Death of nerve cells after cerebral ischemia have a variety of forms,including cell necrosis occurs immediately in ischemic core area and the subsequent apoptosis and autophagy induced by oxidative stress and inflammatory response in the course of reperfusion.After cerebral ischemia,a variety of different molecular mechanisms eventually lead to cell death,and the process involves several signaling pathways.Intervention of different forms and mechanisms of cell death may alleviate cell death after cerebral ischemia.

As an intracellular energy sensor, AMP-activated protein kinase (AMPK) plays an important role in maintaining the energy balance of the cells and organisms. Initially, the effects of AMPK on the processes of pathophysiology in diabetes, obesity and other metabolic diseases were well studied. In recent years, the roles of AMPK in the pathophysioiogical processes, including distribution and acidosis, oxidative stress injury and apoptosis in brain tissue have received increasing attention. At the same time, it also found that artificially regulates the AMPK activity after stroke may change the outcome of neurons. Therefore, AMPK is expected to become a new target in the treatment of ischemic cerebrovascular disease.

As an important component of the “neurovascular unit”,astrocytes provide protective effect for nervous through intaking excessive excitatory amino acids,providing energy substances,maintaining extracellular K + and water balance,scavenging oxygen free radicals and secreting neurotrophic factor during ischemic stroke.This article elaborates the mechanisms of astrocytes participating in ischemic stroke in recent years.

Bone Diseases, Metabolic ; physiopathology ; Bone and Bones ; metabolism ; physiopathology ; Child ; Child Nutrition Disorders ; physiopathology ; Child Nutritional Physiological Phenomena ; physiology ; Humans ; Infection ; physiopathology ; Kidney Failure, Chronic ; physiopathology

Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms ; genetics ; metabolism ; pathology ; MicroRNAs ; genetics ; metabolism ; Paraffin Embedding ; RNA, Neoplasm ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; methods

Objective To explore the relationship between vascular endothelial growth factor (VEGF) concentration in urine and renal vascular damage in children with Henoch Schonlein purpura nephritis (HSPN).Methods The kidney pathological lesion of 78 biopsy-proven HSPN children was assessed with renal vascular damage, glomerular pathological damage, and tubulointerstitial pathological damage semi-quantitative points. The children were divided into 3 groups (light, medium, and heavy group) according to the renal vascular, glomerular, tubulointerstitial, glomerular and tubulointerstitial total pathological points. Blood and urine vascular endothelial growth factor concentration was detected by enzyme linked immunosorbent assay;the localized renal VEGF expression and microvessel density were detected by immunohistochemistry assay in the kidneys. Results The semi-quantitative points of glomerular, tubulointerstitial, renal vascular, and glomerular and tubulointerstitial total points in different groups had significant difference (all P＜0.01);the minor renal vascular damage, the higher light microvessel density, blood and kidney concentration of VEGF, and the VEGF excretion in the urine were also lower in different groups, and there were significant differences (all P＜0.01). Glomerular points were positively related with tubular points, vascular points, kidney total score (r=0.596,0.612, and 0.728;P＜0.05, 0.05, and 0.01 respectively). Microvessel density was highly positively related with blood VEGF and renal VEGF, and negatively rela-ted with urine VEGF (r=0.601, 0.696, and -0.639,all P＜0.01). Conclusion The urinary excretion of VEGF leads to the decrease of local kidney VEGF concentration resulting in the renal vascular injury, which may be the important reason for renal vascular damage and pathology chronic progress in HSPN children.

Objective To Compare different methods of quantitative breast density measurement.Methods The study included sixty patients who underwent both mammography and breast MRI. The breast density was computed automatically on digital mammograms with R2 workstation. Two experienced radiologists read the mammograms and assessed the breast density with Wolfe and ACR classification respectively. Fuzzy C-means clustering algorithm (FCM) was used to assess breast density on MRI. Each assessment method was repeated after 2 weeks. Spearman and Pearson correlations of inter- and intrareader and intermodality were computed for density estimates. Results Inter- and intrareader correlation of Wolfe classification were 0. 74 and 0. 65, and they were 0. 74 and 0. 82 for ACR classification respectively.Correlation between Wolfe and ACR classification was 0. 77. High interreader correlation of 0. 98 and intrareader correlation of 0. 96 was observed with MR FCM measurement. And the correlation between digital mammograms and MRI was high in the assessment of breast density (r = 0. 81, P ＜ 0. 01). Conclusion High correlation of breast density estimates on digital mammograms and MRI FCM suggested the former could be used as a simple and accurate method.

A strain producing eggshell membrane protease (ESM protease) was isolated from the soil and identified as Pseudomonas aeruginosa. The enzyme isolated from the fermentation liquid of this strain and purified by ammonium sulfate precipitation, quadratic anion-exchange chromatography exhibited eggshell membrane degrading activity of 304.5 U/mg. By SDS-PAGE, the protein molecular mass is 32 kD. The N-terminal amino acid sequence of this protease is: Ala, Glu, Ala, Gly, Gly, Val, Ala, Gly, Lys, Glu, Asp, Ala, Ala, Glu, Leu.

Objective To evaluate the safety of a surgical appwach for transabdominal cardial carci- noma.Methods We retrospectively analyzed 326 patients undergoing transabdominal esophagastrostomy or esophagojejunostomy from 1998 to 2006 via the EEA(end-to-end anastomosis)stapler.Results By the surgi- cal approach for transabdominal cardial carcinoma,the average length of reseete esophagus above the carci- noma was about 6～8 cm realized the low average of remnant carcinoma at the margin and operation mortality and anastomotic leakage,which was lower than those in the thoraeotomy appmaeh significantly.Conclusion The transabdominal approach makes a clear operative field in posterio-inferior mediastinum,it is beneficial for radical resection of eardial carcinoma and intramediastinal esophagogastric or esophagojejunal mechanical anastomosis,and it fits to the old,the weakening and with the disease of heart and lung.

Objective To investigate the effects of adenosine monophosphate-activated protein kinase (AMPK) on high-mobility group box 1 (HMGB1) release from PC12 cells after oxygen-glucose deprivation and reoxygenation (OGD/R) and its mediated inflammatory response in BV2 cells.Methods PC12 and BV2 cells were cultured,respectively.The PC12 cells were used to induce a model of oxygen glucose deprivation for 12 h and reoxygenation for 24 h.After giving 5-aminoimidazole-4-carboxamide (AICAR) 5,50 and 100 μmol/L as well as Compound C 0.1,1 and 10 μmol/L activation or inhibition of AMPK phosphorylation,respectively,methyl thiazolyl tetrazolium (MTT) was used to detect the PC12 cell activity.Enzyme-linked immunosorbent assay was used to detect the HMGB1 release level in the PC12 cell culture media.After OGD/R in each group,the PC12 culture media were acted on normal cultured BV2 cells for 24 h respectively.Westem blotting and Enzyme-linked immunosorbent assay were used to detect the NFκB inhibitory protein (inhibitor of NFκB,IκB) phosphorylation level and TNF-α release level in BV2 cells,respectively.Results After OGD/R,the PC12 cell activity was decreased significantly (68.84％±6.60％ vs.100.04％ ± 8.82％;P ＜ 0.01);the AMPK phosphorylation level was increased significantly (1.95 ±0.39 vs.1.00 ±0.20;P＜0.05),and the extracellular HMGB1 release was increased significantly (287.66 ± 26.42 pg/μl vs.53.05 ± 9.11 pg/μl;P ＜ 0.01).Compared with the OGD/R group,AICAR 100 μmol/L significantly increased the survival rate of PC12 cell after OGD/R (78.6％ ± 3.75％ vs.68.84％ ± 6.60％;P ＜ 0.05),promoted AMPK phosphorylation (3.32 ± 0.66 vs.1.95 ± 0.39;P ＜ 0.01),and reduce the release of extracellular HMGB1 (164.06 ± 12.77 pg/μl vs.287.66 ± 26.42 pg/μl;P ＜0.01).In contrast,Compound C 10 μmol/L significantly reduced the cell survival rate of PC12 (40.44％ ±3.79％ vs.68.84％ ±6.60％;P ＜0.01),inhibited AMPK phosphorylation (1.07 ± 0.21 vs.1.95 ± 0.39;P＜0.05),and increased the release of HMGB1 (337.97 ± 18.9 pg/μlvs.287.66 ± 26.42 pg/μl;P＜0.01).The conditioned medium from the AICAR 100 μmol/L group significantly inhibited IκB phosphorylation (1.68 ±0.51 vs.3.09 ± 0.10;P ＜ 0.05) and reduced the release of TNF-α (669.53 ±38.58 pg/μlvs.841.76 ± 45.82 pg/μl;P＜ 0.05) in BV2 cells.The conditioned medium from the compound C 10 μmol/L group significantly promoted IκB phosphorylation (4.98 ± 1.24 vs.3.09 ± 0.10;P ＜0.01) and increased the release of TNF-α (1 035.32 ± 128.06 pg/μl vs.841.76 ± 45.82 pg/μl;P ＜0.05) in BV2 cells.Conclusions Promoting AMPK phosphorylation activation may reduce the release of HMGB1 from PC12 cells after OGD/R,and inhibit its mediated NF-κB inflammatory pathway and reduce the release of TNF-αin BV2 cells,and thus reducing neuroinflammatory injury.On the contrary,inhibiting AMPK phosphorylation may promote the release of HMGB1 from PC12 cells after OGD/R and aggravate its mediated inflammatory reaction in BV2 cells.