, or country) among sex workers in Vancouver, Canada, over a 2.5-year study period (2010–2012). We examined longitudinal correlates of short-term mobility/migration (i.e., worked or lived in another city, province, or country over the 3-year follow-up period) among 646 street and off-street sex workers in a longitudinal community-based study (AESHA). Of 646 sex workers, 10.84 % (n = 70) worked or lived in another city, province, or country during the study. In a multivariate generalized estimating equations (GEE) model, short-term mobility/migration was independently correlated with older age (adjusted odds ratio (AOR) 0.95, 95 % confidence interval (CI) 0.92–0.98), soliciting clients in indoor (in-call) establishments (AOR 2.25, 95 % CI 1.27–3.96), intimate partner condom refusal (AOR 3.00, 1.02–8.84), and barriers to health care (AOR 1.77, 95 % CI 1.08–2.89). In a second multivariate GEE model, short-term mobility for sex work (i.e., worked in another city, province, or country) was correlated with client physical/sexual violence (AOR 1.92, 95 % CI 1.02–3.61). In this study, mobile/migrant sex workers were more likely to be younger, work in indoor sex work establishments, and earn higher income, suggesting that short-term mobility for sex work and migration increase social and economic opportunities. However, mobility and migration also correlated with reduced control over sexual negotiation with intimate partners and reduced health care access, and mobility for sex work was associated with enhanced workplace sexual/physical violence, suggesting that mobility/migration may confer risks through less control over work environment and isolation from health services. Structural and community-led interventions, including policy support to allow for more formal organizing of sex work collectives and access to workplace safety standards, remain critical to supporting health, safety, and access to care for mobile and migrant sex workers.     

The origin and distribution of human lice in the world

Two genera of lice parasitize humans: Pthirus and Pediculus. The latter is of significant public health importance and comprises two ecotypes: the body louse and the head louse. These ecotypes are morphologically and genetically notably similar; the body louse is responsible for three infectious diseases: Louse-borne epidemic typhus, relapsing fever, and trench fever. Mitochondrial DNA studies have shown that there are three obviously divergent clades of head lice (A, B and C), and only one clade of body lice is shared with head lice (clade A). Each clade has a unique geographic distribution. Lice have been parasitizing humans for millions of years and likely dispersed throughout the World with the human migrations out of Africa, so they can be good markers for studying human evolution. Here, we present an overview of the origin of human lice and their role in vector pathogenic bacteria that caused epidemics, and we review the association between lice clades and human migrations.     

一次性纸塑复合材料食具污染物迁移情况研究

目的模拟一次性纸塑复合材料食具日常使用环境,测定其残留的化学物质迁移的情况。方法原子荧光法测定砷、汞、锌,原子吸收光谱法测定铅、铜、镉;化学法测定脱色、荧光、感官评价、挥发性酚、羰基价;气相色谱-质谱法联合测定多环芳烃。结果三种不同模拟条件下,食具中污染物向水或乙酸中转移的数量比较微小;食具脱色和感官评价均为阴性,均未检出挥发性酚,有2个食具的荧光测试结果为阳性;少部分食具检出少量菲、二苯并（a,h）蒽和苯并二萘嵌（ghi）苯外,其余均未检出。结论在本文的模拟条件下,样品食具还是比较安全的。     

UHMWPE 颗粒上调 EMMPRIN、MMPs 表达并增强共培养体系中 THP-1、FLS 迁移、侵袭能力的实验研究

目的：探讨超高分子量聚乙烯（ UHMWPE）颗粒对人单核细胞株THP-1、成纤维样滑膜细胞（ FLS）共培养体系迁移、侵袭能力及对细胞外基质金属蛋白酶诱导剂（ EMMPRIN）与基质金属蛋白酶（ MMPs）表达的影响。方法建立THP-1-FLS细胞共培养体系,应用台盼蓝染色检测THP-1细胞、FLS细胞存活率,Western blot、明胶酶谱、实时定量PCR方法检测样品中的EMMPRIN、MMP-2、MMP-9的表达及活性,并应用RNA干扰技术评估EMMPRIN的作用。结果 UHMWPE颗粒刺激THP-1细胞EMMPRIN表达上调,对FLS的EMMPRIN表达无明显影响。 UHMWPE颗粒刺激FLS的MMP-2、MMP-9表达上调、活性增强,对 THP-1表达 MMPs 无明显影响。 THP-1-FLS 共培养时, UHMWPE颗粒刺激使EMMPRIN、MMP-2、MMP-9表达上调更为显著。颗粒刺激下,THP-1-FLS共培养体系的迁移能力、侵袭能力明显强于无颗粒刺激,并与EMMPRIN的表达水平和MMPs的活性呈明显正相关。行THP-1细胞EMMPRIN基因干扰后,共培养体系的EMMPRIN、MMPs表达均下调,迁移、侵袭能力下降。结论 UHMWPE 颗粒可刺激THP-1-FLS 共培养体系高表达EMMPRIN,上调MMP-2、MMP-9的分泌并增强其活性,提高共培养体系的迁移、侵袭能力。     

结缔组织生长因子通过ERK1/2和PI3K信号通路促进大鼠肝星状细胞迁移和基质金属蛋白酶2表达

目的：研究结缔组织生长因子（CTGF）对大鼠肝星状细胞（HSC）迁移及基质金属蛋白酶2（MMP-2）表达及活化的影响。方法分别应用RT-PCR和Western blotting法检测MMP-2表达,明胶酶谱法检测MMP-2的活性;运用Western blotting法检测ERK1/2和Akt的磷酸化水平。运用Transwell小室检测肝星状细胞迁移能力。结果 CTGF呈剂量依赖性促进大鼠HSC中MMP-2 mRNA和蛋白表达;同时CTGF能够促进HSC迁移,MMP-2特异性抑制剂能够抑制CTGF的促迁移作用。ERK1/2和PI3K抑制剂能够显著抑制CTGF诱导的MMP-2表达以及CTGF促进HSC的迁移作用。结论 MMP-2表达和活性的增强在CTGF促进HSC迁移过程中发挥着重要作用,ERK1/2和PI3K信号通路在CTGF促进MMP-2表达发挥关键作用。