Objective:To investigate the effect of type ⅡNKT cells activated by sulfatide on airway inflammation in a murine model of asthma.Methods:Thirty-two BALB/c mice were randomly divided into four groups:normal control group ( n=8 ) , asthma group (n=8),sulfatide treatment group (n=8) and adoptive transfer group (n=8).The murine model of asthma was established by sensitization with intraperitoneal injection of ovalbumin ( OVA) and intranasal challenge in all animals except for the normal control group where PBS was used instead.Intraperitoneal injection of sulfatide in a sulfatide treatment group, adoptive transfer of sulfatide-activated typeⅡNKT cells in adoptive transfer group and PBS in asthma group were carried out 1 hour before the first challenge.PBS was used for intraperitoneal administration in the normal control group.Lung histology and goblet cell hyperplasia were analyzed by HE or PAS staining.Differential cell count in bronchial alveolar lavage ( BALF) was measured by May-Gruenwald Giemsa;levels of OVA-specific IgE in serum and L-4,IL-5 in BALF were measured by ELISA.The percentages of lung type Ⅱ NKT cells,IL-4+and IFN-γ+typeⅡNKT cells were detected by flow cytometry.Results:Inflammatory cell infiltration in lung tissue and goblet cell hyperplasia in the airway were decreased in sulfatide treatment group and adoptive transfer group.Percentages of eosinophil in BALF,level of OVA-specific IgE in serum,and levels of IL-4,IL-5 in BALF in sulfatide treatment group and adoptive transfer group were significantly lower than those in asthma group (all P<0.05).The percentages of lung IL-4+and IFN-γ+typeⅡNKT cells in sulfatide treatment group was significantly higher than those in asthma group ( P<0.01 ).Conclusion: Type Ⅱ NKT cells activated by sulfatide may inhibit airway inflammation in a murine model of asthma.

Objective: To explore the risk factors for ventricular aneurysm formation in patients after acute myocardial infarction (AMI).
Methods: Our research included 2 groups of AMI patients who received percutaneous coronary intervention (PCI)
in our hospital from 2012-04 to 2014-07 as Ventricular aneurysm group,n=146 and Control group,n=142, in which the AMI patients without ventricular aneurysm formation. The baseline condition with aneurysm related risk factors were analyzed and compared between 2 groups including age, gender, hypertension, hyperlipidaemia, diabetes, smoking, family history, MI history, anterior myocardial wall infarction, angina pectoris, left main (LM) disease, the lesion at proximal left anterior descending (LAD) artery, NYHA classiifcation III/IV, chest pain time ≥ 24 hours and ST-segment elevation ≥ 4 adjacent leads in ECG.
Results: Compared with Control group, the patients in Ventricular aneurysm group had the elder age (OR=1.023, 95% CI 1.000-1.046), higher incidence rates of smoking (OR=1.819, 95% CI 1.130-2.928) and anterior MI (OR=9.162, 95% CI 4.657-18.028), more patients with ≥ 4 adjacent ST-segment elevation (OR=6.571, 95% CI 2.426-17.798), while less patients with angina pectoris (OR=0.557, 95% CI 0.335-0.927, allP<0.05. With adjusted relating factors of age, gender, hypertension, diabetes and angina pectoris, the multivariate Logistic regression analysis indicated that smoking (regression coefifcient: 0.833, OR=2.301, 95% CI 1.283-4.125), anterior MI (regression coefifcient: 1.799, OR=6.041, 95% CI 2.831-12.894) were positively related to ventricular aneurysm formation.
Conclusion: Smoking and anterior MI were strongly related to ventricular aneurysm formation in patients after AMI.

Animals ; Macaca mulatta ; Optic Disk ; Glaucoma ; Craniocerebral Trauma ; Intraocular Pressure ; Low Tension Glaucoma