The stability analyses of the mathematical models of hepatitis C virus infection

There are two mathematical models of Hepatitis C virus (HCV) being discussed; the original model of HCV viral dynamics (Neumann et al., 1998) and its extended model (Dahari et al., 2007). The key aspects of the mathematical models have provided resources for analysing the stability of the uninfected and the infected steady states, in evaluating the antiviral effectiveness of therapy and for estimating the ranges of values of the parameters for clinical treatment. The original model is considered to be a deterministic model because of the predictive nature of the antiviral therapy within the constant target cells. Numerical simulations are carried out in the extended model, to explain the stability of the steady states in the absence or existence of migration in hepatocytes and, drug efficacy in treating HCV infection

From the cell membrane to the nucleus: unearthing transport mechanisms for Dynein

Mutations in the motor protein cytoplasmic dynein have been found to cause Charcot-Marie-Tooth disease, spinal muscular atrophy, and severe intellectual disabilities in humans. In mouse models, neurodegeneration is observed. We sought to develop a novel model which could incorporate the effects of mutations on distance travelled and velocity. A mechanical model for the dynein mediated transport of endosomes is derived from first principles and solved numerically. The effects of variations in model parameter values are analysed to find those that have a significant impact on velocity and distance travelled. The model successfully describes the processivity of dynein and matches qualitatively the velocity profiles observed in experiments

The stability analyses of the mathematical models of hepatitis C virus infection

There are two mathematical models of Hepatitis C virus (HCV) being discussed; the original model of HCV viral dynamics (Neumann et al., 1998) and its extended model (Dahari et al., 2007). The key aspects of the mathematical models have provided resources for analysing the stability of the uninfected and the infected steady states, in evaluating the antiviral effectiveness of therapy and for estimating the ranges of values of the parameters for clinical treatment. The original model is considered to be a deterministic model because of the predictive nature of the antiviral therapy within the constant target cells. Numerical simulations are carried out in the extended model, to explain the stability of the steady states in the absence or existence of migration in hepatocytes and, drug efficacy in treating HCV infection

Molecular recognition of organic ammonium ions in solution using synthetic receptors

Ammonium ions are ubiquitous in chemistry and molecular biology. Considerable efforts have been undertaken to develop synthetic receptors for their selective molecular recognition. The type of host compounds for organic ammonium ion binding span a wide range from crown ethers to calixarenes to metal complexes. Typical intermolecular interactions are hydrogen bonds, electrostatic and cation–π interactions, hydrophobic interactions or reversible covalent bond formation. In this review we discuss the different classes of synthetic receptors for organic ammonium ion recognition and illustrate the scope and limitations of each class with selected examples from the recent literature. The molecular recognition of ammonium ions in amino acids is included and the enantioselective binding of chiral ammonium ions by synthetic receptors is also covered. In our conclusion we compare the strengths and weaknesses of the different types of ammonium ion receptors which may help to select the best approach for specific applications

Social movements and the politicization of chronic poverty

Discussions of chronic poverty emphasize the extent to which poverty endures because of the social relationships and structures within which particular social groups are embedded. In this sense chronic poverty is a socio-political relationship rather than a condition of assetless-ness. Understood as such, processes of social mobilization become central to any discussion of chronic poverty because they are vehicles through which such relationships are argued over in society and potentially changed. This article explores the ways in which social movements, as one form of such mobilization, might affect chronic poverty. Four domains are discussed: influencing the underlying dynamics of the political economy of poverty; challenging dominant meanings of poverty in society; direct effects on the assets of the poor; and engaging with the state. The inherent fragilities of social movements limit these contributions, the most important of which is to destabilize taken-for-granted, hegemonic discourses on poverty and its reduction