ABSTRACT:

This article examines two medical journal research articles on tuberculosis, one published in 1938 and the other in 2014. The two articles, which use animal models to understand aspects of tuberculosis mycobacteria survival in the lungs, rely on markedly different research and biotechnological techniques, reach somewhat opposite conclusions, and reflect different paradigms of tuberculosis pathogenesis: the 1938 article (indirectly invoking Koch’s postulates) was written before the paradigm of so-called “latent” and “reactivation” tuberculosis became widely adopted, while the 2014 article (indirectly invoking the molecular equivalents to Koch’s postulates) works within that paradigm but implicitly questions it. Despite this, both articles exhibit fascinating similarities in terms of how their authors tackled their research questions, formulated their results, and framed their research methodologies. These similarities reflect both the reliance on tenets of the scientific method but also the value of paradigms of disease causation. Using tuberculosis as an example, this article concludes with remarks about how disease paradigms evolve and can stimulate research that leads to advances in disease understanding.

摘要：

本文研究了两篇关于结核病的医学期刊研究文章，一篇发表于 1938 年，另一篇发表于 2014 年。这两篇文章使用动物模型来了解肺结核分枝杆菌在肺部存活的各个方面，依赖于明显不同的研究和生物技术，达到了得出了有些相反的结论，反映了结核病发病机制的不同范式：1938 年的文章（间接援引科赫假设）是在所谓的“潜伏”和“再激活”结核病范式被广泛采用之前撰写的，而 2014 年的文章（间接援引科赫假设的分子等价物）在该范式中起作用，但隐含地质疑它。尽管如此，两篇文章在作者如何解决研究问题方面都表现出令人着迷的相似之处，制定了他们的结果，并制定了他们的研究方法。这些相似之处既反映了对科学方法原则的依赖，也反映了疾病因果关系范式的价值。本文以结核病为例，最后评论了疾病范式如何演变以及如何刺激研究，从而促进疾病理解的进步。