Objective To investigate whether P12，a kind of lipopolysaccharide（LPS）-binding protein（LBP） inhibitory peptide，could suppress the binding of LPS to alveolar macrophages（AMs） in a mouse model of endotoxemia in vivo.Methods Forty mice were randomly divided into five groups，ie.a control group，an endotoxemia group，a low dose P12-treated group，a middle dose P12-treated group and a high dose P12-treated group.Mouse model of endotoxemia was established by LPS injection intraperitoneally in the endotoxemia group and P12-treated groups.P12 was instilled via the tail vein.The effects of P12 on the binding of LPS to AMs were determined by flow cytometric analysis and quantization by mean fluorescence intensity(MFI).The productions of tumor necrosis factor α(TNF-α) in serum of mice were measured by enzyme-linked immunosorbent assay(ELISA).Results MFI in AMs from low，middle and high dose P12-treated groups was 40.08%，30.76% and 24.45%，respectively，which was higher than that of the control group(4.61%)，but less than that of the endotoxemic mice(45.31%).The concentration of TNF-α in serum of low，media and high dose P12-treated mice was (112.69±19.78)pg/mL，(86.34±9.25) pg/mL，(70.48±8.48)pg/mL respectively，which was higher than that of the control group[(24.88±5.82)pg/mL]，but less than that of the endotoxemic mice[(180.17±39.14)pg/mL].Conclusion The results suggest that P12 inhibit the binding of LPS and AMs，thus reduce the proudction of TNF-α stimulated by LPS.
Objective To explore the imaging features of acute exacerbation of idiopathic pulmonary fibrosis ( IPF) under high-resolution computed tomography ( HRCT) . Methods The HRCT imaging features of six patients who met the criteria for acute exacerbation of IPF were analyzed retrospectively. Results The manifestations of IPF on HRCT scan were various in forms and distribution, as multifocal, ground-glass opacity, reticular shadow, honeycombing densities, capillary bronchiectasis,subpleural lines, traction bronchiolectasis and emphysema. The characteristic lesions were newly diffuse bilateral ground-glass opacity at the time of acute exacerbation, superimposed on subpleural reticular and honeycombing densities. Conclusions Chest HRCT findings in acute exacerbation of IPF are characteristic.HRCT is accurate and superior in diagnosis of IPF and in determining acute exacerbation of IPF.
Objective To explore the risk factors of invasive fungal infection ( IFI) in respiratory ward. Methods A multi-center, retrospective, case-control study was carried out. Patients from five general hospitals in Chongqing city, diagnosed as fungal infection, or whose respiratory specimens were fungal positive, were retrospectively screened for IFI. Patients with respiratory infection and colonization of nonfungal cases in the same period of hospitalization were enrolled as control. Results Thirty-four patients diagnosed with IFI and 50 patients diagnosed with bacterial infection were analyzed for the risk factors of IFI. The demographic characteristics of patients including age and gender were not different( P gt; 0. 05) , but hospitalization days, carbapenem antibiotic use, chemotherapy, deep venous catheterization, total parenteralnutrition( TPN) , neutropenia, and renal disfunction were different significantly between the IFI group and the control group. Multiple logistic regression analysis showed that carbapenem antibiotic use ( OR = 6. 753) ,central venous catheterization ( OR = 5. 021) and TPN ( OR = 3. 199) were main risk factors of invasive fungal infection. Conclusion The carbapenem antibiotic use, central venous catheterization and TPN are risk factors for IFI in respiratory ward.
Objective To investigate the effects of immunoliposomes containing vasohibin on pulmonary fibrosis in mice. Methods Liposomes containing vasohibin plasmids were prepared by reverse phase evaporation technique, then combined with VWF antibody to form the immunoliposomes. 30 mice were randomly divided into a control group, a model group, and a vasohibin group. The mice in the model group and the vasohibin group were nasally instilled with bleomysin to induce pulmonary fibrosis. After 3 days, the mice in the vasohibin group were nasally instilled with the immunoliposomes containing vasohibin. The mice were all sacrificed after 14 days. Lung tissue sections were stained by HE and CD31 immunohistochemistry staining. The level of hydroxyproline in lung was measured by colorimetry. Results The resultsdemonstrated that the vasohibin immunoliposome could markedly decrease angiogenesis with the number of ( 46 ±16) compared to ( 78 ±12 ) , and decrease fibroblast proliferation with ( 0. 84 ±0. 12) μg/mg compared to ( 1. 39 ±0. 23) μg/mg. Conclusion The vasohibin immunoliposome can attenuate pulmonaryfibrosis and provide a novel strategy for clinical application in the future.