CCR2, chemokine receptor 2

  • 文章类型: Journal Article
    在过去的几十年里,人们对了解癌症发病机制和进展的分子机制越来越感兴趣,因为它仍然与高发病率和死亡率相关。目前对大型骨肉瘤的治疗通常包括抢救或处死肢体的复杂治疗方法,并结合术前和术后多药化疗和/或放疗,并且仍然与高复发率相关。针对肿瘤细胞特定特征的细胞策略的发展似乎是有希望的,因为它们可以选择性地靶向癌细胞。最近,间充质基质细胞(MSC)通过其在再生医学中的应用,已成为骨科临床实践中重要研究的主题。进一步的研究已经针对使用MSCs进行更个性化的骨肉瘤治疗,利用它们广泛的潜在生物学功能,可以通过使用组织工程方法来促进大缺损的愈合来增强。在这次审查中,我们探讨了MSCs在骨肉瘤治疗中的应用,通过分析MSCs和肿瘤细胞的相互作用,MSCs对靶肉瘤的转导,以及它们在人类骨肉瘤摘除术后骨再生方面的临床应用。
    Over the past few decades, there has been growing interest in understanding the molecular mechanisms of cancer pathogenesis and progression, as it is still associated with high morbidity and mortality. Current management of large bone sarcomas typically includes the complex therapeutic approach of limb salvage or sacrifice combined with pre- and postoperative multidrug chemotherapy and/or radiotherapy, and is still associated with high recurrence rates. The development of cellular strategies against specific characteristics of tumour cells appears to be promising, as they can target cancer cells selectively. Recently, Mesenchymal Stromal Cells (MSCs) have been the subject of significant research in orthopaedic clinical practice through their use in regenerative medicine. Further research has been directed at the use of MSCs for more personalized bone sarcoma treatments, taking advantage of their wide range of potential biological functions, which can be augmented by using tissue engineering approaches to promote healing of large defects. In this review, we explore the use of MSCs in bone sarcoma treatment, by analyzing MSCs and tumour cell interactions, transduction of MSCs to target sarcoma, and their clinical applications on humans concerning bone regeneration after bone sarcoma extraction.
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  • 文章类型: Journal Article
    肝性脑病描述了由于肝功能不全和/或门体分流引起的一系列神经系统并发症。肝性脑病的发病机制与高氨血症和炎症有着长期的联系。最近,异常的胆汁酸信号与急性肝功能衰竭(包括神经元功能障碍)引起的肝性脑病的关键特征有关,神经炎症和血脑屏障通透性。这篇综述总结了最近的研究结果,这些研究表明胆汁酸在肝性脑病中的作用,并推测了胆汁酸信号传导可能的下游后果。
    Hepatic encephalopathy describes the array of neurological complications that arise due to liver insufficiency and/or portal-systemic shunt. The pathogenesis of hepatic encephalopathy shares a longstanding association with hyperammonemia and inflammation. Recently, aberrant bile acid signaling has been implicated in the development of key features of hepatic encephalopathy due to acute liver failure including neuronal dysfunction, neuroinflammation and blood-brain barrier permeability. This review summarizes the findings of recent studies demonstrating a role for bile acids in hepatic encephalopathy and speculates on the possible downstream consequences of bile acid signaling.
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