Objective To investigate the expression of high mobility group protein-B1( HMGB1)and α-smooth muscle actin( α-SMA) in Bleomycin induced pulmonary fibrosis in mice. Methods Twenty C57BL/ 6 male mice were randomly divided into a Bleomycin group and a control group. The Bleomycin group was treated with Bleomycin( 3 mg/kg) by endotracheally injection to induce pulmonary fibrosis. The control group were treated with normal saline( NS) . Then they were sacrificed by abdominal aortic bleeding 10 days after the injection. The right lung was stained with hematoxylin-eosin and Masson trichrome respectively for pathological examination. Immunohistochemistry and RT-PCR were performed to identify the protein and mRNA levels of α-SMA and HMGB1 respectively. Results The mRNA( 0. 89 ±0. 12, 0. 61 ±0. 08) and protein( 13. 66 ±1. 01, 13. 12 ±1. 33) expressions of α-SMA and HMGB1 in the Bleomycin group were all significantly higher than those of the control group( mRNA: 0. 60 ±0. 07, 0. 15 ±0. 02; protein: 8. 18 ±1. 33,7. 92 ±1. 10; all P lt; 0. 01) . Conclusions The expressions of HMGB1 and α-SMA are increased in Bleomycin induced pulmonary fibrosis. HMGB1 participates in the pathological process of pulmonary fibrosis probably by activation of the α-SMA expression.
Objective To systematically review the effectiveness and safety of safflor yellow for unstable angina. Methods Relevant studies of safflor yellow for unstable angina were collected from databases including CENTRAL (Issue 4, 2012), MEDLINE, EMbase, CNKI, VIP, WanFang Data and CBM from January, 2007 to December, 2012. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted data and assessed the quality of the included studies. Then, meta-analysis was performed using RevMan 5.1 software. Results A total of 6 RCTs involving 533 patients were included, which were of low quality. The results of meta-analysis showed: compared with conventional treatment alone, safflor yellow plus routine biomedical treatment significantly improved the symptoms f angina (excellence: OR=2.34, 95%CI 1.79 to 4.87; effectiveness: OR=1.23, 95%CI 0.86 to 1.76). Besides, it significantly improved ECG outcomes (excellence: OR=1.85, 95%CI 1.29 to 2.64; effectiveness: OR=1.43, 95%CI 1.00 to 2.05), obviously improved the hemorheology index and blood lipid, reduced plasma homocysteine concentration, and increased the decreasing of nitroglycerin stop amount. No damage of the liver and kidney were reported. Conclusion Current evidence showed that, safflor yellow plus routine biomedical treatment is effective in the treatment of unstable angina, which is superior to routine biomedical treatment alone. Due to the limited quantity and quality of the included studies, more high quality, double blind, randomized controlled trials are needed to verify the above conclusion.
ObjectiveTo confirm the effect of comprehensive prevention and care measures in reducing the incidence of multi-drug resistance in Intensive Care Unit (ICU) patients. MethodFrom March 1 to August 31 in 2014, we took routine measures to prevent multi-drug-resistant infections in ICU patients, and from September 1 in 2014 to February 28 in 2015, We added a series of comprehensive prevention measures to prevent multi-drug resistant infections including focus on isolation, temperature control of the ward, ward disinfection, quality improvement of basic care, standardized management and disinfection of equipments in ICU. Finally, we compared the detection rate of multi-drug resistant patients before and after the comprehensive nursing intervention. ResultsAfter taking comprehensive care interventions and a six-month monitoring, the detection rate of multi-resistant bacteria occurred in 11.87‰ of the patients. Compared with the previous six months, the detection rate dropped from 16.64‰ to 11.87‰ with a significant difference (χ2=6.346,P=0.012). ConclusionsComprehensive nursing intervention measures taken by the ICU department can effectively reduce multi-drug resistant infections in ICU patients.
Objective To investigate the effects and mechanisms of lactic acid bacteria on MAPK signaling in immune response of dust mite sensitized mice. Methods Forty C57BL/6 mice in Group M, P and L, were sensitized and challenged with mite extract while then the animals in Group N were treated with saline as control. The mice in Group L and P were fed with Lactococcus lactis or Lactobacillus respectively.Three days after the last challenge, all mice were sacrificed for lung pathological examination. IL-10 level in culture supernatant of splenocytes stimulated with mite extract was detected by ELISA. The expression of IL-4/ IFN-γon CD3 +CD4 + cells was detected by flow cytometry. Western blot were performed for detection of MAPK signaling ( P38, ERK, and JNK) from mice’s spleen cells stimulated with mite extract. Results The mice fed with Lactococcus lactis ( Group L) had lower rate of eosinophilic airway inflammation and higher level of IL-10 in the culture supernatant of splenocytes than Group P. Meanwhile, the number of CD4 + T cell with IL-4 expression was decreased revealed by the analysis of flow cytometry. P38 signaling inspleen cells was activated in the mice of Group M, similarly in the mice of Group P, but not of Group L.Conclusion Oral treatment of Lactococcus lactis can induce an immune tolerance in response to mite by up-regulating the level of Tr cells secreting IL-10, thus inhibiting activation of P38 signaling.
ObjectiveTo evaluate the association between extent and severity of acute coronary syndrome and uric acid, leukocytes. MethodsA retrospective analysis of leukocytes, platelets, lipids and uric acid levels were performed on 23 patients with acute myocardial infarction (AMI group), 17 patients with unstable angina (UA group), and 17 healthy subjects (controls) between January and December 2010. ResultsIn the three groups (AMI, UA, and Control), the leukocyte count was respectively (10.4±3.2)×109/L, (6.9±2.4)×109/L and (5.4±1.1)×109/L (P<0.05); neutrophil was (7.4±3.2)×109/L, (4.8±2.3)×109/L, and (3.4±0.8)×109/L (P<0.001); and uric acid was (401.4±94.3), (384.1±74.1) and (285.5±76.8) μmol/L, respectively (P<0.001). Multinomial Logistic regression showed leukocyte was a predictor for AMI (OR=1.712, P=0.003), while uric acid was not (OR=1.006, P=0.255), regarding the UA group as the reference. When the control group was using as reference, leukocyte was an independently significant factor for AMI (OR=2.942, P=0.004) and was not a significant factor for UA (OR=1.718, P=0.125); uric acid was a significant factor for AMI and UA (OR=1.027, P=0.016; OR=1.021, P=0.041). ConclusionUric acid may be associated with the chronic development of coronary heart disease, while leukocytes may play a potential role in plaque destabilization and the onset of AMI.
Objective To explore whether epithelial to mesenchymal transition ( EMT) occurs in bleomycin( BLM) induced pulmonary fibrosis, and the involvement of bronchial epithelial cells( BECs) in the EMT. Methods BLM-induced peribronchial fibrosis in an α-smooth muscle actin-Cre transgenic mouse( α-SMACre /R26R) was examined by pulmonary βgal staining and α-SMA immunofluorescence staining. Results BLMtreated mice showed significantly enhanced βgal staining in subepithelial areas in bronchi, terminal bronchioles and walls of pulmonary vessels. Some alveolar epithelial cells( AECs) in certain peribronchial areas or even a small subset of BECs were also positively stained, as confirmed by α-SMA immunostaining. Conclusions EMT occurs in BLM-induced peribronchial fibrosis mice. BECs, like AECs, have the capacity to undergo EMT and to contribute to mesenchymal expansion in pulmonary fibrosis.