急性肺损伤/急性呼吸窘迫综合征（ALI/ARDS）是指心源性以外的各种肺内外致病因素导致的原发或继发的急性、进行性呼吸衰竭，其病理改变主要表现为肺上皮及内皮细胞的损伤、炎性浸润和透明膜形成，并伴有肺间质纤维化。临床表现为以呼吸窘迫、顽固性低氧血症和非心源性肺水肿为特征的一种急性进行性呼吸困难。采用常规的治疗难以纠正其低氧血症，死亡率高达60%，严重威胁人们的生命健康[1]。自1967年Ashbaugh及其同事首次描述ALI/ARDS以来，医学研究者进行了大量关于ALI/ARDS发病机制及病理生理学的基础及临床研究，但是迄今ALI/ARDS的发病机理仍未完全阐明。近年来越来越多的研究提示凋亡因子（Fas/Fas配体，即Fas/FasL）介导的细胞凋亡在ALI/ARDS的发生发展过程中有着十分重要的作用[2，3]。本文就Fas/FasL的生物学特性及其在ALI/ARDS发病机制中的作用作一综述。
ObjectiveTo review the research progress of pathogenesis mechanism of spinal deformity in neurofibromatosis type 1 (NF1). MethodsRecent literature concerning the pathogenesis mechanism of spinal deformity in NF1 was extensively reviewed, and current developments of the correction of spinal deformity and NF1 and the pathogenesis mechanism were summarized. ResultsThe pathogenesis mechanism of spinal deformity in NF1 is not yet clearly known. Current theories include erosion and stress of neurofibromas, melatonin-related decreased contractility of paraspinal muscles, osteopenia and osteoporosis, sexual precocity and mesoderm dysplasia. ConclusionThe clinical manifestations of NF1 may cause the spinal deformities in patients with NF1. The research of pathogenesis mechanism of spinal deformity in NF1 will be conducive to further understanding, diagnosis and treatment of NF1-related spinal deformity.
Objective To summarize the bioactive substances contained in bacterial extracellular vesicles (EVs) and their mechanisms in mediating bacterial-bacterial and bacterial-host interactions, as well as their mechanisms for use in implant infection-associated clinical guidance. Methods A wide range of publications on bacterial-derived EVs were extensively reviewed, analyzed, and summarized. Results Both gram-negative bacteria (G– bacteria) and gram-positive bacteria (G+ bacteria) can secrete EVs which contain a variety of bioactive substances, including proteins, lipids, nucleic acids, and virulence factors, and mediate bacterial-bacterial and bacterial-host interactions. EVs play an important role in the pathogenic mechanism of bacteria. Conclusion Bioactive substances contained within bacteria-derived EVs play an important role in the pathogenesis of bacterial infectious diseases. In-depth study and understanding of their pathogenic mechanisms can provide new insights which will improve early clinical diagnosis, prevention, and treatment of implant-associated infection. However, at present, research in this area is still in its infancy, and many more in-depth mechanisms need to be further studied.
Seawater drowning leads to acute lung tissue structure injury, lung ventilation and air exchange dysfunction, acute pulmonary edema, and even acute respiratory failure. The pathogenesis of seawater induced acute lung injury is complex, involving inflammatory response, pulmonary edema, pulmonary surfactant, oxidative stress, apoptosis and autophagy. Timely and effective treatment is the key to reduce the mortality and disability rate of patients with seawater induced acute lung injury. This article summarizes the research progress in the pathogenic mechanism and treatment strategy of seawater induced acute lung injury, aiming to provide reference for the comprehensive treatment of seawater induced acute lung injury patients in clinical work and subsequent related research.