microvascular density

微血管密度
  • 文章类型: Meta-Analysis
    设计并进行了一项荟萃分析,以评估肿瘤微血管密度(MVD)对骨肉瘤患者生存率的影响。在总体(OS)和无病(DFS)生存率方面,高MVD和低MVD之间没有差异。低MVD肿瘤在随访第三年表现出较低的DFS。尽管原发转移不影响平均MVD测量值,化疗反应良好的肿瘤有较高的MVD值.虽然肿瘤MVD之间没有显着差异,找到了OS和DFS,良好的辅助治疗反应者的血管形成模式明显较高.
    A meta-analysis was designed and conducted to estimate the effect of tumoral microvessel density (MVD) on the survival of patients with osteosarcoma. There was no difference between high and low MVD regarding the overall (OS) and disease-free (DFS) survival. Low MVD tumors displayed a lower DFS at the third year of follow-up. Although primary metastases did not affect the mean MVD measurements, tumors with a good chemotherapy response had a higher MVD value. Although no significant differences between tumoral MVD, OS and DFS were found, good adjuvant therapy responders had a significant higher vascularization pattern.
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  • 文章类型: Meta-Analysis
    多项研究探讨了前列腺癌(PCa)肿瘤内微血管密度(MVD)与术后生化复发(BCR)风险之间的关系,虽然结果是矛盾的。因此,我们进行了一项荟萃分析,以探讨MVD对PCa中BCR的影响.
    我们搜索了PubMed,MEDLINE,科学直接/爱思唯尔,Cochrane图书馆,CNKI,和EMBase数据库从成立到2022年1月,没有年份或语言限制,并使用NOS指南评估19项符合条件的研究的质量。得出的风险比(HR)和95%置信区间(95CI)用于评估每个终点。使用RevMan进行数据合成以评估MVD在PCa中的预后价值及其异质性,而发表偏倚使用STATA16.0进行检查。
    我们的荟萃分析包括19篇关于PCa术后生化复发的文章(T1-2为4篇,T1-3为6篇,T1-4为9篇),其中,合并3933例患者。肿瘤内MVD对PCa不同分期对BCR的预测能力为T1-2(HR,2.46;95%CI,1.08-5.58;p=0.03;I2=83%),T1-3(HR,2.38,95%CI,1.41-4.01;p=0.001;I2=82%),T1-4(HR,1.61;95%CI,1.19-2.19;p=0.002;I2=61%)。基于欧洲和免疫组织化学抗体无因子VII的亚组分析与主要分析一致。敏感性分析排除那些被判断为在T1-2中存在高偏倚风险的研究,显示HR为2.99[1.70,5.27](I2=38%,p=0.0001),证明MVD风险估计用于评估生化复发的稳健性。
    微血管密度是PCa患者BCR的预测因子,MVD较强的T期PCa与BCR有关。需要进一步的研究来研究PCa不同T阶段的新血管生成,以及MVD是否对EAU推荐的生化复发风险评估工具有益。
    Several studies have explored the relationship between intratumoral microvessel density (MVD) and the risk of postoperative biochemical recurrence (BCR) in prostate cancer (PCa), although the results are contradictory. Therefore, we conducted a meta-analysis to investigate the effect of MVD on BCR in PCa.
    We searched PubMed, MEDLINE, Science Direct/Elsevier, the Cochrane Library, CNKI, and EMBase databases from inception through January 2022, with no year or language restrictions, and used NOS guidelines to evaluate the quality of the 19 eligible studies. The derived hazard ratio (HR) and 95% confidence interval (95%CI) were used to assess each endpoint. Data synthesis was performed with RevMan to assess the prognostic value of MVD in PCa and its heterogeneity, while the publication bias was examined using STATA 16.0.
    Our meta-analysis included 19 articles (4 for T1-2, 6 for T1-3, and 9 for T1-4) on postoperative biochemical recurrence of PCa, among which, 3933 patients were pooled. The predictive ability of intratumoral MVD for different stages of PCa on BCR was T1-2 (HR, 2.46; 95% CI, 1.08-5.58; p = 0.03; I2  = 83%), T1-3 (HR, 2.38, 95% CI, 1.41-4.01; p = 0.001; I2  = 82%), T1-4 (HR, 1.61; 95% CI, 1.19-2.19; p = 0.002; I2  = 61%).The subgroup analyses based on European and immunohistochemical antibody none-factor VII were consistent with primary one. Sensitivity analysis excluding those studies judged to be at high risk of bias in T1-2 showed a HR of 2.99[1.70,5.27] (I2  = 38%, p = 0.0001), demonstrating the robustness of risk estimates of MVD for the assessment of biochemical recurrence.
    Microvessel density is a predictor of BCR among patients with PCa, and earlier T stage PCa with a stronger MVD is associated with BCR. Further studies are needed to investigate neoangiogenesis in different T stages of PCa and whether MVD will be of benefit to the EAU-recommended tool for biochemical recurrence risk assessment.
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  • 文章类型: Journal Article
    颞叶癫痫(TLE)的血脑屏障(BBB)功能失调。在这方面,可能存在微血管变化。这篇综述的目的是概述目前关于癫痫微血管变化的知识,包括癫痫引起的血管生成的临床和临床前证据,barriergenesis和微循环改变。解剖学研究显示海马区微血管密度增加,杏仁核,在各种啮齿动物癫痫模型中,新皮层伴有BBB渗漏。在人类TLE中,传入血管的减少,形态异常血管,并且已经观察到内皮基底膜的增加。临床和实验证据都表明基底膜改变,如字符串容器和突起,指示并可视化内皮细胞增殖和屏障发生之间的不平衡。血管内皮生长因子(VEGF)似乎起着至关重要的作用。血管解剖结构改变后,其生理功能受到神经血管解耦的影响,随后导致灌注不足,实质内稳态被破坏,并可能导致癫痫发作。“因此,癫痫可能是一种以脑微脉管系统紊乱为特征的疾病,其中VEGF起着关键作用。然而,需要来自患者的额外生理数据来验证来自患者活检的模型和组织学研究的发现。
    The blood-brain barrier (BBB) is dysfunctional in temporal lobe epilepsy (TLE). In this regard, microvascular changes are likely present. The aim of this review is to provide an overview of the current knowledge on microvascular changes in epilepsy, and includes clinical and preclinical evidence of seizure induced angiogenesis, barriergenesis and microcirculatory alterations. Anatomical studies show increased microvascular density in the hippocampus, amygdala, and neocortex accompanied by BBB leakage in various rodent epilepsy models. In human TLE, a decrease in afferent vessels, morphologically abnormal vessels, and an increase in endothelial basement membranes have been observed. Both clinical and experimental evidence suggests that basement membrane changes, such as string vessels and protrusions, indicate and visualize a misbalance between endothelial cell proliferation and barriergenesis. Vascular endothelial growth factor (VEGF) appears to play a crucial role. Following an altered vascular anatomy, its physiological functioning is affected as expressed by neurovascular decoupling that subsequently leads to hypoperfusion, disrupted parenchymal homeostasis and potentially to seizures\". Thus, epilepsy might be a condition characterized by disturbed cerebral microvasculature in which VEGF plays a pivotal role. Additional physiological data from patients is however required to validate findings from models and histological studies on patient biopsies.
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