Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell morphology of BAL- fluid and index bronchitis (by Thompson) were evaluated in 52 patients with acute and chronic bronchitis. A significant increase of index bronchitis and percentage of neutrophils in BAL were observed in acute and chronic bronchitis. There was no correlation between index bronchitis and cell in BAL- fluid.
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PMID:[Cellular analysis of bronchoalveolar lavage fluid (BAL) in patients with acute and chronic bronchitis (preliminary study)]. 149 13

The lungs have an important role in the synthesis of angiotensin I converting enzyme (ACE). In BAL fluid and serum the ACE activity was determined in 18 patients with sarcoidosis (11 with high intensity and 7 with low intensity alveolitis), 14 patients with lung cancer and 16 with acute bronchitis. The activity of ACE was examined by a reagent set produced by Boehringer Mannheim Biochemica Test-Combination ACE cat. no. 789/011. The ACE activity in the high intensity alveolitis group of sarcoidosis patients was significantly increased in BAL fluid and serum in comparison to other observed patients. On the other hand, in patients with lung cancer the ACE activity was also increased in comparison to acute bronchitis and referred norms, especially in BAL fluid. This findings suggest a role of neoplastic process in ACE secretion in the airways. Very low correlation observed between ACE activity in serum and BAL fluid indicates a separate mechanism of secretion.
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PMID:[Activity of angiotensin I converting enzyme in serum and bronchoalveolar lavage fluid of patients with sarcoidosis and lung neoplasms]. 166 48

The lungs have an important role in the synthesis of ACE. In BAL fluid and serum the ACE activity was determined in 18 patients with sarcoidosis (11 with high intensity and 7 with low intensity alveolitis), 25 patients with atopic bronchial asthma and 17 with acute bronchitis. The activity of ACE was examined by a reagent set produced by Boehringer Mannheim Biochemica Test-Combination ACE cat. no. 789 011. In the high intensity alveolitis group of sarcoidosis patients the ACE activity was significantly increased in BAL fluid and serum in comparison to other observed patients. On the other hand, in patients with atopic bronchial asthma the ACE activity was also increased in comparison to acute bronchitis and referred norms. These findings suggest a role of atopic processes or administered therapy in ACE secretion in the airways.
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PMID:Activity of angiotensin I converting enzyme in sarcoidosis, atopic bronchial asthma and acute bronchitis. 217 61

A 54-year-old female with bronchial asthma and PIE syndrome induced by disodium cromoglycate (DSCG) was reported. She was referred to our hospital for further examination of the abnormal chest shadows and eosinophilia. She had been treated with DSCG, Cefaclor. Bromhexine and bronchodilator for bronchial asthma and bronchitis. Withdrawal of the drugs except for the bronchodilators alleviated her symptoms. Therefore, drug induced lymphocytes stimulation tests (DLST) were performed for those three drugs. Only DLST for DSCG showed a positive result. She had been asthmatic for ten years and treated by the drug for 18 months prior to admission. The skin test for the drug was negative and a precipitating antibody for the drug could not be found. To obtain a definite diagnosis, bronchial challenge by DSCG was performed, after her symptoms were under control. Severe asthmatic responses were provoked in 6 and 24 hours after the inhalation of DSCG. Bronchoalveolar lavage, performed 8 days after the provocation, revealed increased eosinophils and lymphocytes in BAL fluid. Although several cases of PIE syndrome induced by DSCG have been reported, this seems to be the first report of late and delayed type bronchial response and pulmonary infiltration with eosinophilia provoked by DSCG. The bronchial response to the drug was a late and delayed type reaction and sustained for a long period. This might indicate that PIE syndrome induced by the drug may be caused by a same mechanism as the provoked asthmatic response.
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PMID:[A case of bronchial asthma and PIE Syndrome induced by disodium cromoglycate]. 250 49

Lung transplantation is a potentially curative therapy for the end-stage pulmonary sequelae of sarcoidosis. We reviewed the course of five lung allograft recipients with underlying sarcoidosis (S) at the University of Pittsburgh Medical Center and compared them with a control group (C) of 44 contemporaneous transplant recipients with other respiratory diseases. Sarcoid granulomata have developed in the allografts of 4 S, although these lesions have not yet been demonstrated to result in clinically significant abnormalities. In comparison with C, sarcoidosis patients had significantly greater mean grades of acute rejection during the first 3 months after transplantation (2.1 +/- 0.3 versus 1.6 +/- 0.1, S and C, respectively, p < 0.042) and larger proportions of lung biopsies showing more than mild acute rejection (40 versus 18%, p < 0.012) and lymphocytic bronchitis (30 versus 13%, p = 0.02), as well as a greater percentage of polymorphonuclear leukocytes in BAL returns (34.9 +/- 5.4 versus 19.0 +/- 1.6, p < 0.01). The two groups did not differ, however, in frequency of obliterative bronchiolitis, survival, or pulmonary function. We conclude that lung transplant recipients with underlying sarcoidosis are very likely to develop recurrent disease in the allograft and have more severe acute rejection responses, especially in the first weeks after transplantation. Pulmonary transplantation appears to be an efficacious therapy for end-stage sarcoidosis, but the long-term sequelae of the increased acute rejection and recurrent sarcoidosis in the allograft remain to be determined.
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PMID:Recurrence of sarcoidosis in pulmonary allograft recipients. 823 78

In order to demonstrate how patients with immotile cilia syndrome (ICS) are associated with lower respiratory tract inflammation, bronchoscopy and fractionated BAL were performed on eight ICS patients. Their VC was 84.5 +/- 16.7% (mean +/- SD) and FEV1 73.1 +/- 19.9% of predicted. Endobronchial signs of bronchitis were observed in all patients. The total cell concentrations in the BAL fluid were increased, compared to healthy nonsmokers (n = 10), both in the bronchial (BP) and alveolar portion (AP) (p < 0.01 for both). In the BP, this was mainly due to a high concentration of neutrophils (p < 0.001), whereas in the AP, the concentrations of lymphocytes (p < 0.01) as well as all types of granulocytes (p < 0.001-0.01) were elevated. The signs of active inflammation in the lower respiratory tract were confirmed by the concomitantly elevated (p < 0.001-0.05) concentrations of the soluble BAL components albumin, fibronectin and hyaluronan. Thus, the inflammatory response is not restricted to the ciliated conducting airways, but also occurs in the alveolar space and results-surprisingly-in only a slightly impaired lung function.
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PMID:The immotile cilia syndrome: characterization of the inflammatory response in nonsmoking patients with dysfunction of the cilia. 893 49

Short-term exposure to ambient levels of ozone induces neutrophilic bronchitis. To investigate the early events contributing to inflammatory cell recruitment in the airways we exposed 12 healthy nonsmoking volunteers to 0.12 ppm ozone or filtered air for 2 h on two separate occasions. Spirometry and fiberoptic bronchoscopy were performed immediately and at 1.5 h after the two exposures, respectively. Total protein, albumin, and total and differential cell counts were performed on the bronchial wash and BAL fluid. Bronchial biopsies were embedded in glycol methacrylate and immunostained for inflammatory cells, including neutrophils, mast cells, total T-cells (CD3), T-cell subset CD8, and leukocyte endothelial adhesion molecules, including VCAM-1, ICAM-1, E-selectin, and P-selectin. No significant changes were observed in FEV1, FVC, or any inflammatory indices in the bronchial wash and BAL fluid. In addition, no significant differences were seen in inflammatory cell numbers or percentages of vessels expressing VCAM-1, E-selectin, or ICAM-1 in the biopsies. The percentage of vessels expressing P-selectin increased significantly after ozone exposure: p = 0.016; median (IQR), 28.76 (26.36-36.94) versus 47.06 (38.14-56.86)%. The upregulation of P-selectin could signify an early inflammatory response to ozone such as margination and rolling of the neutrophils on the vessel wall prior to transendothelial migration.
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PMID:Short-term ozone exposure upregulates P-selectin in normal human airways. 915 95

Infectious bronchitis virus, otherwise known as coronavirus, can cause mild upper respiratory tract illnesses in children and adults. Rarely has coronavirus been linked, either by serology or nasal wash, to pneumonia. We report a case of a young woman who, following treatment for stage IIIA breast cancer using a high-dose chemotherapy regimen followed by autologous bone marrow and stem cell transplantation, developed respiratory failure and was found to have coronavirus pneumonia as diagnosed by electron microscopy from BAL fluid. We propose that coronavirus should be considered in the differential diagnosis of acute respiratory failure in cancer patients who have undergone high-dose chemotherapy and autologous hematopoietic support.
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PMID:Coronavirus pneumonia following autologous bone marrow transplantation for breast cancer. 1008 16

The aim of this study was to investigate the cellular and biochemical events associated with repeated exposures to ozone. Twenty-three healthy subjects underwent single exposures to 200 ppb ozone and to filtered air (FA), as well as repeated exposures to 200 ppb ozone on 4 consecutive days, each for 4 h of intermittent exercise. Bronchoalveolar lavage was performed and mucosal biopsies were taken 20 h after the single or the last of the repeated exposures. As compared with FA, the single exposure to ozone caused a decrease in FEV(1), an increase in the percentages of neutrophils and lymphocytes, the concentrations of total protein, IL-6, IL-8, reduced glutathione, urate, and ortho-tyrosine in BAL fluid (BALF), but no changes in the cellular composition of biopsy. After the repeated exposure, the effect on lung function was abolished and differential cell counts in BALF were not significantly different from those after FA. However, the concentrations of total protein, IL-6, IL-8, reduced glutathione, and ortho-tyrosine were still increased. IL-10 could only be detected in BALF after repeated ozone exposures. Furthermore, macroscopic scores for bronchitis, erythema, and hypervulnerability of airway mucosa were increased, as well as numbers of neutrophils in bronchial mucosal biopsies. Our data demonstrate that airway inflammation persists after repeated ozone exposure, despite attenuation of some inflammatory markers in BALF and adaptation of lung function.
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PMID:The effect of repeated ozone exposures on inflammatory markers in bronchoalveolar lavage fluid and mucosal biopsies. 1085 57

Although host defense mechanisms protect the health of the respiratory tract, deficiencies or excessive host responses such as inflammation can create sino-nasal and pulmonary illnesses. Analysis of expectorated secretions (sputum) is traditional, but selective site specific samples (surface washing) seem more applicable for studying illnesses such as rhinitis, bronchitis, or aveolitis. Regional samples should contain representative components (cells and proteins) that ideally reflect changes in adjacent tissue; however, biopsy of contiguous mucosa and lung parenchyma is required for a comprehensive analysis that can link surface samples and tissue pathology. Clinical strategies must be flexible so that maximal information about the host can be obtained through investigation of healthy normals, volunteer-patients with latent illness that can be induced locally and observed in situ, and patients with active illness. Implicit in studying inflammation is the adaptation of new analytic methods to surface or topical samples such as nasal, bronchial and bronchoalveolar lavage (BALF). More correlations between respective components in nasal fluids, bronchial and BAL specimens seem indicated, so that more readily available samples can be used for clinical monitoring. Moreover, further correlations between bronchial and BAL cells and immunohistochemical analysis of tissue for cells are needed.
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PMID:Sampling local respiratory tract sites for inflammation. 1143 34


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