血管内皮生长因子研究进展

血管内皮生长因子（ＶＥＧＦ）是一种能特异地作用于血管内皮细胞的生长因子。在生理和病理情况下均有表达本文就ＶＥＧＦ的分子特征,ＶＥＧＦ受体及信号传导机制,表达调节和生物学特征作一综述。     

血管内皮生长因子与血管生成

本综述了血管内皮生长因子结构特点、体内分布,正常及病理条件下的表达水平变化及其生物学功能,并对血管通透性与血管生成之间的关系进行了评述。     

胎儿稽留流产与染色体异常的关系及其影响因素分析

目的：探讨B超联合FISH实验室诊断技术分析胎儿稽留流产与染色体非整倍体关系并对其他影响因素进行综合分析。方法：采用FISH技术对广西267例B超诊断为稽留流产孕妇的胎儿绒毛组织行13,16,18,21,22,X,Y染色体数目检测,荧光显微镜下观察结果;采用SPSS13．0对相关数据进行统计分析。结果：267例稽留流产胎儿绒毛组织中,染色体数目异常95例,异常率35．6％,数目异常以三体最常见,其次为四体,少见部分单体;异常病例样本中存在多种染色体混合嵌合体现象,如混合嵌合三体（2n＋1／2n）,混合嵌合四体（2n＋2／2n）,混合嵌合单倍体、三体、四体（2n-1／2n＋l／2n＋2／2n）等;稽留流产与患者年龄、流产史、孕周具有显著相关性。结论：染色体数目异常与染色体混合嵌合均是稽留流产的重要原因,同时稽留流产发生与患者高龄、多次流产史、早期妊娠密切关系。     

血管内皮细胞生长因子及其受体的分子生物学研究进展

血管内皮细胞生长因子（ｖａｓｃｕｌａｒ ｅｅｎｄｏｔｈｅｌｉａｌ ｃｅｌｌ ｇｒｏｗｔｈ ｆａｃｔｏｒ,ＶＥＧＦ）是最直接的血管内皮细胞促分裂素,它通过其受体（ＶＥＧＦＲ）介导其活性,不同ＶＥＧＦ剪接体与不同类型的ＶＥＧＦＲ结合,通过胞内信号传导,发挥不同的生物学效应。本总结了ＶＥＧＦ及其受体的结构、特点、分类、分子生物学特征、二的连续及由ＶＥＧＦ诱导的胞内信号传导作用,并简单讨论了它们可能的     

VEGF异常与胎儿生长受限

VEGF正常表达是妊娠正常进行的关键环节,其对胎盘血管形成、胎盘绒毛细胞和子宫螺旋动脉的发生发展起着至关重要的作用.VEGF异常导致子宫、胎盘血管发育障碍,胎儿缺血缺氧,最终导致胎儿生长受限.本文主要从VEGF对胎盘血管生成、胎盘绒毛膜炎、绒毛细胞凋亡、子宫螺旋动脉重塑异常及生殖微生物等方面的影响进行简要综述,为今后临...     

孕激素及人绒毛促性腺激素与药物流产后异常子宫出血的关系

目的:分析孕激素和人绒毛膜促性腺激素(h CG)与药物流产后异常子宫出血的关系。方法:选择2017年1月至2017年12月我院妇产科收治的药物终止妊娠的妇女150例,患者口服米非司酮配伍米索前列醇药物终止早期妊娠。将药物流产后子宫出血时间≤14 d作为对照组(n=75),14d作为异常组(n=75)。比较两组患者在药物流产后10 d、14 d、18 d、22 d血清中孕激素和h CG含量,分析两组患者孕激素和h CG含量相关性。结果:两组患者在年龄、月经周期、孕次、受孕天数、体重等方面比较无统计学差异(P0.05)。异常组在药物流产后10 d、14 d、18 d、22 d血清孕激素和h CG含量均高于对照组(P0.05)。两组患者在药物流产后10 d、14 d、18 d、22 d孕激素含量呈先降低再升高的趋势(P0.05)。对照组患者在药物流产后10 d、14 d、18 d、22 d血清hCG含量逐渐降低(P0.05);异常组在药物流产后10 d、14 d血清h CG含量比较无统计学差异(P0.05),在药物流产后18 d、22 d血清hCG含量低于药物流产后10 d、14 d,且药物流产后22 d低于药物流产后18 d(P0.05)。对全部样本的全部时点数据合并进行Pearson相关检验分析,孕激素和h CG含量呈正相关关系(P0.05)。结论:药物流产后异常子宫出血妇女血清的孕激素、hCG含量较高,两者呈正相关关系。药物流产后10 d、14 d监测血清HCG值无明显下降提示有异常子宫出血的可能,联合监测孕激素、hCG含量有利于药物流产后异常子宫出血的预测和治疗。     

血管内皮生长因子C的研究进展

血管内皮生长因子Ｃ（ＶＥＧＦ－Ｃ）是一种特异性血管、淋巴管内皮细胞调节因子,其结构与ＶＥＧＦ具有同源性。ＶＥＧＦ－Ｃ通过受体ＣＥＧＦＲ－２和ＶＥＧＦＲ－３发挥作用,其ｍＲＮＡ的表达具有一定的组织特点,并受多种因素的调节。ＶＥＧＦ－Ｃ对于胚胎发育,细胞分化、活体内外血管、淋巴管内皮细胞均有重要的调节作用。     

抗肿瘤血管生成治疗的研究进展及应对策略

抗血管生成疗法作为癌症治疗的重要方法之一,能够显著抑制肿瘤的生长与转移。然而,在临床应用中仍无法避免抗血管生成药物耐药性的产生,且目前对其耐药机制的研究尚不完善,严重阻碍了临床治疗进程。因此,基于抗血管生成药物耐药机制的研究,寻找新的靶点,以及整合新的治疗方案,对于改善肿瘤的临床治疗效果意义重大。基于此,本文主要从血管生成在肿瘤发展中的作用机制、抗血管生成治疗药物的应用现状及其介导的耐药机制、未来的研究策略等方面综述了抗肿瘤血管生成治疗的最新研究进展。     

几种与肿瘤血管生成有关的调控因子研究进展

肿瘤血管能够导致肿瘤疯狂生长,也是肿瘤细胞扩散和转移的秘密通道。因此对肿瘤血管的生成的研究就成为了当前研究的热点。本文对VEGF、MMP、EGFR、bFGF等重要的促血管生成因子与肿瘤血管生成、生长关系的临床证明、病理组织学研究、基因学研究以及以此为靶点的药物治疗的研究现状,尤其是中药治疗研究情况作综述。     

习惯性流产伴罕见Rob(13;21)的异常核型分析

病例　　患者,女,29岁,汉族,身高156cm,体重52kg;职业农民表型无异常,非近亲婚配,否认家族遗传史。孕期及孕前期无毒物、化学、放射物的接触史,无特殊病史。因连续流产4次而就诊。细胞遗传学检查　　外周血染色体分析,普通核型计数,分析50个分裂相,均为45条,D、G组各少一条,多一条衍生染色体。经G带技术分析了20个核型均为45,XX,der(13;21)(q10;q10)。其丈夫核型正常,其他家庭成员拒绝检查。患者的13号、21号染色体分别在着丝粒区发生断裂,两者的长臂在着丝粒区附近彼此连接,形成了一条新的染色体,两者的短臂也可能连接成一条小染色体…     

VEGF-null cells require PDGFR alpha signaling-mediated stromal fibroblast recruitment for tumorigenesis

We generated VEGF-null fibrosarcomas from VEGF-loxP mouse embryonic fibroblasts to investigate the mechanisms of tumor escape after VEGF inactivation. These cells were found to be tumorigenic and angiogenic in vivo in spite of the absence of tumor-derived VEGF. However, VEGF derived from host stroma was readily detected in the tumor mass and treatment with a newly developed anti-VEGF monoclonal antibody substantially inhibited tumor growth. The functional significance of stroma-derived VEGF indicates that the recruitment of stromal cells is critical for the angiogenic and tumorigenic properties of these cells. Here we identified PDGF AA as the major stromal fibroblast chemotactic factor produced by tumor cells, and demonstrated that disrupting the paracrine PDGFR alpha signaling between tumor cells and stromal fibroblasts by soluble PDGFR alpha-IgG significantly reduced tumor growth. Thus, PDGFR alpha signaling is required for the recruitment of VEGF-producing stromal fibroblasts for tumor angiogenesis and growth. Our findings highlight a novel aspect of PDGFR alpha signaling in tumorigenesis.     

The Xenopus platelet-derived growth factor α receptor: cDNA Cloning and demonstration that mesoderm induction establishes the lineage-specific pattern of ligand and receptor gene expression

We have cloned the Xenopus PDGF α receptor cDNA and have used this clone, along with cDNA encoding PDGF A, to examine their expression pattern in Xenopus embryos and to determine the factors responsible for lineage specificity. Recombinant Xenopus α receptor expressed in COS cells exhibits PDGF-A-dependent tyrosine kinase activity. We find that receptor mRNA is present in cultured marginal zone tissue explants and in animal cap tissue induced to form mesoderm either by grafting to vegetal tissue or by treatment with recombinant activin A. In contrast, PDGF A mRNA is expressed in cultured, untreated animal cap tissue and is suppressed by mesoderm induction. These results suggest that ectodermally produced PDGF A may act on the mesoderm during gastrulation and that mesoderm induction establishes the tissue pattern of ligand and receptor expression. © 1993Wiley-Liss, Inc.     

Preoperative administration of GnRH-a plus tibolone to premenopausal women with uterine fibroids: evaluation of the clinical response, the immunohistochemical expression of PDGF, bFGF and VEGF and the vascular pattern

Aim of the study is to compare the effects of preoperative therapy with tibolone plus gonadotropin-releasing hormone analogue (GnRH-a) in premenopausal women with those of GnRH-a alone on clinical response, uterine volume, immunohistochemical expression of platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) and vascular features of myomas. Seventy women with symptomatic uterine fibromatosis were treated for four months with leuprorelin acetate alone or plus tibolone. Untreated patients were submitted to uterine surgery directly. Uterine volume, hematological data, BMD, myoma-related symptoms and hot flushes were evaluated at the admission and before surgery. Immunohistochemical expression of PDGF, bFGF and VEGF, vascular changes and CD105 expression, as a marker of angiogenesis, were evaluated in myomas obtained after surgery. Uterine volume and myoma-related symptoms reduced and hematological variables increased in treated patients. BMD decreased in patients treated with GnRH-a alone. Hot flushes were less in GnRH-a plus tibolone group than in GnRH-a group. Immunohistochemical expression of PDGF, bFGF and VEGF, vascularization and angiogenesis reduced in treated patients in comparison with untreated ones. In conclusion, the administration of tibolone plus GnRH-a before uterine surgery does not change the clinical and immunohistochemical effects of GnRH-a alone.