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In early April 2009, cases of human infection with 2009 pandemic influenza A (H1N1) virus were identified in Mexico. The virus then spread rapidly to other regions of the world. From October 2009, sporadic imported cases of novel influenza A (H1N1) were continuously confirmed in Suzhou. The aim of the study was to review the chest CT findings in 63 patients with laboratory-confirmed novel swine-origin influenza A (H1N1) virus (S-OIV) infection.Chest CT examinations were collected from 63 S-OIV infected patients during their hospital stay. Three experienced radiologists inspected images to qualitatively and quantitatively characterize S-OIV induced image changes. CT scores of lesion severity were calculated based on the percentage of affected area to determine severity of infectious lesions. Patients were divided into two groups based on the leukocyte counts. Lesion patterns, local distributions, and quantitative measures were investigated and compared between the two groups.Various degrees of bilateral multifocal lesions of ground-glass opacities were found with or without consolidations on the chest CT images. The lesions were both bronchocentric and centrilobular. Patients with elevated leukocyte counts had more extensive lesions, in terms of severity and affected area, than the patients with normal leukocyte counts. The lesion severity scores of patients in the elevated leukocyte group were significantly higher than those of the normal leukocyte group in terms of the entire lung area (P0.01), and upper (P0.05) and lower (P0.01) lobes as well. There were changes in the CT characteristics seen at follow-up as demonstrated by lesions absorption (P0.01), especially in the upper lobe of the lung (P0.01), but less so in the middle lobe/lingual and lower lobe of the lung (P0.05).The most common CT findings in S-OIV infection patients were bilateral multifocal distributed ground-glass opacities and consolidations. The lesions were located dominantly at bronchocentric and centrilobular areas. Lung lesions were more obviously absorbed in upper lobes between two examinations. The observations and analysis from this study provide information that may be useful in image understanding and patient management for future pandemic influenza.

Glucocorticoid (GC) insensitivity/GC resistance is an important etiological and prognostic factor in multiple diseases and pathophysiological processes such as scald, shock and asthma. The function of GC was mediated by glucocorticoid receptor (GR). Scald not only decreased the expression of GR but also reduced the affinity of GR, which played an important role in GC resistance in scalded rats. Whereas the molecular mechanism responsible for the decrease of GR affinity resulted from scald remains unclear. Recent studies showed that the changes of heat shock proteins (hsp) especially hsp90 and hsp70 of GR heterocomplex were associated with GR low affinity in vitro.The affinity of GR in hepatic cytosols and in the cytosols of SMMC-7721 cells were determined by radioligand binding assay and scatchard plot. GR heterocomplex in cytosols were captured by coimmunoprecipation and the levels of hsp90 and hsp70 of GR complex were detected by quantitative Western blotting.Similar with that of hepatic cytosol of scalded rats, a remarkable decrease of GR affinity was also found in the cytosol of heat stressed SMMC-7721 cells. The level of hsp70 of GR complex in hepatic cytosol of scalded rats (30% total body surface area immersion scald) and in cytosol of heat stressed human hepatocarcinoma cell line SMMC-7721 were both increased by 1.5 fold, whereas no change of hsp90 in GR heterocomplex was found. According to the correlation analysis, there may be a positive relationship between increased hsp70 of GR complex and decreased GR affinity in the cytosols.The primary results indicated that the level of hsp70 of GR heterocomplex was increased in the hepatic cytosol of scalded rats and the cytosol of heat stressed SMMC-7721 cells. The increase of hsp70 of GR complex might be associated with the decrease of GR affinity.