Ancient Chinese scholars believed there were two natural, complementary and contradictory forces in our universe: yin and yang (or in simplified Chinese
,在繁体中文中
那and in pinyin (standard Mandarin romanisation) yīnyáng). Yin represents the female, negative aspects, darkness, softness, moisture, night-time, even numbers, and docility. Yang represents the male, positive aspects, brightness, hardness, dryness, day-time, odd numbers, and dominance. Yin and yang are continually in a state of flux and always looking for a balance point. One moves, the other responds. Ancient scholars therefore treated this phenomenon as a natural universal law.
在这个问题中European Respiratory Journal(ERJ), Man等等。1假设是纤连蛋白对C反应蛋白(CRP)的比例是比每种分离的生物标志物更合适的工具,以评估慢性阻塞性肺病的预后(COPD)。使用肺部健康研究III数据2,他们更新(并改进了)他们以前的CRP研究3.。看来,在这个描述的轻度至中度COPD患者中,纤连蛋白对CRP的对数转化比的关系(在UG·mL中-1)和死亡率是L形,并且超过150左右的阈值,几乎没有观察到死亡。如果这个简单的想法证实了,它可能具有巨大的预后意义。在数学上,在任何L形状与不利结果的关系中,比率越高,更好4.。In a ratio of fibronectin to CRP, this could happen either through a higher fibronectin concentration (more repair) or through a lower CRP (less inflammation).
当然,人类的研究等等。1is hypothesis-generating and deserves to be tested in other samples of COPD individuals with a more varied severity and from different settings.
该research by Man等等。1由于在原始临床试验中为不同目的收集数据,是机会主义。5.,所以研究本问题ERJhas intrinsic limitations, some of them already highlighted by the authors. As in any cross-sectional analysis, causality cannot be inferred. Whether a COPD phenotype expressing more inflammation and/or less repair is associated with a higher likelihood of death, could be a spurious association or a consequence rather than a cause. Whether or not plasma measurements of CRP and fibronectin really reflect what is occurring in the lungs is speculative, and the precise role of both molecules in the process of lung (not plasma) damage and repair is still poorly defined. In fact, acute inflammation is the first step of a successful repair process6.两种过程之间的清晰分离模糊。作为男人等等。1讨论,在一个时间,进行测量point, so the reproducibility of this ratio as well as their direct relationship to other important dimensions of the disease has to be explored. In fact, there was no consistency of the reported association with decline in lung function or respiratory-specific mortality (communication from the authors), which is in contradiction with the initial hypothesis. Finally, the patients studied by Man等等。1有轻度到温和的copd;因此,在患有更严重的疾病的患者中,结果可能是不同的。尽管如此,这是一个重要的研究,因为它开启了一个新的研究途径,解决了其他分子的局限性和/或测试了可以更好地反映这一COPD的yīnyáng的有效性7.。
寻找COPD生物标志物是一场比赛,并设定了一些评估和使用当前和未来结果和标记的规则8.。该study by Man等等。1可能会鼓励其他人帮助解开关于炎症和修复是否是朋友或敌人的争议9.-11.。一些剩下的未知数和解决它们的一些可能的方法已经在其他地方列出12.。Very recently, Curtis等等。13.提出并证实了另一种关于COPD发病机制的另一个假设,基于“金发姑娘”假设。基本上,这个假设表明没有炎症不良;这一切都取决于如何以及何时,就像孩子的童话故事一样。在给定的窗户的肺部窗户中,“太少”或“太多”的修复和炎症可能涉及适应性免疫反应在控制先天反应方面的成功。一方面,当我们目前了解它时,这可能会产生COPD自然历史的进展;另一方面,它可能会解释一些在烟草曝光的许多包装率后具有正常肺功能的“健康”吸烟者。即使是非炎症状态也不能被动地从没有炎症刺激的情况下被动地出现;相反,健康的维持可能需要特定基因产品的积极作用来抑制对潜在炎症刺激的反应,这些炎症刺激不保证全部反应6.。
通过治疗干预措施拟查可能的疾病修饰。任何抗炎或预防管理和药理学治疗的疗效的细平衡必须抵御任何潜在的不良事件,以便在人为修改炎症和修复之间进行仔细平衡,旨在维持肺稳态。
Almost a decade ago, Rennard14.表明,香烟吸烟诱导后的修复过程可导致愈合或更多疾病,并表明损伤是否导致异常纤维化组织的积累可能取决于来自几种来源的复杂因素的复杂平衡。与Yīnyáng符号系统一样,慢性阻塞性肺病的修复和炎症可能以复杂的方式互连,在不同时间和条件下具有正和负反馈。它们中的每一个都包含另一个元素或种子,它们不能没有彼此存在。
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