Pulmonary diseases cusecs a large portion of mortality in the world. There is no more cure for pulmonary diseases and many approaches are needed for finding ways to cure. Nowadays, implantation and drugs are only ways for curing those people who are facing with these diseases. Tissue engineering and regenerative medicine have been appeared as multidisciplinary field and also, they presents new therapeutic approaches for pulmonary diseases. One of these therapeutic approaches is decellularization which removes cellular but leaves intact important extracellular matrix (ECM) proteins and three-dimensional (3D) architecture and also, this approach has been studied for in-vitro and ex-vivo. In this study, we aimed to investigate a comparison of different concentrations of Triton X-100 and Sodium dodecyl sulfate detergents in lung decellularization in order to evaluate the effects of different concentrations and times of mentioned detergents on three dimensional and ECM proteins lung. Two detergents (Triton-X100 and Sodium dodecyl sulfat) were used with different concentrations for decellularizing rat lungs for maintaining of three-dimensional lung architecture and ECM protein compositions which have significant roles in differentiation and migration of stem cells. Results showed that SDS 0.05%, 0.1% and Triton-X100 0.1% could maintain 3D, elastin and collagen better than other concentrations in 24 and 48 h- decellularization. We concluded that these approaches can help to achieve three-dimensional architecture and extracellular matrix of lung with minimum destruction for next step such as recellularization and in-vivo study.

Background and Objectives: Non-thermal atmospheric-pressure plasma or cold plasma is defined as an ionized gas. This study aimed to investigate the effect of cold plasma on Pseudomonas aeruginosa strains. Also, the expression level of the alp virulence gene before and after treatment with cold plasma was compared with the Housekeeping gene gyrA. Materials and Methods: P. aeruginosa isolates recovered from hospitalized burn patients at Shahid Motahari Burns Hos- pital, Tehran, Iran. The Kirby Bauer disk diffusion method was used to determine the antimicrobial susceptibility test. Then, the antibacterial effect of atmospheric non-thermal plasma was evaluated on P. aeruginosa in as in vitro and in vivo studies at different times on Muller Hinton agar and in mouse model (treated by plasma every day/ 90 sec). The histopathological study was evaluated by Hematoxylin-Eosin staining. Data were analyzed using SPSS software by the Chi-square test and Pvalues less than 0.05 considered as statistically significant. Results: Results indicated that non-thermal atmospheric plasma inhibited the growth of P. aeruginosa. The non-thermal helium plasma accelerates wound healing for 6 days. Results showed that cold plasma decreased virulence gene expression alp after treatment. Therefore, cold plasma can be suggested as a complementary therapeutic protocol to reduce bacterial infection and accelerate wound healing and reduce the expression of virulence genes of pathogens. Conclusion: Cold plasma showed pathogen inhibitory properties of P. aeruginosa and virulence alkaline protease and wound healing properties in animal models, so this inexpensive and suitable method can be presented to the medical community to disinfect burn wounds and improve wound healing.

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Airway remodeling is a pathophysiologic process at the clinical, cellular, and molecular level relating to chronic obstructive airway diseases such as chronic obstructive pulmonary disease (COPD), asthma and mustard lung. These diseases are associated with the dysregulation of multiple molecular pathways in the airway cells. Little progress has so far been made in discovering the molecular causes of complex disease in a holistic systems manner. Therefore, pathway and network reconstruction is an essential part of a systems biology approach to solve this challenging problem. In this paper, multiple data sources were used to construct the molecular process of airway remodeling pathway in mustard lung as a model of airway disease. We first compiled a master list of genes that change with airway remodeling in the mustard lung disease and then reconstructed the pathway by generating and merging the protein-protein interaction and the gene regulatory networks. Experimental observations and literature mining were used to identify and validate the master list. The outcome of this paper can provide valuable information about closely related chronic obstructive airway diseases which are of great importance for biologists and their future research. Reconstructing the airway remodeling interactome provides a starting point and reference for the future experimental study of mustard lung, and further analysis and development of these maps will be critical to understanding airway diseases in patients.