Crossover equation of state models applied to the critical behavior of Xenon

The turbidity ( τ ) measurements of Güttinger and Cannell (Phys Rev A 24:3188–3201, 1981) in the temperature range 28mK≤T−Tc≤29K along the critical isochore of homogeneous xenon are reanalyzed. The singular behaviors of the isothermal compressibility ( κT ) and the correlation length ( ξ ) predicted from the master crossover functions are introduced in the turbidity functional form derived by Puglielli and Ford (Phys Rev Lett 25:143–146, 1970). We show that the turbidity data are thus well represented by the Ornstein–Zernike approximant, within 1 % precision. We also introduce a new crossover master model (CMM) of the parametric equation of state for a simple fluid system with no adjustable parameter. The CMM model and the phenomenological crossover parametric model are compared with the turbidity data and the coexisting liquid–gas density difference ( ΔρLV ). The excellent agreement observed for τ , κT , ξ , and ΔρLV in a finite temperature range well beyond the Ising-like preasymptotic domain confirms that the Ising-like critical crossover behavior of xenon can be described in conformity with the universal features estimated by the renormalization-group methods. Only 4 critical coordinates of the vapor–liquid critical point are needed in the (pressure, temperature, molecular volume) phase surface of xenon

Secretory leukocyte protease inhibitor gene deletion alters bleomycin-induced lung injury, but not development of pulmonary fibrosis

Idiopathic pulmonary fibrosis is a progressive, fatal disease with limited treatment options. Protease-mediated transforming growth factor-β (TGF-β) activation has been proposed as a pathogenic mechanism of lung fibrosis. Protease activity in the lung is tightly regulated by protease inhibitors, particularly secretory leukocyte protease inhibitor (SLPI). The bleomycin model of lung fibrosis was used to determine the effect of increased protease activity in the lungs of Slpi− / − mice following injury. Slpi− / −, and wild-type, mice received oropharyngeal administration of bleomycin (30 IU) and the development of pulmonary fibrosis was assessed. Pro and active forms of matrix metalloproteinase (MMP)-2 and MMP-9 were measured. Lung fibrosis was determined by collagen subtype-specific gene expression, hydroxyproline concentration, and histological assessment. Alveolar TGF-β activation was measured using bronchoalveolar lavage cell pSmad2 levels and global TGF-β activity was assessed by pSmad2 immunohistochemistry. The active-MMP-9 to pro-MMP-9 ratio was significantly increased in Slpi− / − animals compared with wild-type animals, demonstrating enhanced metalloproteinase activity. Wild-type animals showed an increase in TGF-β activation following bleomycin, with a progressive and sustained increase in collagen type I, alpha 1 (Col1α1), III, alpha 1(Col3α1), IV, alpha 1(Col4α1) mRNA expression, and a significant increase in total lung collagen 28 days post bleomycin. In contrast Slpi− / − mice showed no significant increase of alveolar TGF-β activity following bleomycin, above their already elevated levels, although global TGF-β activity did increase. Slpi− / − mice had impaired collagen gene expression but animals demonstrated minimal reduction in lung fibrosis compared with wild-type animals. These data suggest that enhanced proteolysis does not further enhance TGF-β activation, and inhibits sustained Col1α1, Col3α1, and Col4α1 gene expression following lung injury. However, these changes do not prevent the development of lung fibrosis. Overall, these data suggest that the absence of Slpi does not markedly modify the development of lung fibrosis following bleomycin-induced lung injury

Control of foliar diseases in barley:towards an integrated approach

Barley is one of the world's most important crops providing food and related products for millions of people. Diseases continue to pose a serious threat to barley production, despite the use of fungicides and resistant varieties, highlighting the impact of fungicide resistance and the breakdown of host plant resistance on the efficacy of control measures. This paper reviews progress towards an integrated approach for disease management in barley in which new methods may be combined with existing measures to improve the efficacy of control in the long-term. Advances have been made in genetic mapping of resistance (R) genes and in identifying novel sources of genes in wild barley populations and land races. Marker assisted selection techniques are being used to pyramid R genes to increase the durability of resistance. Elicitors to induce host resistance used in combination with fungicides can provide effective disease control in the field and could delay the evolution of fungicide insensitivity. Traits that may contribute to disease tolerance and escape have been identified and the extent of genetic variation within barley germplasm is being determined. Tools are being developed to integrate the above methods via an assessment of the risk of economic injury occurring from disease to guide decisions on the requirement for fungicide treatment. Barriers exist to the adoption of integrated management approaches from growers and end-users further down the supply chain (e. g. acceptance of variety mixtures) and policy incentives from government may be required for it to be taken up in practice. © 2012 KNPV