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1.
Ann Otol Rhinol Laryngol ; 107(10 Pt 1): 891-7, 1998 Oct.
Article in English | MEDLINE | ID: mdl-9794621

ABSTRACT

Basic fibroblast growth factor (bFGF) is a polypeptide that is mitogenic for a wide variety of cell types. We used Northern blot analysis and immunohistochemistry to determine if bFGF is expressed in the nasal polyp tissue; bFGF messenger RNA was detectable in the polyps examined by Northern blot analysis. Strong immunostaining for bFGF was found in blood vessels and along the basement membrane of the epithelial cell layers. Basal epithelial cells and some infiltrating mononuclear cells also stained for bFGF. Proliferating cell nuclear antigen colocalized with bFGF to basal epithelial cells, endothelial cells, and areas of focal epithelial metaplasia. The polyp tissue was double-labeled with a mouse monoclonal antitryptase, a specific mast cell marker, and anti-bFGF. A significant number (65% +/- 19%) of the bFGF-positive mononuclear cells in the polyp tissues were positive for tryptase. These findings suggest that bFGF may contribute to the endothelial and epithelial proliferation in nasal polyp tissues and that mast cells are one source of this growth factor.


Subject(s)
Fibroblast Growth Factor 2/genetics , Nasal Polyps/genetics , Nose Neoplasms/genetics , Adolescent , Adult , Animals , Blotting, Northern , Child , Epithelium/pathology , Female , Gene Expression Regulation, Neoplastic/physiology , Humans , Immunoenzyme Techniques , Male , Mice , Microscopy, Fluorescence , Nasal Mucosa/pathology , Nasal Polyps/pathology , Nose Neoplasms/pathology , Proliferating Cell Nuclear Antigen/genetics
2.
Pediatr Pulmonol ; 25(4): 231-7, 1998 Apr.
Article in English | MEDLINE | ID: mdl-9590483

ABSTRACT

In our cystic fibrosis clinic, all patients older than 6 years perform spirometry at each visit just before being seen by the health care team. Upon review, we determined that our perceived rationale for this practice was that the medical history fails to detect deterioration in a sizable minority of patients whose pulmonary decline can be detected by spirometry. Furthermore, the literature and our own experience indicates that physical examination frequently will not detect changes in pulmonary status until the changes are advanced. As part of an ongoing quality/cost assessment, we decided to challenge our rationale for performing routine spirometry. Using standard methodology, we developed a six-item Likert style questionnaire, the purpose of which was to assess perceived changes in pulmonary symptoms since the last clinic visit. The questionnaire had an acceptable degree of internal consistency (Cronbach's alpha = 0.92), although the question about sputum production showed the least correlation with responses to other items. We administered the questionnaire to 103 consecutive different patients and examined the association between reported changes in symptoms and actual changes in spirometric outcomes. Overall, there was a statistically significant, but clinically weak association between symptom scores and change in FEV1, r2 = 0.16, P < 0.001. Twenty-three patients had a decline in FEV1 of > or = 10% from one clinic visit to the next. Depending on the method used to place symptom scores into categories indicating that pulmonary symptoms were "worse," "same," or "better" than at the last clinic visit, 40-60% of these 23 patients indicated they felt the "same" or "better." We conclude that spirometry is a justifiable part of all clinic visits for patients with cystic fibrosis, assuming that one would want to detect and treat declines in pulmonary status before they become advanced.


Subject(s)
Cystic Fibrosis/diagnosis , Spirometry , Cystic Fibrosis/physiopathology , Disease Progression , Forced Expiratory Volume , Humans
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