Cluster-associate viscosity model of tin chloride in comparison with the Frenkel model

Determining the viscosity of inorganic molten compounds like tin chloride is critically important for material processing, chemical synthesis, and energy applications. However, experimental limitations have restricted the development of accurate viscosity models. This study tests a new cluster-associate model for predicting the viscosity of molten tin chloride across a wide temperature range. The model links viscosity to the structure and dynamics of molecular clusters in the melt. The aim of this study is to establish a correlation between viscosity and cluster formation within a liquid, using tin chloride as an example. The data were calculated using a newly developed equation based on the concept of randomized particles. The temperature range studied was from the melting point to the boiling point. To verify the accuracy of the cluster-associate model, it was compared with the Frenkel equation using logarithmic coordinates. Simulations were performed on tin chloride, which yielded results showing a linear relationship between the degree of cluster association and the activation energy of fluidity. The proportionality coefficient reflects the activation energy associated with a single cluster. The Frenkel equation in the logarithmic coordinate scale was compared with the cluster-associate model. The functional dependence and correspondence of these models are indicated by their high coefficient mutual correlation. The proposed viscosity model underwent testing for the entire liquid state range of the substance, and calculations confirmed its validity. This enables reliable use of the suggested model for both high- and low-temperature extrapolation, including the critical point region.     

Asthmatic Eosinophils Alter the Gene Expression of Extracellular Matrix Proteins in Airway Smooth Muscle Cells and Pulmonary Fibroblasts

The impaired production of extracellular matrix (ECM) proteins by airway smooth muscle cells (ASMC) and pulmonary fibroblasts (PF) is a part of airway remodeling in asthma. This process might be influenced by eosinophils that migrate to the airway and abundantly secrete various cytokines, including TGF-β. We aimed to investigate the effect of asthmatic eosinophils on the gene expression of ECM proteins in ASMC and PF. A total of 34 study subjects were recruited: 14 with allergic asthma (AA), 9 with severe non-allergic eosinophilic asthma (SNEA), and 11 healthy subjects (HS). All AA patients underwent bronchial allergen challenge with D. pteronyssinus. The peripheral blood eosinophils were isolated using high-density centrifugation and magnetic separation. The individual cell cultures were made using hTERT ASMC and MRC-5 cell lines and the subjects’ eosinophils. The gene expression of ECM and the TGF-β signaling pathway was analyzed using qRT-PCR. We found that asthmatic eosinophils significantly promoted collagen I, fibronectin, versican, tenascin C, decorin, vitronectin, periostin, vimentin, MMP-9, ADAM33, TIMP-1, and TIMP-2 gene expression in ASMC and collagen I, collagen III, fibronectin, elastin, decorin, MMP-2, and TIMP-2 gene expression in PF compared with the HS eosinophil effect. The asthmatic eosinophils significantly increased the gene expression of several canonical and non-canonical TGF-β signaling pathway components in ASMC and PF compared with the HS eosinophil effect. The allergen-activated AA and SNEA eosinophils had a greater effect on these changes. In conclusion, asthmatic eosinophils, especially SNEA and allergen-activated eosinophils, imbalanced the gene expression of ECM proteins and their degradation-regulating proteins. These changes were associated with increased gene expression of TGF-β signaling pathway molecules in ASMC and PF.