Normal perfusion pressure breakthrough is a serious complication that may occur in the treatment of cerebral arteriovenous malformations. This article reviews the progress in research on normal perfusion pressure breakthrough in recent years. It mainly investigates its pathogeneses, predictive methods and prevention and treatment strategies.

Objective To investigate the effect of repetitive transcranial stimulation (rTMS) on learning and memory and on the neuron and synapse ultrastructures of the CA3 region of the hippocampus.Methods Forty Sprague-Dawley (SD) rats were randomly divided into 4 groups (n =l0 in each group):a normal control group,a depression group,an rTMS group and a sham group.Unpredictable mild stress was used to establish depression models in the rats of the latter3 groups.The sucrose water consumption test and open-field test were used to evaluate any depressive behavior of each group.The rTMS group rats were given 15 Hz rTMS for 21 days while the sham group received sham stimulation.The orientational navigation and spatial probe tests were performed on each group using a Morris water maze to evaluate their learning and memory abilities.In addition,changes in the ultrastructure of the CA3 region of the hippocampus were detected using transmission electron microscopy.Results The modelling induced significant differences in the sucrose water consumption test results and in horizontal and vertical behavior in the open-field tests.Escape latency and spatial probe time were significantly different between the rTMS group and the sham and depression groups.There was no significant difference in the behavioral indexes between the depression group and the sham group.Electron microscopy showed pathological changes in the ultrastructures of the neurons and synapses in the CA3 region of the hippocampus among the depression group,while in the rTMS group those ultrastructures tended to be basically normal.Conclusion rTMS can improve learning and memory during depression,at least in rats.A possible mechanism is that rTMS can induce changes in the ultrastructures of neurons and synapses in the CA3 region of the hippocampus.

Pubmed Database was undertaken to identify relevant articles of brain tumor stem cells published from January 2000 to January 2008. Books on stem cells and brain tumor stem cells were retrieved. The data were selected primarily, 39 articles related to brain tumor stem cells were selected. Of the 39 inclusive articles, 8 were on review of the brain tumor stem cells theory, 31 were about the research and experiment of brain tumor stem cells. Data synthesis shows that the CD133+ cells isolated from brain tumor have the stem cell-like properties of endless cell proliferation, uncontrolled self-renewal and multi-directional differentiation, but brain tumor stem cells have more vigorous capacity to increase than normal neural stem cells. The brain tumor stem cells express the same gene product as the normal neural stem cells, but the nuclear type of the brain tumor stem cells is abnormal. Brain tumor stem cells maybe the products of gene mutation from the normal neural stem cells. Brain tumor stem cells are the bad seeds of brain cancer, and play a key role in the progress of tumorigenesis, growth, invasion, metastasis, drug resistance and recurrence. Thus, studies on brain cancer stem cells have crucial effects on analyzing the mechanism of occurrence and development, as well as radical cure of brain tumor.

Cerebral ischemia represents one of the leading causes of death and disability in modern time, but only few options exist for the treatment of ischemia-related disease. Neural cell replacement can reconstruct the nerve conduction circuit unit and lead to functional recovery partly in patients. The mechanism lies in: the stem cells transplanted into the lesion can differentiate into functional glial cells or neurons, and they can substitute the functions of dead neurons; to activate the endogenous neural stem cells; to excrete cytokines and improve the local environments, such as inflammatory reactions, tissue necrosis and glial scar formation. Transplantation of bone marrow mesenchymal stem cells, umbilical cord blood, embryonic stem cells and adipose mesenchymal cells have been used for stem cells transplantation in treatment of cerebral ischemia in animal models. So far, the underlying mechanisms of the cell replacement therapy for stroke lesions have remained unknown, and this therapy faces predominantly two major problems: one is how cell grafts survive in an ischemic environment; the other is how cell grafts substitute or rescue neural cells with many different phenotypes.

Oncogene-induced senenscence(OIS) is defined as a stable proliferative arrest of normal cells upon overexpression of aberrant proliferative signals of oncogenes through MAPK and PI3K pathway.The molecular mechanism of OIS is related to the formation of heterochromatin and DNA-damage check-point response.The markers of OIS includ senescence-associated ?-galactosidase and senescence-associated heterochromatin foci.With the growing recognization of OIS,the new models of tumor progression are emerging.The further investigation on the mechanism of OIS is of great significance to understanding of the tumorigenesis and provide new ideas and methods of cancer treatment.

Objective:To investigate varied electromyographic types in the patients with hemimasticatory spasm(HMS).Methods:Surface electromyography was recorded to study electromyographic features of 16 cases with HMS.Results:Spasm was found in mandibular rest position in 2 cases and in tooth contact position in 14 cases.During the involuntary spasm of the 14 cases, motor unit potential could be classified into three types:continuous(8 cases), rhythmic(3 cases) and irregular(3 cases).Conclusion:The electromyographic feature of hemimasticatory spasm is characterized by continuous motor unit potential discharge. The spasm is mostly triggered by tooth contact.

Objective:Study on the expression of Fas and Fas ligand (FasL) in gastric cancer and its possible significance.Methods:Fifty-eight paraffin-embedded gastric cancer tissues and twenty-six non-cancer tissues were tested for the expression of Fas and FasL protein by immunohistochemistry.Results:The positive rate of Fas in cancer cells of gastric cancer tissues was significantly lower than that in gastric epithelial cells of the control tissues(19.0% and 61.5%,respectively;?~2=14.918;P=0.000).The positive rate of FasL showed no significant difference between cancer cells of gastric cancer tissues and gastric epithelial cells of the control tissues(63.8% and 53.8%,respectively).Conclusion:The Fas-FasL system is unbalanced.It may be related to the carcinogenesis of gastric epithelial cells and might be responsible for the immune excape of these cells.

AimTo investigate the influence of tetramethylpyrazine(ligustrazine, Lig) on oxygen consumption and superoxide during the respiratory burst of human neutrophils. MethodsIt was observed by using ESR spin trapping, spin probe oxymetry and luminol-dependent chemiluminesence(CL) . Results Lig had no influence on oxygen consumption during the respiratory burst of neutrophils(P＞0.05), but had remarkable inhibition on CL response generated by neutrophils(P＜0.01), and had scavenging effect on O2 and OH ·generated by neutrophils, which were demonstrated in xanthine/ xanthine oxidase system and Fentons reaction(P＜0.01) . ConclusionLig has no inhibiting effect on oxygen metabolic function of neutrophils,but protects tissue from injury caused by activated neutrophils through scavenging oxygen radicals.

Objective To observe the effect of rhTRAIL on survivin gene expression of human lung adeno-carcinoma A549 xenografted tumor in nude mice,and investigate the possible inhibitory mechanism of rhTRAIL on the implanted-tumor growth.Methods The solid tumor model was formed in nude mice with human lung adeno-carcinoma cell line.A549.24 mice were randomly divided into the four groups,rhTRAIL single treated group (1 μg/mL),rhTRAIL combined with cisplatin (DDP) treated group,cisplatin treated (1.5mg/kg) and 0.9％ sodium chloride injection(NS) control group.The rhTRAIL and DDP were injected once every other day by intraperitoneal injection to mice in the treated groups,lasting eight times,the same volume of saline solution was injected to the control group.After these,mice were killed and dissected completely.The expression level of survivin mRNA and protein in the tumor tissues was detected by real-time polymerase chain reaction (RT-PCR) and immunohistochemistry,respectively.And the expression of survivin gene in serum of each group was tested by ELISA.Results The expression levels of survivin mRNA in implanted-tumor tissues in rhTRAIL,rhTRAIL combined with DDP,DDP and NS group were (48.7 ± 2.5) ％,(53.1 ± 4.6) ％,(99.1 ± 5.3) ％ and (95.6 ± 3.7) ％,respectively.While the protein expressions of survivin gene in those groups were (0.319 ± 0.025),(0.483 ± 0.058),(0.635 ± 0.041) and (0.619 ± 0.017),respectively.Moreover,the serum levels of survivin were (71.9 ± 7.05),(80.26 ± 10.80),(112.75 ± 15.41) and (105.03 ± 20.37),respectively.The data showed that the expression levels of rhTRAIL and rhTRAIL combined with DDP group were lower than that of DDP-treated group or the NS control group (P ＜ 0.0 5).Compared with the rhTRAIL combined with DDP group,the survivin gene expression level of rhTRAIL-single treated group decreased a little lower,but the difference was not significant (P ＞ 0.05).Conversely,the survivin gene level was increased to some degree compared with the NS control group,and uniformly there was no significant difference (P ＞ 0.05).Conclusion rhTRAIL can downregulate the expression level of survivin gene of human lung adeno-carcinoma A549 xenografted tumor in nude mice.It may be one of the possible inhibitory mechanisms of rhTRAIL on the implanted-tumor growth that rhTRAIL can downregulate survivin gene expression and promote tumor cell apoptosis.

Objective To explore the effects of repetitive transcranial magnetic stimulation on behaviors and hippocampus neuronal apoptosis in rats with chronic stress-induced depression.Methods 40 male SD rats of SPF grade were randomly divided into normol control group (n =8) and model preparation group (n =30) after screening.Rats in model preparation group were singly housed and given chronic unpredictable mild stress(CUMS) to build depression model.Excluding unsuccessful modeling rats,the model preparation group was divided into three groups:model group(n=8,without any treatment),rTMS group (n=8,with the intervention of 10 Hz rTMS) and shame group (n=8,simulation of rTMS environment without rTMS stimulus).The changes of behaviors in each group were detected by weight measurement,sucrose consumption test and open-field test.The changes of morphology of hippocampal neurons were detected by Nissl's staining.The changes of Bax in hippocampal neuron were detected by Immunohistochemical staining.Results (1) Behavioral results showed stress for 21 d could make rat behavior scores decrease significantly(all P＜0.05),and rTMS intervention could significantly improve their behavior scores (all P＜0.01).Compared with model group,the weight reduction rate (0.32±0.05)％,the score of sucrose consumption test(7.03 ± 1.02) and the score of open field test(8212.41 ± 1416.15,8.75 ± 1.58) in rTMS group was higher(P ＜0.01).(2) Nissl staining showed stress for 21 d could make the number of hippocampal CA3 neurons was reduced,cell morphology was poor,and the number of Nissl bodies was reduced.rTMS intervention could increase the number of hippocampal CA3 neurons,cell morphology was integral and the number of Nissl bodies was increased.(3) Immunohistochemistry results showed stress for 21 d could cause the number of Bax cell were significantly increased(P＜0.01),and rTMS intervention can make the number of Bax cell were significantly lower(P＜0.01).Conclusion rTMS intervention improves the depressive behavior in chronic stress depression model rats and inhibits the apoptosis,which might work through inhibition of neuron apoptosis and decline of Bax expression in hippoeampal neurons.