To explore the influences of pregnancy and iodine intake on thyroid function and immune functions, 210 pregnant women and 290 fertile women were chosen from iodine excess area, and the average ages of them were (27. 69±4. 73 )and (30. 62±6. 01 )years respectively. Fasting blood and urine were collected in the morning. The urinary iodine level was determined by arsenic-cerium catalytic contact. Serum free triiodothyronine ( FT3 ), free thyroxine ( FT4 ), and sensitive thyroid-stimulating hormone ( sTSH ) levels were measured by chemiluminescence.Thyroid peroxidase antibody (TPOAb)and thyroglobulin antibody (TGAb)were measured by radioimmunoassay. The median urinary iodine in the pregnant and fertile women were I 240. 70 and 949. 21 μg/L, respectively. There were 84. 3% pregnant women and 81.0% fertile women admitting excess iodine intake. The prevalence of overall thyroid diseases was 22. 9% in the pregnant women and 30. 3% in the fertile women. The prevalence of hyperthyroidism,subclinical hyperthyroidism, hypothyroidism, and subclinical hypothyroidism was0. 5%, 1.9%, 0. 5%, and 20. 0% in the former group, and 2. 8%, 0. 3%, 0. 3%, and 26. 9% in the latter. Both FT3 and FT4 levels of the pregnant women were lower than those of fertile women [(4. 03±0. 59 vs 4. 71 ± 1.04)pmol/L, ( 13. 35 ± 1.59 vs 14. 27 ±3.63 )pmol/L,both P＜0. 01], and the positive rate of TGAb of pregnant women was also lower than that of fertile women (7. 1% vs14. 1%, P=0. 014). The prevalence of thyroid diseases and positive rate of thyroid autoantibodies is high in women with excess iodine intake. Compared with fertile women, pregnancy may lead to decreas~s in level of thyroid hormones and positive rate of TGAb. Their iodine intake should be controlled, and the thyroid function and autoimmunity antibodies should be monitored.

The present study aimed to explore the neuroprotective effect and possible mechanisms of rhGLP-1 (7–36) against transient ischemia/reperfusion injuries induced by middle cerebral artery occlusion (MCAO) in type 2 diabetic rats. First, diabetic rats were established by a combination of a high-fat diet and low-dose streptozotocin (STZ) (30 mg/kg, intraperitoneally). Second, they were subjected to MCAO for 2 h, then treated with rhGLP-1 (7–36) (10, 20, 40 µg/kg i.p.) at the same time of reperfusion. In the following 3 days, they were injected with rhGLP-1 (7–36) at the same dose and route for three times each day. After 72 h, hypoglycemic effects were assessed by blood glucose changes, and neuroprotective effects were evaluated by neurological deficits, infarct volume and histomorphology. Mechanisms were investigated by detecting the distribution and expression of the nuclear factor erythroid-derived factor 2 related factor 2 (Nrf2) in ischemic brain tissue, the levels of phospho-PI3 kinase (PI3K)/PI3K ratio and heme-oxygenase-1 (HO-l), as well as the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA). Our results showed that rhGLP-1 (7–36) significantly reduced blood glucose and infarction volume, alleviated neurological deficits, enhanced the density of surviving neurons and vascular proliferation. The nuclear positive cells ratio and expression of Nrf2, the levels of P-PI3K/PI3K ratio and HO-l increased, the activities of SOD increased and the contents of MDA decreased. The current results indicated the protective effect of rhGLP-1 (7–36) in diabetic rats following MCAO/R that may be concerned with reducing blood glucose, up-regulating expression of Nrf2/HO-1 and increasing the activities of SOD.
Animals ; Blood Glucose ; Brain ; Diet, High-Fat ; Hypoglycemic Agents ; Infarction ; Infarction, Middle Cerebral Artery ; Malondialdehyde ; Neurons ; Neuroprotective Agents ; Phosphotransferases ; Rats* ; Reperfusion ; Reperfusion Injury* ; Streptozocin ; Superoxide Dismutase