The dissociation conditions of methane hydrates in confined small pores were measured by the gradual temperature increase method. Significant downward shifts of the dissociation temperature were observed in porous glasses, which had small pores ranging from 100 to 500 Å in diameter, compared with that of the bulk hydrate at a given pressure. Systematic measurements revealed that the temperature offset was in inverse proportion to the pore diameter. The Arrhenius plot of the dissociation conditions suggests that the heat of methane-hydrate dissociation tended to be small compared to that of bulk hydrates in pores smaller than 300 Å in diameter. Applying the Gibbs−Thomson effect to the quantitative analysis of the phenomenon indicated that the dissociation condition of methane hydrates in small pores shifted because of changes in the water activity. The apparent interfacial free energy between methane hydrates and water in the confined condition was estimated to be approximately 3.9 × 10-2 J m-2, which is comparable to that between ice and water in the similar condition.

These results suggest that initial evaluation of serum KL-6 level can predict survival in patients with IPF.

Mizuno S, Bogaard HJ, Kraskauskas D, Alhussaini A, Gomez-Arroyo J, Voelkel NF, Ishizaki T. p53 Gene deficiency promotes hypoxia-induced pulmonary hypertension and vascular remodeling in mice. Am J Physiol Lung Cell Mol Physiol 300: L753-L761, 2011. First published February 18, 2011 doi:10.1152/ajplung.00286.2010.-Chronic hypoxia induces pulmonary arterial remodeling, resulting in pulmonary hypertension and right ventricular hypertrophy. Hypoxia has been implicated as a physiological stimulus for p53 induction and hypoxia-inducible factor-1␣ (HIF-1␣). However, the subcellular interactions between hypoxic exposure and expression of p53 and HIF-1␣ remain unclear. To examine the role of p53 and HIF-1␣ expression on hypoxia-induced pulmonary arterial remodeling, wild-type (WT) and p53 knockout (p53KO) mice were exposed to either normoxia or hypoxia for 8 wk. Following chronic hypoxia, both genotypes demonstrated elevated right ventricular pressures, right ventricular hypertrophy as measured by the ratio of the right ventricle to the left ventricle plus septum weights, and vascular remodeling. However, the right ventricular systolic pressures, the ratio of the right ventricle to the left ventricle plus septum weights, and the medial wall thickness of small vessels were significantly greater in the p53KO mice than in the WT mice. The p53KO mice had lower levels of p21 and miR34a expression, and higher levels of HIF-1␣, VEGF, and PDGF expression than WT mice following chronic hypoxic exposure. This was associated with a higher proliferating cell nuclear antigen expression of pulmonary artery in p53KO mice. We conclude that p53 plays a critical role in the mitigation of hypoxia-induced small pulmonary arterial remodeling. By interacting with p21 and HIF-1␣, p53 may suppress hypoxic pulmonary arterial remodeling and pulmonary arterial smooth muscle cell proliferation under hypoxia. p21; hypoxia-inducible factor-1␣, vascular endothelial growth factor; platelet-derived growth factor PULMONARY HYPERTENSION COMMONLY occurs in highland residents and in patients with pulmonary disorders associated with chronic hypoxia, most notably patients with chronic obstructive pulmonary disease, and may ultimately lead to right heart failure and death (4,23,27,34,35,41). Prolonged hypoxic exposure is associated with cellular and histological changes in the pulmonary vascular wall. The major characteristic pathological findings of pulmonary vascular remodeling are increased wall thickening of pulmonary vessels and muscularization of small arteries. In animals, hypoxia has been shown to cause pulmonary vascular wall thickening by inducing pulmonary arterial smooth muscle cell (PASMC) proliferation (44,46). Several in vitro studies have shown that hypoxia stimulates proliferation of pulmonary vascular cells (9,14,24,26,40).Under normal physiological conditions, the majority of pulmonary vascular cells are in a quiescent state, and proliferation of PASMCs requires the cells to enter the cell cycle. The most important molecular event necessary...

(18)F-FDG PET is considered to be useful for the diagnosis and evaluation of disease activity along with HRCT findings, and in monitoring response to chemotherapy in patients with PM.

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P Pn ne eu um mo on ni it ti is s d du ur ri in ng g i in nt te er rf fe er ro on n a an nd d/ /o or r h he er rb ba al l d dr ru ug g t th he er ra ap py y i in n p pa at ti ie en nt ts s w wi it th h c ch hr ro on ni ic c a ac ct ti iv ve e h he ep pa at ti it ti is s ABSTRACT: We report four cases of acute pneumonitis due either to interferon, or a herbal drug, " "Sho-saiko-to" ", or both in combination, in patients with chronic active hepatitis, focusing on its pathogenesis and response to prednisolone therapy. These cases shared common clinical features: fever, dry cough, dyspnoea, hypoxaemia, diffuse infiltrates both on chest radiography and chest computed tomography, restrictive pulmonary functional impairment, and alveolitis on examination of transbronchial lung biopsy, all of which suggest acute interstitial pneumonia. Furthermore, lymphocytosis was observed in association with the dominant CD8+ T-cell subset in bronchoalveolar lavage fluid. A lymphocyte stimulation test using peripheral blood was positive to interferon in one case and to Sho-saiko-to in another. All patients responded to oral prednisolone therapy. Peripheral soluble interleukin-2 receptor levels decreased in parallel with improvement in the clinical course. All patients were free of symptoms with a follow-up of 1-3 yrs.We conclude that interferon-and/or Sho-saiko-to-induced acute pneumonitis may be due to allergic-immunological mechanisms rather than toxicity, and that peripheral levels of soluble interleukin-2 receptor appear to be good markers of disease activity.

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