[Evolution, controversies, and exploration of the nature of the definition of acute respiratory distress syndrome].

Acute respiratory distress syndrome (ARDS) is a collection of clinical syndromes characterized by a variety of heterogeneous causes. It includes diffuse lung diseases of various etiologies that ultimately lead to refractory hypoxia and severe acute respiratory failure. Despite advances in research and treatment of ARDS, its incidence and mortality continue to pose significant challenges in clinical practice. Since its inception in 1967, the definition of ARDS has undergone several revisions that have generated controversy and influenced the implementation of diagnostic and treatment strategies. At present, ARDS remains a formidable obstacle to both diagnosis and treatment. This article undertakes a comprehensive review of the evolution of ARDS definitions, examines the current diagnostic paradigm, and explores its far-reaching consequences. Our aim is to identify research directions, both in the realm of basic science and clinical practice, that are consistent with the nature of this complex disorder.

[Pathogenesis and assessment of exertional dyspnea in chronic obstructive pulmonary disease].

Chronic obstructive pulmonary disease (COPD) is a common respiratory system disease that seriously affects the quality of life and has a high mortality rate. Exertional dyspnea is the most common symptom in COPD patients with complexed pathogenesis and limited therapeutic drug effects. In this paper, we reviewed the relevant mechanisms and assessment, in order to improve understanding of the pathogenesis of exertional dyspnea in COPD, to emphasize the importance of accurate assessment, and to explore effective interventions that can effectively improve the degree of dyspnea and even delay or reverse the decline in lung function.

[Identification of study populations in the clinical study of chronic obstructive pulmonary disease: Surface-based or essence-based].

Chronic obstructive pulmonary disease (COPD) is a heterogeneous disorder characterized by chronic bronchitis, emphysema, or both. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) has had a tremendous impact on the diagnosis and treatment of COPD. This article reviewed the evolution of the definition of COPD in GOLD and the change of its treatment strategy. In addition, in light of relevant clinical studies, the paper attempted to illustrate the importance of understanding the heterogeneous nature of COPD, and analyzed the possible consequences of ignoring this nature, including confusion with bronchial asthma caused by lung function as the "gold standard" and excessive use of inhaled glucocorticoids (ICS). It is suggested that in clinical practice, the essential characteristics of COPD patients should be clarified by collecting a variety of information in order to provide personalized treatment for patients' assessment, therapy and rehabilitation. At the same time, more basic and clinical research on COPD should be conducted, based on the nature of the disease, to explore new treatment methods.

microRNA-182 inhibits the proliferation and migration of glioma cells through the induction of neuritin expression.

Astrocytomas are the most common type of glial tumors and carry a poor prognosis. However, the pathogenesis of astrocytomas remains to be elucidated. Neuritin, a novel member of the neurotrophic factors family, has been shown to be associated with tumor malignancy, via the regulation of apoptosis and proliferation. In the present study, microRNA-182 (miR-182) was cloned and transfected into the U251 human astrocytoma cell line, in order to investigate its regulatory effects on the proliferation and migration of these cells, as well as its association with the expression of neuritin. The results showed that miR-182 specifically targets the gene encoding neuritin, NRN1, as demonstrated by a reduction in the protein and mRNA levels of NRN1. In addition, overexpression of miR-182 affected cell cycle regulation and cell migration capacity in vitro, which may have been associated with the promotion of apoptosis by this molecule. In conclusion, endogenous miR-182 may be involved in the pathogenesis of astrocytoma, which is associated with the miR-182-regulated gene, NRN1.