Objective To investigate the effect of recent blood glucose control level of diabetes on prognosis in the patients with general surgery. Methods To analyze the clinical data of 126 diabetic patients with general surgery and the relatiouship among the average hospitalized length,medical cost and the complications of sugery due to glycosylated hemoglobin. Results Comparing with controls, diabetic patients HbA1c＞7.5% had more days longer than those HbA1c＜6.5 % at the time of average in-hospital duration, stitch removing, food-taking and using antibiotics after the operation,Diabetics HbA1c＜6.5 % with cholecystolithiasis, thyroid adenoma had lower surgery cost than those HbA1c＞7.5 %. Conclusion To intensify the control of blood glucose of the patients of limited or selective general surgery as to lower glycosylated hemoglobin＜6.5 % is very important for improving prognosis, and decreasing the complications and medical cost of the operation.

Objective To explore the effects of iodine on apoptosis and proliferation of the thyroid cells. Methods Wistar rats of one month wean were randomly divided into five groups(low iodine-LI, normal iodine-NI, fivefold high iodine-5 HI, tenfold high iodine-10 HI, fiftyfold high iodine-50 HI), and fed on water containing different concentration of iodine. All groups got prospective iodine intake, that is 0.6, 6.15, 30.75, 61.5, and 307.5 mg/d. After 7 days, 14 days, 28 days, the rats were sacrificed. The proliferation, apoptosis, and apoptosis related genes expression in the thyroid cells were determined by TUNEL, immunohistochemistry and RT-PCR. Results As for short-term of iodine deficiency, no significant change was seen in the mRNA expression of fas and fasL genes, while in the iodine excess groups,the expreesion showed an up-regulation trend as iodine intake increased. Fas and FasL proteins expressions were consistent in LI and NI groups and all of them were negative or weak positive. In the HI groups the stain density increased with iodine intake and treatmnet period increased. Expression of PCNA was enhanced by short-term iodine deficiency, but not by short-term iodine excess. Apoptosis was not observed in all groups. Conclusion Both short-term iodine deficiency and iodine excess have no obvious effects on thyrocytes apoptosis. Proliferation can be induced by short-term iodine deficiency, not by iodine excess. Wistar rats present a strong tolerance to long-term iodine excess.

Objective To study the effects of excessive iodine intake through the meal on the expression of mRNA of placental NIS in pregnant rat and breast NIS in lactating rats. Methods Wistar rats, weaning one month, were randomly divided into three groups according to the body weights, i.e., normal iodine (NI), ten fold high iodine(10HI), one hundred fold high iodine(100HI), the ratio of female and male was 2∶1. Iodine intake of the groups were about 6.15, 61.5 and 615.0 mg/d respectively. After 3 months of treatment, the urine iodine was determined by As-Ce-catalytic spectrophotometry. The rats mated and had offspring. Their placenta and breasts were taken on the seventeenth day of pregnancy and tenth day of lactation respectively. Then NIS mRNA expression was determined by RT-PCR. Results The urine iodine increased with the increase of the iodine intake. The urine iodine and iodine intake showed the parallel magnification. Compared with the NI group,AR value of the placental NIS mRNA in 100HI group and the breast NIS mRNA in 10HI and 100HI group significantly decreased. Conclusion Excessive iodine intake may down-regulate the expression of the placental and breast NIS, which presents a protective effect on offspring.

Objective To evaluate the effects of iodine on antioxidative capability by observing activity of antioxidative enzymes and related gene expression, and peroxide content in the brain of rat offspring. Methods One-month weaning Wistar rats were divided into four groups(low iodine-LI, normal iodine-NI, ten-fold high iodine-10HI and fifty-fold high iodine-50HI), and fed with water containing different iodine concentration by adding potassium iodate respectively. Rats mate randomly after three months.The offspring were sacrificed at 28 days after birth, then the activity of SOD and GSH-Px, and MDA content in brain tissue were tested, and the SOD and GSH-Px mRNA expression were measured by RT-PCR. Results Compared with the NI group, only in LI group MDA content were increased significantly (P

Objective To study the effect of different dosage KIO3 on anti-oxidative capability of the blood.Methods The Wistar rats were randomly divided into 6 groups and given KIO3 through food at different dosages,low iodide(LI),normal iodide(NI),5 fold high iodide(5HI),10 fold high iodide(10HI),50 fold high iodide(50HI)and 100 fold high iodide(100HI).3,6 and 12 months later,the rats were sacrificed and blood glutathione peroxidase(GPx)activity,superoxide dismutase(SOD)activity and malondialdehyde(MDA)content were determined.Results After 3,6 and 12 months of treatment,the GPx activity in LI group was significantly lower than that in NI group.Furthermore,after 12 months of low iodide intake,the SOD activity in LI group was higher than that in NI group.The GPx activity in 100HI group was lower than that in NI group after 3 months of administration,but no difference was seen between these two groups after 6 and 12 months of treatment.No difference was found in the GPx activity of NI group and those of 5HI,10HI and 50HI groups.The SOD activity in 50HI and 100HI groups was higher than that in NI group after 12 months of administration.There was no difference in MDA content among NI group and 4 high iodide groups.Conclusion Low iodide intake may damage the anti-oxidative capability of blood in normal rats.Blood has a strong anti-oxidative ability and compensative capabilities to compete with high iodate intake.

To explore the relationship between thyroid autoantibodies and thyroid function in school children aged 8-10 years,adults,pregnant women,and lactating women in China,in order to provide reference for the prevention and monitoring of thyroid disease.Healthy 8-10 years old school children (693 cases),adults (698 cases),pregnant women(325 cases),and lactating women(332 cases) from six iodine sufficient areas were enrolled.Serum TSH,FT4,and FT3 were determined by chemiluminescent immunoassay,while antithyroid antibody by radioimmunoassay.The positive rate of thyroid autoantibodies in females was significantly higher than that in the male (5.6％ vs 2.0％ in school children,and 22.8％ vs 3.2％ in adults) ; while positive rate of autoantibodies in pregnant and lactating women (8.9％,8.7％) were significantly lower than that in the other healthy adult women (22.8％).The incidence of abnormal thyroid function in antibody-positive people was higher than that in negative ones in all groups,and abnormal thyroid function showed mainly as subclinical hypothyroidism.In addition,lactating women with negative autoantibodies presented a higher incidence of abnormal thyroid function,mainly as low FT4.The abnormal thyroid function is related with the positive thyroid autoantibodies,indicating that it is essential to follow-up these people with positive antibodies in order to facilitate prevention,early diagnosis,and treatment of thyroid disease.Reference data for thyroid hormones in lactating women should be establisbed as soon as possible.

Objective:To compare the proliferation and osteogenic differentiation between human bone marrow mesenchymal stem cells from orofacial bone(OMMSCs)and those from long bone(BMMSCs).Methods:OMMSCs were isolated from orthognathic surgical sites and cultured by limited dilution.BMMSCs were obtained from bone marrow of volunteers and isolated by density gradient centrifugation method.The surface markers of the cells were detected by flowcytometry.Single-colony formation,CCK assay and cell circle analyses were conducted.Osteogenic differentiation ability was evaluated by ALP activity test and Alizarin red staining after osteogenic induction culture.Results:The cell surface markers STRO-1 and CD105 of both stem cells were positive,CD34,CD31 and CD45 were negative. OMMSCs generated significantly higher numbers of colonies than BMMSCs.In addition,OMMSCs had a higher proliferation rate and more cells in proliferative(S +G2 )stage than BMMSCs.After osteogenic induction for 3,5,7 and 10 d,OMMSCs showed higher levels of ALP activity.OMMSCs formed significantly more mineralized nodules than BMMSCs after 21-day ostogenic induction.Conclusion:The proliferation and osteogenic differentiation capacity of OMMSCs are higher than those of BMMSCs.

Objective To observe and compare the different orthotopic models of papillary thyroid cancer ( PTC) cell lines of RET/PTC1 rearrangement and BRAFV600E mutation in nude mice. Methods Human PTC cell lines TPC-1, BHP5-16 and BHP2-7 were used. The genotypes of RET/PTC1 rearrangement and BRAFV600E mutation were determined by realtime-PCR and DNA sequencing analysis. The cells(2×105) were injected into the thyroid gland of nude mice. The nude mice were executed at 4th, 12th week, and then their thyroid tumors were removed and weighed. The levels of thyroid hormone were detected using chemiluminescent immunoassay. Results Both TPC-1 and BHP2-7 cells were identified as RET/PTC1 rearrangement by real time-PCR, and the expression of RET/PTC1 rearrangement in BHP2-7 cell was higher than that of TPC-1 cell. BRAFV600E mutation was found in BHP5-16 cell by DNA sequencing analysis, but was not found in TPC-1 and BHP2-7 cells. There were different characteristics in three orthotopic nude model groups. Tumorigenic rates of TPC-1 and BHP5-16 groups were 100%, but the growth of tumor was more rapid in BHP5-16 group than that in TPC-1 group, with more weight tumor. The changes of thyroid hormone levels in BHP5-16 group and TPC-1 group were the same, which were normal at 4th week and sharply decreased at 12 th week(P<0. 05). However, the tumorigenic rate of BHP2-7 group was only 6. 25%. Compared with normal control group, there was no statistical difference in the levels of thyroid hormone in BHP2-7group(P>0. 05). Conclusions It showed difference in the orthotopic models of PTC cell lines of RET/PTC1 rearrangement and BRAFV600E mutation in nude mice. BRAFV600E mutation has obvious impacts on increasing tumorigenic rate and promotion of tumor growth in the orthotopic model. It should not be ignored that advanced thyroid tumor will lead to the destruction of thyroid function.

Objective To observe the effects of different iodine intake on the thyroid tumor growth and thyroid function in the orthotopic nude mice model of human papillary thyroid carcinoma (PTC) cell line TPC-1.Methods Human PTC cell line TPC-1 (2 × 105) was injected into the left thyroid gland of nude mice.After the operation,the nude mice were randomly divided into three groups:low iodine group (LI),normal iodine group (NI),and high iodine group(HI,50 folds of normal iodine) based on the iodine levels contained in their diet.4 and 12 weeks later,the nude mice were executed,then their thyroid tumors were removed and weighted.The levels of urinary iodine were measured with As3+-Ce4+ catalytic spectrophotometry using ammonium persulfate digestion method.The thyroid hormone level was detected using chemiluminescent immunoassay.The morphology and structure of thyroid tumor tissue was observed by microscope.Results The iodine intervention feeding was successful according to urinary iodine level of LI,NI,and HI groups,paralleled to their iodine intakes.However,the difference of the weight of thyroid tumor in three groups had no statistical significance(P＞0.05).At 4 weeks,compared with control group,the levels of thyroid hormones were normal in NI group,while lower T4 and normal T3 were found in LI group.However,T4 was higher and T3 was lower in HI group (P＜0.05).At 12 weeks,the levels of thyroid hormones all were decreased due to the enlargement of thyroid gland tumor in NI,LI and HI groups.T4 and T3 in LI group were the lowest among three groups,even T4 was below detection limit.T4 was normal and T3 was lower in HI group as compared to control group.Conclusion Iodine intake may not significantly affect tumor growth in the orthotopic nude mice model of human PTC cell line TPC-1,but it has a significant effect on the synthesis of thyroid hormones.

ObjectiveTo investigate the effects of maternal thyroid dysfunction during pregnancy caused by iodine deficiency of different degrees on doublecortin ( DCX ) and synaptophysin ( p38 ) expressions in fetal brain.Methods Wistar female rats were randomly divided into four groups:adequate iodine ( AI),mild iodine deficiency ( MiID ),moderate iodine deficiency ( MoID ),and severe iodine deficiency ( SID ),according to the total daily iodine supply( fed on an iodine deficient diet with different dosages of KI added in drinking water).Three months later the rats were mated.Serum TSH and thyroid hormones were determined in maternal rats on gestational day 20 using chemiluminescent immunoassay.The iodine contents in urine and histological changes of thyroid gland were observed in pregnant rats.The mRNA and protein levels of DCX and synaptophysin ( p38 ) were analyzed in fetal brain by using real time quantitative RT-PCR and western blotting respectively.Results( 1 ) Iodine contents in urine of pregnant rats were reduced with the decrease of their iodine supply.Compared with group AI,serum TSH was significantly increased [ ( 2.95 ± 1.70 vs 1.31 ± 0.55 ) mU/L,P ＜ 0.05 ],and both TT4 and FT4 were significantly decreased [ ( 14.3±4.1 vs 28.4±19.3 ) nmol/L,P＜0.05 ] and [ ( 10.8±3.6 vs 20.2±8.0) pmol/L,P＜0.01 ] in pregnant rats of SID group.Whereas,a slight rise in TSH,and a mild decline in both TT4and FT4 were found in MoID and MiID groups.However,there were no significant changes in TT3 and FT3 levels among these four groups.( 2 )Histological characteristics of thyroid gland in pregnant rats showed a typical goiter with small follicular hyperplasia and lack of colloid in SID group,moderate follicular hyperplasia with decreased colloid in MoID group; but mild cellular hyperplasia without decrease in follicular size and colloid in MiID group.( 3 ) The mRNA levels of DCX were increased in fetal brains of three iodine deficiency groups compared with AI group,but a statistical significance was found in MoID group.The protein levels of DCX in all experiment groups were significantly increased.Both mRNA and protein expressions of synaptophysin ( p38 )were significantly down-regulated in three iodine deficiency groups.Conclusions Maternal thyroid dysfunction caused by iodine deficiency,even by mild or moderate iodine deficiency,may lead to retardation of fetal neuronal and synaptic growth.