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Background and Objective: Correlations between the image analysis of CT scan, lung function and quality of life in patients with idiopathic pulmonary fibrosis (IPF) remain unclear. This study aimed to investigate the impacts of pulmonary blood‐vessel distribution and the extent of fibrosis on the lung function and quality of life of patients with IPF. Methods: Patients were enrolled in an IPF registry and had completed pulmonary function tests, chest HRCT, St. George Respiratory Questionnaire (SGRQ) and echocardiography. Pulmonary blood‐vessel distribution, specific image‐derived airway volume (siVaw) and fibrosis extent (siVfib) were quantitatively calculated by functional respiratory imaging on HRCT. Results: The study subjects were categorized into DLco <40% pred. (n = 40) and DLco ≥40% pred. (n = 19) groups. Patients with DLco <40% pred. had significantly higher scores of SGRQ, composite physiologic index (CPI), exercise oxygen desaturation (∆SpO2), siVaw, lower FVC% pred. and 6‐minute walking distance% pred. The proportion of small blood vessels in the upper lobes (BV5PR‐UL) was significantly correlated with CPI, DLco % Pred., FVC% pred., SGRQ and ∆SpO2. Only BV5PR‐UL had a significant impact on all indices but not BV5PR in the lower lobes (BV5PR‐LL). siVfib was significantly negatively correlated with BV5PR‐UL, DLco% pred. and FVC% pred., as well as positively correlated with CPI, ∆SpO2 and siVaw. Conclusion: BV5PR‐UL and siVfib had significant correlations with lung function and may become important indicators to assess the severity of IPF and the impact on quality of life. The pulmonary small vessels proportion in upper lobes of lung and fibrotic extent of whole lung obtained from functional respiratory imaging analysis have significant correlations with lung function and may become important indicators to assess the severity of IPF and the impact on quality of life. [ABSTRACT FROM AUTHOR]

Purpose Chronic obstructive pulmonary disease (COPD) with eosinophilic airway inflammation may represent a unique phenotype, possibly with shared features of COPD and asthma. The role of exhaled nitric oxide (eNO) in identifying COPD patients with sputum eosinophilia was examined in this study. Methods Ninety COPD patients without past medical history of asthma or allergic diseases were prospectively enrolled, and their eNO, lung function, and cellular profile of induced sputum were measured. Eosinophil cationic protein and IgE in sputum and venous blood also were determined. Subjects with and without sputum eosinophilia (>3 %) were compared. The role of eNO in the prediction of sputum eosinophilia was assessed in a logistic regression model. Results Patients with sputum eosinophilia had significantly higher levels of eNO (29 vs. 18 ppb, p = 0.01) than those without. The difference in serum total IgE (168 vs. 84.9 IU/ml, p = 0.057) and percentages of positive allergen test results (48.3 vs. 29.5 %, p = 0.082) showed a trend toward significance. The sputum eosinophil level was significantly correlated to the eNO level (r = 0.485, p 23.5 ppb) in the prediction of sputum eosinophilia were 3.909 (confidence interval (CI) 1.542-9.91, p = 0.004) and 4.329 (CI 1.306-14.356, p = 0.017), respectively. Conclusions eNO is a good marker to identify COPD patients with eosinophilic airway inflammation., Author(s): Kun-Ta Chou[sup.1] [sup.2] [sup.3] [sup.4] , Kang-Cheng Su[sup.1] [sup.5] , Shiang-Fen Huang[sup.1] , Yi-Han Hsiao[sup.1] , Ching-Min Tseng[sup.1] , Vincent Yi-Fong Su[sup.1] , Shih-Chieh Hung[sup.3] , Diahn-Warng Perng[sup.1] [sup.4] [...]

Background Expression of transforming growth factor (TGF)-[β.sub.1] and increases in angiogenesis and deposition of extracellular matrix are the key features of tracheal granulation formation. The aim of this study was to investigate the potential role of thalidomide in preventing granulation tissue formation from the aspect of cellular effects in vitro, including fibroblast proliferation, vascular endothelial growth factor (VEGF) release, and collagen production. Methods Human lung fibroblasts were obtained from bronchus and cultured. The effects of thalidomide on cell proliferation, migration, TGF-[β.sub.1]-induced VEGF, and signal pathway were investigated. Results Thalidomide (20 µM) not only inhibited cell proliferation after 24 h [fold increase of cell number, 0.85 ± 0.09 vs. 1.47 ± 0.14 (treatment vs. control group); P < 0.01] and 48 h of incubation (0.85 ± 0.10 vs. 1.97 ± 0.12; P < 0.001), it also inhibited cell migration and slowed wound closure at 24 h (P < 0.001). Thalidomide significantly attenuated TGF-[β.sub.1]-induced VEGF expression at both the mRNA and protein levels. Incubation of thalidomide with cells stimulated with TGF-[β.sub.1] significantly inhibited their production of collagen. Thalidomide inhibited Smad3, STAT3, and subsequent p44/42 kinase phosphorylation. Conclusion Thalidomide may inhibit human fibroblast proliferation and it is worthy of further in vivo investigation. Keywords Thalidomide * Lung fibroblasts * STAT3 * Smad3 * TGF-[β.sub.1], Introduction Prolonged tracheotomy and endotracheal intubation may cause airway obstruction due to occupation of the airway lumen by the growth of exuberant granulation tissue. Granulation tissue is one of the [...]

Background: While Candida pneumonia is life-threatening, biomarker measurements to early detect suspected Candida pneumonia are lacking. This study compared the diagnostic values of measuring levels of (1, 3)-β-D-glucan in endotracheal aspirate, bronchoalveolar lavage fluid, and serum to detect suspected Candida pneumonia in immunocompromised and critically ill patients.Methods: This prospective, observational study enrolled immunocompromised, critically ill, and ventilated patients with suspected fungal pneumonia in mixed intensive care units from November 2010 to October 2011. Patients with D-glucan confounding factors or other fungal infection were excluded. Endotracheal aspirate, bronchoalveolar lavage fluid and serum were collected from each patient to perform a fungal smear, culture, and D-glucan assay.Results: After screening 166 patients, 31 patients completed the study and were categorized into non-Candida pneumonia/non-candidemia (n = 18), suspected Candida pneumonia (n = 9), and non-Candida pneumonia/candidemia groups (n = 4). D-glucan levels in endotracheal aspirate or bronchoalveolar lavage were highest in suspected Candida pneumonia, while the serum D-glucan level was highest in non-Candida pneumonia/candidemia. In all patients, the D-glucan value in endotracheal aspirate was positively correlated with that in bronchoalveolar lavage fluid. For the detection of suspected Candida pneumonia, the predictive performance (sensitivity/specificity/D-glucan cutoff [pg/ml]) of D-glucan in endotracheal aspirate and bronchoalveolar lavage fluid was 67%/82%/120 and 89%/86%/130, respectively, accounting for areas under the receiver operating characteristic curve of 0.833 and 0.939 (both P < 0.05), respectively. Measuring serum D-glucan was of no diagnostic value (area under curve =0.510, P = 0.931) for the detection of suspected Candida pneumonia in the absence of concurrent candidemia.Conclusions: D-glucan levels in both endotracheal aspirate and bronchoalveolar lavage, but not in serum, provide good diagnostic values to detect suspected Candida pneumonia and to serve as potential biomarkers for early detection in this patient population. [ABSTRACT FROM AUTHOR]

Gesture-recognition is an important component for many intelligent human-computer interaction applications. For example, a realtime sign-language recognition system would detect and interpret hand gestures. Many vision-based sign-language recognition methods have been proposed over the years with mix results of usability. Some system are limited to recognize only a few gestures, while others require the use of 3D camera to provides depth information to improve recognition accuracy. In this paper, a Kinect-based Taiwanese sign-language recognition system is proposed. Three main features are extracted from the signing gestures, namely hand positions, hand signing direction, and hand shapes. The hand positions are readily available through the input sensor. The signing direction is determined using HMM on trajectory of the hand movement, and a SVM is trained and used to recognize the hand shapes. Experimental results show that the proposed system achieved an 85.14 % recognition rate. [ABSTRACT FROM AUTHOR]

Background and objective Bile acid ( BA) aspiration is associated with various lung diseases. It was hypothesized that BA may induce changes in alveolar epithelium permeability and contribute to the pathogenesis of lung injury. Methods Human alveolar epithelial cells were grown in monolayer and stimulated with a major component of BA, chenodeoxycholic acid ( CDCA). Transepithelial electrical resistance ( TER) and paracellular fluxes were measured to assess permeability alteration. Prostaglandin E2 ( PGE2) production was measured, and its effect on TER and junctional proteins ( JP) was also examined. Reverse transcription polymerase chain reaction and Western blots were used to investigate the expression of messenger RNA and JP. Results CDCA induced significant p38 and c-Jun N-terminal kinase ( JNK) phosphorylation, cytosolic phospholipase A2 ( cPLA2) and cyclooxygenase-2 ( COX-2) messenger RNA expression, PGE2 production, TER reduction and decay of JP (including occludin, zonula occludens-1 ( ZO-1) and E-cadherin, in which ZO-1 had maximal change). CDCA also increased paracellular fluxes, which was abolished by dexamethasone. Both CDCA and PGE2 contributed to TER reduction in an identical trend and a dose-response manner. PGE2 also reduced ZO-1 expression, which was similar to that observed by CDCA stimulation. Pretreatment with inhibitors of p38 ( SB203580), JNK ( SP600125), cPLA2 (mepacrine) and COX-2 ( NS398) as well as dexamethasone reversed the CDCA-induced PGE2 production, TER reduction and decay of ZO-1. Conclusions The increase in alveolar permeability was associated with decay of JP. BA may induce permeability alteration through the upregulation of mitogen-activated protein kinase, cPLA2, COX-2, PGE2 and JP, which may contribute to the pathogenesis of BA-associated lung injury. [ABSTRACT FROM AUTHOR]

Abstract: Background: Treatment of COPD with a combination of long-acting β2 agonists and corticosteroids is currently used worldwide. The mechanisms of the anti-inflammatory effects and their associations with histone deacetylase (HDAC) activity remain unclear. Methods: Human alveolar macrophages were isolated and stimulated with H2O2 in the presence of varying concentrations of long-acting β2 agonists and corticosteroids. Supernatants were collected for IL-8 and MMP-9 measurements. Cell lysates were analyzed for HDAC (mainly HDAC1/HDAC2) activity. Quantitative real-time PCR was performed to determine the levels of IL-8 and MMP-9 mRNA. Results: Both long-acting β2 agonists, salmeterol and formoterol, and corticosteroids, fluticasone and budesonide, showed anti-inflammatory effects to a certain extent on H2O2-induced IL-8 and MMP-9 release in alveolar macrophages. Combinations of long-acting β2 agonists and corticosteroids exerted greater effects to suppress mediator release, and both transcription and translation of IL-8 and MMP-9 were inhibited. It seemed that the levels of IL-8 and MMP-9 after H2O2 stimulation were inversely associated with the activity of HDAC. H2O2 stimulation resulted in a significant decrease in HDAC activity and was associated with an increase in mediator release. In contrast, treatment with long-acting β2 agonists, corticosteroids or theophylline restored the H2O2-induced decrease in HDAC activity and inhibited mediator release. Conclusion: Combinations of long-acting β2 agonists and corticosteroids exerted greater effects on the suppression of mediator release in relation to the enhancement of HDAC activity. This supports at least in part the likely contribution of anti-inflammatory effects of long-acting β2 agonists and corticosteroids to the clinical benefits seen in COPD patients. [Copyright &y& Elsevier]