Objective To investigate the expression of NF-κBp65 in hippocampus after the XST intervention therapy in the SD rats with global cerebral I/R injury and testify the protective effect of XST after global cerebral I/R injury.Methods 72 healthy SD rats were randomly divided into 3 groups,sham operation(SO) group ( n =24),I/R group( n =24) and XST group( n =24).The model of acute global cerebral ischemia/reperfusion (including:I/R and XST group) injury was produced by means of simple Pulsinelli- brierley's four arteries occlusion method.H.E.staining was performed to detect the number of surviving neurons and TUNEL was used to detect the rate of neurons apoptosis.The expression activation of NF-κB p65 in hippocampus comu-ammonis ( CA1 ) region were examined by immunohistochemical method (SABC).Results The survival pyramidal neurons in the XST group continued to increase,and it was significantly more than the I/R group at each time-point after reperfusion[ (99.23 ±4.22)/mm vs (75.83 ±7.17 )/mm,(80.93 ± 5.36)/mm vs (51.50 ± 8.26 )/mm,(103.24 ± 5.48 )/mm vs (35.67 ± 13.17 )/mm,( 126.22 ± 7.54 )/mm vs (9.83 ± 4.71 )/mm ],the differences were statistically significant ( P ＜0.01 ).The apoptosis rate of pyramidal cell in the XST group at each time-point were more significantly reduced than the I/R group [ ( 8.82 ± 2.71 ) ％ vs ( 22.58 ± 4.68 ) ％.( 19.15 ± 6.23 ) ％ vs (42.68 ± 3.04 ) ％,( 11.82 ± 2.87 ) ％ vs ( 55.51 ± 6.81 ) ％,( 8.44 ± 3.23 ) ％ vs ( 71.69 ± 7.71 ) ％ ],the differences were statistically significant ( P ＜0.01 ).The positive neurons of NF-κBp65 expression in the XST group at different time-points were significantly less than the L/R group[ ( 13.20 ±2.50) vs ( 18.00 ± 1.87),(8.20 ±5.31) vs (41.60±3.65),(6.70±3.36) vs (55.30±5.10),(7.10±3.57) vs (72.80 ±4.71)],the differences were statistically significant ( P ＜ 0.05,P ＜ 0.01 ).Conclusions After global cerebral ischemia/reperfusion,XST could protect the brain from global cerebral ischemia/reperfusion injury by holding up the expression of NF- kappaB p65,and inhibiting neuronal apoptosis,and increasing the number of surviving neurons.Thus,the results of this experiment could provide a powerful and weighty objective indication for XST being used during cerebral resuscitation.

Objective:To evaluate the clinical effects of conjoint fascial sheath suspension and frontalis muscle flap suspension in correction of severe blepharoptosis.Methods:The databases of China National Knowledge Infrastruction (CNK), WANGFANG DATA, VIP, PubMed, Cochrane Library and Web of Science (SCIE) databases were searched. All relevant studies were collected from February 2002 to April 2019, and the clinical effects of conjoint fascial sheath suspension and frontalis muscle flap suspension in correction of severe blepharoptosis were studied. The correction effective rate, complication rate and recurrence rate between two operations were Meta analyzed.Results:A total of seven randomized controlled trial studies including 387 eyes of 315 patients were subject to final analysis. The conjoint fascial sheath suspension group had 158 patients (192 eyes) and frontalis muscle flap suspension group had 157 patients (195 eyes). The results showed that the correction effective rate of conjoint fascial sheath suspension was higher than frontalis muscle flap suspension. There were statistically significant difference between the two groups ( P<0.05). The rate of complication and recurrence were lower. There were statistically significant difference between the two groups ( P<0.05). Conclusions:The clinical effects of conjoint fascial sheath suspension are better than frontalis muscle flap suspension in correction of severe blepharoptosis.

Inflammatory bowel disease (IBD) is a formidable disease due to its complex pathogenesis. Macrophages, as a major immune cell population in IBD, are crucial for gut homeostasis. However, it is still unveiled how macrophages modulate IBD. Here, we found that LIM domain only 7 (LMO7) was downregulated in pro-inflammatory macrophages, and that LMO7 directly degraded 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) through K48-mediated ubiquitination in macrophages. As an enzyme that regulates glycolysis, PFKFB3 degradation led to the glycolytic process inhibition in macrophages, which in turn inhibited macrophage activation and ultimately attenuated murine colitis. Moreover, we demonstrated that PFKFB3 was required for histone demethylase Jumonji domain-containing protein 3 (JMJD3) expression, thereby inhibiting the protein level of trimethylation of histone H3 on lysine 27 (H3K27me3). Overall, our results indicated the LMO7/PFKFB3/JMJD3 axis is essential for modulating macrophage function and IBD pathogenesis. Targeting LMO7 or macrophage metabolism could potentially be an effective strategy for treating inflammatory diseases.