Simulation of Phenol Adsorption in a Packed Bed Column

Water pollution is a very persistent problem. The intensive throwing up of different toxic substances without control constitutes a real danger for humanity. Phenolic compounds are common contaminants in wastewater, generated by petroleum and petrochemical, coal conversion and phenol producing industries. The phenols are considered as priority pollutants since they are harmful to organisms at low concentrations because of their potential harm to human health. United State Environmental Protection Agency(EPA) regulations call for lowering phenol content in wastewaterto less 1 mgL-1 before discharging. This study focusses on the feasibility of using activated carbon to remove phenol from waste water in industry. Simulation by Aspen Adsorption is conducted to investigate the feasibility. Several sensitivity analyses such as changing the parameters which affected the rate of adsorption are discussed. Besides that, it is found that the scaling up of the column is not practicable in industry

Type-1 Collagen differentially alters β-catenin accumulation in primary Dupuytren's Disease cord and adjacent palmar fascia cells

<p>Abstract</p> <p>Background</p> <p>Dupuytren's Disease (DD) is a debilitating contractile fibrosis of the palmar fascia characterised by excess collagen deposition, contractile myofibroblast development, increased Transforming Growth Factor-β levels and β-catenin accumulation. The aim of this study was to determine if a collagen-enriched environment, similar to <it>in vivo </it>conditions, altered β-catenin accumulation by primary DD cells in the presence or absence of Transforming Growth Factor-β.</p> <p>Methods</p> <p>Primary DD and patient matched, phenotypically normal palmar fascia (PF) cells were cultured in the presence or absence of type-1 collagen and Transforming Growth Factor-β1. β-catenin and α-smooth muscle actin levels were assessed by western immunoblotting and immunofluorescence microscopy.</p> <p>Results</p> <p>DD cells display a rapid depletion of cellular β-catenin not evident in patient-matched PF cells. This effect was not evident in either cell type when cultured in the absence of type-1 collagen. Exogenous addition of Transforming Growth Factor-β1 to DD cells in collagen culture negates the loss of β-catenin accumulation. Transforming Growth Factor-β1-induced α-smooth muscle actin, a marker of myofibroblast differentiation, is attenuated by the inclusion of type-1 collagen in cultures of DD and PF cells.</p> <p>Conclusion</p> <p>Our findings implicate type-1 collagen as a previously unrecognized regulator of β-catenin accumulation and a modifier of TGF-β1 signaling specifically in primary DD cells. These data have implications for current treatment modalities as well as the design of <it>in vitro </it>models for research into the molecular mechanisms of DD.</p