Objective To investigate the effects of the c-Jun N-terminal kinase (JNK)pathway on isoflurane induced neuronal apoptosis and the proteins expression of phospho-JNK,Bcl-2 and Bax in the hippocampi of neonatal rats.Methods Forty-eight neonatal rats at postnatal day 7 (P7) were randomly assigned into 4 groups:DMSO control group (group D),SP600125 control group (group SP30),isoflurane + DMSO group (group Iso +D),isoflurane + SP600125 group (group Iso + SP30).Rats were exposed to air (control group) or 1.1％ isoflurane (isoflurane group) for 4 h.The JNK inhibitor SP600125 at 30 μg or 12％ DMSO 5 μl was intraventricularly administered 20 min before the exposure.The brains of some rats in each group were perfused and embedded by paraffin 6 h after the exposure.Neuronal apoptosis in the hippocampi CA1 area was detected by TUNEL (n =6).The fresh hippocampi of other rats in each group were dissected 6 h after the exposure and the proteins expression of phospho-JNK,Bcl-2 and Bax were detected by Western blot (n =6).One way ANOVA were used for data analysis among groups.Results The number of TUNEL positive cells in the hippocampal CA1 regions in group Iso +D (135.72 ±21.26 per mm2) increased by 5 folds compared with group D (24.07 ± 1.35 per mm2) (P＜0.01) ;while the number of apoptotic cells in group Iso + SP30 (42.49 ± 5.56 per mm2) decreased by 84％ (P ＜ 0.05)compared with group Iso + D.The expression of phospho-JNK p46 kd in group Iso + D increased by 44.1％ (P ＜0.01),while both phospho-JNK at p46kd and at p54kd in group Iso + SP30 decreased significantly (P＜0.05,P ＜0.01) compared with group Iso + D.The protein expression of Bax increased 1.5 folds (P＜0.05) and Bcl-2 decreased by 42.2％ (P＜0.05) in group Iso + D compared to group D;while SP600125 significantly decreased expression of Bax (P ＜0.05) and increased expression of Bcl-2 (P＜0.01).Conclusion JNK activation contributes to isoflurane-induced neuroapoptosis in the developing brain.Maintaining Bcl-2 expression and inhibiting Bax expression may be involved in the neuroprotective effects of SP600125.

Objective This study aims to investigate the effect of Lipoxin A4 receptor on acute lung injury (ALI) induced by intestine ischemia-reperfusion (IIR). Methods Thirty-two 8-week old SD rats were randomly divided into four groups: sham, intestine ischemia-reperfusion (IIR), IIR + BML111 (BML-111), Boc-2 + IIR +BML111 (Boc-2). BML-111 (1 mg/kg) was given intraperitoneally at the onset of reperfusion in the BML-111 and the Boc-2 group. Boc-2 (50 μg/kg) was given intraperitoneally after anesthesia in the Boc-2 group. Rats were subjected to superior mesenteric artery occlusion consisting of 45-min ischemia and 6-h reperfusion, and the sham laparotomy was served as controls. The lung pathology was assayed by the H&E staining. Lung water content was detected using dry/wet ratio. Concentrations of TNF-α, IL-1β, and IL-6 in lung tissue were determined by ELISA. The protein expression of p38 MAPK and NF-κB of lung was assayed by western blot. Results IIR induced serious ALI, with poor lung pathology and increased lung water content, elevation of TNF-α, IL-1β, and IL-6 levels in lung, accompanied with activation of p38 MAPK/NF-κB pathway. However, BML-111 could inhibit the activation of p38 MAPK/NF-κB pathway, leading to the reductions of TNF-α, IL-1β, and IL-6 in lung and attenuation of IIR-induced ALI. Conclusion BML-111 treatment could attenuate inflammation in lung after IIR injury via inactivating the p38 MAPK/NF-κB signaling pathway.

Objective To investigate the accumulative 3-year morbidity of diabetes in the residents aged 40 years and above in a community of Guiyang and the risk factors. Methods A total of 10140 permanent residents aged over 40 years in a community of Guiyang were selected from May 2011 to October 2011 using randomized sampling. This population was followed up again in 2014. Questionnaires, physical examination, blood lipids and oral glucose tolerance test were performed among the subjects of study for two surveys with the same criteria. Finally, 5958 subjects with complete data and without baseline diabetes at the two time points were enrolled in this study for analysis. Results The 3-year accumulative morbidity of diabetes in this population was 6. 13％ (6. 59％ in males, 5. 65％ in females). The main factors influencing the incidence of diabetes mellitus were age (OR = 1. 589, 95％ CI 1. 395-1. 809, P<0. 01), body mass index ( OR = 2. 012, 95％ CI 1. 632-2. 479, P<0. 01), pulse rate ( OR =1. 019, 95％ CI 1. 012-1. 025, P<0. 01), family history (OR = 1. 700, 95％ CI 1. 299-2. 225, P<0. 05), fasting plasma glucose at baseline(OR = 3. 132, 95％ CI 2. 478-3. 958, P<0. 01), 2 h plasma glucose at baseline( OR =1. 698,95％ CI 1. 574-1. 832, P < 0. 01), total cholesterol ( OR = 1. 350, 95％ CI 1. 060-1. 719, P < 0. 05), triglyceride(OR=2. 196, 95％ CI 1. 758-2. 743, P<0. 01),high density lipoprotein-cholesterol(OR = 0. 540, 95％CI 0. 375-0. 776, P < 0. 01), and low density lipoprotein-cholesterol ( OR = 1. 614, 95％ CI 1. 094-2. 382, P<0. 05). Conclusion 3-year morbidity of diabetes in Guiyang was 6. 13％ . The incidence of diabetes is notably correlated with aging, faster pulse frequency, overweight and obesity, higher baseline blood glucose, and dyslipidemia.

Objective:To explore the predictive value of brachial-ankle pulse wave velocity (baPWV)>1 400 cm/s in fragility fracture in middle-aged and elderly population.Methods:From May to October 2011, questionnaire survey was conducted on a total of 3 265 males over 50 years old and postmenopausal females in Yunyan District, Guiyang City, and physical examination was carried out to measure their metabolic related indicators such as blood lipids, QUS calcaneus bone densities, and brachial-ankle pulse wave velocities. According to their baPWV, the enrolled subjects were divided into a normal baPWV group and an elevated baPWV group. Follow-up was performed for 38 months, and the incidence of fractures was tracked. Finally, 2 637 subjects with complete baseline and follow-up data were enrolled in this research for analysis.Results:The 3-year total incidence of fragility fracture was 5.08%. In particular, the rate of fragility fractures among males in the normal baPWV group was 1.6%, and that in the elevated baPWV group was 2.0%. There was no statistically significant difference between the two groups ( P>0.05). The rate of fragility fracture events among postmenopausal females in the normal baPWV group was 4.4%, and that in the elevated baPWV group was 7.1%. There was statistically significant difference between the two groups ( P<0.05). Further multivariate COX regression (or proportional hazards regression) analysis showed that the bone density T value ( HR 0.839, 95% CI 0.741-0.952, P=0.006) and baPWV ( HR 1.700, 95% CI 1.046-2.763, P=0.042) were related with risk of fragility fractures in postmenopausal women. Conclusion:A baPWV greater than 1 400 cm/s could be independently associated with the risk of fragility fractures in postmenopausal females and might be an independent risk factor for predicting fragility fractures. However, such differences were not as evident in middle-aged and elderly male patients.