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 CytoJournal , 2007, DOI: 10.1186/1742-6413-4-11 Abstract: Background The combination of cytology and biopsies improves the recognition and typing of small cell (SCLC) versus non small cell (NSCLC) lung cancers in the fiberoptic bronchoscopy assessment of centrally located tumours. Methods We studied whether bronchial aspirates performed before biopsies (BA) and washings performed after biopsies (BW) could increase the diagnostic yield of fiberoptic bronchoscopy. A series of 334 consecutive samples taken in patients with suspicious fiberoptic bronchoscopy findings was studied. Two hundred primary tumours were included in the study. The actual diagnosis was based on surgical tissue specimen analysis and/or imaging techniques. The typing used was that of the 1999 WHO/IASLC classification. Results The diagnosis of malignancy and tumour typing were analyzed according to the sequential (combined) or single use of tests. Malignancy was assessed by cytology in 144/164 (87.8%) positive biopsy cases and in 174/200 tumour cases (87.0%). BA before biopsies allowed 84.0% of cancers to be diagnosed, whereas BW after biopsies allowed 79.0% of cancers to be found (p = ns). However, combining biopsies with BW allowed 94.0% of cancers to be diagnosed, whereas 82.0% were diagnosed by biopsies alone (p < 0.001). The highest diagnostic yield was obtained with the combination of BA, biopsies and BW, with 97.0% sensitivity. Exact concordance in typing was obtained in 83.8% of cases. The six surgically resected cases (3.0%) with negative cytology and biopsy results included four squamous cell carcinomas with necrotizing or fibrous surface and two adenocarcinomas, pT1 stage. Conclusion Fiberoptic bronchoscopy may reach a yield of close to 100% in the diagnosis and typing of centrally located, primary lung cancers by combining bronchial aspirates, biopsies and washings.
 Egyptian Journal of Hospital Medicine , 2010, Abstract: To determine the different presentations encountered upon diagnosis of ABPA among patients with bronchial asthma and the two-year-follow-up results. Patients and method All patients with bronchial asthma and ABPA were included in the study .Specially formulated sheet was done include age, gender, duration of bronchial asthma ,new clinical,radiological,and laboratory findings suggestive of ABPA and two year follow up of them. Diagnosis of ABPA was based on Rosenberg-Patterson criteria. Result Fifteen patients with ABPA 3.9% out of 385 patients with bronchial asthma were included in our study, (5males)and (10 females) there mean age was 28.8 years , and mean duration of asthma was 8.9 years, and they represent all stages of asthma severity. Fleeting shadows mainly in the upper lobes were the most common radiological findings observed in nine patients (60%), five patients (33.3%) had proximal bronchiectasis detected by high resolution chest ct-scan, one of our patients had collapsed consolidation. All patients had moderate to severe eosinophilia and positive immediate skin test for aspergillus. Conclusion As the prevalence of ABPA is not uncommon among patients with bronchial asthma regardless the severity and the level control of asthma, high index of suspicious for ABPA should be maintained when followed up any patient with bronchial asthma.
 BMC Cancer , 2005, DOI: 10.1186/1471-2407-5-155 Abstract: We used immunohistochemistry to determine the presence, relative levels, and localization of proteins that mediate anti-apoptotic pathways in developing human bronchial neoplasia.Bronchial epithelial protein levels of the phosphorylated (active) form of AKT kinase and the caspase inhibitor cIAP-2 were increased in more advanced grades of bronchial IEN lesions than in normal bronchial epithelium. Additionally, the percentage of biopsies with nuclear localization of p65/RELA in epithelial cells increased with advancing pathology grade, suggesting that NF-κB transcriptional activity was induced more frequently in advanced IEN lesions.Our results indicate that anti-apoptotic pathways are elevated in bronchial IEN lesions prior to the onset of invasive carcinoma and that targeting these pathways therapeutically may offer promise in prevention of non-small cell lung carcinoma.Lung cancer is the leading cause of cancer mortality in both men and women in the United States [1]. Non-small cell lung carcinomas arise from the respiratory epithelium and progress through well-defined pathological stages prior to becoming invasive and metastatic tumors. While many studies have identified lung tumor markers of clinical or prognostic significance, survival rates for this deadly disease have remained essentially unchanged for the past 30 years. The slow advance in treating lung cancer is due in part to continued gaps in our understanding of the molecular mechanisms of lung tumorigenesis. Thus, studies that aid in our understanding of molecular mechanisms of lung tumorigenesis are important steps towards developing better detection, prevention and treatment of this disease.Evasion of apoptosis by tumor cells is a critical step during tumorigenesis. The serine/threonine kinase Akt is a critical mediator of anti-apoptotic signaling in eukaryotic cells and is activated in a signaling cascade downstream of Ras activation and phosphoinositide-3-kinase (PI3K) [2]. Amplification of PI3K is c
 Kazem Amoli Acta Medica Iranica , 1994, Abstract: Chronic bronchopulmonary disorders occurred in a large number of rustic females who used to bake bread at their dwellings under unhgyienic conditions. Bronchoscopy revealed advanced pathological changes with characterised black areas infiltrating the bronchial walls. Findings in ten patients who referred with acute chronic respiratory symptoms and a positive history of indoor pollution are described with an emphasis on their bronchoscopic changes.
 Journal of Postgraduate Medicine , 1996, Abstract: A 38 year old male was diagnosed to have allergic bronchopulmonary aspergillosis which responded remarkably to prednisolone therapy.
 Ritesh Agarwal World Journal of Radiology , 2010, Abstract: Allergic bronchopulmonary aspergillosis (ABPA) is a complex hypersensitivity syndrome triggered against antigens of Aspergillus fumigatus, a fungus that most commonly colonizes the airways of patients with bronchial asthma and cystic fibrosis. It presents clinically with refractory asthma, hemoptysis and systemic manifestations including fever, malaise and weight loss. Radiologically, it presents with central bronchiectasis and recurrent episodes of mucus plugging. The mucus plugs in ABPA are generally hypodense but in up to 20% of patients the mucus can be hyperdense on computed tomography. This paper reviews the literature on the clinical significance of hyperattenuated mucus in patients with ABPA.
 Alan P. Knutsen Journal of Allergy , 2011, DOI: 10.1155/2011/785983 Abstract: Allergic bronchopulmonary aspergillosis (ABPA) is a Th2 hypersensitivity lung disease in response to Aspergillus fumigatus that affects asthmatic and cystic fibrosis (CF) patients. Sensitization to A. fumigatus is common in both atopic asthmatic and CF patients, yet only 1%–2% of asthmatic and 7%–9% of CF patients develop ABPA. ABPA is characterized by wheezing and pulmonary infiltrates which may lead to pulmonary fibrosis and/or bronchiectasis. The inflammatory response is characterized by Th2 responses to Aspergillus allergens, increased serum IgE, and eosinophilia. A number of genetic risks have recently been identified in the development of ABPA. These include HLA-DR and HLA-DQ, IL-4 receptor alpha chain (IL-4RA) polymorphisms, IL-10 ？1082GA promoter polymorphisms, surfactant protein A2 (SP-A2) polymorphisms, and cystic fibrosis transmembrane conductance regulator gene (CFTR) mutations. The studies indicate that ABPA patients are genetically at risk to develop skewed and heightened Th2 responses to A. fumigatus antigens. These genetic risk studies and their consequences of elevated biologic markers may aid in identifying asthmatic and CF patients who are at risk to the development of ABPA. Furthermore, these studies suggest that immune modulation with medications such as anti-IgE, anti-IL-4, and/or IL-13 monoclonal antibodies may be helpful in the treatment of ABPA. 1. Introduction Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease due to bronchial colonization by Aspergillus fumigatus that occurs in susceptible patients with asthma and cystic fibrosis (CF). The first published description of ABPA as an entity came from the United Kingdom in 1952 [1], while the first cases in the United States were reported a decade later [2, 3]. ABPA affects approximately 1%–2% of asthmatic patients and 7%–9% of CF patients [4–6]. If unrecognized or poorly treated, ABPA leads to airway destruction, bronchiectasis, and/or pulmonary fibrosis, resulting in significant morbidity and mortality. The diagnosis of ABPA is based on clinical and immunologic reactivity to A. fumigatus. The minimal criteria required for the diagnosis of ABPA are: (1) asthma or cystic fibrosis with deterioration of lung function, for example, wheezing, (2) immediate Aspergillus skin test reactivity, (3) total serum IgE ≥ 1000？IU/mL, (4) elevated Aspergillus specific IgE and IgG antibodies, and (5) chest radiographic infiltrates. Additional criteria may include peripheral blood eosinophilia, Aspergillus serum precipitating antibodies, central bronchiectasis, and
 Mathematics , 2014, Abstract: We study a two-person game based on the well-studied brushing process on graphs. Players Min and Max alternately place brushes on the vertices of a graph. When a vertex accumulates at least as many brushes as its degree, it sends one brush to each neighbor and is removed from the graph; this may in turn induce the removal of other vertices. The game ends once all vertices have been removed. Min seeks to minimize the number of brushes played during the game, while Max seeks to maximize it. When both players play optimally, the length of the game is the game brush number of the graph $G$, denoted $b_g(G)$. By considering strategies for both players and modelling the evolution of the game with differential equations, we provide an asymptotic value for the game brush number of the complete graph; namely, we show that $b_g(K_n) = (1+o(1))n^2/e$. Using a fractional version of the game, we couple the game brush numbers of complete graphs and the binomial random graph $\mathcal{G}(n,p)$. It is shown that for $pn \gg \ln n$ asymptotically almost surely $b_g(\mathcal{G}(n,p)) = (1 + o(1))p b_g(K_n) = (1 + o(1))pn^2/e$. Finally, we study the relationship between the game brush number and the (original) brush number.
 Journal of Immunology Research , 2011, DOI: 10.1155/2011/843763 Abstract: Allergic bronchopulmonary aspergillosis (ABPA) is a Th2 hypersensitivity lung disease in response to Aspergillus fumigatus that affects asthmatic and cystic fibrosis (CF) patients. Sensitization to A. fumigatus is common in both atopic asthmatic and CF patients, yet only 1-2% of asthmatic and 7–9% of CF patients develop ABPA. ABPA is characterized by wheezing and pulmonary infiltrates which may lead to pulmonary fibrosis and/or bronchiectasis. The inflammatory response is characterized by Th2 responses to Aspergillus allergens, increased serum IgE and eosinophilia. A number of genetic risks have recently been identified in the development of ABPA. These include HLA-DR and HLA-DQ, IL-4 receptor alpha chain (IL-4RA) polymorphisms, IL-10-1082GA promoter polymorphisms, surfactant protein A2 (SP-A2) polymorphisms, and cystic fibrosis transmembrane conductance regulator gene (CFTR) mutations. The studies indicate that ABPA patients are genetically at risk to develop skewed and heightened Th2 responses to A. fumigatus antigens. These genetic risk studies and their consequences of elevated biologic markers may aid in identifying asthmatic and CF patients who are at risk to the development of ABPA. Furthermore, these studies suggest that immune modulation with medications such as anti-IgE, anti-IL-4 and/or IL-13 monoclonal antibodies may be helpful in the treatment of ABPA. 1. Introduction Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease due to bronchial colonization by Aspergillus fumigatus that occurs in susceptible patients with asthma and cystic fibrosis (CF). The first published description of ABPA as an entity came from the United Kingdom in 1952 [1], while the first cases in the United States were reported a decade later [2, 3]. ABPA affects approximately 1-2% of asthmatic patients and 7–9% of CF patients [4–6]. If unrecognized or poorly treated, ABPA leads to airway destruction, bronchiectasis, and/or pulmonary fibrosis, resulting in significant morbidity and mortality. 2. Biology of Aspergillus fumigatus A number of fungi may lead to allergic bronchopulmonary mycoses (ABPM), but the genus Aspergillus contains the predominant organisms causing these pulmonary disorders; Aspergillus fumigatus is the species most commonly associated with ABPM. It is a ubiquitous, saprophytic mold found in both outdoor and indoor air, in potting soil, crawl spaces, compost piles, mulches, freshly cut grass, decaying vegetation, and sewage treatment facilities [7, 8]. A. fumigatus is found worldwide including the United States, where it is
 Southwest Journal of Pulmonary and Critical Care , 2011, Abstract: Bronchial atresia is a rare congenital disorder characterized by localized atresia or stenosis of a segmental bronchus. Imaging features typically include mucus impaction in distal airways associated with regional lung hyperlucency. Pathologic features of bronchial atresia have been rarely been reported. This case demonstrates CT features of this disorder as well as the unusual finding of increased lung uptake of 18F-fluorodeoxyglucose on PET scan. This finding led to a surgical lung biopsy to exclude infectious or neoplastic disorders. This case provides radiologic-pathologic correlation in a patient with congenital bronchial atresia and demonstrates that localized, mildly increased uptake on PET scan be associated bronchial atresia.
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