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

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.

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 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.

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.

AAIM:To investigate the effect of atorvastatin ( ATO) on electrical remodeling, atrial ion channel protein expression and cardiac function in atrial tachypacing rabbits, and to explore the potential electrical mechanism of ATO in the prevention of atrial fibrillation.METHODS:The rabbits were subjected to atrial tachypacing at 600 min-1 in the absence or presence of treatment with atorvastatin (ATP and ATO groups) for 48 h, and the other 10 as sham group without pacing ( NP group) .The tachypacing model was performed by attaching pacing and testing electrodes to left atrial and connecting with custom animal cardiac pacemaker in the open-chest situation.The animals in ATO group were pretrea-ted with ATO for 7 d and continued during tachypacing.Serial atrial effective refractory period ( AERP) was measured in each rabbit at baseline, 8 h, 16 h, 24 h, 32 h, 40 h and 48 h with different cycle lengths.The changes of cardiac func-tions and cardiac structure were observed by cardiac ultrasonic cardiogram before and after atrial tachypacing.The expres-sion of atrial ion channel proteins CaLα1 and Kv4.3 was detected by Western blotting.RESULTS:Compared with NP group, AERP at cycle lengths of 150 and 200 ms, the adaption of AERP, and the levels of CaLα1 and Kv4.3 expression were all decreased in ATP and ATO group, especially in ATP group.Left atrial dimension ( LAD) was increased in pacing groups as compared with NP group (P<0.05) after pacing delivery for 48 h, while no difference between the formers was observed.No significant change of the left ventricular dimension ( LVD) and ejection fraction ( LVEF) among groups be-fore and after pacing was found.CONCLUSION:Atrial tachypacing significantly shorten AERP, resulting in poor adap-tion of AERP, while ATO pretreatment significantly attenuates the atrial electrical remodeling in rabbits, but had no effect on cardiac structure.ATO suppresses the down-regulation of atrial ion channel proteins CaLα1 and Kv4.3 expression after 48 h, which may be the potential ionic mechanism of atrial electrical remodeling for ATO.