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Biomedical subjects

U Costabel

Publications and source records attributed to U Costabel.

At least 163 records · Page 9Linked to original sources
PubMed1990

[Cytologic and immunocytologic findings in bronchoalveolar lavage as a contribution to the differential diagnosis of chronic lung hemorrhage].

In the present paper, the results of cytological and immunocytological investigations of the broncho-alveolar lavage fluid obtained from 13 patients with pulmonary haemorrhage were studied for their differential-diagnostic usefulness. Five patients each were suffering from idiopathic pulmonary haemosiderosis (IPH) and the Goodpasture syndrome (GPS), one patient had a Wegener's granulomatosis, and two patients presented with vasculitis (VA) which was not amenable to further histological characterization. Parameters that proved particularly suitable for differentiation were the total cell count, the number of haemosiderin-positive macrophages, the extent of the expression of the transferrin receptor (OKT 9) on the macrophages, and the relationship of OKT 4 and OKT 8-positive lymphocytes.

Anti-Glomerular Basement Membrane Disease↗
PubMed1990

[Detection of the activation of alveolar lymphocytes in alveolar proteinosis].

In 7 patients with pulmonary alveolar proteinosis, differential cytology and lymphocyte subsets in BAL fluid were investigated. The study showed that pulmonary alveolar proteinosis is another disorder characterized by a lymphocytic alveolitis and activation of T-lymphocytes (expression of HLA-DR antigens and IL-2 receptors). Our data indicate that immunological mechanisms involving T-cell activation may contribute to be pathogenesis of pulmonary alveolar proteinosis.

Adult↗
PubMed1990

[Surfactant phospholipids in bronchoalveolar lavage fluid in smokers with healthy lungs and non-smokers].

The surfactant phospholipids were determined in the BA1 fluid of 9 smokers and 9 non-smokers with no disease of the lungs. The total phospholipid content was reduced significantly in smokers to 10 +/- 6 nmol/ml as compared with 24 +/- 10 nmol/ml in the non-smokers (p less than 0.02). The composition of major phospholipid fractions (phosphatidyl-choline and phosphatidyl-ethanolamine) did not differ between the two groups. Possible reasons for this reduction of surfactant in smokers are discussed.

Bronchoalveolar Lavage Fluid↗
PubMed1989

Tuberculous pleural effusions: lymphocyte phenotypes in comparison with other lymphocyte-rich effusions.

This study investigated whether the analysis of T cell subsets and of activation markers on T cells in pleural fluids can be helpful for diagnostic purposes in tuberculous pleurisy and other lymphocyte-rich pleural effusions. Pleural effusion fluids were obtained from 18 patients with tuberculous pleurisy (TB), 21 with effusions following radiotherapy (RT) for a malignant disease, and 11 with congestive heart failure (CHF). Lymphocyte subsets were analyzed by a battery of monoclonal antibodies using an immunoperoxidase method. The majority of the lymphocytes were CD3-positive T cells (TB, 86 +/- 7% of lymphocytes; RT, 81 +/- 8%; CHF, 84 +/- 12%). The ratios of CD4-positive helper-inducer to CD8-positive suppressor-cytotoxic T cells were higher than those reported for the peripheral blood but not significantly different between the study groups (TB, 3.3 +/- 1.9; RT, 2.8 +/- 1.4; CHF, 2.5 +/- 1.1). The activation marker studies revealed that only a few pleural T cells were positive for CD38, CD25 (interleukin-2 receptor), HLA-DR antigen, and OKT9 (transferrin receptor), the proportion of CD25-positive T cells being higher in TB and in RT than in CHF and the proportion of HLA-DR-positive T cells being higher in TB than in CHF (P less than 0.05). Significant differences were not observed relative to the natural killer-cytotoxic phenotypes staining positive for Leu-7 or for CD16. Thus, we concluded that phenotypic analysis of lymphocytes is of limited diagnostic usefulness to differentiate tuberculous from other nonmalignant effusions.

Adolescent↗
PubMed1989

Determination of carbonyl groups in oxidatively modified proteins by reduction with tritiated sodium borohydride.

Oxidatively modified proteins have been implicated in a variety of physiologic and pathologic processes. Oxidative modification typically causes inactivation of enzymes and also the introduction of carbonyl groups into amino acid side chains of the protein. We describe a method to quantify oxidatively modified proteins through reduction of these carbonyl groups with tritiated borohydride. The technique was applied to purified, oxidatively modified glutamine synthetase and to bronchoalveolar lavage fluid from dogs and from humans. Since the protein content of lung lavage fluid is low, a very sensitive method was required to measure the oxidized residues. Reduction of the carbonyl group generated during oxidation of proteins with tritiated borohydride provided excellent sensitivity. Incorporation of tritium was directly proportional to the amount of protein with a range from 10 to 1000 micrograms. Should moieties other than amino acids be labeled, they are easily removed by rapid benchtop hydrolysis of the protein followed by chromatography on Dowex 50.

Amino Acids↗
PubMed1989

Immunocytology in malignant pleural mesothelioma. Expression of tumor markers and distribution of lymphocyte subsets.

We studied the reactivity of malignant mesothelioma cells with tumor markers and the phenotypes of lymphocyte subsets in pleural effusions from 14 patients with malignant mesothelioma. For identification of cell surface antigens with monoclonal antibodies, the adhesive slide assay was used. The reaction pattern of mesothelioma cells was found to be CEA negative, Leu M1 negative, EMA positive, BMA-120 positive, My 4 positive, and BA-2 positive. The surface morphology of mesothelioma cells may be of additional help for diagnosis. By these markers, the distinction between mesotheliomas and carcinomas is facilitated. The differentiation of reactive benign mesothelial hyperplasia from malignant mesothelioma by surface marker staining is not yet possible, however. In many effusions in this study, a concomitant T-lymphocytosis was observed with a non-specific increase in the CD4/CD8 ratio, as known for other pleural diseases.

Aged↗
PubMed1989

[Alveolitis in hypersensitivity pneumopathies].

In the pathogenesis of hypersensitivity pneumonitis several immune mechanisms are in play. The initial phase appears to be an immune complex reaction occurring 4 to 8 hours after antigen inhalation, and is characterized by an early increase in neutrophils in the alveolar washing and histopathologically there are oedema, neutrophil infiltration in the alveolar walls, and vasculitis. After 12 hours and for several days there is a cell mediated immune response and the alveolitis consists of cytotoxic cells and suppressor cells whose target is perhaps to modulate the diminution of the B cell response in the production of antibodies by plasma cells. During this phase the lymphocytes of CD8 positive phenotype, the NK cells and occasionally some plasma cells are increased in the alveolar lavage. The characteristic histological appearance is a mononuclear infiltrate predominantly of lymphocytes and some plasma cells and foamy macrophages. After several weeks and for several months a delayed hypersensitivity reaction may lead to a discrete increase in the CD4 cells in the broncho-alveolar lavage and the formation of granulomas. Finally after several months and for several years the repeated immunological activity and damage to the alveolar wall leads to the secretion of proteolytic enzymes and to growth factors to attract fibroblasts leading to pulmonary fibrosis and to a honeycomb lung with a concomitant increase in alveolar neutrophils as in other diseases characterised by pulmonary fibrosis.

Alveolitis, Extrinsic Allergic↗
PubMed1988

[AIDS and the lung].

Explore the source record for details and available documents.

Acquired Immunodeficiency Syndrome↗
PubMed1988

[Systemic necrotizing vasculitis with bronchial asthma and eosinophilia: Churg-Strauss syndrome].

Two cases of the Churg-Strauss syndrome are reported, seen within the past year. The first concerned a 31-year-old woman with a rapidly progressive illness characterized by bronchial asthma, leukocytosis and eosinophilia, abdominal pain, diarrhoea and purpura. In the second case, a 47-year-old man had granulomatous epididymitis and interstitial nephritis before the asthma and eosinophilia developed. In both the diagnosis was confirmed by lung biopsy. Immunosuppressive treatment achieved rapid regression of all symptoms and of the eosinophilia, without recurrence so far.

Adult↗
PubMed1988

Human macrophage maturation and heterogeneity: restricted expression of late differentiation antigens in situ.

Terminal maturation of human macrophages is an important step for creation of cell diversity amongst site-specific subpopulations and their functional competence in situ. As monocytes undergo differentiation in vitro, they start to express lineage-restricted antigens specific for differentiation stages beyond the blood monocyte level as detected by monoclonal antibodies of the MAX series. We have analyzed the expression of MAX.1, MAX.2, MAX.3 and MAX.11 on exudate-type macrophages from pleural and peritoneal cavity and the alveolar space, as well as on resident and activated tissue macrophages in cryostat sections of spleen, lymph node, tonsil, liver, gut mucosa, skin, placenta, kidney and bone. It was found that "free" macrophages in serous cavities expressed MAX antigens in a heterogenous pattern, whereas none of the organ-specific tissue macrophages subsets did so (with the exception being the weak label of MAX.2 on Kupffer cells). Only during allograft rejection were infiltrating macrophages found to express MAX antigens but not at sites of "non-specific" inflammation or granuloma formation. However, Cyclosporin A treatment seems to suppress the induction of MAX antigen expression on intragraft macrophages. In addition, freshly harvested MAX-negative exudate macrophages converted to the complete Max+ phenotype on further cultivation. Isolated Kupffer cells were able only to express the MAX.2 antigen in culture but still did not react with the MAX.1 and MAX.3 monoclonal antibodies. Some MAX antigens are co-expressed on glomerular mesangial cells, dendritic reticulum cells and placental cells (MAX.1/.11) as well as on capillary endothelium within tissues of active immune response (MAX.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1988

Proteases and antiproteases related to the coagulation system in plasma and ascites. Prediction of coagulation disorder in ascites retransfusion.

To improve the ability to predict the occurrence of coagulation disorders in ascites retransfusion and, in addition, to better define the nature of the coagulation disorder, several proteases and antiproteases were analyzed in ascites and plasma before ascites retransfusion in 17 patients. Plasminogen, alpha 2-antiplasmin, antithrombin III, and fibrin(ogen) degradation products in ascites were significantly altered in patients who later developed abnormal coagulation as compared to those who did not. Only plasminogen and alpha 2-antiplasmin in ascites achieved a sufficient predictive value for the occurrence of coagulation abnormalities. The pattern of the coagulation abnormalities observed strongly suggests fibrinolysis induced by the infusion of plasminogen activators as the cause of the coagulation disorder in ascites retransfusion procedures.

Antithrombin III↗