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In the framework of the DCMB (Développement Concerté de Matrices de Bolomètres) collaboration we develop low temperature bolometer arrays for large field, high resolution imaging in astrophysics. DCMB is a R&D effort funded by CNES and CNRS involving a number of French laboratories. Two parallel developments have been made in this collaboration based on the NbSi alloy either semi-conducting or superconducting depending on the Nb concentration. Multiplexing schemes have been developed and demonstrated for these two options. Here we focus on high impedance bolometers and present two examples of array developments in progress: first, a 23 pixels array for the balloon-borne instrument OLIMPO and, second, 204 pixels for ground based observations with the 30 m IRAM telescope. [ABSTRACT FROM AUTHOR]

An increasing number of drugs are recognized to induce distinctive patterns of infiltrative lung disease (ILD), ranging from benign infiltrates to life-threatening adult respiratory distress syndromes. In addition to drugs, biomolecules such as proteins and cytokines, and medicinal plants are also capable of inducing respiratory disease, some being severe and/or irreversible. For several reasons it is difficult to estimate the exact frequency of drug-induced infiltrative lung disease (DI-ILD). The risk for DI-ILD and the clinical patterns vary depending on a variety of host and drug factors. Although establishing the diagnosis is often difficult, systematic evaluation of the possible role of almost any kind of drugs in ILD is warranted, as stopping a drug may favourably influence prognosis. However, prognosis depends on the drug and the type of DI-ILD. Corticosteroids may suppress the inflammatory reaction, but for many drugs, proof of the effect of corticosteroids is lacking. Advances in prevention and prediction are needed. A user-friendly database of respiratory adverse drug reactions was made available on the web, to provide quick information in this area.

The purpose of this review is to describe the present state of knowledge regarding host susceptibility factors that may determine the occurrence, development and severity of interstitial lung disease (ILD) caused by exogenous agents. First, host susceptibility may pertain to differences in the delivery and/or persistence of the noxious agent in the lung. The deposition and clearance of inhaled particles or fibres may vary depending on innate anatomical or physiological characteristics, and on acquired changes, such as nasal disease or smoking-induced alterations. Genetically- or environmentally-induced interindividual differences in the expression of pulmonary biotransformation enzymes may form the basis for, or contribute to the risk of, drug-induced interstitial lung disease. Secondly, there are genetic and acquired variations in various enzymatic and nonenzymatic defence systems that protect cells and tissues against oxidative stress, which is often involved in the pathogenesis of interstitial lung disease caused by particles, fibres, metals, organic agents and drugs. Thirdly, the occurrence of immunological sensitization is dependent on both genetic and environmental factors. This has been demonstrated in chronic beryllium lung disease and in hypersensitivity pneumonitis. Fourthly, the propensity of individuals to develop particular types of inflammation, such as granulomas, is probably under genetic control. The regulation and resolution of inflammation and fibrogenesis caused by dust particles are also partly determined by genetic factors, involving cytokine networks and growth factors. In conclusion, although the issue of genetics pervades the entire discussion of host susceptibility, genes are not the only determinants of health and disease. Environmental factors may be equally important in shaping host susceptibility. Therefore, research must be focused on both the genetic bases and the environmental determinants of interstitial lung disease, in order to provide mechanism-based prevention strategies, early detection of, and improved therapy for these conditions.

Amiodarone hydrochloride is a diiodinated antiarrhythmic agent widely used in the treatment of cardiac disorders. With the increasing use of amiodarone, several untoward effects have been recognized and neuropathy following amiodarone therapy has recently been reported. The present studies were carried out to study the effect of amiodarone on rat brain synaptosomal ATPases in an effort to understand its mechanism of action. Na+, K+-ATPase and oligomycin sensitive Mg2+ ATPase activities were inhibited by amiodarone in a concentration dependent manner with IC50 values of 50 microM and 10 microM respectively. [3H]ouabain binding was also decreased in a concentration dependent manner with an IC50 value of 12 microM, and 50 microM amiodarone totally inhibited [3H]ouabain binding. Kinetics of [3H]ouabain binding studies revealed that amiodarone inhibition of [3H]ouabain binding is competitive. K+-activated p-nitrophenyl phosphatase activity showed a maximum inhibition of 32 per cent at 200 microM amiodarone. Synaptosomal ATPase activities did not show any change in rats treated with amiodarone (20 mg kg-1 day-1) for 6 weeks, when compared to controls. The treatment period may be short, since the reported neurological abnormalities in patients were observed during 3-5 years of treatment. The present results suggest that amiodarone induced neuropathy may be due to its interference with sodium dependent phosphorylation of Na+, K+-ATPase reaction, thereby affecting active ion transport phenomenon and oxidative phosphorylation resulting in low turnover of ATP in the nervous system.