Autophagy and inflammation.

Autophagy is a homeostatic mechanism involved in the disposal of damaged organelles, denatured proteins as well as invaded pathogens through a lysosomal degradation pathway. Recently, increasing evidences have demonstrated its role in both innate and adaptive immunity, and thereby influence the pathogenesis of inflammatory diseases. The detection of autophagy machinery facilitated the measurement of autophagy during physiological and pathophysiological processes.

Regulatory mechanisms of TGF-β1-induced fibrogenesis of human alveolar epithelial cells.

Pulmonary fibrosis is characterized by an extensive activation of fibrogenic cells and deposition of extracellular matrix (ECM). Transforming growth factor (TGF)-β1 plays a pivotal role in the pathogenesis of pulmonary fibrosis, probably through the epithelial- to-mesenchymal transition (EMT) and ECM production. The present study investigates potential mechanism by which TGF-β1 induces EMT and ECM production in the fibrogenesis of human lung epithelial cells during pulmonary fibrosis.

Increased Lung Ischemia-Reperfusion Injury in Aquaporin 1-Null Mice Is Mediated via Decreased Hypoxia-Inducible Factor 2α Stability.

Aquaporin (AQP) 1, a water channel protein expressed widely in vascular endothelia, has been shown to regulate cell migration, angiogenesis, and organ regeneration. Even though its role in the pathogenesis of lung ischemia-reperfusion (IR) injury has been defined, the functional role of AQP1 during long-term IR resolution remains to be clarified. Here, we found that AQP1 expression was increased at late time points (7-14 d) after IR and colocalized with endothelial cell (EC) marker CD31.

Autophagy protects against ischemia/reperfusion-induced lung injury through alleviating blood-air barrier damage.

Background: Understanding the role and underlying regulation mechanism of autophagy in ischemia/reperfusion (I/R)-induced lung injury may provide potentially new pharmacologic targets for treatment of acute lung injury. The aim of this study was to adjust autophagy with pharmacologic agents to determine its functional significance in I/R-induced lung injury.

Methods: Human pulmonary microvascular endothelial cells (HPMVECs) and mice were pre-conditioned with autophagy inhibitor chloroquine or promoter rapamycin before they were challenged with oxygen-glucose deprivation/oxygen-glucose restoration (OGD) and lung I/R, respectively.

Protective effects of keratinocyte growth factor-2 on ischemia-reperfusion-induced lung injury in rats.

Ischemia-reperfusion (I/R) is a common cause to compromise tissue injury via endothelial and epithelial barrier dysfunction and damage. Keratinocyte growth factor (KGF)-2 could play an important role in the repair of alveolar epithelial damage and maintain the capillary barrier function. The present study aimed to investigate the potential effects of KGF-2 on I/R-induced lung injury in rats and the related mechanisms.

Bioinformatics insights into acute lung injury/acute respiratory distress syndrome.

Bioinformatics is the application of omics science, information technology, mathematics and statistics in the field of biomarker detection. Clinical bioinformatics can be applied for identification and validation of new biomarkers to improve current methods of monitoring disease activity and identify new therapeutic targets. Acute lung injurt (ALI)/Acute respiratory distress syndrome (ARDS) affects a large number of patients with a poor prognosis.

A short-term educational program improved physicians' adherence to guidelines for COPD and asthma in Shanghai.

Background: Chronic pulmonary diseases such as chronic obstructive pulmonary disease (COPD) and asthma exert increasing burden on society while the management of them is far from adequate. The objective of this study is to evaluate adherence to guidelines through a patient study, and then investigate the effects of a short-term quality improvement educational program among clinicians in Shanghai, China.

Methods: A prescription survey was performed in a random sample of 100 COPD and asthma outpatients to assess their pharmacological therapy.

Effects of phosphoinositide 3-kinase on protease-induced acute and chronic lung inflammation, remodeling, and emphysema in rats.

Background: Phosphoinositide 3-kinase (PI3K) plays an important role in tissue inflammatory reactions and fibrotic processes. The objective of this study was to evaluate the potential mechanism and therapeutic effects of PI3K inhibitor on pancreatic elastase (PE)-induced acute and chronic lung inflammation, edema, and injury.

Methods: Rats were terminated at 7 or 28 days after an intratracheal challenge with PE and intranasal instillation with a PI3K inhibitor, SHBM1009.

Genetic network and gene set enrichment analysis to identify biomarkers related to cigarette smoking and lung cancer.

Objectives: Cigarette smoking is the most demonstrated risk factor for the development of lung cancer, while the related genetic mechanisms are still unclear.

Methods: The preprocessed microarray expression dataset was downloaded from Gene Expression Omnibus database. Samples were classified according to the disease state, stage and smoking state.

Profiling the human response to physical exercise: a computational strategy for the identification and kinetic analysis of metabolic biomarkers.

Background: In metabolomics, biomarker discovery is a highly data driven process and requires sophisticated computational methods for the search and prioritization of novel and unforeseen biomarkers in data, typically gathered in preclinical or clinical studies. In particular, the discovery of biomarker candidates from longitudinal cohort studies is crucial for kinetic analysis to better understand complex metabolic processes in the organism during physical activity.

Findings: In this work we introduce a novel computational strategy that allows to identify and study kinetic changes of putative biomarkers using targeted MS/MS profiling data from time series cohort studies or other cross-over designs.

Potential clinical application of KGF-2 (FGF-10) for acute lung injury/acute respiratory distress syndrome.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an acute life-threatening form of hypoxemic respiratory failure with a high mortality rate, and there is still a great need for more effective therapies for such a severe and lethal disease. Dysfunction of endothelial and epithelial barriers is one of the most important mechanisms in hypoxia-associated ALI/ARDS. The acceleration of the epithelial repair process in the injured lung may provide an effective therapeutic target.

Preventive and therapeutic effects of phosphoinositide 3-kinase inhibitors on acute lung injury.

Background: Phosphoinositide 3-kinases (PI3Ks) are involved in a number of biologic responses. Recent preclinical studies demonstrated that the PI3K-dominant signal pathway could play an important role in the development of acute lung injury, although the mechanism remains unclear.

Methods: CD-1 mice were administered different PI3K inhibitors either intranasally or intragastrically once a day for 3 days before intratracheal instillation of lipopolysaccharide at 4 h and 24 h.

COPD in China: the burden and importance of proper management.

Although, to our knowledge, there has been no exhaustive or credible review of the evidence of the disease burden of COPD in China, COPD has become an increasing public health concern to the Chinese medical community. The purpose of this article is to review the evidence and evaluate and clarify the disease burden of COPD in China with the aim of improving effective management. We reviewed previous studies of COPD in China, which included data on prevalence, mortality, disease burden, risk factors, diagnosis, and management by searching related Web sites, including PubMed, ProQuest, and Thomson Reuters' Web of Knowledge, as well as major Chinese databases and government Web sites.

Involvement of type II pneumocytes in the pathogenesis of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality, but the cellular and molecular mechanisms are still not fully understood. Type II pneumocytes are identified as the synthesizing cells of the alveolar surfactant, which has important properties in maintaining alveolar and airway stability. Lung surfactant can reduce the surface tension and prevent alveolar collapse and the airway walls collapse.