Standard models fail to predict the observed mass transfer dynamics and to identify kLa correctly. In order to capture the concentration gradient in the gas phase, we refine a standard ordinary differential equation (ODE) model and obtain a system of partial integro-differential equations (PIDE), for which we derive
an approximate analytical solution. Specific reactor configurations, in particular a relatively short Smad inhibitor bubble residence time, allow a quasi steady-state approximation of the PIDE system by a simpler ODE model which still accounts for the concentration gradient. Moreover, we perform an appropriate scaling of all variables and parameters. In particular, we introduce the dimensionless overall efficiency ?, which is more informative than kLa since it combines the effects of gas inflow, exchange, and solution.
Current standard models of mass transfer in laboratory-scale aerated STRs neglect the gradient in the gas concentration, which arises from highly efficient bubbling systems and high cellular exchange rates. The resulting error in the identification of ? (and hence kLa) increases dramatically with increasing mass transfer efficiency. Notably, the error differs between cell-free and culture-based methods of parameter identification, potentially confounding the determination of the biological enhancement buy STI571 of mass transfer. Our new model provides an improved theoretical framework that can be readily applied to aerated bioreactors in research and biotechnology.
Ricolinostat cell line Biotechnol. Bioeng. 2012; 109: 29973006. (C) 2012 Wiley Periodicals, Inc.”
“Multiple system atrophy (MSA) is a neurodegenerative disorder characterized by striatonigral degeneration and olivo-pontocerebellar atrophy. Neuronal degeneration is accompanied by primarily oligodendrocytic accumulation of alpha-synuclein (alpha syn) as opposed to the neuronal inclusions more commonly found in other alpha-synucleinopathies such as Parkinson’s disease. It is unclear how alpha syn accumulation in oligodendrocytes may lead to the extensive neurodegeneration observed in MSA; we hypothesize that the altered expression of oligodendrocyte-derived neurotrophic factors by alpha syn may be involved. In this context, the expression of a number neurotrophic factors reportedly expressed by oligodendrocytes [glial-derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), and insulin-like growth factor 1 (IGF-1), as well as basic fibroblast growth factor 2 (bFGF2), reportedly astrocyte derived] were examined in transgenic mouse models expressing human alpha syn (h alpha syn) under the control of either neuronal (PDGF beta or mThy1) or oligodendrocytic (MBP) promoters.