Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to characterize, and determine the significance of, pulmonary activity on labelled leukocyte images. This retrospective review included 137 immunocompetent patients who had undergone 111In labelled autologous leukocyte chest imaging and chest X-ray within 7 days. Pulmonary activity was classified as normal, focally increased, or diffusely increased. Images were correlated with chest X-rays and final diagnoses. One hundred and twelve patients (82%) had normal pulmonary activity. Seventy-six had normal chest X-rays; none had pulmonary infection. Thirty-six patients had chest X-ray abnormalities; only one had pulmonary infection. Twenty-five patients had abnormal pulmonary activity. In 13 patients it was segmental or lobar in distribution. The chest X-ray was abnormal in 12: pneumonia (11) and cystic fibrosis (one). The chest X-ray was normal in one patient with pneumonia. Two patients with non-segmental pulmonary activity did not have pulmonary infection. The chest X-ray was abnormal in one (pulmonary edema) and normal in one (sepsis). Ten patients had diffuse pulmonary activity. Chest X-ray was abnormal in two patients: adult respiratory distress syndrome (ARDS) (one) and drug toxicity (one). No patient with diffuse pulmonary activity had pulmonary infection. In summary, negative labelled leukocyte imaging excludes pulmonary infection with a high degree of certainty (the negative predictive value was 99% in this series), and can exclude pneumonia as the cause of a chest X-ray abnormality. Focal pulmonary activity strongly suggests pneumonia, while diffuse pulmonary activity is unlikely to indicate infection.
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PMID:Pulmonary activity on labelled leukocyte images: patterns of uptake and their significance. 1202 11

We evaluated the safety of agents that enhance gene transfer by modulating paracellular permeability. Lactate dehydrogenase (LDH) and cytokine release were measured in polarized primary human airway epithelial (HAE) cells after lumenal application of vehicle, ethyleneglycol-bis-(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA), sodium caprate (C10), or sodium laurate (C12). Lung toxicity was assessed after tracheobronchial instillation to murine airways and the relative ability of these agents to enhance in vivo adenoviral gene transfer was evaluated. Lumenal C12 increased LDH release in vitro, but C10 and EGTA did not. Increased levels of interleukin 8 (IL-8) were secreted from EGTA-pretreated cystic fibrosis HAE cells after apical application of Pseudomonas aeruginosa (10(8) CFU/ml), whereas IL-8 secretion from C10- and C12-pretreated cells was not different from controls. In vivo toxicity studies demonstrated no effect of EGTA, C10, or C12 on weight gain, lung edema, or bronchoalveolar lavage fluid (BALF) albumin. EGTA increased BALF cell counts, neutrophils, and murine (m) macrophage inflammatory protein 2, mKC, mIL-6, and mIL-1 beta levels. C10 had no effect on BALF cell counts or LDH, but increased murine tumor necrosis factor alpha. C12 increased BALF LDH, neutrophils, and mIL-6 levels. Histopathological analysis revealed mild focal lung inflammation more frequently in the EGTA, C10, and C12 groups than in vehicle controls, with greater intensity in the C12 group relative to the other groups. C10 and C12 also increased airway responsiveness to methacholine challenge compared with control and EGTA groups. Adenoviral gene transfer to murine trachea in vivo was enhanced more efficiently by C10 than by C12 or EGTA. Thus, the different toxicities may permit the selection of agents that enhance gene transfer with minimal adverse effects.
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PMID:Safety and efficiency of modulating paracellular permeability to enhance airway epithelial gene transfer in vivo. 1280 37

Noninvasive ventilation (NIV), i.e. without tracheal intubation, has been reintroduced for the treatment of respiratory failure to reduce the complications of mechanical ventilation. Nowadays, NIV with positive pressure is the preferred method, applied through a mask held in place by a harness. Several masks can be used (nasal, bucconasal facial) and a variety of means can be used to keep them in place. Many respirators can be selected, ranging from those traditionally used in the intensive care unit(ICU) to specific NV respirators and conventional ICU respirators with specific software for NIV. Many respiratory modalities can be used according to the respirator (biphasic positive airway pressure [BIPAP], proportional assist ventilation, pressure support, synchronized intermittent mandatory ventilation [SIMV], etc.). NIV is mainly indicated in exacerbations of chronic respiratory failure: neuromuscular diseases, pretransplantation cystic fibrosis, and obstructive sleep apnea syndrome. It is also indicated in acute respiratory failure: pneumonia, status asthmaticus, and acute lung edema. The main contraindications are a weakened airway protection reflex(absent cough reflex) and hemodynamic instabiity. The advantages of NIV derive mainly from avoiding the complications associated with invasive ventilation. NIV also presents some disadvantages, especially the greater workload involved to ensure good patient adaptation to the respirator. The most common sequelae of NIV are skin lesions due to pressure on the nasal bridge.
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PMID:[Mechanical ventilation in pediatrics (III). Weaning, complications and other types of ventilation. Noninvasive ventilation]. 1456 42

Ion transport is essential for maintenance of transmembranous and transcellular electric potential, fluid transport and cellular volume. Disturbance of ion transport has been associated with cellular dysfunction, intra and extracellular edema and abnormalities of epithelial surface liquid volume. There is increasing evidence that conditions characterized by an intense local or systemic inflammatory response are associated with abnormal ion transport. This abnormal ion transport has been involved in the pathogenesis of conditions like hypovolemia due to fluid losses, hyponatremia and hypokalemia in diarrhoeal diseases, electrolyte abnormalities in pyelonephritis of early infancy, septicemia induced pulmonary edema, and in hypersecretion and edema induced by inflammatory reactions of the mucosa of the upper respiratory tract. Components of membranous ion transport systems, which have been shown to undergo a change in function during an inflammatory response include the sodium potassium ATPase, the epithelial sodium channel, the Cystic Fibrosis Transmembrane Conductance Regulator and calcium activated chloride channels and the sodium potassium chloride co-transporter. Inflammatory mediators, which influence ion transport are tumor necrosis factor, gamma interferon, interleukins, transforming growth factor, leukotrienes and bradykinin. They trigger the release of specific messengers like prostaglandins, nitric oxide and histamine which alter ion transport system function through specific receptors, intracellular second messengers and protein kinases. This review summarizes data on in vivo measurements of changes in ion transport in acute inflammatory conditions and in vitro studies, which have explored the underlying mechanisms. Potential interventions directed at a correction of the observed abnormalities are discussed.
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PMID:Changes in ion transport in inflammatory disease. 1657 Nov 16

Amiloride-sensitive Na+ channels belong to the epithelial Na+ channel (ENaC)-degenerin superfamily of ion channels. In addition to their key role in sodium handling, they serve diverse functions in many tissues. Improper functioning of ENaC has been implicated in several diseases, including salt-sensitive hypertension (Liddle's syndrome), salt-wasting syndrome (pseudohypoaldosteronism type I), pulmonary edema, and cystic fibrosis. We have utilized planar lipid bilayers, a well-defined system that allows simultaneous control of "internal" and "external" solutions, to study ENaCs.
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PMID:Epithelial sodium channel in planar lipid bilayers. 1692 41

The reported pluripotential capabilities of many human stem cell types has made them an attractive area of research, given the belief they may hold considerable therapeutic potential for treating a wide range of human diseases and injuries. Although the bulk of stem cell based research has focused on developing procedures for the treatment of pancreatic, neural, cardiovascular and haematopoietic diseases, the potential for deriving respiratory cell types from stem cells for treatment of respiratory specific diseases has also been explored. It is suggested that stem cell derivatives may be used for lung replacement/regeneration therapeutics and high though-put pharmacological screening strategies for a variety of respiratory injuries and diseases including: cystic fibrosis, chronic obstructive pulmonary disease, respiratory distress syndrome, pulmonary fibrosis and pulmonary edema. This review will explore recent progress in characterizing adult respiratory and bone marrow derived stem cells with respiratory potential as well as the endogenous mechanisms directing the homing of these cells to the diseased and injured lung. In addition, the potential for embryonic stem cell based therapies in this domain as well as the histological, anatomical and molecular aspects of respiratory development will be summarized.
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PMID:Deriving respiratory cell types from stem cells. 1822 Sep 3

Chronic obstructive lung diseases are characterized by the inability to prevent bacterial infection and a gradual loss of lung function caused by recurrent inflammatory responses. In the past decade, numerous studies have demonstrated the importance of nucleotide-mediated bacterial clearance. Their interaction with P2 receptors on airway epithelia provides a rapid 'on-and-off' signal stimulating mucus secretion, cilia beating activity and surface hydration. On the other hand, abnormally high ATP levels resulting from damaged epithelia and bacterial lysis may cause lung edema and exacerbate inflammatory responses. Airway ATP concentrations are regulated by ecto nucleoside triphosphate diphosphohydrolases (E-NTPDases) which are expressed on the mucosal surface and catalyze the sequential dephosphorylation of nucleoside triphosphates to nucleoside monophosphates (ATP --> ADP --> AMP). The common bacterial product, Pseudomonas aeruginosa lipopolysaccharide (LPS), induces an acute reduction in azide-sensitive E-NTPDase activities, followed by a sustained increase in activity as well as NTPDase 1 and NTPDase 3 expression. Accordingly, chronic lung diseases, including cystic fibrosis (CF) and primary ciliary dyskinesia, are characterized by higher rates of nucleotide elimination, azide-sensitive E-NTPDase activities and expression. This review integrates the biphasic regulation of airway E-NTPDases with the function of purine signaling in lung diseases. During acute insults, a transient reduction in E-NTPDase activities may be beneficial to stimulate ATP-mediated bacterial clearance. In chronic lung diseases, elevating E-NTPDase activities may represent an attempt to prevent P2 receptor desensitization and nucleotide-mediated lung damage.
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PMID:E-NTPDases in human airways: Regulation and relevance for chronic lung diseases. 1840 79

The epithelial Na(+) channel (ENaC) is a major regulator of salt and water reabsorption in a number of epithelial tissues. Abnormalities in ENaC function have been directly linked to several human disease states including Liddle's syndrome, psuedohypoaldosteronism, and cystic fibrosis and may be implicated in states as diverse as salt-sensitive hypertension, nephrosis, and pulmonary edema. ENaC activity in epithelial cells is highly regulated both by open probability and number of channels. Open probability is regulated by a number of factors, including proteolytic processing, while ENaC number is regulated by cellular trafficking. This review discusses current understanding of apical membrane delivery, cell surface stability, endocytosis, retrieval, and recycling of ENaC and the molecular partners that have so far been shown to participate in these processes. We review known sites and mechanisms of hormonal regulation of trafficking by aldosterone, vasopressin, and insulin. While many details of the regulation of ENaC trafficking remain to be elucidated, knowledge of these mechanisms may provide further insights into ENaC activity in normal and disease states.
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PMID:Regulation of the epithelial sodium channel by membrane trafficking. 1850 77

Stem/progenitor cells can be used to repair defects in the airway wall, resulting from e.g., tumors, trauma, tissue reactions following long-time intubations, or diseases that are associated with epithelial damage. Several potential sources of cells for airway epithelium have been identified. These can be divided into two groups. The first group consists of endogenous progenitor cells present in the respiratory tract. This group can be subdivided according to location into (a) a ductal cell type in the submucosal glands of the proximal trachea, (b) basal cells in the intercartilaginous zones of the lower trachea and bronchi, (c) variant Clara cells (Clara v-cells) in the bronchioles and (d) at the junctions between the bronchioles and the alveolar ducts, and (e) alveolar type II cells. This classification of progenitor cell niches is, however, controversial. The second group consists of exogenous stem cells derived from other tissues in the body. This second group can be subdivided into: (a) embryonic stem (ES) cells, induced pluripotent stem (iPS) cells, or amniotic fluid stem cells, (b) side-population cells from bone marrow or epithelial stem cells present in bone marrow or circulation and (c) fat-derived mesenchymal cells. Airway epithelial cells can be co-cultured in a system that includes a basal lamina equivalent, extracellular factors from mesenchymal fibroblasts, and in an air-liquid interface system. Recently, spheroid-based culture systems have been developed. Several clinical applications have been suggested: cystic fibrosis, acute respiratory distress syndrome, chronic obstructive lung disease, pulmonary fibrosis, pulmonary edema, and pulmonary hypertension. Clinical applications so far are few, but include subglottic stenosis, tracheomalacia, bronchiomalacia, and emphysema.
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PMID:Tissue engineering and the use of stem/progenitor cells for airway epithelium repair. 2057 96

Pulmonary fluid clearance is regulated by the active transport of Na(+) and Cl(-) through respiratory epithelial ion channels. Ion channel dysfunction contributes to the pathogenesis of various pulmonary fluid disorders including high-altitude pulmonary edema (HAPE) and neonatal respiratory distress syndrome (RDS). Nasal potential difference (NPD) measurement allows an in vivo investigation of the functionality of these channels. This technique has been used for the diagnosis of cystic fibrosis, the archetypal respiratory ion channel disorder, for over a quarter of a century. NPD measurements in HAPE and RDS suggest constitutive and acquired dysfunction of respiratory epithelial Na(+) channels. Acute lung injury (ALI) is characterized by pulmonary edema due to alveolar epithelial-interstitial-endothelial injury. NPD measurement may enable identification of critically ill ALI patients with a susceptible phenotype of dysfunctional respiratory Na(+) channels and allow targeted therapy toward Na(+) channel function.
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PMID:Nasal potential difference to detect Na+ channel dysfunction in acute lung injury. 2111 43


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