神经重症患者常面临急性脑损伤、颅内压升高及脑血流障碍等复杂病理生理问题,这些问题需要精准的监测手段以支持诊断和干预。传统神经监测方法以临床检查为主,但发现的变化往往是晚期体征,不足以发现和预防继发性脑损伤。近年来,多模态脑监测(MMM)技术的发展为神经重症监测提供了新的可能。MMM涵盖脑组织氧监测、脑血流监测、颅内压监测、脑电监测及脑代谢监测等多种手段,从多维度动态评估脑功能和病理状态。本文详细探讨了上述监测方法的原理、技术特点、临床应用及其在神经重症管理中的优势与局限性。没有一种单一的监测手段是适合所有患者,MMM是当前的趋势。随着该技术的进一步推广和应用,可为神经重症患者提供更为及时和个性化的治疗。Patients with severe neurological diseases in the neuroscience intensive care unit often face complex pathophysiological problems such as acute brain injury, increased intracranial pressure, and cerebral blood flow obstruction, which require precise monitoring techniques to support diagnosis and intervention. Traditional neurological monitoring methods are mainly based on clinical examination, but changes found during the examination are often late signs and insufficient to detect and prevent secondary brain injury. In recent years, the development of multimodal brain monitoring (MMM) technology has provided new possibilities for neurocritical care monitoring. MMM covers oxygen monitoring of brain tissue, cerebral blood flow monitoring, intracranial pressure monitoring, electroencephalography (EEG) monitoring, and cerebral metabolism monitoring, which evaluate brain function and pathological states from multiple dimensions and in a dynamic manner. This article discusses the principles, technical features, clinical applications, and advantages and limitations of the monitoring methods in detail. No single monitoring method is suitable for all patients, and MMM is the current trend. With the further promotion and application of this technology, it can provide more timely and personalized treatment for neurosurgical intensive care patients.
目的分析糖尿病患者低血糖恐惧感的影响因素,并结合影响因素结果讨论聚焦解决干预模式的方法。方法选取2023年1—12月福州市第二总医院收治的120例出现低血糖的糖尿病患者,应用中文版低血糖恐惧感调查-忧虑量表(Chinese Version Hypogly...
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目的分析糖尿病患者低血糖恐惧感的影响因素,并结合影响因素结果讨论聚焦解决干预模式的方法。方法选取2023年1—12月福州市第二总医院收治的120例出现低血糖的糖尿病患者,应用中文版低血糖恐惧感调查-忧虑量表(Chinese Version Hypoglycemia Fear SurveyⅡ-Worry Scale,CHFSⅡ-WS)评估,分析糖尿病患者低血糖恐惧感影响因素。结果经单因素分析发现,不同糖尿病患者年龄、糖尿病病程、半年内低血糖发生次数、低血糖严重程度、自我管理能力的糖尿病患者的CHFSⅡ-WS评分比较,差异均有统计学意义(P均<0.05)。多元线性回归分析结果显示:年龄>60岁、糖尿病病程≥10年、半年内低血糖发生>6次、重度低血糖是低血糖恐惧感的危险因素,糖尿病自我管理行为量表评估结果好为低血糖恐惧感的保护因素(P均<0.05)。结论年龄、糖尿病病程、半年内低血糖发生次数、低血糖严重程度、自我管理能力是糖尿病患者低血糖恐惧的影响因素,针对存在危险因素的糖尿病患者采取聚焦解决干预模式,以降低患者低血糖恐惧感。
特发性肺纤维化(IPF)是一种进行性且最终致命的纤维化肺病,可以导致进行性的肺功能下降,其发展被认为与遗传、环境、免疫、炎症、自噬、衰老等因素有关。TRIM蛋白是一个高度保守的E3泛素连接酶家族,参与多个过程:包括细胞内信号传导、发育、细胞凋亡、蛋白质质量控制、先天免疫、自噬和致癌作用,近年来,有关TRIM蛋白在疾病中的研究越来越多,研究表明它们可以参与细胞内信号传导、发育、细胞凋亡、蛋白质质量控制、先天免疫、自噬和致癌等多个过程,它们的失调会导致癌症、免疫疾病或发育障碍等疾病,参考肺纤维化所涉及的发生发展机制,TRIM蛋白在各器官纤维化中的研究也逐渐展开,本文将主要论述TRIM蛋白在肺纤维化中的研究进展。Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal fibrotic lung disease that can lead to progressive decline in lung function, and its development is thought to be related to genetic, environmental, immune, inflammatory, autophagy, aging and other factors. TRIM proteins are a highly conserved family of E3 ubiquitin ligases involved in several processes: It includes intracellular signaling, development, apoptosis, protein quality control, innate immunity, autophagy and carcinogenesis. In recent years, more and more studies on TRIM proteins in diseases have shown that they can participate in many processes such as intracellular signaling, development, apoptosis, protein quality control, innate immunity, autophagy and carcinogenesis. Their disorders can lead to cancer, immune diseases or developmental disorders and other diseases, referring to the occurrence and development mechanism involved in pulmonary fibrosis, the study of TRIM protein in various organ fibrosis is also gradually launched, this paper will mainly discuss the research progress of TRIM protein in pulmonary fibrosis.
特发性肺纤维化(IPF)是一种不明原因导致的慢性、进行性、间质性肺部疾病,以弥漫性肺泡炎和肺泡结构紊乱并最终导致肺间质纤维化为主要特征。IPF预后普遍较差,诊断后的中位生存时间仅为3~5年,约5%~20%的患者病程中可出现急性加重,急性加重后中位生存时间相较之前将进一步减少。目前现有的治疗手段无法彻底治愈IPF,治疗目的主要为延缓疾病进展。本文旨在对现有IPF的致病机制进行回顾与总结,以期为寻找合适的治疗靶点及新的治疗途径提供新的思路。Idiopathic pulmonary fibrosis (IPF) is an unexplained, chronic, progressive, interstitial lung disease characterized by diffuse alveolitis and alveolar structural disturbances that eventually lead to interstitial fibrosis. The prognosis of IPF is generally poor, with a median survival time of 3~5 years after diagnosis, with acute exacerbations occurring in about 5%~20% of patients. After acute exacerbation, the median survival time will be further reduced compared with the previous one. Currently available treatments do not provide a complete cure for IPF, and the main goal of treatment is to slow down the progression of the disease. The aim of this paper is to review and summarize the existing pathogenic mechanisms of IPF, with a view to providing new ideas for finding suitable therapeutic targets and new therapeutic pathways.
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