Objective To explore the trend of Th_1/Th_2 bias in Hashimoto thyroiditis(HT)and their effects on the pathogenesis of HT.Methods The proportion and mean fluorescence intensity(MFI)of CCR5 and CD30 were examined on peripheral T lymphocytes by flow cytometry in patients with Hashimoto thyroiditis(HT)(n=21)and healthy controls(n=45).Results The proportion of both CD4~+CCR5~+and CD~+4 CD30~+ cells were significantly increased in HT group(P

To explore the dose- and time- dependent relationship between the chronic iodine excess and thyroid structure, ultrastructure, and thyroid function in autoimmune-prone NOD. H-2h4 mice. Chronic iodine excess leads to iodine-induced goiter with an ultrastructure of follicle epithelial cells injury in a dose and time dependent way.

Objective To investigate the effect of subclinical hypothyroidism during pregnancy on hippocampus insulin-like growth factor Ⅰ (IGF-Ⅰ) signaling pathway in rat offspring.Methods A total of 60 female Wistar rats were evenly divided into control(CON),subclinical hypothyroidism(SCH),and clinical hypothyroidism (CH) groups.The hippocampus of progenies were collected on the postnatal day 3,postnatal day 7 to measure protein kinase B (Akt) and phosphorylated-Akt (p-Akt) by Western blot,IGF-Ⅰ and insulin-like growth factor Ⅰ receptor (IGF-Ⅰ R) by Elisa.Morris water maze and field excitatory postsynaptic potential long-term potentiation were measured at the postnatal 40 day.Results Western blot and Elisa revealed that levels of IGF-Ⅰ,IGF-Ⅰ R,and p-Akt of pups from SCH group were lower than that of CON group and were higher than CH group on day 3 (P ＜ 0.05).On day 7,the levels of IGF-Ⅰ,IGF Ⅰ R,and p-Akt of pups from SCH group were lower than CON group (P＜ 0.05),but no difference was observed in p-Akt and IGF-Ⅰ R level between SCH group and CH group (P ＞ 0.05).Latencies of all groups had shortened in Morris water maze test with increasing of training trials.The slope of field excitatory postsynaptic potenial was increased in all groups after Theta burst stimulation.The amplification percentage of slope of field excitatory postsynaptic potenial in SCH group's was lower than control group's but was higher than CH group's(all P values＜0.05).Conclusions Maternal subclinical hypothyroidism impairs long-term potentiation induction in hippocampus of rat might be associated with the levels of IGF-Ⅰ,IGF-Ⅰ R,and p-Akt.

Objective To investigate the efficacy and optimal time of levothyroxine (L-T4) treatment in pregnant rats with subclinical hypothyroidism.Methods Female adult Wistar rats were divided into six groups (n =10 per group):control,hypothyroid (H),subclinical hypothyroid (SCH),and SCH treated with L-T4 starting from the tenth,thirteenth,and seventeenth gestational day (GD10,GD13 and GD17),to restore normal thyroid hormone levels.Spatial learning was assessed in progenies by a water maze test and fEPSPs recording.Results Progenies from the SCH and H groups demonstrated significantly longer mean latency in the water maze test and a lower amplification percentage of the fEPSPs' amplitude and slope compared with the offspring of the control group.L-T4 treatment in the GD10 and GD13 groups significantly shortened mean latency and increased the amplification percentage of the fEPSPs' amplitude and slope as compared with the progeny of rats with subclinical hypothyroidism.However,L-T4 treatment in the GD17 group showed only minimal effect on spatial learning of offspring.Conclusion Maternal subclinical hypothyroidism may impair spatial learning in the offspring; L-T4 treatment started early during pregnancy may alleviate this adverse effect.

A total of 1151 subjects were enrolled in this study.Metabolic syndrome (MS) was diagnosed according to the International Diabetes Federation (IDF) criteria.Significant differences in waist circumference,body mass index(BMI),diastolic blood pressure(DBP),systolic blood pressure(SBP),fat mass,Fat％ in different serum TSH levels were found.There were positive relation between fasting plasma glucose,DBP,SBP,and serum FT4 levels,between high density lipoprotein-cholesterol,DBP,SBP,waist circumference,fat mass,Fat％,and serum FT3 levels,even after adjustment for age and sex.Serum FT3 and FT4 levels were higher in the MS group than those in the control group.

Thyrocytes expressing MHC class Ⅱ molecules were separated from transgenic mice and were co-cultured with autologous spleen T lymphocytes. T cells did not proliferate and were not activated, but CD4+ T cells were promoted into apoptosis.

Objective To explore the correlation between anti-thyroid autoantibodies and hepatitis C virus (HCV) infection. Methods Four hundred and sixty-two samples with positive thyroid peroxidase antibody (TPOAb) and (or) thyroglobulin antibody (TgAb) were collected. Three hundred and eighty age and gender matched subjects with negative TPOAb and TgAb were selected as controls. The anti-HCV antibody was examined in all the cases using the third-generation enzyme-linked immunosorbent assay (ELISA), HCV RNA qualitative examination was examined further in those who had positive anti-HCV antibody. Meanwhile, 195 subjects with hepatitis C, 150 healthy subjects and 150 subjects with hepatitis B were tested for thyroid-related markers. The data were analyzed by independent-sample t test and chi square test. Results The HCV infection rate in 462 thyroid autoantibodies positive subjects was 1.30% and 0.53% in 380 thyroid autoantibodies negative subjects. There was no significant difference of the HCV infection rate between two groups (X2=1.322, P>0.05). In the subjects with hepatitis C, 30.8% were TPOAb positive, 30.8% were TgAb positive, which were significantly different from those of healthy subjects and subjects with hepatitis B (X2=21.496,X2=30.454;P<0.01). Conclusions HCV infection rate does not increase in subjects with abnormal thyroid autoimmunity. However, positive rate of thyroid autoantibodies increases in subjects with hepatitis C, which suggests that thyroid-related markers should be examined in hepatitis C patients.

Objective To investigate the effect of iodine excess on thyroid follicle epithelial ultrstructure and the relationship between thyroid iniury and autoimmune thyroiditis. Methods NOD.H-2h4 mice and Kunming mice were randomly divided into four groups receiving plain water,5 fold,10 fold,and 100 fold excessive iodine water.4,8 and 24 weeks after receiving iodine water,the mice were killed.After fixation with osmic acid and dual staining with uranyl chloride and citrate lead,thyroid gland ultrstructure was examined with electron microscopy.Resuits Iodine treated NOD.H-2h4 mice exhibited marked accumulation of peroxisome and secondary lysosomes,apoptosis and necrosis of thyroid epithelial cell.damage of thyroid follicles and lymphocvtic infiltration.The observed changes induced by iodine were in a dose dependent way.Conclusion The oxidative iniury on the thyroid epithelial cells induced by iodine excess might be the prerequisite for the creation of autoimmune thyroiditis.

Objective To investigate the effect of VPA and molecular hydrogen(H2)on phenotypes of microglia treated with hypoxia. Methods Mouse hypoxic BV2 microglia were treated with VPA or H2. The levels of phenotypic markers of supernatant and cells were detected by ELISA, flow cytometry and real?time PCR,respectively. Results Hypoxia significantly increased mRNA level of M1 marker(iNOS)and reduced mRNA levels of M2 markers(CD206 and TGF?β)in BV2(P<0.05). Besides,the ratio between the mRNA levels of M1 increased(P<0.05). VPA significantly reduced protein level(CD16/32)and mRNA production(iNOS)of M1 markers in hypoxia?treated BV2(P<0.05). The ratio be?tween the mRNA levels of M1 markers and M2 markers(CD16:CD206,CD32:CD206,iNOS:CD206 and iNOS:TGF?β)were also significantly decreased(P<0.05). H2 significantly reduced both protein levels(TNF?α,CD16/32 and iNOS)and mRNA production(iNOS)of M1 markers and increased secretion of M2 marker(IL?10)in hypoxia?treated BV2(P<0.05). The ratio between the mRNA levels of M1 markers and M2 markers(CD16:CD206,iNOS:CD206 and iNOS:TGF?β)were also highly declined(P<0.05). Conclusion Hypoxia can induce microglial cells toward pro?inflammatory phenotype. Both VPA and H2 can inhibit hypoxia?induced inflammatory effect on microglia.

Objective To explore the chronic effects of mild and moderate iodine excess and iodine restriction on apoptosis of thyrocytes. Methods Wistar rats were exposed to 4 different doses of iodine: 4 μg/d (control), 6 μg/d (1.5 fold iodine excess), 12 μg/d (3 fold iodine excess), and 24 μg/d (6 fold iodine excess) for 1, 2, 4 and 8 months. Some rats treated for 8 months were fed with 4 μg/d iodine for another 3 months. Urinary iodine concentration was monitored by arscnic/cerium catalyzing spectrophotography. Apoptosis was determined by flow cytometry after Annexin V-FTTC staining and uhrastructure assessment under electronic microscope. Cell cycle kinetics was analyzed by flow eytometry after propidium iodine staining. Fluorescent measurement by DCFH-DA probe was used to determine the intracellular reactive oxygen species (ROS) level. Expressions of apoptic proteins were analyzed by flow cytometry and immunohistochemistry. Results Apoptotosis rate and ROS production in thyrocytes were significantly increased in 3 and 6 fold iodine excess groups after 4 months and 8 months (all P < 0.05), which was reversed with iodine restriction. 6 fold iodine exposure was proved to cause a reduction of cells in GOG1-phase (64% and 67% vs 80%, both P < 0. 05) and a concomitant accumulation in S-phase (5% and 6% vs 3%, both P <0.05) after 4 months and 8 months. Expressions of Fas, FasL and TRAIL proteins in 3 and 6 fold iodine excess groups after 8 months were increased by 2 to 4 times compared with control group and did not return to normal after iodine restriction. Bcl-2 and Bax remained constant. Positive correlations were observed among iodine amount, apoptosis rate and ROS level in 6 fold iodine excess group after 8 months (r = 0. 637-0.790, P < 0.01). Conclusion Chronic iodine excess results in thyrocyte apoptosis due probably to generation of ROS.