PubMed Health⌕ Search

Biomedical subjects

O H Yoo

Publications and source records attributed to O H Yoo.

14 recordsLinked to original sources
PubMed1992

Identification of two zinc metalloendopeptidases in alveolar macrophages of rats, guinea pigs, and human beings.

Neutral endopeptidases EC 3.4.24.11 and EC 3.4.24.15, widely distributed zinc metalloendopeptidases, degrade a number of biologically active peptides including substance P, bradykinin, neurotensin, and luteinizing hormone-releasing hormone. In this study we measured EC 3.4.24.11 and EC 3.4.24.15 activity in alveolar macrophages, key inflammatory cells in the lung that produce and respond to a large number of bioactive substances including chemotactic peptides, with the substrates glutaryl-ala-ala-phe-2-naphthylamide and tertiary butoxycarbonyl-phe-ala-ala-phe-paraaminobenzoate, respectively. We found that specific activity of EC 3.4.24.15, defined as activity inhibited with N-[(1RS)-carboxy-3-phenylpropyl]-ala-ala-phe-paraaminobenzoate+ ++, was significantly higher (p < 0.001) in cells from Sprague-Dawley rats (485 +/- 123 nmol/mg protein.hr) than in cells from Hartley guinea pigs (138 +/- 94 nmol/mg protein.hr), healthy human male smokers (121 +/- 73 nmol/mg protein.hr) and healthy human male nonsmokers (94 +/- 12). In contrast, activity of EC 3.4.24.11, defined as activity inhibited with N-[(1RS)-carboxy-3-phenylpropyl]-phe-paraaminobenzoate, was significantly higher (p < 0.001) in cells from human smokers (689 +/- 167 nmol/mg protein.hr) and nonsmokers (762 +/- 136 nmol/mg protein.hr) than in cells from rats (52 +/- 12 nmol/mg protein.hr) and guinea pigs (34 +/- 14 nmol/mg protein.hr). An additional activity in alveolar macrophages toward tertiary butorycarbonyl-phe-ala-ala-phe-paraaminobenzoate was inhibited with L-3-carboxy-trans-2,3-epoxypropionyl-leucylamido-(4-guanido) butane, a specific inhibitor of cysteine proteinases, a finding of interest because in general enzymes in this class show little activity at neutral pH.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminobenzoic Acid↗
PubMed1991

Cystatin C and cathepsin B production by alveolar macrophages from smokers and nonsmokers.

The capacity of alveolar macrophages (AM) obtained from smokers and nonsmokers to secrete cathepsin B and its inhibitor cystatin C was examined because of the concept that an imbalance in the production of proteolytic enzymes and/or their inhibitors could be responsible for the lung damage seen in smokers. Quantitation of immunoprecipitates on Western blots showed that the amount of total cystatin C secreted into the culture medium by AM of smokers was significantly greater than the amount secreted by cells obtained from nonsmokers, whereas the difference between the amount of cathepsin B secreted by the AM of smokers and that from nonsmokers did not appear significant. The cystatin C found in the medium conditioned by AM of nonsmokers appeared to be more heterogeneous in molecular size, presenting either as a single band of about 14 Kd or as a high-molecular-weight triplet of about 69 Kd, 63 Kd, and 57.3 Kd. Furthermore, in some cases there were single or doublet bands at 14 Kd as well as the high-molecular-weight triplets. In contrast, smokers AM-conditioned medium uniformly possessed both the low-and the high-molecular-weight cystatin C. Cathepsin B was not detected in Western blots at its reported molecular weights but was identified at the exact area occupied by the higher molecular weight cystatin C, i.e., at bands corresponding to 69 Kd, 63 Kd, and 57.3 Kd. Therefore, it is clear that in culture media of AM, cystatin C and cathepsin B are present as proteinase-antiproteinase complexes. The observation also suggests that in smokers an excess of cystatin C may be elaborated, which, if further substantiated, would show for the first time a likely role for this proteinase inhibitor in vivo.

Adult↗
PubMed1990

Successful retrieval of fractured tracheostomy cannula by flexible fiberoptic bronchoscopy.

The fracture and aspiration of tracheostomy tubing is not rare. It may go unnoticed by the patient. The equipment is prone to shearing at the flange and fracture along its body. Its integrity should be routinely tested, and a policy instituted for the discarding of old equipment. Fiberoptic bronchoscopy is advantageous in that it can be performed quickly and easily, it avoids general anesthesia, and it is more adaptable to foreign body retrieval than the nasopharyngoscope because of its forceps channel, through which varied retrieval instruments can be passed.

Bronchoscopy↗
PubMed1989

Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome: diagnosis using minilavage samples.

Over a 30-month period, we evaluated 74 patients with acquired immunodeficiency syndrome (AIDS) for suspected opportunistic pulmonary infection. All had abnormal findings on chest roentgenogram. Sixty patients (81%) were found to have Pneumocystis carinii pneumonia (PCP). We assessed the yield of various diagnostic methods, and found that bronchoalveolar lavage samples obtained by the instillation of 20 to 50 ml of normal saline (minilavage) contained detectable organisms in 51 of 53 patients (sensitivity of 96%) when the samples were embedded in plastic, cut in thick sections (1 micron), stained with toluidine blue O, and evaluated by light microscopy. In comparison, the diagnostic yield was 94% for lung biopsy, 85% for touch preparation of lung tissue, 32% for bronchial washing, and 14% for brush biopsy. It is significant that minilavage samples embedded in plastic were positive in all seven patients who did not have transbronchial lung biopsy because they were at high risk for complications. We conclude that the process of embedding minilavage samples in plastic and evaluating thick sections stained with toluidine blue O is a sensitive method of diagnosing PCP in patients with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Cathepsin D activity is increased in alveolar macrophages and bronchoalveolar lavage fluid of smokers.

Cathepsin D activity was determined in alveolar macrophages (AM) and cell-free bronchoalveolar lavage fluid (BALF) from volunteers who were current cigarette smokers and compared with that found in lifetime nonsmokers. Enzyme activity was determined with a highly sensitive and specific substrate [D-Phe-Ser(0-CH2-C6H5)-Phe-Phe-Ala-Ala-pAB]. Specific activity was more than three times higher in AM from smokers than in cells from nonsmokers (37,880 +/- 2,090 versus 10,300 +/- 1,200; p less than 0.001) and approximately seven times higher in BALF from smokers than from nonsmokers (3,620 +/- 490 versus 515 +/- 165; p less than 0.001). This study demonstrated that cigarette smoke is a potent inducer of cathepsin D activity in AM in vivo. Because cathepsin D is capable of degrading a variety of proteins, the finding of high concentrations of the enzyme in AM and BALF from smokers, along with previous observations of elevated cathepsin B activity, suggests that lysosomal enzymes may cause or contribute to structural lung damage associated with cigarette smoking.

Adult↗
PubMed1987

Nonfatal pulmonary edema after "freebase" cocaine smoking.

Pulmonary edema is known to develop in users of heroin and methadone. Its association with cocaine use is usually a postmortem finding. There has been only 1 report of pulmonary edema being diagnosed clinically after cocaine use. In that case the cocaine was used intravenously, and death occurred within 3 h after the onset of symptoms. Here we describe a patient who developed acute pulmonary edema after smoking "freebase" cocaine. The pulmonary edema resolved spontaneously within 72 h. The cause of the acute reversible pulmonary edema was probably related to both pressure- and permeability-related changes.

Acute Disease↗
PubMed1986

Increased cathepsin B-like activity in alveolar macrophages and bronchoalveolar lavage fluid from smokers.

Cathepsin B-like activity was determined in alveolar macrophages (AM) and cell-free bronchoalveolar lavage fluid (BALF) obtained from volunteers who were current cigarette smokers and compared with that found in lifetime nonsmokers. Enzyme activity was determined with benzyloxycarbonyl-Leu-Leu-Arg-2-naphthylamide as the substrate. Specific activity of the enzyme was more than twice as high in AM from smokers than in cells from nonsmokers (35,600 +/- 2,250 versus 16,000 +/- 860; p less than 0.001) and about 10 times as high in BALF from smokers than in that from nonsmokers (3,060 +/- 380 versus 300 +/- 25; p less than 0.001). Because cathepsin B is capable of degrading structural lung proteins and inactivating alpha-1-proteinase inhibitor, and the elastinolytic activity of AM may be mediated through cysteine proteinases such as cathepsin B, the finding of high concentrations of an enzyme with cathepsin B-like activity in AM and BALF from smokers suggests the need to explore the role of the enzyme in structural lung damage associated with cigarette smoking.

Adult↗
PubMed1983

Bronchioalveolar carcinoma arising in areas previously irradiated for Hodgkin's disease.

A man who received therapeutic irradiation to limited areas of each lung for intrapulmonary Hodgkin's disease developed bronchioalveolar carcinoma in the same areas more than 20 years later. This is the first report of a malignant process developing in areas of the lung that had been previously irradiated for treatment of a primary lung condition.

Adenocarcinoma, Bronchiolo-Alveolar↗