Cardiovascular disease is the leading cause of mortality worldwide. Atherosclerosis constitutes most cardiovascular disease etiologies. Atherosclerosis is a chronic inflammatory and lipid-driven disease affecting the intima of blood vessels, resulting in an increase in its thickness and, therefore, narrowing of the arterial lumen. Many blood and immune cells have been shown to be implicated in atherosclerosis pathophysiology. Neutrophils are among those cells with their novel function of forming neutrophil extracellular traps. Neutrophil extracellular traps are mesh-like structures formed and released on activation of neutrophils. These structures consist of decondensed chromatin, histones, and other components, including nuclear and cellular proteins, cytoskeleton, proteases, and azurophilic granules. Neutrophil extracellular traps contain these elements and hold other circulating elements in the blood, such as tissue factor, fibrin, and other coagulation factors. Neutrophil extracellular traps are also implicated in the pathogenesis of atherothrombosis, which evolves as a consequence of atherosclerosis. In this review, we aim to demonstrate the process of neutrophil extracellular traps formation, release, and interaction with other blood cells, meaning it could be possible to use neutrophil extracellular traps as a therapeutic target in deceleration of atherosclerosis progression. Impact statement Fatal consequences of atherosclerosis and atherothrombosis give research in this field great importance. This review provides recent information about the implications of neutrophils in the pathophysiology of atherosclerosis and atherothrombosis via formation and release of neutrophil extracellular traps (NETs), thereby enhancing our understanding on how the process of atherosclerosis develops and how its consequences occur. Information provided in this review suggests NETs as a new therapeutic target and a rich point for research. This review gives answers to questions about the mechanisms of atherosclerosis and atherothrombosis progression through studying the implications of NETs in these processes.
Background and Importance: Brown-Sequard Syndrome (BSS) is a rare neurological condition resulting from a hemisection injury to or unilateral compression on the spinal cord. The common causes of BSS that are amenable to be treated surgically can be divided into traumatic and non-traumatic injuries. Traumatic injuries are often reported as the main cause of BSS. However, non-traumatic injuries of the spinal cord are more seen in recent years. This study aims to classify and update surgically treatable causes of BSS. Case Presentation: Retrospective data of 17 patients operated for BSS between 2008 and 2020 were included. The long-term outcomes of these patients were evaluated. In addition, a comprehensive search in PubMed, Scopus, and CINAHL was conducted for the retrieval of all relevant studies. Results: Magnetic Resonance Image (MRI) of our patients revealed Cervical Disc Herniation (CDH), spinal canal stenosis with cervical spondylosis, epidural hematoma, and ossification of the posterior longitudinal ligament. The postoperative outcomes of our cases ranged from partial to complete recovery. While the patients with acute epidural hemorrhage achieved complete recovery after surgery, neurological deficits in the other patients, especially those with severe cervical spinal canal stenosis, persisted despite adequate surgical decompression. The systematic literature review revealed that CDH is the most common non-traumatic surgically treatable cause of BSS, followed by spinal cord herniation and spinal epidural hematoma. Conclusion: Non-traumatic injuries of the spinal cord accompanied by narrowed cervical spinal canal pathologies are prominent surgically treatable causes of BSS. Contrary to the definition made 100 years ago, BSS can occur spontaneously due to underlying pathologies rather than major traumatic injuries.
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