The differentiating of neurons and other distinct cell types during embryonic development requires the selective activation or repressing of many different sets of genes. Gene expression patterns in neurons are modulated by multiple extracellular and intracellular stimuli. The transcriptional regulation of individual gene is mediated by small DNA sequences such as silencer and enhancer, and the expression pattern can be determined by the integration of the effects of a very large number of these cis-acting elements. These DNA elements either activate or repress promoter activity depending upon the nature of the transcription factors that bind to them. It is possible that there are different regulatory mechanisms of gene expression in the nerve system.

Multimedia Services has drawn much attention from both industrial and academic researchers due to the emerging consumer market, how to provide High-Availability service is one of most important issues to take into account. In this paper, a dynamic fault tolerant algorithm is presented for highly available distributed multimedia service, then by introducing SLB(server load balancing) into fault tolerance and switching servers in different ways according to their functions, the proposed schema can preserve reliability and real-time of the system .The analysis and experiments indicate that resuming server's faulty by this method is smooth and transparent to the client The proposed algorithm is effectively improving the reliability of the multimedia service.

ObjectiveToinvestigatetherolesofbrain-derivedneurotrophicfactor(BDNF)and tyrosine receptor kinase B (TrkB) in ischemic postconditioning. Methods Wistar rats w ere randomly assigned to three groups:a sham operation (9 rats), an ischemic postconditioning, and an ischemia-reperfusion group. According to the reperfusion time, the latter 2 groups w ere redivided into 6, 12, 24, 48, and 72 h subgroups (9 rats in each subgroups). A middle cerebral artery occluded by suture method for a cerebral ischemia-reperfusion model. Triphenyl tetrazolium staining w as used to detect infarct volume (P=4). Immunohisto-chemical staining w as used to detect the expression levels of BDNF and TrkB proteins (P=5). Results The infarct volumes in the ischemic postconditioning group w ere reduced significantly compared w ith those in the ischemia-reperfusion group (6 h:143.3 ±8.7 mm3 vs.166.8 ±7.5 mm3, t=4.104, P=0.006;12 h:151.7 ±7.8 mm3 vs.171.6 ±9.1 mm3, t=3.314, P=0.016; 24 h: 159.2 ±9.3 mm3 vs.177.1 ± 7.6 mm3, t=3.000, P=0.024;48 h:166.9 ±9.6 mm3 vs.184.9 ±9.0 mm3, t=2.732, P=0.034;72 h:172.0 ±9.1 mm3 vs.198.1 ±8.2 mm3, t=2.640, P=0.039), and the positive cel numbers of BDNF (6 h:23.98 ±4.07 vs.18.63 ±2.5, t=2.479, P=0.038;12 h:27.64 ±3.18 vs.22.01 ±3.14, t=2.817, P=0.023;24 h:34.82 ±4.17 vs.28.46 ±4.05, t=2.446, P=0.040; 48 h:34.30 ±3.27 vs.26.29 ± 3.26, t=3.872, P=0.005;72 h:28.77 ±3.53 vs.23.64 ±3.54, t=2.297, P=0.051) and TrkB (6 h:33.83 ±3.90 vs.21.51 ±3.86, t=5.012, P<0.001; 12 h:38.59 ±4.84 vs.23.41 ±3.67, t=5.586, P<0.001;24 h:46.07 ±3.06 vs.28.78 ±3.61, t=8.169, P<0.001; 48 h:47.90 ±3.30 vs.29.51 ± 3.81, t=8.160, P<0.001; 72 h:42.78 ±4.07 vs.27.46 ±3.19, t=6.623, P<0.001) per high-pow er field at each time point in the ischemic postconditioning group w ere significantly more than those in the ischemia-reperfusion group. Conclusions Ischemic postconditioning upregulates the expressions levels of BDNF and TrkB proteins after ischemia-reperfusion and reduces cerebral infarct volumes. BDNF/TrkB may play an important neuroprotective effect in ischemic postconditioning.

Objective To investigate the change rule and correlation of heme oxygenase-1(HO-1)/carbon monoxide(CO)and the influence of simvastatin and amlodipine in athemsclemtic progress.Methods The rabbits received 1％cholesterol diet(n=24)for eight weeks.After eight weeks,rabbits were fed with normal diet for eight weeks.The rabbits in model group(n=8)were administrated with cholesterol diet.The rabbits in simvastatin group(n=8)were administrated with simvastatin.The rabbits in amlodipine group(n=8)were administrated with amlodipine.The levels of serum lipids and plasma carbon monoxide were obtained at the beginning,the 8th week and the 16th week.The expression of heme oxygenase-1 in the thoraoia aortic tissue were observed with immunohistochemistry technique.Results By the end of 16th week,the levels ofserum lipids and plasma carbon monoxide in model group were obviously increased,however,the expression of heine oxygenase-1 were markedly decreased.Compared with model group.The levels～rurfl lipi&and plasma carbon monoxide in simvastatin group were significantly decreased,while the expression of heme oxysenase-1 in aortic great reduced.The levels flerum lipids in amlodipine group were not significant ckmged,the levels of plasma carbon monoxide were obviously decreased,while tlle expression ofheine oxygenase-1 in aortic great reduced.Conclusions In atheresclerofic progress,heme oxygenase-1(HO-1)/carbon monoxide(CO)appared the reciprocal relationship,and amlodipine may suppress athemsclemtie progress by decreasing the system.

Objective To investigate the effect of cerebral ischemic preconditioning (IP) on the expressions of angiopoietin-1 (Ang-1) and its receptor Tie-2 mRNA in cerebral ischemia in rats.Methods Ninety-nine Wistar rats were randomly assigned to three groups:sham operation (n =9),non-ischemic preconditioning (NIP) (n =45),and IP (n =45).The latter two groups were redivided into 5 subgroups:ischemia-reperfusion 1,3,7,14,and 21 days (n =9 in each group).A model of transient middle cerebral artery occlusion (MCAO) was induced by the intraluminal suture method for focal IP (ischemia for 10 minutes and restoring perfusion).Infarct volume was determined by 2,3,5-triphenyltetrazolium staining.The expression levels of Ang-1/Tie-2 mRNA were detected by in situ hybridization.Results The infarct volumes in the 1 -,3-,and 7-day subgroups of the IP group were significantly smaller than those in the relative subgroups of the NIP group (all P＜ 0.05).The expression of Ang-1 mRNA in the 3- and 7-day subgroups of the IP group and the expression of Tie-2 mRNA in the 1-,3-,and 7-day subgroups of the NIP group were upregulated significantly (all P ＜ 0.05).The infarct volume in the 3-day subgroup of the IP group was reduced most significantly (P ＜ 0.05).The expression of Ang-1 mRNA in the 7-day subgroup was upregulated significantly,and the peak expression of its receptor Tie-2 mRNA appeared at day 3 after IP and continued to day 7.Pearson correlation analysis showed that the expression levels of Ang-1/Tie-2 mRNA were significantly negatively correlated with infarct volume (P ＜0.01).Conclusions The expression of Ang-1/Tie-2 mRNA in the IP group was upregulated within the time window of ischemic tolerance (1 - 7 days after preconditioning),in which Ang-1 may mainly act on the later stage of the cerebral ischemic tolerance.

AIM To investigate the role and mechanism of a novel antiepileptic drug topiramate on amygdala kindling in rats. METHODS The effects and mechanism of topiramate on kindling were examined by the establishment of amygdala kindling model and combination with other drugs. The influence of topiramate on seizures induced by semicarbazide hydrochloride(SCZ) was also observed. RESULTS Topiramate (50～200 mg?kg -1 ,ig) dose-dependently inhibited the seizure severity in amygdala kindling ( P

Glycemic variability is closely related to diabetes complications,and might play a more valuable role in clinical risk assessment.The glycemic variability could effect the prognosis of cardiovascular disease and ischemic stroke.Meanwhile,it has a close relationship with the presence, development and severity of diabetic nephropathy.Moreover,as an independent risk factor for the damage of macro- and microvessels,it has a positive relationship with the severity of target organ.Therefore,the strategy to regulate glycemic variability is a valuable measure of glycemic control,and may be of great significance to strengthen the effect of diabetes treatment and reduce the damage on target organs.

Objective To investigate the role of phosphatidyl inositol 3 kinase (PI3K)/Akt pathway in the protection of focal cerebral ischemia reperfusion injury in rats with limb ischemic postconditioning (LIP) by detecting the expression levels of p-Akt protein, and caspase-9 and Bcl-2 mRNAs after remote LIP. Methods Forty-two Wistar rats were randomly assigned to 3 groups: sham operation, ischemia-reperfusion (IR) and LIP groups. The middle cerebral artery ischemia-reperfusion injury model was induced by the suture method in the IR group and the LIP group. In the LIP group, three circulatory LIP ( 5 min ischemia/5 min reperfusion) in the contralateral femoral artery were performed before reperfusion 2 h after cerebral ischemia. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining. The expression of p-Akt protein was detected by immunohistochemical staining and the expression levels of cystin-9 and Bcl-2 mRNAs were detected by in situ hybridization. Results Compared with the IR group, the infarct volume in the LIP group was significantly reduced ( P<0.05). The expression levels of p-Akt protein and Bcl-2 mRNA significantly increased (all P<0.05), and the expression level of caspase-9 mRNA significantly decreased (P<0.05). Conclusions LIP can reduce the volume of cerebral infarction in focal cerebral ischemia-reperfusion injury in rats. Its mechanism may be involved in up-regulation of p-Akt protein and Bcl-2 mRNA expression and down-regulation of caspase-9 mRNA expression, suggesting that LIP can alleviate cerebral ischemia-reperfusion injury through PI3K/Akt pathway.

As an important tool to evaluate cardiac autonomic function, heart rate variability (HRV) is closely associated with ischemic stroke. The change of HRV can not only increase the incidence and recurrence risk of ischemic stroke, but also affect the severity of the disease and the risk of complications, resulting in poor outcomes. Effective intervention for patients with stroke to restore their autonomic nerve function is expected to become a new target for the treatment of ischemic stroke. This article reviews the research progress of the correlation between HRV changes and ischemic stroke.

Cardiovascular diseases (CVDs) are a leading factor driving mortality worldwide. Iron, an essential trace mineral, is important in numerous biological processes, and its role in CVDs has raised broad discussion for decades. Iron-mediated cell death, namely ferroptosis, has attracted much attention due to its critical role in cardiomyocyte damage and CVDs. Furthermore, ferritinophagy is the upstream mechanism that induces ferroptosis, and is closely related to CVDs. This review aims to delineate the processes and mechanisms of ferroptosis and ferritinophagy, and the regulatory pathways and molecular targets involved in ferritinophagy, and to determine their roles in CVDs. Furthermore, we discuss the possibility of targeting ferritinophagy-induced ferroptosis modulators for treating CVDs. Collectively, this review offers some new insights into the pathology of CVDs and identifies possible therapeutic targets.
Humans ; Cardiovascular Diseases ; Ferroptosis ; Iron ; Trace Elements