颈部迁移性异物一例

患者男,39岁,因发现左颈部一肿物伴疼痛10 d于2004年9月6日入我院.查体:左颈胸锁乳突肌下段前方皮肤稍隆起,可触及一约0.5 cm×1.0 cm,边界不清、活动欠佳、轻触痛包块.

中国流动人口及其卫生问题

一、流动人口的内涵国际上对流动人口的通用称法是"迁移人口"("Migrant Population"或者"Migrants"、"Migration").根据国际人口科学联盟编写的《多语种人口学词典》[1],"迁移"是指"空间移动的一种形式,包括常住址的改变,并常跨越行政边界.这种常住址的改变可以是长期的,半长期的,甚至是短期的".国际上公认的人口迁移定义是指:为居住的目的而进行跨越一定区域界限的人口移动.一般在时间上规定,移入某地居住一年即为该地的移民.

人类原始生殖细胞的起源、迁移、增殖及凋亡过程

人类原始生殖细胞(PGC)是人卵母细胞的祖细胞,是人类生存及繁衍后代的重要细胞.PGCs起源于性腺外,经迁移到达生殖嵴与体细胞共同组成生殖腺;之后,PGCs在性腺内经增殖、分化等一系列复杂的变化终形成成熟的卵子.认识PGCs的起源、迁移、增殖、分化等过程对生殖医学具有重要意义.目前对禽类及小鼠PGCs的研究已取得深入进展,由于人PGCs不易获得,且受到伦理、道德及宗教方面的制约,有关人生殖细胞的研究进程较缓慢,对人PGC的起源及迁移过程等都不甚清楚,现就生殖细胞的起源、迁移、增殖及凋亡过程的研究进展作一概述.

MIF与恶性肿瘤相关研究进展

1966年Bloom等首次发现了由活化T淋巴细胞分泌的可抑制单核巨噬细胞移动的细胞因子并将其命名为巨噬细胞移动抑制因子(Macrophage migration inhibitory factors,MIF)[1].有研究报道MIF在乳腺癌、肝癌、肺癌、前列腺癌、胃癌、膀胱癌、及食管癌等肿瘤细胞中过度表达[2～3].因此MIF在恶性肿瘤中的作用越来越受到人们重视.本文就MIF与恶性肿瘤相关性作一阐述.

Low-density lipoprotein receptor-related protein 1 (LRP1, also known as CD91), a multifunctional endocytic and cell signaling receptor, is widely expressed on the surface of multiple cell types such as hepatocytes, ifbroblasts, neu-rons, astrocytes, macrophages, smooth muscle cells, and malignant cells. Emerging invitro and invivo evidence demonstrates that LRP1 is critically involved in many processes that drive tumorigenesis and tumor progression. For example, LRP1 not only promotes tumor cell migration and invasion by regulating matrix metalloproteinase (MMP)-2 and MMP-9 expression and functions but also inhibits cell apoptosis by regulating the insulin receptor, the serine/threonine protein kinase signaling pathway, and the expression of Caspase-3. LRP1-mediated phosphorylation of the extracellular signal-regulated kinase pathway and c-jun N-terminal kinase are also involved in tumor cell proliferation and invasion. In addition, LRP1 has been shown to be down-regulated by microRNA-205 and methylation ofLRP1 CpG islands. Furthermore, a novel fusion gene,LRP1-SNRNP25, promotes osteosarcoma cell invasion and migration. Only by understanding the mechanisms of these effects can we develop novel diagnostic and therapeutic strategies for cancers mediated by LRP1.

The inhibitory effect of SEMA3C/3D mutations on Neuro-2a cells migration and axonal growth in patients with Hirschsprung's disease

Objective:To explore the effect and mechanism of SEMA3C/3D mutations on axonal growth of neurons and cell migration in Hirschsprung's disease (HSCR) patients.Methods:HEK293T cells were transfected with wild-type and mutant SEMA3C/3D plasmids.The supernatants that contained SEMA3C/3D-AP fusion proteins were collected and added into the Neuro-2a cells.The changes in the cell morphology were observed by immunofluorescence staining.The expression and phosphorylation levels of cofilin,ERM and CRMP2 were determined by western blotting.The cell migration rate was measured by transwell assay.Results:Compared with wild type SEMA3D,SEMA3D-P615T mutant suppressed cofilin phosphorylation in Neuro-2a cells (P ＜ 0.05).The neural cells treated by five mutant SEMA3C/3D-AP fusion proteins presented different levels of axon atrophy,growth cone collapse,and sometimes,loss of normal structure.SE MA3C-S329G,SEMA3C-V337M and SEMA3D-P615T mutants cells exhibited a significantly reduced migration rate as compared with wild-type SEMA3C/3D treated cells (P ＜ 0.01).Conclusion:SEMA3C and SEMA3D mutations in HSCR patients could lead to the inhibition of Neuro-2a cells' migration and axonal growth.The mechanism of SEMA3D-P615T mutant might be related to down-regulation of the expression of p-cofilin,which consequently lead to cytoskeleton structure collapse and migrating ability decrease.Our study might provide important clues for the pathogenesis of HSCR.

Construction,identification and biological feature study of human hepatocellular carcinoma cells stably expressing HBeAg

Objective:To construct a HepG2 cell line which stably expressing Hepatitis B e antigen (HBeAg) and investigate mthe effects of HBeAg on the proliferation,migration and invasion of HepG2 cells.Methods:The lentivirus carrying HBeAg gene was constructed and packaged.HepG2 cells were infected with the lentivirus and screened with puromycin to obtain HepG2 cells which stably expressing HBeAg (HepG2-HBeAg cells).The expression levels of HBeAg mRNA and protein were detected by RT-qPCR and Western blot,respectively.The content of HBeAg secretion in cell supernatant in both HepG2-HBeAg cells and control cells (HepG2-NC cells and HepG2 cells) were detected by IFMA assay.Furthermore,CCK-8 proliferation assay,colony formation assay and transwell migration and invasion assays were conducted to compare the abilities of cell proliferation,migration and invasion,respectively.Results:The expression of HBeAg in the HepG2-HBeAg cell was significantly higher than those in HepG2 cells and HepG2-NC cells.Secreted HBeAg in the supernatant of HepG2-HBeAg cells was 26.33 ± 2.13 PEIU/mL but was undetectable in supernatant of control cells.The proliferation,migration and invasion were all significantly lower in HepG2-HBeAg cells compared to control cells (P＜0.01).Conclusion:A HepG2 cell line which stably expressing HBeAg was constructed successfully,and the over-expression of HBeAg could attenuate the proliferation,migration and invasion of hepatoeellular carcinoma cells.

Epithelial to Mesenchymal Transition: Biology and Clinical Translation

Epidlelial to mesenchymal transition(EMT)is a fundamental molecular process by which cancer cens gain increased migration,nvasion and me-tastasis.

β-咔啉类生物碱对SGC-7901细胞迁移、细胞侵袭和相关通路基因的影响

目的 探索β-咔啉类生物碱对SGC-7901细胞迁移、细胞侵袭,和PI3 K/AKT及MAPK/ERK通路基因mRNA,以及蛋白水平的抑制作用.方法 通过CCK-8法测定不同浓度条件下β-咔啉类生物碱对胃癌SGC-7901细胞增殖的抑制率;通过Transwell小室测定β-咔啉类生物碱对SGC-7901细胞迁移、侵袭能力的影响;利用qRT-PCR、Westem blotting技术检测相关基因mRNA及蛋白的表达差异.结果 随着β-咔啉类生物碱浓度增加,人胃癌SGC-7901细胞增殖抑制率逐渐升高,IC50=13.364μg/mL;阳性对照组(5-FU,5μg/mL)、β-咔啉类生物碱组中Transwell小室内SGC-7901细胞均可见显著减少(P＜0.01),且β-咔啉类生物碱组SGC-7901细胞数目较阳性对照组明显降低(P＜0.01);阳性对照组、β-咔啉类生物碱实验组GRB2 、PI3Kp85a、FAK基因mRNA表达水平较空白对照组显著降低(P＜0.05),而STAT3、ERK1、ERK2基因mRNA表达水平无统计学差异(P＞ 0.05);β-咔啉类生物碱组PI3Kp85a、p-ERK1/2、AKT蛋白表达水平显著低于空白对照组1与阳性对照组(P＜0.05).结论 较5-FU,β-咔啉类生物碱具有更有效的抑制胃癌SGC-7901细胞迁移1与侵袭能力,而该机制可能与β-咔啉类生物碱抑制PI3Kp85a、p-ERK1/2、AKT蛋白表达水平有关.

Objective:The aim of this study was to investigate the effects of plumbagin (PL), a naphthoquinone derived from the medicinal plant plumbago zeylanica, on the invasion and migration of human breast cancer cells. Methods:Human breast cancer MDA-MB-231SArfp cells were treated with different concentrations of plum-bagin for 24 h. The effects of plumbagin on the migration and invasion were observed by a transwell method. The expressions of IL-1α, IL-1β, IL-6, IL-8, TGF-β, TNFα, MMP-2 and MMP-9 mRNA in M DA-MB-231SArfp cells were detected using Real-Time PCR. MDA-MB-231SArfp cells were treated with plumbagin at different concentrations for 45 minutes. The activation of STAT3 was detected by western blot. Following this analysis, STAT3 in MDA-MB-231SArfp cells was knocked out using specific siRNA. mRNA levels of IL-1α, TGF-β, MMP-2 and MMP-9 were then detected. Consequently, MDA-MB-231SArfp cells were injected intracardially into BALB/c nude mice to construct a breast cancer bone metastatic model. The mice were injected intra-peritoneally with plumbagin. Non-invasive in vivo monitoring, X-ray imaging and histological staining were performed to investigate the effects of plumbagin on the invasion and migration of breast cancer cells in vivo. Results: The in vitro results showed that plumbagin could suppress the migration and invasion of breast cancer cells and down-regulate mRNA expressions of IL-1α, TGF-β, MMP-2 and MMP-9. Western blotting demonstrated that plumbagin inhibited the activation of STAT3 signaling in MDA-MB-231SArfp cells. The inactivation of STAT3 was found to have an inhibitory effect on the expressions of IL-1α, TGF-β, MMP-2 and MMP-9. In vivo studies showed that plumbagin inhibited the metastasis of breast cancer cells and decreased osteolytic bone metastases, as well as the secretion of MMP-2 and MMP-9 by tumor cells at metastatic lesions. Conclusions:Plumbagin can suppress the invasion and migration of breast cancer cells via the inhibition of STAT3 signaling and by downregulation of IL-1α, TGF-β, MMP-2 and MMP-9.

Objective:To study the expression of aminopeptidase N (CD13) in renal carcinoma and the effect of CD13 expression vector transfection on biological behavior of cancer cells.Methods:Renal carcinoma tissue and normal kidney tissue were collected and APN (CD13) contents in tissue were detected; renal carcinoma cell lines kevt-3 were cultured, 0 μg/mL, 10 μg/mL, 20 μg/mL, 40 μg/mL and 80 μg/mL of CD13 expression vector were transfected, and then migration ability, ATP generation capacity, and mRNA contents of migration and angiogenesis genes in cells were detected.Results:mRNA contents of APN in renal carcinoma tissue were higher than those in normal kidney tissue; the higher the clinical stage and pathological grade were, the higher the mRNA contents of APN in renal carcinoma tissue were; mRNA levels of APN in renal carcinoma tissue with lymph node metastasis were higher than those without lymph node metastasis;CD13 expression vector transfection could dose-dependently increase kevt-3 cell migration rate, ATP generation amount as well as mRNA contents of VEGF, HIF-1α, MMP9 and MMP10.Conclusion: Expression of aminopeptidase N (CD13) in renal carcinoma tissue abnormally increases; overexpression of CD13 can promote renal carcinoma cell migration and increase ATP generation as well as VEGF, HIF-1, MMP9 and MMP10 expression.

Objective:To explore molecular mechanism and biological function of miR-155 and its target genes on endometriosis.Methods: The expression of miR-155 in Ems patient and healthy control were assayed by RT-PCR. After miR-155 mimic and inhibitor were transfected into Ems endometrial cells for 48 h, the viability of cell was detected by MTT assay. Transwell migration and invasion assay were used to detect cell migration and invasion. The expression of cell apoptotic protein Bax and Bcl-2, matrix metalloproteinase (MMP 2) and MMP 9 were assayed by western blot.Results: The expression of miR-155 in Ems patient was more than that in the health control (P<0.01). After miR-155 mimic and inhibitor were transfected into Ems endometrial cells for 48 h, miR-155 over-expression could increase cell viability, and promoted cell migration and invasion, which was related to down-regulation of Bax along with up-regulation of Bcl-2, MMP 2 and MMP 9.Conclusion:These results suggested miR-155 lower expression inhibit endometrial cell proliferation and migration of the Ems.