Publications by authors named "Stanflin N"

In chronic obstructive pulmonary disease (COPD) patients airway mucosa is infiltrated by macrophages and T lymphocytes, potentially reactive to pathogens. We studied the antigen-specificity and the effector functions of in vivo activated T lymphocytes isolated from BAL (Bronchoalveolar lavage) of 5 Moraxella catarrhalis (Mc)-infected and 5 Mc-non-infected COPD patients. Mc-specific T cells were detected only in BAL or peripheral blood of Moraxella catarrhalis-infected patients.

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Background: Induced sputum (IS) is a noninvasive tool, which can be used to collect cellular and soluble materials from lung airways.

Objective: To evaluate if IS may be a useful and safe tool for the detection of airway inflammation in patients with interstitial lung disease (ILD) in systemic sclerosis (SSc).

Methods: Sixty-eight patients with SSc and ILD as well as 18 healthy individuals (controls) were selected and submitted to IS examination.

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Lung macrophages may play a relevant role in oxidative processes producing both superoxide anion (O(2)(-)) and NO. In this view, an antioxidant therapy can be useful in the treatment of systemic sclerosis (SSc) patients. N-Acetylcysteine (NAC) is able to expand natural antioxidant defenses by increasing intracellular gluthatione concentration and it has been proposed as an antioxidant therapy in respiratory distress syndromes.

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The purpose of this contribution is to place a higher value on the existence of a turn-over of bronchial and pulmonary elastic fibers: the former would derive from the smooth muscle cells of the bronchial wall, the latter from the interstitial myofibroblasts of the alveolar septa. The reduction of the number of the elastic fibers in the bronchial wall during chronic atrophic bronchitis depend on the atrophy of the bronchial smooth muscle cells; in the alveolar septa the hyperplasia of the elastic fibers during pulmonary fibroses depend on the myofibroblastic proliferation, while the reduction of the elastic fibers number during pulmonary enphysema depend on the reduction in the number of myofibroblasts.

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Considering the role proposed for myofibroblasts in inflammatory and hyperelastotic lung diseases, the possibility arises that these cells are involved in bronchial pathology, including asthma. To address this issue, we have analyzed by light microscopy, histochemistry and immunohistochemistry the structure of extra- and intra-pulmonary bronchi of patient died of asthma. We have demonstrated hyperplasia of connective tissue cells and fibers in the mucosa, all around the lumen of extra- and intra-pulmonary bronchi.

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On the possible ontogeny of the cells of a "granular cell tumor" of the human trachea. In a young patient affected with pulmonary tuberculosis during bronchoscopy a "granular cell tumor" of the membranous part of trachea was occasionally evidentied. After pathologic examination, the specimen is analyzed in order to assess the kind of cells that are present in the lesion: the ultrastructural and immunohistochemical study shows Schwann cells which particularly well developed lysosomal complement.

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The occurrence of Mycobacterium xenopi (MX) isolates is not homogeneous in various geographic zones. In the Florence area, between 1975-1989, strains of MX from 64 different patients have been isolated. The review of bacteriological and clinical data of 46 of them, from whose sputum MX had been grown, allowed to diagnose for 26% the commensal nature of this finding, for 41% the concomitance with a tubercular infection and for the remaining 33% the pathogenicity of this microorganism.

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A new framework for pulmonary fibroses may be obtained by distinguishing the "true" forms (solely collagen hyperplasia) from the "false" forms or mesenchymal fibril lung diseases (collagen, reticular and elastic hyperplasia with neo-angiogenesis): the "true fibroses" are then divisible into those not causing architectural subversion of the lung and those which bring it about. Pulmonary architectural subversion is common to true granulomatous fibroses and mesenchymal fibril lung diseases: it is, in our opinion, the product of a combination of factors, including the hyperactivity of a fibroblast sub-population normally in the minority, stimulated by T lymphocytes which are activated by an autoimmune response to type I collagen produced in excess.

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