Air quality indices: a review

National directives on air quality oblige nations to monitor and report on their air quality, allowing the public to be informed on the ambient pollution levels. The last is the reason for the always increasing interest, demonstrated by the number of publications on this topic in recent years, in air quality/pollution indices: since the concentration of individual pollutants can be confusing, concentration measurements are conveniently transformed in terms of an air quality index. In this way, complex situations are summarized in a single figure, letting comparisons in time and space be possible. In this paper we will give an overview about the Air Quality/Pollution Indices proposed in literature and/or adopted by countries, trying also to categorize them into homogeneous groups. For the classification different approaches can be followed. Since in real life exposure to mixtures of chemicals occurs, with additive, synergistic or antagonistic effects, here we will distinguish between indices that consider the conjoint effect of pollutants and indices only based on the actual most dangerous pollutant. This brief review on air pollution indices shows, on one side, the wide interest in the problem, on the other, the lack of a common strategy which allows to compare the state of the air for cities that follow different directives. The main differences between the indices will be also described.     

Simulating the G-protein cAMP pathway with a two-compartment reactive lattice gas

Cellular signaling (or signal transduction) is the process by which extracellular signals are converted into cellular responses. Mathematical models of signaling pathways may help understanding their general regulatory principles, as well as the roles of the different components often involved in more than one pathway.

The aim of the present work is to describe a discrete model in time and space to study the dynamics of the population of molecules involved in a specific pathway. To this purpose, we use a multi-compartment stochastic cellular automaton to simulate one of the best understood cell signaling pathways: the GPCR-pathway.

We then show the effect on the signal-carrying efficiency of condensing a molecular species, which is pivotal to the reaction pathway, in a closed region of the cytosol.

We find that localization increases the robustness of the translocation mechanism only above a density threshold. For homogeneous settings, by increasing the concentration above a critical value, the translocation is obstructed by mere physical occupation constraints of the signal-carrying molecule. This conclusion is in line with previous findings, according to which in highly dense regions of the cytosol, convection by autocatalytic activation of adjacent molecules might be more efficient than diffusion as a main signal propagation mechanism.     

Artemis is a phosphorylation target of ATM and ATR and is involved in the G2/M DNA damage checkpoint response

Mutations in Artemis in both humans and mice result in severe combined immunodeficiency due to a defect in V(D)J recombination. In addition, Artemis mutants are radiosensitive and chromosomally unstable, which has been attributed to a defect in nonhomologous end joining (NHEJ). We show here, however, that Artemis-depleted cell extracts are not defective in NHEJ and that Artemis-deficient cells have normal repair kinetics of double-strand breaks after exposure to ionizing radiation (IR). Artemis is shown, however, to interact with known cell cycle checkpoint proteins and to be a phosphorylation target of the checkpoint kinase ATM or ATR after exposure of cells to IR or UV irradiation, respectively. Consistent with these findings, our results also show that Artemis is required for the maintenance of a normal DNA damage-induced G2/M cell cycle arrest. Artemis does not appear, however, to act either upstream or downstream of checkpoint kinase Chk1 or Chk2. These results define Artemis as having a checkpoint function and suggest that the radiosensitivity and chromosomal instability of Artemis-deficient cells may be due to defects in cell cycle responses after DNA damage.