Millions of microorganisms make up the complex microbial ecosystem found in the human gut. The immune system’s interaction with the gut microbiota is essential for preventing inflammation and maintaining intestinal homeostasis. Numerous metabolic products that can cross-talk between immune cells and the gut epithelium are metabolized by the gut microbiota. Traumatic injury elicits a great and multifaceted immune response in the minutes after the initial offense, containing simultaneous pro- and anti-inflammatory responses. The development of innovative therapies that improve patient outcomes depends on the gut microbiota and immunological responses to trauma. The altered makeup of gut microbes, or gut dysbiosis, can also dysregulate immunological responses, resulting in inflammation. Major human diseases may become more common as a result of chronic dysbiosis and the translocation of bacteria and the products of their metabolism beyond the mucosal barrier. In this review, we briefly summarize the interactions between the gut microbiota and the immune system and human disease and their therapeutic probiotic formulations. We also discuss the immune response to traumatic injury.

Since cyclic guanosine monophosphate‐adenosine monophosphate synthase (cGAS)–stimulator of interferon genes (STING) signaling pathway was discovered in 2013, great progress has been made to elucidate the origin, function, and regulating mechanism of cGAS–STING signaling pathway in the past decade. Meanwhile, the triggering and transduction mechanisms have been continuously illuminated. cGAS–STING plays a key role in human diseases, particularly DNA‐triggered inflammatory diseases, making it a potentially effective therapeutic target for inflammation‐related diseases. Here, we aim to summarize the ancient origin of the cGAS–STING defense mechanism, as well as the triggers, transduction, and regulating mechanisms of the cGAS–STING. We will also focus on the important roles of cGAS–STING signal under pathological conditions, such as infections, cancers, autoimmune diseases, neurological diseases, and visceral inflammations, and review the progress in drug development targeting cGAS–STING signaling pathway. The main directions and potential obstacles in the regulating mechanism research and therapeutic drug development of the cGAS–STING signaling pathway for inflammatory diseases and cancers will be discussed. These research advancements expand our understanding of cGAS–STING, provide a theoretical basis for further exploration of the roles of cGAS–STING in diseases, and open up new strategies for targeting cGAS–STING as a promising therapeutic intervention in multiple diseases.

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Background: Virtual reality (VR) technology has emerged as a promising tool for cognitive rehabilitation in patients with neuropsychiatric disorders. These patients often endure significant cognitive impairments, which are associated with decreased quality of life and increased disease burden. Traditional treatments are limited in improving cognitive functions, making VR-based interventions an area of growing interest. Objective: This meta-analysis aims to evaluate the efficacy of VR-based interventions on cognitive function in patients with neuropsychiatric disorders by synthesizing data from randomized controlled trials (RCTs). Methods: Following PRISMA guidelines, we conducted a comprehensive search across PubMed, Web of Science, MEDLINE, EMBASE, and Cochrane Library for RCTs from January 2010 to December 2024. Studies were included if they evaluated the impact of VR-based interventions on cognitive outcomes in patients with neuropsychiatric disorders. Data extraction and risk of bias assessment were performed independently by 2 researchers. Meta-analyses were conducted using random-effects models, and standardized mean differences (SMDs) as effect size. Results: A total of 21 RCTs involving 1051 participants were included. Overall, VR-based interventions significantly improved cognitive functions of patients with neuropsychiatric disorders (SMD 0.67, 95% CI 0.33-1.01, z=3.85; P<.001). Subgroup analyses revealed significant benefits for cognitive rehabilitation training (SMD 0.75, 95% CI 0.33-1.17, z=3.53; P<.001), exergame-based training (SMD 1.09, 95% CI 0.26-1.91, z=2.57; P=.01), and telerehabilitation and social functioning training (SMD 2.21, 95% CI 1.11-3.32, z=3.92; P<.001). Conversely, immersive cognitive training, music attention training, and vocational and problem-solving skills training did not yield significant improvements (z=1.86, P=.06; z=0.35, P=.72; z=0.88, P=.38; respectively). Disease-type subgroup analyses indicated significant improvements in schizophrenia (SMD 0.92, 95% CI 0.22-1.62, z=2.58; P=.01), and mild cognitive impairment (SMD 0.75, 95% CI 0.16-1.35, z=2.47; P=.01), but not in brain injuries, Parkinson disease, or stroke (z=0.34, P=.73; z=1.26, P=.21; z=1.16, P=.24; respectively). Conclusions: This meta-analysis revealed that VR-based interventions can improve cognitive functions among individuals with neuropsychiatric disorders, with notable improvements observed in cognitive rehabilitation training, exergame-based training, and tele-rehabilitation and social functioning training. These results offer valuable evidence supporting the use of VR technology in rehabilitation for neuropsychiatric conditions and inform the optimization of future intervention approaches.

High-altitude polycythemia (HAPC) is a common chronic altitude disease caused by living in low-pressure and low-oxygen environment. At present, there is still no effective cure for HAPC. HIF-2α may play an important role in the development of HAPC in regulating the increased red blood cell excessively induced by HIF-EPO and the blood vessel formation induced by VEGF-VEGFR. Here, we established a rat HAPC model and treated it with the HIF-2α inhibitor PT2385. We mainly evaluated the therapeutic effect of PT2385 on HAPC rats by observing the changes in rat phenotype, tissue and organ damage, red blood cell and hemoglobin content, angiogenesis, lipid peroxidation reaction, and inflammatory factors. The results showed that PT2385 treatment improved the congestion phenotype characteristics, inhibited increased erythrocytes and hemoglobin, reduced blood vessel formation, lipid peroxidation, and inflammation, and reduced tissue and organ damage in HAPC rats. This study preliminarly explains the physiological, pathological, and immunological effects of PT2385 treatment for HAPC. It provides a new idea, a reliable experimental basis, and theoretical support for the clinical prevention and treatment of HAPC.

随着我国居民生活方式和疾病谱发生变化，全生命周期健康已被提升至国家战略高度。近十年来，全球护理研究者已逐渐开始关注人体各生命周期中精准护理的相关研究，应用多组学探索肿瘤患者或慢病患者等相应症状的发生机制和新型生物标志物，以期更精准地进行症状管理，但目前尚未形成全生命周期健康与疾病的精准护理学的系统理论，科学研究领域和内涵仍需不断的拓展和创新。护理学科应充分发挥多学科交叉融合优势，以精准有效地解决全生命周期的健康问题为目标，通过对可量化的护理关键客观指标进行精准界定，对全生命周期健康问题的早期识别，厘清全生命周期健康问题的发生与变化规律，并探明调控机制；研发精准有效的非药物、非手术的护理相关技术与产品，以实现更为精准的护理干预，从而有效促进疾病康复，提升健康水平。