Diabetic nephropathy is one of the most serious microvascular complications, which is related to many growth factors. Growth factors are a kind of cytokines that can stimulate cells to grow, which includes transforming growth factor-? (TGF-?), hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), connective tissue growth factor (CTGF), and so on. Different growth factors can cause glomerular hypertrophy or proliferation, perinephric angiogenesis, tubulointerstitial fibrosis and the like respectively. To know the relationship between the growth factors and diabetic nephropathy could provide a prospective mean to reduce the diabetic mortality rate. This paper reviews the recent researches about the growth factors and diabetic nephropathy to provide a scientific basis for clinical treatment.

Objective To study the effect of different iodine intake on the antioxidation of rat thyroid. Methods The rats were divided into 6 groups, low iodide (LI), normal iodine (NI), high iodide including five fold (5HI), ten fold (10HI), fifty fold (50HI), one hundred fold (100HI) and given potassium iodide (KI) at different dosages through food respectively. After 6 and 12 months of treatment, the rats were sacrificed respectively and the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD), the content of malondialdehyde (MDA) in the thyroid were determined. Results The activity of GPx , SOD and the MDA content in LI group were significantly higher than those in NI group. There was no difference in the SOD and GPx activity and MDA content among NI, 5HI and 10HI groups. The MDA content in 50HI group was lower than that in NI group after treated for 12 months, but no difference was found between them after treated for 6 months. Compared with NI group, the GPx activity, SOD activity and MDA content in 100HI group increased after 6 months of treatment, however, decreased after 12 months of treatment. Conclusion Low iodine intake can induce oxidative damage of the thyroid gland in normal rats, high iodine (100 fold) intake for a long period (12 months) may decrease the activity of anti-oxidases in thyroid without obvious oxidative damage, that shows the anti-oxidative system of rat thyroid has a tolerance to high iodine intake.

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.

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

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 investigate the activation of β-sheet breaker peptide H102 on ERK signal transduction pathway in brain of PAP double transgenic mice. Methods PAP double transgenic mice were randomly divided into model group and H102 treatment group (n=10 for each group). A group of C57BL/6J mice with the same genetic background was served as controls. H102 (5.8 mg/kg) 5 μL was infused by intranasal administration to mice in H102 treatment group, and equal volume of blank solution of H102 (chitosan, BSA) was given to mice in control group and model group. The ability of spatial reference memory was tested by Morris water maze after 30 days of treatment. Then immunohistochemistry tests and Western blot technique were used to detect the content of RAS, P-MEK and P-ERK proteins in mouse brain. Results (1) The ability of learning and memory was significantly lower in model group than that of control group. The ability of learning and memory was significantly improved in treatment group than that in model group (P<0.05). (2) The contents of RAS, P-MEK and P-ERK in mouse brain were significantly lower in model group than those of control group, and these protein ex-pressions were significantly increased in treatment group than those in model group (P<0.01). Conclusion β-sheet break-er peptide H102 can activate ERK signal transduction pathway in brain of PAP double transgenic mice, increase PAS, P-MEK and P-ERK levels in nerve cells, and improve the ability of learning and memory in PAP mice.

Objective To set up the reference range for thyroid hormones and thyrotropin (TSH) of 8-10 years old school children in certain regions of China to provide reference criteria for diagnosis,treatment,and monitoring of thyroid diseases and related research.Methods A cross-sectional survey was conducted in primary school children aged 8-10 years from six iodine sufficient areas.664 normal school children were selected for establishing reference ranges of thyroid hormones and TSH after crucial screening through questionnaire and laboratory investigation.The serum hormone levels were determined by using chemiluminescent immunoassay (Bayer's reagents),and the reference range of each hormone was displayed as its 95％ central interval.Results The reference ranges of TSH,FT4,FT3,TT4,and TT3 were 1.03-8.42 mIU/L,13.44-20.59 pmol/L,4.75-6.96pmol/L,75.29-152.66 nmol/L,and 1.76-3.35 nmol/L,respectively.There was no significant difference in hormone levels between boys and girls.The eight years old group had slightly higher TT4 level compared with the other age groups.The rural children had higher TSH and TT3 levels and lower FT4 level than the urban children.Conclusion The thyroid hormone and TSH levels are substantially different between school children and adults.Therefore,it is necessary to establish the reference range of thyroid function indices for normal school children in order to diagnose,treat,and monitor thyroid diseases.