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.

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.

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.

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.

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.

Objective To study the surgery factors on chronic subdural hematoma(CSH)recurrence.Methods Two hundred and thirty-six patients with CSH were treated with trepanation and drainage.It was analyzed retrospectively on location of burr-hole,location of drainage tube,volume of intracranial pneumatocele,residual hematoma and drainage time etc.Results Half hematoma was in 177cases,two sides hematoma was in 59 cases,total was 295 hematomas.Twenty-seven hematomas were recurrent,9 cases were two sides hematoma,and 18 cases were half hematoma.There was no significant difference between recurrence rate and age,sex,drunkenness,hemorrhagic tendency,half or two sides hematoma,location of burr-hole,location of drainage tube,volume of intracranial pneumatocele and residual hematoma(P＞0.05).The recurrence rate was 9.2％(27/295).There was significant difference in recurrence rate between drainage time ≥ 3 d and＜3 d[3.5％(5/143)vs.14.5％(22/152),P＜0.01].In age ≥ 60years patients,there was significant difference in recurrence rate between drainage time ≥ 3 d and＜3 d[3.4％(4/119)vs.16.2％(18/111),P＜0.01].But in age＜60 years patients,there was no significant difference in recurrence rate between drainage time ≥ 3 d and＜3 d[4.2％(1/24)vs.9.8％(4/41),P＞0.05].Conclusion It should be taken more than 3 d of drainage time for old patients with CSH,while shorten time for young patients with CSH.

Objective: To investigate the effects of glucagon-like peptide-1(GLP-1)on high glucose-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and the mechanism involved. Methods: HUVECs were cultured under varying conditions for 48 h, and the cell viability was spectrophotometrically measured by MTT assay. Flow cytometry detected the ratio of cell apoptosis. Western blot detected the protein levels of p-Akt and p-eNOS, while NO assay kit detected the NO concentration.
Results: Treatment of high glucose (33 mmol/L) for 48 h signiifcantly decreased the HUVECs viability and induced the apoptosis of HUVECs, concomitant with decreased Akt and eNOS phosphorylation leves and subsequent NO production. Treatment with GLP-1 (3 nmol/L) for 48 h in the high glucose group increased the HUVECs viability (P<0.01), decreased the ratio of HUVECs early apoptosis (P<0.05), ameliorated the reduced protein levels of p-Akt and p-eNOS caused by high glucose, and increased the NO production (P<0.05). The anti-apoptotic effect and the increased NO production of GLP-1were inhibited by PI3K inhibitor wortmannine (100 nmol/L) or eNOS inhibitor L-NAME (100μmol/L). The effect on p-Akt, p-eNOS of GLP-1 was inhibited by wortmannine (100 nmol/L) while L-NAME (100μmol/L) did not have any influence on the expression of p-Akt.
Conclusion: GLP-1 can ameliorate high glucose-induced HUVECs apoptosis, which is probably related to the up-regulation of PI3K/Akt/eNOS pathway.