聚焦超声治疗老年变应性鼻炎的疗效

老年人生理功能逐渐下降,特别是免疫系统的老化现象尤为明显,机体对外来特异性抗原的免疫应答能力下降,变应性鼻炎(AR)发病率较其他年龄段少[1].患AR的老年人多同时伴有全身其他疾患,治疗方案选择复杂.本文对难治性老年AR的治疗方案进行了初步研究.     

老人肺

老人肺是指呼吸系的生理性老化,但肺部是与外界接触的器官,因此,老人肺很难排除大气污染、吸烟等环境及病理性因素的影响。本文综述了老年人随增龄出现的肺部形态学、生理学、生化学改变,老人肺的临床及X线特点,以及提出阻抑老人肺功能早衰的几点建议。     

老年人重症肺部感染临床分析

老年人随着年龄增长，因其免疫功能减退、呼吸系统老化、肺功能减退等诸多因素．常伴有原发或基础疾病存在，极易患肺部感染。现对我科2001年至今收治住院的老年人重症肺感染200例的临床特点进行分析。     

老人肺

老人肺是指呼吸系的生理性老化，但肺部是与外界接触的器官，老肺很难除大气污染，吸烟等环境及病性因素的影响。本综述了老年人随增龄出现的肺部形态学、生理学、生化学改变、老人肺的临床及Ｘ线特点，以及提出阻抑老人功能早衰的几点建议。     

老年肺与吸烟肺的影像学研究进展

随着人口老龄化进程和生活环境空气污染,老年性肺部疾患明显增加,国内外有关肺老化影像学研究也越来越多,但某些早期病变与肺老化没有明显界限,甚至与肺老化过程同时存在,难以区分与鉴别;吸烟也是引起多种呼吸系统疾病的重要原因,而且与肺老化的影像学表现有不少相似之处,故本文就老年肺与吸烟肺的影像学研究进展进行阐述。1机制与病理基础国外学者Verbeken等[1]在20世纪90年代初开始提出了老年肺(senilelung)的组织病理学概念,认为老年肺表现为肺泡腔均匀扩大,而肺泡壁完整,其腔壁也随年龄增长逐渐均匀增厚,最终可引起老年     

老年肺部感染问题浅议

老年肺部感染在老年人感染性疾患中最常见，它是老年人重要的死亡原因之一。由于老年人多伴有基础疾患，呼吸道防御机制和免疫功能减退，所以容易发生肺部感染．临床症状多不明显，X线征象也多不典型，因而老年人肺部感染常被漏诊和误诊。     

肺内前列腺素的动力学

在肺的血流调节支气管平滑肌的舒缩以及肺部炎症或变态反应等的发生机制中都有化学介质的参与。近年来认识到肺除了进行气体交换,它还是一个重要的化学介质的合成和代谢器官。所以探讨化学介质在肺内的合成、代谢和与肺部疾患的关系,将对肺部疾患的诊治有很大的帮助。由于肺是化学介质前列腺素生物合成、释放和灭话的主要场所,亦是人体中含前列腺素浓度很高的组织之一,前列腺素代谢异常与肺部疾患的关系逐渐引起重视。本文     

老年人肺部疾病的介入治疗

一、前言 老年人肺部疾病的介入治疗,是指应用支气管动脉的栓塞及灌注药物来治疗某些老年人的肺部疾患.     

肺叶切除术后并发症的防治

肺叶切除主要用以处理原发性肺癌、转移性肺肿瘤和良性肺部疾患(赘生物、炎症、肉芽肿、先天性疾病、退行病变、肺囊肿和诊断不明的肺部疾患),亦偶尔用以治疗肺部损伤,无年龄限制。肺叶切除的范围包括所有肺部病变组     

老年人多器官衰竭的肺启动机制及防治策略研究

老年人多器官衰竭(MOFE)肺启动学说是MOFE的预防和治疗的一个切入点.MOFE的发生与非老年人的多器官衰竭(MOF)不同,老年人由于器官老化功能减退,常合并基础疾病,且免疫低下,常以肺部感染、心血管疾病诱发 MOFE;中青年人多半无明显基础疾病,器官功能和免疫功能也多正常,常以创伤、大手术和败血症等诱发MOF.     

端粒与衰老及特发性肺纤维化的相关性研究

随着老龄化社会的到来,与衰老相关慢性病的发病率呈增长趋势,衰老性疾病已引起国内外多学者的广泛关注。特发性肺纤维化是一种细胞复制性衰老疾病,易受年龄的影响。端粒、端粒酶已被证实为导致衰老的重要机制之一,其在肺部衰老和疾病的发生、发展过程中起着重要作用。进一步研究了解端粒与衰老及特发性肺纤维化的关系,将有助于临床治疗方案的选择,为提高疾病转归提供理论依据。     

Cellular senescence in normal and premature lung aging

The incidence of chronic respiratory diseases (e.g., chronic obstructive pulmonary disease, COPD) and interstitial lung diseases (e.g., pneumonia and lung fibrosis) increases with age. In addition to immune senescence, the accumulation of senescent cells directly in lung tissue might play a critical role in the increased prevalence of these pulmonary diseases. In the last couple of years, detailed studies have identified the presence of senescent cells in the aging lung and in diseased lungs of patients with COPD and lung fibrosis. Cellular senescence has been shown for epithelial cells of bronchi and alveoli as well as mesenchymal and vascular cells. Known risk factors for pulmonary diseases (cigarette smoke, air pollutions, bacterial infections, etc.) were identified in experimental studies as being possible mediators in the development of cellular senescence. The present findings indicate the importance of cellular senescence in normal lung aging and in premature aging of the lung in patients with COPD, lung fibrosis, and probably other respiratory diseases.     

慢性阻塞性肺疾病与心血管疾病相关性研究进展

众所周知,慢性阻塞性肺疾病是一种常伴随有显著肺外表现的慢性炎症性疾病,心血管疾病风险增加即此类肺外表现之一。慢性阻塞性肺疾病与心血管疾病之间相关机制复杂,吸烟、衰老、缺氧、全身性炎症、氧化应激及用药等多种因素均可能参与其中。现就其潜在关联机制的研究现状予以综述。     

Aging and interstitial lung diseases: unraveling an old forgotten player in the pathogenesis of lung fibrosis

Aging is a natural process characterized by a progressive functional impairment and reduced capacity to respond adaptively to environmental stimuli. Aging is associated with increased susceptibility to a variety of chronic diseases, including type 2 diabetes mellitus, cancer, and neurological diseases. Lung pathologies are not the exception, and the prevalence of several interstitial lung diseases (ILDs), primarily idiopathic pulmonary fibrosis, has been found to increase considerably with age. Although our understanding of the biology of aging has advanced remarkably in the last 2 decades, the molecular mechanisms linking aging to ILD remain unclear. Immunosenescence, oxidative stress, abnormal shortening of telomeres, apoptosis, and epigenetic changes affecting gene expression have been proposed to contribute to the aging process, and aging-associated diseases. Here, we review the emerging concepts highlighting the putative aging-associated abnormalities involved in some human ILDs.     

Klotho及其基因多态性与衰老相关性疾病关系研究进展

Klotho基因是一种与寿命和衰老表型（如动脉硬化、骨质疏松、肺气肿等）相关的基因,该基因缺陷的小鼠会出现与人类衰老相似的临床表型。随着增龄,与衰老相关性疾病也日益增多,成为影响人类健康长寿的重要因素,为此本文从分子遗传学角度上就klotho基因及其多态性与衰老相关性疾病的关系研究进展做综合分析,以寻求该基因在衰老相关性疾病的发生和发展中所起作用的线索。     

Molecular composition of the alveolar lining fluid in the aging lung

As we age, there is an increased risk for the development of pulmonary diseases, including infections, but few studies have considered changes in lung surfactant and components of the innate immune system as contributing factors to the increased susceptibility of the elderly to succumb to infections. We and others have demonstrated that human alveolar lining fluid (ALF) components, such as surfactant protein (SP)-A, SP-D, complement protein C3, and alveolar hydrolases, play a significant innate immune role in controlling microbial infections. However, there is a lack of information regarding the effect of increasing age on the level and function of ALF components in the lung. Here we addressed this gap in knowledge by determining the levels of ALF components in the aging lung that are important in controlling infection. Our findings demonstrate that pro-inflammatory cytokines, surfactant proteins and lipids, and complement components are significantly altered in the aged lung in both mice and humans. Further, we show that the aging lung is a relatively oxidized environment. Our study provides new information on how the pulmonary environment in old age can potentially modify mucosal immune responses, thereby impacting pulmonary infections and other pulmonary diseases in the elderly population.     

The rehabilitation potential of geriatric patients from the cardiologic viewpoint

The potential of rehabilitation for geriatric patients depends on physiological considerations about the aging organism, as well as diseases, accompanied by the natural aging process. A common feature of the aging process of human organs is a general loss of adaptability that contributes to hypocirculation. The potential for rehabilitation may be considerably limited by diseases which burden the circulatory system (atherosclerosis, coronary heart disease, hypertension, and hypotension). Cardiac arrhythmias occurring during rehabilitation procedures call for special care. Mode and intensity of the rehabilitation program will be determined by cardiac and circulatory reactions following active rehabilitation procedures. Isometric exercise stress in conjunction with pressure breathing leads to an excessive rise of blood pressure in systemic and pulmonary circulation. Therefore dynamic muscle actions should be preferred as the most reasonable active training, but there is the possibility of heart-circulation problems arising, depending on the intensity of training.     

Mitochondrial disease: a pulmonary and critical-care medicine perspective

The clinical spectrum of mitochondrial diseases has expanded dramatically in the last decade. Abnormalities of mitochondrial function are now thought to participate in a number of common adult diseases, ranging from exercise intolerance to aging. This review outlines the common presentations of mitochondrial disease in ICUs and in the outpatient setting and discusses current diagnostic and therapeutic options as they pertain to the pulmonary and critical-care physician.     

Aging of the lung: Pulmonary disease in the elderly

Anatomical and physiologic evidence for pulmonary problems most prevalent in the aged is reviewed. The lungs begin to age in utero. True aging must be distinguished from chronic environmental damage. The lung is essentially an “outdoor organ” vulnerable to the environment. Biochemically, aging is caused by both endogenous and exogenous free radical injury, inflicted by an over-balance of oxidants with respect to anti-oxidants. Glucose may also play a role in the aging process, by binding non-enzymatically with proteins in lung to form irreversible advanced glycosylation end-products. Physiological age-related lung changes result in: decreasing lung volumes and maximal rates of airflow; decreasing forced vital capacity (accelerated in smokers); hyperinflation (confirmed by the increased RV/TLC ratio); increased closing volume or capacity; decreased diffusing capacity; and hyporesponsive respiratory center and peripheral chemoreceptors. The clinical consequence of these age-related changes in the lung is disease in the elderly. Lung cancer and emphysema also occur as a result of chronic exposure to cigarette smoke and other environmental pollutants. Age-dependent pulmonary changes combine with non-pulmonary age-prevalent changes to cause additional diseases. Bacterial pneumonias, aspiration pneumonia, tuberculosis, and pulmonary thromboembolism are examples of these.     

Abnormal lung aging in chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis

Aging is a natural process characterized by progressive functional impairment and reduced capacity to respond appropriately to environmental stimuli and injury. The incidence of two common chronic respiratory diseases (chronic obstructive pulmonary disease [COPD] and idiopathic pulmonary fibrosis [IPF]) increases with advanced age. It is plausible, therefore, that abnormal regulation of the mechanisms of normal aging may contribute to the pathobiology of both COPD and IPF. This review discusses the available evidence supporting a number of aging mechanisms, including oxidative stress, telomere length regulation, cellular and immunosenescence, as well as changes in a number of antiaging molecules and the extracellular matrix, which are abnormal in COPD and/or IPF. A better understanding of these abnormalities may help in the design of novel and better therapeutic interventions for these patients.