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 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.

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.

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

Objective To research Henoch-Schonlein purpura purpura (HSP) and renal pathology in children.Methods 31 hospitalized HSP children that with normal urine routine and accepted renal biopsy in our hospital.Results There were different levels of kidney pathological damage in this group of 31 cases,the results of light microscope were from grade Ⅱ to grade Ⅵ The proportion was grade Ⅱ(35.48％,11 of 31),grade Ⅲ (54.83％,17 of 31),and grade Ⅳ,Ⅴ and Ⅵ (each 1 case of 31,3.23％ ).lmmunofluorescence pathology results were showed as following:merely IgA depositional (48.38％,15 of 31 ),IgA + IgG depositional ( 19.36％,6 of 31 ),IgA + IgM depositional ( 19.36％,6of 31 ),IgA + igG + IgM depositional ( 12.90％,4 of 31 ).Microalbuminuria had been founded in 14 cases,and the microalbuminuria level of 10 cases were higher than normal value( 10 of 14,71.43％ ).Conclusions HSP children had renal pathologic dysfunction,even the urine routine were normal,and the detection of urine microalbumin was a significant marker in the early stage.

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 establish a cell line with overexpression of rat serotonin1A receptor (5-HT1AR).Methods Human neuroblastoma cells-SH-SY5Y were donated by cancer institute attached to the 4 th Affiliated Hospital, Hebei Medical University. Total RNA was extracted from brain tissues of male SD rats and rat 5-HT1A R was obtained by RT-PCR. Plasmid pc-DNA3. 1/hisC containing the rat 5-HT1AR (pc-DNA3.1/hisC-Rat-5-HT1AR)was constructed and transfected into SH-SY5Y cells. The transfected cells were isolated by G418 selection and SH-SY5Y-Rat-5-HT1A R cells were obtained. Expression of 5-HT1A R was detected by Western blot analysis. Cell viability was evaluated by MTT assay. SH-SY5Y-Rat-5-HT1AR cells were further observed for 5-HT1AR by immuno-fluorescence staining. Results Plasmid pc-DNA3. 1/hisC-Rat-5-HT1AR was successfully constructed by linking Rat-5-HT1A R with pc-DNA3.1/hisC and transfected into SH-SY5Y. The SH-SY5Y-Rat-5-HT1A R cells were more slender than SH-SY5Y cells with less and longer processes. MTT showed that the viability of SH-SY5Y-Rat-5-HT1A R cells was much lower than SH-SY5Y. Rat 5-HT1A R was expressed efficiently on the membrane of SH-SY5Y-Rat-5-HT1A R cells. Conclusion A cell line with overexpress of rat 5-HT1A R is successfully established.

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.

Objective To investigate the changes in the concentration of myocardin in children with lupus nephritis (LN) under different degree of vessel damage.Methods Forty-nine children diagnosed with LN by routine tissue immunolfuorescence, light microscope, and electron microscope were included, and 30 healthy children were included as control group. The pathological classiifcations were performed according to the ISN/RPS 2003 LN pathological classiifcation criterion. According to the Katafuchi evaluation method, the semi quantitative assessment of glomerular and kidney tubule damage was carried out, and the degree of vascular damage was evaluated at the same time. Double antibody sandwich method was used to detect the concentration of serum myocardin.Results The glomerular and kidney tubules damage in children with LN were signiifcantly aggravated with higher pathological classification (P<0.05). Glomerular damage was positively correlated with renal interstitial damage (r=0.96, P<0.01). The degree of vascular damage was related to the degree of glomerular injury and renal interstitial injury, while it was no related with the results of clinical tests. There were different concentrations of myocardin among mild-, moderate-, severe-vessel damage and control groups (F=378.61,P<0.001), and the concentration of myocardin in moderate- and severe-vessel damage groups were obviously lower than those in control group and mild-vessel damage group (P<0.01) while there was no difference between control group and mild-vessel damage group (P>0.05). According to pathological type, there were signiifcant differences in the concentration of myocardial between control group and different pathological types (F=626.793,P<0.01). FromⅡ,Ⅲ,Ⅲ+Ⅴ,Ⅳ toⅣ+Ⅴ, the concentrations of myocardial were decreased systematically, and there were statistic differences between groups (P all<0.05).Conclusion The concentration of myocardin in children with LN can relfect the renal vascular damage to a certain extent. Elevation of myocardin concentration may be helpful for the repair of vascular damage.

ObjectiveStudy the relationship among CaSR expression, tubulointerstitial damage,metabolic disturbance of calcium and phosphorus and microvascular density around the tubulointerstitium in children with steroid-resistant nephrotic syndrome.Methods36 cases of children with primary nephrotic syndrome were divided into hormone-sensitive group and steroid-resistant group.Semi-quantitative scores for tubulointerstitial pathological evaluation of the extent of damage, automatic biochemical analyzer for the determination of serum calcium (Ca), phosphorus (P) concentration of renal tubular epithelial CaSR expression and microvessel microvascular density around the tubulointerstitium were determined by immunohistochemical assay.ResultsMore severe the tubulointerstitial damage, lower level of serum Ca and higher level of serum P were observed [(2.26 ± 0.15) mmol/L]in children of the steroid-resistant group and the steroid-sensitive group [(1.90 + 0.12) mmol/L, P ＜ 0.05].CaSR expression (4.63 + 0.78) of renal tubular epithelial cells in the steroid- sensitive group was significantly lower than that in the steroid-resistant group (6.56 + 1.22, P ＜ 0.05), but microvascular density was significantly higher in the steroid- sensitive group(2.98 +0.35 vs 2.02 +0.24, P ＜0.05).When the tubulointerstitial damage was mild, CaSR expression (4.15 +0.58) in renal tubular epithelial cells in the steroid- sensitive group (4.26 ±0.61) was lower than the steroid-resistant group(3.12 ± 0.33; 3.01 ± 0.21), and microvascular density was higher,but the difference was not significant(P ＞0.05).In the moderate tubulointerstitial damage, CaSR expression in renal tubular epithelial cells in the steroid- sensitive group (5.35 ± 0.64) was significantly lower than the resistant group (7.37 +0.81, P ＜0.01), and microvascular density was significantly higher than the resistant group (2.81 ±0.16, 2.02 ±0.14, P ＜0.05).Compared by mild and moderate tubulointerstitial damage in children with the steroid-resistant, CaSR expression (11.46 ± 1.38) in children with severe tubulointerstitial damage was significantly increased, and microvascular density (1.15 ± 0.11) was significantly decreased (all P ＜ 0.01).ConclusionsCaSR expression was increased and microvascular density around the tubulointerstitium was decreased in children with steroid-resistant nephrotic syndrome.Dut to steroid resistance, the cytotoxic of steroid damaged the renal tubular epithelial cells, the metabolic disturbance of calcium and phosphorus and the damage of blood vessel endothelium finally resulted in severe tubulointerstitial damage.