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)

The rate of reaction of several radioprotective agents or their active metabolites with 4-hydroxynonenal (4HNE) was studied and compared to the rate of reaction with cysteine (Cys) and glutathione (GSH). The agents studied were: mercapto ethylamine (MEA); 2(3-aminopropyl) aminoethanethiol (WR1065); S-2-aminoethylisothiouronium bromide-hydrobromide (AET); 1,4-dithiothreitol (DTT); 1,4-dithioerythritol (DTE); N-2(2-mercaptopropionyl)-glycine (MPG); penicillamine hydrochloride (PA); N-acetylcysteine (NAC); 2-3 dimercapto-1 propane sulfonic acid (DMPS); 2,3-dimercaptopropanol (BAL), and meso 2,3 dimercapto succinic acid (DMS). All of them reacted with 4HNE. MEA and WR1065 were the most reactive thiols, and PA and DMS were the least reactive thiols. All the others reacted at rates comparable to or higher than that of cysteine or GSH. The potential role of this type of interactions in the protective action of these drugs against deleterious effects of radiation or carbon tetrachloride is analyzed.
Free Radic Biol Med 1994 Dec
PMID:Reaction of 4-hydroxynonenal with some thiol-containing radioprotective agents or their active metabolites. 786 76

Many patients with asthma have increased wheezing with colds. We hypothesized that rhinovirus colds might increase asthma by augmenting airway allergic responses (histamine release and eosinophil influx) after antigen challenge. Seven allergic rhinitis patients and five normal volunteers were infected with rhinovirus type 16 (RV16) and evaluated by segmental bronchoprovocation and bronchoalveolar lavage. Segmental challenge with saline and antigen was performed 1 mo before infection, during the acute infection, and 1 mo after infection. Lavage was performed immediately and 48 h after antigen challenge. Data were analyzed by two-way analysis of variance, and a P value of < or = 0.05 was considered to be significant. All volunteers inoculated with RV16 developed an acute respiratory infection. BAL fluid obtained from allergic rhinitis subjects during the acute viral infection, and 1 mo after infection, showed the following significant RV16-associated changes after antigen challenge: (a) an enhanced release of histamine immediately after local antigen challenge; (b) persistent histamine leak 48 h afterwards; and (c) a greater recruitment of eosinophils to the airway 48 h after challenge. These changes were not seen in non-allergic volunteers infected with RV16 and challenged with antigen, nor in allergic volunteers repetitively challenged with antigen but not infected with RV16, nor in RV16 infected allergic volunteers sham challenged with saline. We conclude that rhinovirus upper respiratory infection significantly augments immediate and late allergic responses in the airways of allergic individuals after local antigen challenge. These data suggest that one mechanism of increased asthma during a cold is an accentuation of allergic responses in the airway which may then contribute to bronchial inflammation.
J Clin Invest 1994 Dec
PMID:A common cold virus, rhinovirus 16, potentiates airway inflammation after segmental antigen bronchoprovocation in allergic subjects. 798 75

Summer-type hypersensitivity pneumonitis (SHP) is the most prevalent type of HP in Japan, and the major causative agent of the disease is T. cutaneum. The major antigenic substance of the yeast is serotype-related polysaccharide. Home environmental factors indicate that SHP is a sick house syndrome. Immunologically, both humoral and cellular hypersensitivities are involved in the induction of the disease. The levels of specific IgG and IgA antibodies and complements in BAL fluids from SHP patients are well correlated to the clinical course. On the other hand, BAL lymphocytes in SHP patients are mostly T lymphocytes, mainly due to an increase in CD8+ subpopulations of lymphocytes; this leads to a decrease in the ratio of CD4+ to CD8+. These T cells belong to CD45RO+ memory T lymphocytes and LFA-11 alpha high+ cytotoxic T lymphocytes as assessed by their cell surface phenotypes. However, functions of these BAL T lymphocytes remain undefined. Host factors such as HLA-DQw3 and cigarette smoking may participate in the development of the disease. In conclusion, the pathogenesis of SHP is considered to be a combination of immune complex disease and cellular hypersensitivity to T. cutaneum.
Nihon Kyobu Shikkan Gakkai Zasshi 1993 Dec
PMID:[Pathogenesis of summer-type hypersensitivity pneumonitis]. 800 74

The mouse monoclonal anti-BAL antibody induced apoptosis in a pre-B acute lymphocytic leukemia cell line within 2 days of incubation, after being crosslinked by a secondary antibody. The antibody specifically recognized a 37 kDa membrane protein that was expressed on a wide spectrum of normal and malignant cells, but induced programmed cell death in only very few of these cells. In this study, we have followed the initial kinetics of the antibody-induced cell death in the human acute lymphocytic leukemia cell line KM-3, by microcalorimetric measurements in conjunction with determination of the cellular proliferation rate and DNA fragmentation. An increase in metabolic activity was observed already after incubating the cells for 20 min with crosslinked anti-BAL antibody, which was several hours before significant growth inhibition and DNA fragmentation were detected. These data show for the first time that the initiation phase of antibody-induced apoptosis is an active, energy-dependent process and not merely an effect of receptor blocking.
Cancer Lett 1993 Dec 10
PMID:Antibody-induced apoptosis in a human leukemia cell line is energy dependent: thermochemical analysis of cellular metabolism. 829 20

We have examined the ability of HepG2 human hepatoblastoma cells and 7800 C1 Morris rat hepatoma cells to convert 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-cholestanoic acid (THCA) and 3 alpha, 7 alpha-dihydroxy-5 beta-cholestanoic acid (DHCA) to cholic acid and chenodeoxycholic acid, respectively. Cell extracts from both these cell lines could neither form cholic acid from THCA nor from the activated form, THCA-CoA. This suggests that both cell lines are defective in two enzyme activities involved in the pathway, the microsomal THCA-CoA ligase and the peroxisomal THCA-CoA oxidase. Furthermore, we show that the subsequent enzymes are active in the conversion to bile acids, because the product of the THCA-CoA oxidase, 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-cholest-24-enoyl-coenzyme A (delta 24-THCA-CoA) or delta 24-THCA in the presence of THCA-CoA ligase, are converted to cholic acid by both cell lines. HepG2 cells were able to slowly form chenodeoxycholic acid and cholic acid from 5 beta-cholestane-3 alpha, 7 alpha-diol and 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha-triol, respectively, in 24- and 96-h incubations. The rate of cholic acid formation was lower than the rate for chenodeoxycholic acid and there was a clear accumulation of THCA. 7800 C1 Morris cells had no ability to form cholic acid or chenodeoxycholic acid after 96 h incubation. We conclude that these two cell lines have defects in two enzyme activities involved in the peroxisomal oxidation in bile acid formation, the microsomal THCA-CoA ligase and the peroxisomal THCA-CoA oxidase.
J Lipid Res 1993 Dec
PMID:Human hepatoblastoma cells (HepG2) and rat hepatoma cells are defective in important enzyme activities in the oxidation of the C27 steroid side chain in bile acid formation. 830 Dec 25

In general, lung involvement in connective tissue disorders has not been as well defined as has isolated interstitial lung disease; this applies particularly to bronchiolitis, which occurs infrequently. The low prevalence of bronchiolitis may reflect difficulties in making the diagnosis in mild to moderate disease; at present, most reported disease is severe. This is likely to account for the lack of therapeutic success in obliterative bronchiolitis and in many patients with follicular bronchiolitis. There is a need for earlier intervention if treatment is to be effective, and thus there is a need to refine the noninvasive diagnosis of bronchiolitis. This goal is unlikely to be achieved without the systematic noninvasive evaluation and surveillance of large groups of patients with connective tissue diseases. The role of the pulmonary function laboratory in identifying early bronchiolitis remains entirely uncertain; whether silent "small airways disease," defined physiologically, predicts the eventual development of bronchiolitis is unclear. The reversibility of this asymptomatic lesion with inhaled steroid therapy and the role of inhaled treatment in bronchiolitis, in general, have not been evaluated. More work needs to be done to determine the predictive value of CT appearances and BAL findings, to try to identify a subgroup of patients at greater risk of developing severe bronchiolitis. Further histocompatibility studies may serve as a basis for the selection of patients with an increased likelihood of developing airways disease. The role of open lung biopsy requires further clarification. Better noninvasive evaluation should reduce the need for this invasive procedure; in some patients, however, including those with concomitant interstitial lung disease, histologic assessment will remain an essential component of management. In recent years, in contrast to early reports, it has become apparent that organizing pneumonia has a better prognosis than fibrosing alveolitis in the connective tissue diseases; overall, stability or regression of disease, usually with corticosteroid therapy, was documented in 28 of 39 reported cases. In these patients, a tissue diagnosis serves to identify the need for aggressive therapeutic intervention. Finally, the compilation of larger clinical series would improve our understanding of severe bronchiolitis. This is likely to require multicenter collaboration, which often is impracticable; without this approach, however, the description of bronchiolitis will remain anecdotal.
Clin Chest Med 1993 Dec
PMID:Bronchiolitis in association with connective tissue disorders. 831 70

The purpose of this prospective postmortem study was to assess the diagnostic accuracy of bronchoscopic techniques (bronchoalveolar lavage [BAL] and protected specimen brush [PSB]) and nonbronchoscopic techniques (blind bronchial sampling [BBS] and mini-BAL) in the diagnosis of ventilator-associated pneumonia (VAP). The results of each technique were compared with histology and culture of lung tissue specimens obtained by surgical pneumonectomies in 38 patients who died after at least 72 h of mechanical ventilation. Histology was positive for VAP in 18 patients and negative in 20 patients. There were 12 definite VAP (positive histology and positive lung cultures) and 6 histologic VAP (positive histology and negative cultures). Clinical pulmonary infection score (CPIS) at a threshold of 6 achieved a sensitivity of 72% and a specificity of 85%. When the CPIS was combined with the logarithmic concentration of the predominant microorganism obtained from the BBS sample culture, specificity was increased to 95%, for a threshold of 10. Using 10(3) cfu/ml as the threshold of positivity for cultures obtained with PSB and mini-BAL samples and 10(4) cfu/ml for cultures obtained with BBS and BAL, the respective sensitivities of these techniques for definite VAP were 42, 67, 83, and 58%. The sensitivity of BBS was significantly higher than that of PSB (p < 0.05). The area under the receiver operator characteristic curve was significantly greater for BBS than PSB (p < 0.05). Given that it is more sensitive and noninvasive, BBS is preferable to PSB for the diagnosis of VAP.
Am J Respir Crit Care Med 1995 Dec
PMID:Bronchoscopic or blind sampling techniques for the diagnosis of ventilator-associated pneumonia. 852 Jul 66

Drug-induced eosinophilic lung disease commonly presents as a simple pulmonary eosinophilia-like syndrome consisting of transient pulmonary infiltrates, peripheral eosinophilia, and mild pulmonary symptoms that disappear promptly upon withdrawal of the offending medication. However, a more fulminant presentation most resembling acute eosinophilic pneumonia has been recently described. We present a patient with BAL-confirmed eosinophilic pneumonia (EP) and respiratory failure after a trazodone overdose. This is the first case of EP associated with trazodone and only the third drug-mediated EP reported to precipitate respiratory failure.
Am J Respir Crit Care Med 1995 Dec
PMID:Eosinophilic pneumonia and respiratory failure associated with a trazodone overdose. 852 Jul 92

A simple radioimmunoassay for detection of secreted and intracellular annexin II in human cells is presented. Annexin II is a multifunctional protein in human cells and may have a role in several types of cancers. No enzymatic activity has been associated with the protein, thus making its detection difficult. Using purified annexin II from human placenta, we have developed a sensitive radioimmunoassay protocol. A linear response was observed up to a concentration of 0.5 microgram purified protein in the assay. Using this radioimmunoassay protocol, annexin II can be detected in undiluted clinical human samples such as bronchoalveolar lavages and various tissue extracts. We demonstrate the applicability of this technique to measure intracellular annexin II in extracts of a human adenocarcinoma cell line (HeLa) and secreted annexin II from bronchoalveolar lavage fluid from a human patient. Using HeLa cell extracts and BAL, we observed a linear response with up to 10 micrograms total protein in the assay. We further demonstrate the applicability of this technique to measure differences in intracellular and secreted annexin II in the human pancreatic adenocarcinoma cell lines CD-11, CD-18 and Capan-2. While CD-11 and CD-18 do not secrete annexin II, the cell line Capan-2 secretes high levels of the protein.
J Immunol Methods 1995 Dec 15
PMID:Detection of secreted and intracellular annexin II by a radioimmunoassay. 855 Oct 43

In summary, orthomyxo- and paramyxoviruses cause clinically important infections in transplant patients. Patients often develop lower respiratory tract involvement and sometimes respiratory failure, which almost is uniformly fatal. Bone marrow transplant recipients appear to be at higher risk of severe disease than are solid-organ recipients, but well defined criteria to predict those patients who will be severely affected are not available. Factors associated with more severe disease include the type of viral pathogen, with pneumonia occurring more commonly with RSV and PIV infection, and the degree of immunosuppression of the patient, particularly the pre-engraftment phase in bone marrow transplant recipients. Because mortality is associated with development of pneumonia, prompt diagnosis and studies for concurrent infections are essential. Evaluation of fever and upper respiratory tract symptoms in patients in the peritransplant period should include sampling of nasopharyngeal and throat for virus isolation and antigen detection for respiratory viruses. If patients develop lower respiratory tract symptoms, early bronchoscopy with BAL is indicated. No specific antiviral therapy has proved effective in the treatment of established respiratory viral infections of transplant patients. Aerosolized ribavirin or, in the instance of influenza A virus infection, oral rimantadine might be considered as early therapy to prevent severe lower respiratory disease. Intravenous ribavirin, currently available on a compassionate use basis, might be considered for treating measles virus infection. In patients with lower tract disease due to RSV, the addition of immunoglobulin with high neutralizing antibody titers to RSV or intravenous ribavirin are additional considerations to forestall respiratory failure. Controlled studies of these interventions are needed in transplant patients before their use can be recommended routinely.
Infect Dis Clin North Am 1995 Dec
PMID:Orthomyxoviral and paramyxoviral infections in transplant patients. 874 76


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