Subject(s)
Antineoplastic Agents/adverse effects , Carcinoma, Non-Small-Cell Lung/drug therapy , Lacrimal Apparatus Diseases/chemically induced , Lacrimal Apparatus/drug effects , Lung Neoplasms/drug therapy , Pemetrexed/adverse effects , Carcinoma, Non-Small-Cell Lung/pathology , Humans , Lacrimal Apparatus/physiopathology , Lacrimal Apparatus Diseases/diagnosis , Lacrimal Apparatus Diseases/physiopathology , Lacrimal Apparatus Diseases/therapy , Lung Neoplasms/pathology , Male , Middle Aged , Quality of Life , Treatment OutcomeABSTRACT
Pseudoaneurysm due to cancer is uncommon generally and is extremely rare in lung cancer. We report two cases of false aneurysms due to lung cancer that spontaneously regressed upon chemotherapy without intervention. Both patients had squamous cell carcinoma of the lung and the diagnosis of a pseudoaneurysm was made using computed tomography. There was no evidence of severe bronchial hemorrhage and the pseudoaneurysms were small and well-encased. Chemotherapy was performed and the pseudoaneurysms resolved.
ABSTRACT
Airway smooth muscle growth contributes to the mechanism of airway hyperresponsiveness (AHR) in asthma. Although current steroid use demonstrates anti-inflammatory activity, there is little reported on the action of corticosteroid on smooth muscle of the asthmatic airway. The present study investigated the effect of inhaled corticosteroid on the thickening of airway smooth muscle in bronchial asthma. We developed a mouse model of airway remodeling including smooth muscle thickening in which ovalbumin (OVA)-sensitized female BALB/c-mice were repeatedly exposed to intranasal OVA administration twice a week for 3 months. Mice were treated intranasally with fluticasone during the OVA challenge. Mice chronically exposed to OVA developed sustained eosinophilic airway inflammation compared with control mice. In addition, the mice chronically exposed to OVA developed features of airway remodeling, including thickening of the peribronchial smooth muscle layer. Intranasal administration of fluticasone inhibited the development of eosinophilic inflammation, and importantly, thickening of the smooth muscle layer. Moreover, intranasal fluticasone treatment reduced the transforming growth factor (TGF)-beta 1 level in bronchoalveolar lavage fluid and regulated active TGF-beta 1 signaling with a reduction in the expression of phospho-Smad2/3 and the concomitant up-regulation of Smad7 in lung tissue sections. These results suggest that intranasal administration of fluticasone can modulate the remodeling of airway smooth muscle via regulation of TGF-beta 1 production and active TGF-beta 1 signaling.
Subject(s)
Androstadienes/pharmacology , Anti-Inflammatory Agents/pharmacology , Asthma/pathology , Muscle, Smooth/drug effects , Administration, Intranasal , Androstadienes/administration & dosage , Animals , Anti-Inflammatory Agents/administration & dosage , Asthma/immunology , Bronchi/drug effects , Bronchi/pathology , Bronchoalveolar Lavage Fluid/cytology , Chronic Disease , Enzyme-Linked Immunosorbent Assay , Female , Fluticasone , Lung/drug effects , Lung/pathology , Mice , Mice, Inbred BALB C , Muscle, Smooth/pathology , Ovalbumin/immunology , Transforming Growth Factor beta1/biosynthesisABSTRACT
Asbestos is a very important material for industrial use. However, the need for a substitute for asbestos fiber is currently on the rise due to its high disease causing potential. This study evaluated the potential bio-hazardous effects of TAFMAG, a natural fibrous silicate produced in China, in comparison with chrysotile, a typical toxic asbestos. The physicochemical properties of TAFMAG were very similar to those of chrysotile when it was examined by a scanning electron microscope (SEM) and X-ray diffraction (XRD) analyses. Both of TAFMAG and chrysotile showed high content of magnetite and Fenton activity when compared with wollastonite, a non-asbestos fiber with a known low toxicity. When their cellular toxicity was assessed, TAFMAG showed no or less comparable to that of chrysotile in the hemolysis and lipid peroxidation of erythrocytes, and also on a MTT assay in RLE-6TN, a rat alveolar epithelial cell line. Pre-treatment of fibers with desferrioxamine, an iron chelator, showed that iron content of TAFMAG and chrysotile might be important in their cellular toxicity. These results suggest that TAFMAG is potentially toxic when inhaled into the lung and appropriate laws and regulations should be established for its use.