Thyroid hormones (TH) play an imp or tant role in the development and maturity of the mammalian brain. Maternal TH de ficiency, even subclinical hypothyroidism, leads to poor neurodevelopment of the fetus. Screening of pregnant women for hypothyroidism is recommended. Identific ation of the TH-responsive genes in the developing brain and investigation on t heir functions are helpful to provide insights into the molecular mechanisms by which TH influence brain development.

Thyroid-stimulating hormone receptor(TSHR)is an important autoantigen whose cleavage and shedding can induce autoimmunity.The TSHR is the main functional receptor of the thyroid.The shedding of the ? subunit plays an important role in the forming of TSAb and balancing between TSAb and TBAb.Research on the cleavage and shedding of the TSHR extracellualar domain helps to gain a deep insight into the structure and function of TSHR,illuminate the pathogenesis of autoimmune thyroid disease and find out a new therapy.The structure of TSHR,the mechanism and the significance of its cleavage and shedding are reviewed in this article.

Objective To study the effect of hypothyroidism on oxidative stress status in developing rat brain and to further explore the mechanism of impaired brain development caused by hypothyroidism. Methods Perinatal hypothyroidism was induced by administering propylthiouracil(PTU) solution to the dams by gavage.The oxidative stress indexes were measured in brain homogenate of normal and hypothyroid pups which were sacrificed on the 21st d after birth. Results As compared to the control,the following indexes were found to be increased in the hypothyroid group: protein carbonyl contents,thiobarbital acid reactive substances,reduced glutathione,total antioxidative capacity,activities of superoxide dismutase and glutathione peroxidase(P0.05). Conclusion Hypothyroidism during rat brain development may cause oxidative stress,which may be related to the brain damage caused by hypothyroidism.

Objective To explore the effects of oxidative stress in porcine iliac endothelial cells(PIECs) induced by high glucose. Methods After being intervened by high glucose for some time, dihydroethidium (DHE) or dihydrorhodamine 123 (DHR123) was used as a reactive oxygen species(ROS) capture. The mean fluorescent intensity(MFI) of above probes which were the products of intracellular oxidation was detected by fluorescent microscopy and flow cytometry, and the level of ROS was thus measured. With lucigenin as chemiluminescence agent, luminescence changes were detected by chemiluminescence analyzer after addition of NADPH to observe the effect of high glucose on activity of NADPH oxidase(NOX). Results Intracellular MFI was markedly elevated with the concentration of high glucose and time of exposure to high glucose. It was revealed by flow cytometry that the NOX activity was significantly activated compared with normal medium treated PIECs(P

Objective: To study the protective effects of tetrahydropalmatine (THP) against ischemia－reperfusion induced hippocamp lesion in rats. 　MethodS: A model of ischemia-reperfusion induced brain lesion was set up by ligation of common carotid arteria in rats, and the protective effects of THP was observed.　Results: It was found that, with administration of THP, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and Na+, K+-ATPase as well as Ca2＋－ATPase were increased (P＜0.05, respectively), while malondialehyde (MDA) was decreased to 42.5% (P＜0.01) during brain ischemia－reperfusion.　Conclusion:The results suggested that THP can protect the rat against ischemia－reperfusion induced brain lesion.

Objective To investigate the effect of triiodothyronine on the expression of alpha subunit of C protein Co (Coa) gene in cultured rat cerebral cortex neurons. Methods Primary cultured neurons of rat were prepared from the cerebral cortex at embryonic day 19. The neurons were cultured in DMEM supplemented with 15% fetal calf serum. After 7 days, the neurons were cultured in different media; DMEM supplemented with 15% fetal calf serum (group A), DMEM supplemented with 15% fetal calf serum stripped of thyroid hormone (group B), 0.5nmol/L T3-containing DMEM supplemented with 15% fetal calf serum stripped of thyroid hormone (group C) , 5nmol/L T3-containing DMEM supplemented with 15% fetal calf serum stripped of thyroid hormone (group D) and 50nmol/L T3-containing DMEM supplemented with 15% fetal calf serum stripped of thyroid hormone (group E). The neurons were cultured for another 7 days and total RNA was extracted. Goa mRNA leves were measured by competitive RT-PCR. Results As compared with group A, Coa mRNA leves in group B, D and E were low (P 0.05). Conclusion T, has dual effects on the expression of Coa gene in cultured rat cerebral cortex neurons. T3 down-regulated Coa mRNA in cultured neuron. However, in the absence of T3, Goa mRNA was also very low. Thyroid hormone may exert their action on brain development by regulating the the expression of Goa gene.

Objective To explore the effect of advanced glycation end products(AGEs) on the oxidative stress in porcine vascular endothelial cells(PIECs). Methods After being intervened by AGEs for some time,cell viability was detected by MTT.2′,7′-dichlorofluorescein diacetate(DCFH-DA) was used as a reactive oxygen species(ROS) capture agent.The fluorescent intensity of 2′,7′-dichlorofluorescein(DCF),which was the product of cellular oxidation of DCFH-DA,was detected by flow cytometry,and the level of ROS was thus measured. Results Viability of PIECs was inhibited by AGEs in a dose-and time-dependent fashion(P

Objective To explore the effects of high glucose on oxidative stress of human peritoneal mesothelial cells(HPMCs).Methods HPMCs were cultured in vitro and identified by immunohistochemistry, and cells of second generation were selected. After HPMCs were treated by glucose with different concentrations for some time, MTT method was employed to detect the cell viability. 2’,7’-dichlorofluorescein diacetate (DCFH-DA) was used as a reactive oxygen species (ROS) capture. The cell viability of HPMCs and ROS level were analysed after being intervened by glucose with different concentrations and for different time. Results Viability of HPMCs was significantly inhibited in a dose-and time-dependent manner by high glucose(P

Objective To explore the association between disrupted in schizophrenia 1(DISC1) genepolymorphism and schizophrenia and different subtype depression.To verify if DISC1 gene is the common predisposing gene for schizophrenia and depression.Methods The genotypes and alleles in 260 cases of schizophrenicpatients,96 cases of depressive patients with psychotic symptoms,124 cases of depressive patients without psychotic symptoms,and 100 normal controls were examined with polymerase chain reaction(PCR),denaturing polyacrylamide gel elcctmphoresis separation technique.The association was analyzed between DISC1 gene single nncleotide polymorphisms(SNP) locus rs821616 and schizophrenia and different subtype depression.Results The frequeneies of the genotypes T/T,A/T,and A/A were 3.5%,28.0%and 69.5%respectively,the frequencies of alleles T and A were 9.6%and 90.4% respectively in schizophrenia group.The frequencies of the genotypes T/T,A/T,and A/A were 3.1%,24.0% and 72.9% respectively,the frequencies of alleles T and A were 15.6% and84.4% respectively in depression 1 group;The frequencies of the genotypes T/T,A/T,and A/A were 2.4%,23.4% and 74.2% respectively,the frequencies of alleles T and A were 15.3% and 84.7% respectively in depression 2 group;The frequencies ofthe genotypes T/T,A/T,and A/A were 1.0%,16.0% and 83.0% respectively,the frequencies of alleles T and A were 17.0% and 83.0% respectively in control group.There were significant differences in the frequencies of the genotypes (Chi-Square=8.072,P=0.045)and alleles(Chi-Square=8.564,P=0.036) of DISC1 gene among the four groups with non-parametric Kruskal-Wallis test.After pairwisecomparison each other in the four groups we found that there were significant differences in the frequencies of thegenotypes(Z=-2.802,P=0.005)and alleles(Z=-2.837,P=0.005) of DISC1 gene between patients withschizophrenia and normal controls with non-parametric Mann-Whitney test(two-tailed),there were no significantdifferences between other groups(P>0.05).Conclusion Our results suggest that DISC1 gene polymorphism is associated with schizophrenia significantly,but it is not associated with different subtype depression.This finding do not support the viewpoint that DISC1 gene is the common predisposing gene for schizophrenia and depression.

Ataxia Telangiectasia Mutated Proteins ; Breast ; metabolism ; pathology ; Breast Neoplasms ; metabolism ; pathology ; Carcinoma, Ductal, Breast ; metabolism ; pathology ; Carcinoma, Intraductal, Noninfiltrating ; metabolism ; pathology ; Cell Cycle Proteins ; metabolism ; Checkpoint Kinase 2 ; DNA-Binding Proteins ; metabolism ; Female ; Humans ; Lymphatic Metastasis ; Neoplasm Grading ; Protein-Serine-Threonine Kinases ; metabolism ; Tumor Burden ; Tumor Suppressor Protein p53 ; metabolism ; Tumor Suppressor Proteins ; metabolism