Objective To study the inhibitory effect of methylmercury chloride(MMC) on rat C6 glioma cells in vitro.Methods The rat C6 glioma cells were cultivated in vitro and divided into control group and MMC-treated group(0.08-10.00 ?mol?L-1 MMC were divided into 8 groups with concentration gradient).MTT assay was performed to evaluate the proliferation inhibitory effect and cytotoxicity effect of MMC with different concentrations on cultured rat C6 glioma cells,and flow cytometry was used to assess the effects of MMC treatment on cell apoptosis and cell cycle in rat C6 glioma cells.Results 1.25,2.50,5.00 and 10.00 ?mol?L-1 MMC could inhibit the proliferation of cultured rat C6 glioma cells in vitro,the viabilities of MMC treated C6 glioma cells were significantly lower than those in control group(P

Objective To study the anti-neuroglioma effect of methyl-mercuric chloride(MMC) by observing the morphological changes of apoptotic neuroglioma cells induced with MMC in rats with brain neuroglioma.Methods The rat models of neuroglioma were established,and divided into two groups.The rats in experimental group were lavaged with MMC 1 week after injected with C6 glioma cells,10 mg?kg-1every day,the rats in control group were treated with sodium chloride at the same dose.24 d after inoculation all rats were sacrificed except natural death,the brain tissues were obtained,and the pathohistological changes were observed under light microscope and transmission electron microscope.Results The macropathological result showed that the tumor volume in experimental group was smaller than that in control group.Under light microscope,in experimental group the growth density of C6 ghioma cells was lower than that in control group,and the apoptotic cells with smaller volume and karyopyknosis were found.The result of transmission electron microscope showed that in experimental group,the glioma cells had some changes such as karyopyknosis,chromoplasm margination,nuclear fragmentation and vacuolar degeneration and so on.Conclusion MMC has inhibitory effect on the proliferation of C6 glioma in rats in vivo,its mechanism may be related to inducing the apoptosis of neuroglioma cells.

Objective To study the inhibitory effect of triethyltin chloride(TETC) on proliferation of rat C6 glioma cells in vitro and its mechanism and provide basis for research on TETC in treatment for glioma.Methods MTT assay was performed to determine the inhibitory rate of 0.5,1.0 and 2.0 ?mol?L-1 TETC on rat C6 glioma cells for 24 and 48 h.The changes of nucleus of C6 glioam cells treated with 0.5,1.0 and 2.0 ?mol?L-1 TETC for 48 h were observed by fluorescent microscope.Flow cytometry was used to assess the effects of 0.5,1.0 and 2.0 ?mol?L-1 TETC on cell cycle and apoptosis in rat C6 glioma cells for 48 h.Results 0.5,1.0 and 2.0 ?mol?L-1 TETC inhibited the proliferation of C6 glioma cells in vitro,and the inhibitory rates were 7.92%,9.51%,19.03% and 15.62%,36.16%,41.92% in 24 h TETC treated group and 48 h TETC treated group,respectively.The inhibitory rate of TETC on C6 glioma cells determined by MTT assay increased in a dose-dependent and time-dependent manner,and there were significant differences of the inhibitory rates at 48 h between control and various doses groups as well as between various doses groups(P

Objective To study the inhibitory effects of triethyltin chloride(TETC) on proliferation and the morphological changes of rat C6 glioma cells in vivo.Methods C6 glioma cells were autotransplanted into 16 Wistar rats,and the rats were divided into experiment group and control group.TETC was injected into each rat through intraperitoneal route at the dose of 1 mg?kg-1?d-1 and the injection lasted 4 d in experiment group,and the physiological saline was injected into each rat in the same way as experiment group in control group.The weights of C6 glioma were measured and the proliferation rate of the tumor was calculated after 14 d.The morphological changes of C6 glioma cells were observed by HE staining and electron microscope.Results The weight of C6 glioma in TETC group was lighter than that in control group(P

Objective To study the effects of methylmercury chloride(MMC) on protein kinase C(PKC) activities in rat developing cerebellum.Methods The animals in experimental groups were fed standard rat chow with(0.75 mg) MMC(ExpⅠ),1.5 mg MMC(ExpⅡ) and 3.0 mg MMC(ExpⅢ)respectively for 90 d before gestation to(30 d) post parturition.Cerebella of pups from each group on postnatal days(PND) 3,7,17,21 and 30 were dissected. All the samples were separated into cytosol and membrane subcellular fractions and assayed for PKC activity by the improved method from Takai′s.Results Membrane and cytosolic PKC activities of pups′ cerebella from certain experimental groups were significantly higher than those of corresponding control group,PKC activities of rats from ExpⅡ,ExpⅢ and PND 3,7,14 in ExpⅠwere significantly higher than those in control group((P

Depression is a common complication after stroke.It is often associated with disability,cognitive impairment,and increased mortality.This article reviews the epidemiology,risk factors,predictive factors,and pathophysiology mechanisms of post-stroke depression.

Flavonoids are widely used today in the treatment of ischemic stroke. The therapeutic effects and functions of flavonoids are, therefore, generating more and more interest.

Objective To explore the molecular defects of CYP17A1 gene in a family with 17?-hydroxylase deficiency. Methods Clinical features and laboratory data were collected from the pedigree with 17?-hydroxylase derficiency and the proband was hospitalized in Shanghai Clinical Center for Endocrine and Metabolic Diseases. PCR and subclone sequencing were performed to screen the mutations of CYP17A1 gene. Results The patient was diagnosed as 17?-hydroxylase deficiency according to the clinical presentations, laboratory examination and blood level of steroid hormones. A new type of mutation was identified as a base deletion and a base transversion (TAC/AA) at codon 329 in the patient. It produced a missense mutation of Tyr→Lys at codon 329 and the open reading frame shift following this codon. The patient was homozygous mutation and her parents were heterozygote carrying TAC329AA mutation. Conclusion 17?-hydroxylase deficiency in this family was caused by CYP17A1 mutation (TAC329AA) which was first identified as a complex defects of missense mutation and the open reading frame shift at codon 329.

Objective Measurement of ankle brachial index (ABI) is a simple method of assessing lower limb arterial blood supply,while measurement of toe brachial index (TBI)has only been advocated as an alternative.The aim of this study was to obtain information about whether TBI should be taken in type 2 diabetes,even when ABI is normal,and to evaluate the relationship between TBI and atherosclerosis.Methods In a crosssection study,ABI,TBI,and carotid intimal-medial thickness (IMT) were measured on 979 outpatients with type 2 diabetes in Ruijin Hospital.Those with normal ABI (0.9 ≤ABI ＜ 1.3,n = 945) were divided into two groupsnormal TBI group(TBI≥0.6,n=893) and low TBI group(TBI＜0.6,n=52),and then the clinical and laboratory data were compared between these two groups.Furthermore,the relationship between TBI and atherosclerosis was investigated.Atherosclerosis was defined as the maximum IMT ≥ 1.1 mm.Results Low ABI and low TBI were detected in 1.3% and 6.6% of the patients,respectively.Comparison of the clinical and laboratory data between the two groups showed that age and HbA1C values were significantly higher in the low TBI group.Furthermore,TBI was inversely associated with IMT(β=-0.217,P＜0.01),an indicator for atherosclerosis of the carotid artery.Multiple logistic regression analysis revealed that decline of TBI was an independent risk factor of atherosclerosis (OR=1.30,95% CI 1.01-1.69,P＜0.05).Conclusion In type 2 diabetes,the decline of TBI is associated with atherosclerosis,indicating the necessity for diabetic patients to detect TBI,even when ABI is within normal range,in order to detect peripheral artery disease in early stage,and reduce the risk for atherosclerosis.

patients. Maintenance of systolic BP<120 mm Hg(1 mm Hg=0.133 kPa) and diastolic BP<80 mm Hg may reduce the risk of atherosclerosis in type 2 diabetes.