Relationship between disease activity and choroidal thickness in patients with inflammatory bowel disease / 眼科新进展

Objective To investigate the relationship between inflammatory bowel disease (IBD) activity and choroidal thickness,and evaluate the utility of a choroidal thickness measurement in assessing IBD activity.Methods A total of 100 eyes of 50 patients of IBD with different disease activity,including 23 patients of ulcerative colitis,27 patients of Crohn's disease (CD).Ninety-six eyes of 48 healthy volunteers were recruited as control group.Choroidal thickness was measured using enhanced depth imaging(EDI)optical coherence tomography.Results Compared with the subfoveal choroidal thickness (294.37 ± 35.04) μm in healthy volunteers,the subfoveal choroidal thickness (349.28 ± 76.57) μm in UC patients with severe disease activity,the subfoveal choroidal thickness (326.71 ± 59.71) μm and (354.24 ± 66.34) μm,respectively,in CD patients with moderate and severe disease activity were found to be increased significantly (all P ＜ 0.05).Conclusion Choroidal thickness should be considered as a potential marker to assess the disease activity in patients with IBD,especially in patients with CD.

Azithromycin inhibits proliferation of rat airway smooth muscle cells though TRAF6/NF-κB/VEGF signaling pathway / 重庆医学

Objective To explore the mechanism of azithromycin (AZM) for inhibiting the proliferation of rat airway smooth muscle cells (ASMCs).Methods Thirty Sprague-Dawley (SD) rats were divided into the control group,asthma model group and AZM group.The rat model of asthma was established by ovalbumin (OVA) sensitization and stimulation in vitro.The airway related parameters of rat lung tissue were determined by using the medical image analysis system.Primary passage ASMCs were isolated and cultured using the tissue-sticking method,and the vascular endothelial growth factor (VEGF) overexpression vector or tumor necrosis factor receptor-associated factor 6 (TRAF6) overexpression vector was transfected into ASMCs in the AZM group.The protein levels of VEGF,NF-κB p65 and TRAF6 were detected by Western blotting,and the proliferation of ASMCs was evaluated by CCK-8 kit.Results AZM significantly inhibited the increase of thickness of total airway wall,thickness of inner airway wall and thickness of airway smooth muscle layer in asthma rats (P<0.05),also significantly inhibited the proliferation of ASMCs in the asthma model group (P<0.05).AZM significantly inhibited the protein expression of VEGF and NF-κB p65 induced by asthma (P<0.05),and the overexpression of VEGF significantly reduced the inhibiting effects of AZM on proliferation of ASMCs (P<0.05).AZM significantly inhibited the high expression of TRAF6 induced by asthma (P<0.05),and the overexpression of TRAF6 significantly reduced the inhibiting effects of AZM on expression of VEGF and NF-κB p65 as well as proliferation of ASMCs (P<0.05).Conclusion AZM can suppress the proliferation of ASMCs,its partial mechanism may be realized through inhibiting TRAF6/NF-κB/VEGF signaling pathway.

Changes in endogenous nitric oxide and effects of inhaled nitric oxide on pulmonary artery hypertension in chronically hypoxic rats / 中国病理生理杂志

AIM: To investigate the role of nitric oxide (NO)in the development of chronically hypoxic pulmonary artery hypertension (PAH) and the hemodynamic effects of inhaled NO on pulmonary circulation. METHODS: 67 male adult SD rats were randomly divided into 7 groups: (1) control ( n= 9);(2) chronically intermitent hypoxia (CIH, 6 h/d, 7 d/w) 1 week( n= 7); (3) CIH 2 weeks ( n= 11); (4) CIH 3 weeks ( n= 11); (5) CIH 1 week+L-NAME (NO synthase inhibitor, 30 mg/kg, by gavage, n= 10); (6)CIH 3 weeks+L-Arg (NO precursor, 10 mg/kg, by gavage, n= 9); (7) CIH 3 weeks+inhaled NO (0.0004% for 20 min, n= 10) to determine the mean pulmonary artery pressure (MPAP), weigh the right ventricle (R) and ventricular segment plus left ventricle (S+L), and calculate R/(S+L) (g/g) and R/Wt (Wt: body weight, g/kg). RESULTS: 1.MPAP increased compared with control [(3 2?0.3 ) kPa vs (1.8?0.3) kPa, P

An Experimental Study of Pathogenesis of Acute Lung Injury Induced by Complement Activation in Conscious Goat, Roles of Leukocytes and Prostaglandins / 第三军医大学学报

The roles of leukocytes and prostaglandins in mediating alterations of pulmonary hemodynainics and lung fluid exchange after intravenous autologous zymo-san-activated plasma (ZAP) challenge is investigated in 14 conscious goats with chronic lung-lymph-fistula. In the control group, ZAP infusion causes the mean pulmonary arterial pressure (Ppa) markedly elevate, lung lymph flow (QI) and the lymph-to-plasma protein concentration ratio (L/P) increase. There is a significant correlation between Ppa and the content of plasma TXB2. In antiPMNs serum-induced leukopenia group, the extent of increment in Pp a is not as obvious as the normal goats, and no marked change is observed in QI, L/P and content of TXB2. These results indicate: l.TXA2 releases from leukocytes may affect lung fluid exchange during ZAP infusion; 2. leukocytes may play an important role in ZAP-induced lung injury.