Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The involvement of melengestrol acetate (MGA) in susceptibility to developing pulmonary edema and emphysema following oral administration of 3-methylindole (3MI) was investigated using 10 Suffolk ewes receiving 0 or 0.15 mg of MGA daily (n = 5). Blood, urine and ruminal fluid were collected immediately prior to 3MI dosing (0.2 g/kg BW) and 1, 2, 3, 4, 5, 6, 12 and 24 h (blood); 3, 6, 9, 12 and 15 h (urine) and 1, 2, 3 and 12 h (ruminal fluid) afterward. Ewes receiving MGA experienced earlier (P < 0.05) onset of respiratory distress than the control ewes (2.5 vs 4 h), and upon euthanasia at 96 h, their lung weight relative to body weight tended (P < 0.10) to be lower. Ruminal 3MI concentrations did not differ between treatments (P > 0.05). Ewes receiving MGA had higher (P < 0.05) concentrations of 3MI metabolites in plasma prior to dosing than did control ewes, and these values tended to remain higher throughout the sampling period. Immunoreactivity assays indicated more pneumotoxin present in the lungs of MGA-treated ewes than controls. Lung damage was apparently more acute and accelerated in the MGA-treated ewes than in the controls. Urinary 3MI mercapturate concentrations differed (control > MGA-treated, P < 0.05) at 9, 12, and 15 h, but this difference was not apparent when urinary production (as estimated by creatinine concentration) was considered. The implications of these findings for MGA-treated feedlot heifers are currently under investigation.
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PMID:Effect of melengestrol acetate on development of 3-methylindole-induced pulmonary edema and emphysema in sheep. 979 92

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
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PMID:Lung disease at high altitude. 1063 92

A 15-year-old patient has been admitted to the intensive care unit for severe respiratory distress syndrome that developed as a result of pneumonia. Interstitial lung edema was confirmed by computer-aided tomography. It was successfully treated by positive pressure ventilation (PPV). Although PEEP did not exceed 7 cm H2O, PPV was complicated by interstitial emphysema, pneumomediastinum, and bilateral pneumothorax as a result of barotrauma. Pulmonary artery pressure (PAP) and pulmonary capillary wedge pressure (PCWP) were monitored. High PCWP values were inconsistent with the diagnosis of acute respiratory distress syndrome. The authors suggest that high PCWP was caused by high intraalveolar pressure, pneumomediastinum, and venule constriction in the hypoxic sites of the lung.
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PMID:[A case of respiratory distress syndrome complicated by the development of interstitial emphysema and pneumomediastinum]. 1090 Jul 27

The aim of this study was to assess the frequency of new abnormalities on routine chest radiographs of ventilated, very low birth weight (VLBW) infants during the acute stage of their illness. Infants were identified who had had at least three daily routine chest radiographs. The appearance of their subsequent radiographs was compared to that obtained on the 1st day of ventilatory support and the timing of new abnormalities (malposition of the endotracheal or nasogastric tube, pulmonary interstitial emphysema, pleural effusion, pulmonary oedema, lobar collapse or consolidation) noted. A total of 100 radiographs were examined from 30 VLBW infants, median gestational age 27 weeks (range 23-32 weeks). New abnormalities were present on the radiographs of 24 infants and on 50% of the radiographs examined. The commonest abnormalities noted were pulmonary interstitial emphysema, collapse and consolidation. Conclusion. Routine daily chest radiographs in mechanically ventilated, very low birth weight infants during the acute stage of their respiratory illness can yield new information important in patient care, new abnormalities being demonstrated in 50% of radiographs examined.
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PMID:Routine daily chest radiographs in ventilated, very low birth weight infants. 1127 73

Mechanical ventilation-induced air-space enlargement was investigated in a porcine model of multifocal pneumonia. Following the intrabronchial inoculation of Escherichia coli, 9 piglets (22 +/- 2 kg) were ventilated with a tidal volume (VT) of 15 ml/kg for 43 +/- 15 h. Five noninoculated piglets ventilated for 60 h with the same VT served as control animals. Following death, the lungs were fixed and lung morphometry was assessed. In inoculated animals, unventilated infected and normally ventilated noninfected pulmonary lobules coexisted. In normally ventilated lung regions (1) emphysema-like lesions were present, (2) mean alveolar area and mean linear intercept were significantly greater in inoculated than in control animals, and (3) the degree of alveolar distension correlated with the decrease in respiratory compliance. In unventilated lung areas (1) pseudocysts were frequent, (2) alveolar edema was rare, (3) bronchiolectasis was frequent, (4) mean bronchiolar area was greater in inoculated than in control animals, and (5) the degree of bronchiolar distension correlated with the increase in inspiratory plateau pressure. In conclusion, in piglets with severe bronchopneumonia, air-space enlargement rather than pulmonary edema was the major feature of mechanical ventilation-induced lung barotrauma and resembled lesions previously reported in critically ill patients ventilated using high inspiratory pressures.
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PMID:Mechanical ventilation-induced air-space enlargement during experimental pneumonia in piglets. 1128 41

The ground-glass pattern is a common but nonspecific finding on CT. In certain clinical circumstances, it can suggest a specific diagnosis, indicate a potentially treatable disease, and guide a clinician to an appropriate area for biopsy. A pattern of centrilobular ground-glass nodules is fairly specific for the diagnosis of hypersensitivity pneumonitis with the appropriate clinical history. The tree-in-bud pattern indicates disease affecting the small airways. The differential diagnosis is lengthy; however, the most common process leading to this CT appearance is infection. Although commonly associated with M. tuberculosis, many infectious organisms can produce this pattern. When honeycombing is seen on HRCT, a confident diagnosis of lung fibrosis can be made. The most common causes of interlobular septal thickening on HRCT are pulmonary edema, pulmonary hemorrhage, and lymphangitic spread of cancer, and smooth thickening is characteristic of all three. Diffuse lung cysts in patients who are not immunocompromised generally signify Langerhans' cell histiocytosis, lymphangioleiomyomatosis, or centrilobular emphysema. Centrilobular emphysema can be diagnosed when the centrilobular artery is seen as a small nodular opacity in the center of the cyst. Langerhans' cell histiocytosis is often associated with parenchymal nodules, helping to distinguish it from lymphangioleiomyomatosis. When a nodular pattern is seen on HRCT, the differential diagnosis is very long, but can be narrowed by noting whether the nodules are random, centrilobular, or perilymphatic in distribution. A mosaic pattern of lung attenuation can represent an infiltrative, small airway, or vascular process. The distinction can often be made by noting the size of the pulmonary vessels in the abnormal areas of lung, and whether air trapping is present on expiratory scanning. Computed tomographic signs can be useful indicators of a specific disease process. For instance, the air bronchogram sign indicates that an opacity is intrapulmonary in location, and signals the possibility of two types of neoplasm: lymphoma and bronchioloalveolar cell carcinoma. An air crescent sign indicates recovery of the immune system in an immunocompromised patient with invasive pulmonary aspergillosis. The fallen lung sign is diagnostic of a bronchial transection in the correct clinical setting. The gloved finger sign is very suggestive of allergic bronchopulmonary aspergillosis. The halo sign is highly suggestive of early angioinvasive pulmonary aspergillosis in patients with acute leukemia. When a split pleura sign is seen, the diagnosis is often empyema, although other causes of pleuritis can lead to a similar CT appearance.
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PMID:CT signs and patterns of lung disease. 1169 64

The electrical resistivity of lung tissue can be related to the structure and composition of the tissue and also to the air content. Conditions such as pulmonary oedema and emphysema have been shown to change lung resistivity. However, direct access to the lungs to enable resistivity to be measured is very difficult. We have developed a new method of using electrical impedance tomographic (EIT) measurements on a group of 142 normal neonates to determine the absolute resistivity of lung tissue. The methodology involves comparing the measured EIT data with that from a finite difference model of the thorax in which lung tissue resistivity can be changed. A mean value of 5.7 +/- 1.7 omega(m) was found over the frequency range 4 kHz to 813 kHz. This value is lower than that usually given for adult lung tissue but consistent with the literature on the composition of the neonatal lung and with structural modelling.
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PMID:Neonatal lungs--can absolute lung resistivity be determined non-invasively? 1245 9

The aim of this pictorial essay is to illustrate the distribution of normal findings and various lung diseases on coronal reconstructions as compared with cross-sectional high-resolution CT images. The volumetric CT images were obtained at 120 kVp, 200 mA/rotation, pitch 6:1, and a high-spatial-frequency reconstruction algorithm. The scans were performed using 2.5-mm collimation and reconstructed at 1.25-mm intervals. Coronal reconstructions were obtained at 2.5-mm slice thickness and 2.5-mm intervals. The pictorial includes images of normal anatomy, emphysema, idiopathic pulmonary fibrosis, Langerhans cell histiocytosis, sarcoidosis, bronchiolitis obliterans organizing pneumonia, desquamative interstitial pneumonia, nonspecific interstitial pneumonia, lymphocytic interstitial pneumonia, pulmonary edema, tuberculosis, cytomegalovirus pneumonia, bronchiectasis, and panbronchiolitis.
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PMID:Multidetector spiral high-resolution computed tomography of the lungs: distribution of findings on coronal image reconstructions. 1236 68

Pulmonary surfactant, a complex of lipids and proteins, maintains alveolar integrity and participates in the control of host defense and inflammation in the lung. Surfactant proteins A, B, C, and D are important components of surfactant that play diverse roles in the surface tension reducing as well as host defense and inflammation control functions of surfactant. Hyperoxia or exposure of cells/tissues to elevated levels of oxygen occurs when high levels of oxygen are used to treat a variety of pulmonary disorders that include respiratory distress syndrome of premature infants, emphysema, sarcoidosis, end-stage lung diseases, and others. The lung serves as a primary target organ in hyperoxia, and hyperoxic lung injury is characterized by pulmonary edema, inflammation, and respiratory failure. Hyperoxic lung injury is associated with significant changes in the expression of surfactant proteins that likely serves as an adaptive response to elevated oxygen levels. In most animal species studied, hyperoxia increases the tissue expression of surfactant protein mRNAs. A limited number of studies have indicated that the increased tissue expression of surfactant protein mRNAs is associated with increased levels of surfactant proteins in the bronchoalveolar lavage.
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PMID:Regulation of surfactant protein gene expression by hyperoxia in the lung. 1471 50

Central bronchi and pulmonary arteries are surrounded and enveloped by a strong connective-tissue sheath termed the peribronchovascular interstitium, extending from the level of the pulmonary hila into the peripheral lung. Thickening of the peribronchovascular interstitium can be seen in a wide variety of diseases. The CT appearance can be smooth, nodular, or irregular depending on the underlying cause. Many of the diseases affecting the peribronchovascular interstitium are entities that show a predilection for lymphatic routes, such as sarcoidosis, pulmonary lymphangitic carcinomatosis, silicosis, and lymphoproliferative disorders. There are other entities that mainly affect the peribronchovascular interstitium without a predominant perilymphatic distribution, such as hydrostatic pulmonary edema, cryptogenic organizing pneumonia, Kaposi's sarcoma, interstitial pulmonary emphysema, and interstitial hemorrhage. Although there is an overlap in radiologic features, some CT findings are useful in differentiating among these entities. When CT shows mainly peribronchovascular abnormality, the differential diagnosis is considerably reduced, and it is generally possible to reach the correct diagnosis by considering the clinical context. We illustrate the CT findings and pathologic correlation for a number of different disorders that mainly affect the peribronchovascular interstitium.
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PMID:Diseases affecting the peribronchovascular interstitium: CT findings and pathologic correlation. 1575 80


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