Epidemiological investigation on endemic fluorosis along the Yellow River alluvial plain of Shandong province / 中华流行病学杂志

Objective To investigate the current prevalent status of endemic fluorosis in the floodplain area of the lower Yellow River in Shandong province. Methods According to "The National Technical Scheme for Endemic Disease Control in 2008", 16 counties were chosen to carry out the epidemiological survey of endemic fluorosis. Three villages were chosen in each county, to determine the fluoride content of drinking water and to check the dental fluorosis of children aged 8 to 12 year old, the skeletal fluorosis of adults over 16 years of age. Both children and adults were tested for urine fluoride. The content of fluoride in drinking water and urine was determined by F-ion selective electrode while dental fiuorosis of children aged 8 to 12 years old was diagnosed by Dean's method and adults skeletal fluorosis by the National Standard for "Diagnosis of endemic skeletal quality' villages in 16 counties, among which 19 villages had water fluoride content ≤ 1.00 mg/L and accounted for 73.08% ( 19/26), 7 villages had water fluoride content ＞ 1.00 mg/L and accounted for quality' villages in 16 counties, 5 villages had water fluoride content ≤ 1.00 mg/L (accounted for 22.73% ), 17 villages had water fluoride content ＞1.00 mg/L(accounted for 77.27% ), with the highest water fluoride content as 3.38 mg/L. The overall rate of dental fluorosis among children aged 8to 12 years old was 52.18% (1042/1997), with the index of dental fluorosis as 1.17 and the rate of dental damage as 8.01% (160/1997). The urinary fluoride values above 1.40 mg/L were found in 65.00% (845/1300) of children aged 8 to 12 years old, with the highest urinary fluoride concentrations as 18.53 mg/L. The rate of skeletal fiuorosis by clinic and X-rays in adults older than 16 years old were 4.35% ( 1121/25 781 ) and 11.36%(5/44), respectively. The urinary fluoride values above 1.60 mg/L were found as 63.92%(606/948) in adults older than 16 years old, with the highest urinary fluoride concentrations as 21.35 mg/L. Conclusion The status of endemic fluorosis had not been effectively controlled and the situation for endemic fluorosis control was still critical in the floodplain area of the lower Yellow River in Shandong province, suggesting that the preventive approaches on endemic fluorosis control should be strengthened.

Melatonin suppressing the proliferation of E2-induced pituitary prolactin-secreting tumor in rat involves the effects of estrogen receptor / 中国应用生理学杂志

<p><b>AIM</b>To investigate effects of melatonin on estrogen receptor at the primary stage of melatonin (MLT) inhibiting the proliferation of 17-beta-estradiol (E2)-induced pituitary prolactin-secreting tumor (prolactinoma) and its mechanisms in the rat.</p><p><b>METHODS</b>MLT inhibiting the proliferation of 17-beta-E2-induced prolactinoma was created by administrating different concentration of melatonin subcutaneously at 18:00 in every group of SD rat in vivo. We also examined the expression of MLT receptor in prolactinoma cells and the effects of MLT on the expression of estrogen receptor (ER) by in situ hybridization and the effects of MLT on the binding of ER to estrogen response element (ERE) by electrophoretic mobility shift assay (EMSA)in primary culture cells iv vitro.</p><p><b>RESULTS</b>The results showed that the weights of prolactinomas in MLT groups, in which 0.25 mg or 0.50 mg/day/rat melatonin was administrated subcutaneously at 18:00, were decreased significantly (P < 0.01 and P < 0.05). The expression of MLT1a and MLT1b were shown in pituitary prolactinoma cells. Compared with the prolactinoma, the expression of ER and the bind of ER to ERE in prolactinoma treated with 0.25 mg/day/rat or 0.50 mg/day/rat MLT was decreased (P < 0.01 and P < 0.01).</p><p><b>CONCLUSION</b>These data indicate that some dosage of MLT inhibit the development of E2-induced prolactinoma in SD rat. One of the mechanisms is involved in suppressing the expression of estrogen receptor and partly inhibiting the bind of ER to ERE.</p>

Melatonin inhibits the proliferation of pituitary prolactin-secreting tumor by suppressing the enhancer elements mutation of PRL gene in the rat / 生理学报

In order to investigate the molecular mechanisms of the inhibition of the proliferation of 17-beta-estradiol (E(2))-induced pituitary prolactin-secreting tumor (prolactinoma) by melatonin (MLT) in the rat, we examined the inhibitory effects of MLT on the proliferation of E(2)-induced prolactinoma of the rat and the suppressing effects of MLT on the enhancer elements mutation of PRL gene in vivo and in vitro. The results showed that the weights of prolactinomas in MLT groups, in which 0.25 mg or 0.50 mg per day per rat of MLT was administered subcutaneously at 18:00, were decreased significantly. Out of the dosage of MLT, such as 0.05, 1.00 mg and 2.00 mg per day per rat, the antitumor action of MLT is less or disappointing. Polymerase chain reaction (PCR) and DNA sequencing showed five mutations in the enhancer elements of PRL gene in prolactinoma, such as -1885 point mutation (C --> G), -1857 - -1855 substitution (ACA --> G), -1792 - -1791 insertion G, -1383 - -1382 insertion (GGTGTGTG), -1265 - -1250 deletion (GTGTGTGTGTGTGTGT). Excluding of -1885 point mutation (C --> G), the mutation in the prolactinoma treated with 0.25 mg per day per rat MLT was decreased, such as -1792 - -1791 without insertion of G, -1856 - -1855 deletion AC, -1385 - -1384 deletion TG, -1250 - -1253 deletion GTGT. Firefly luciferase reporter gene systems showed that the luminosity of enhancer elements-luciferase reporter fusion gene in normal pituitary, prolactinoma treated without or with 0.25 mg per day per rat MLT were (13448.17+/-3012.74), (161831.67+/-60996.01), and (10212.17+/-634.71) OD units. Compared with the normal pituitary, the activity of PRL gene enhancer elements in prolactinoma was increased by 11 times (P<0.001). Compared with the prolactinoma, the activity of PRL gene enhancer elements in prolactinoma treated with MLT was decreased by 93.69% (P<0.001). Analysis of the space structure of PRL gene enhancer elements showed that the bending index in prolactinoma was higher than that in prolactinoma treated with MLT, which was higher than that in the normal pituitary. These results demonstrate that one of the important molecular mechanisms of MLT inhibiting the proliferation of prolactinoma is related to the reduction of enhancer elements mutation of PRL gene. These data also suggest that MLT-induced attenuation of enhancer elements mutation of PRL gene is involved in decreasing the bending index and attenuating the higher expression of PRL gene.

Baroreceptor reflex in heart failure / 生理学报

Congestive heart failure is a syndrome that is usually initiated by a reduction in pump function of the heart, i.e. a decrease in cardiac output. Initially, a reduction in cardiac output leads to unloading of baroreceptor reflex that, in turn, increases heart rate through vago-sympathetic mechanisms and total peripheral resistance via an increase in sympathetic outflow to vascular beds. In this review we are thinking on how baroreceptor reflex plays a role in the abnormal control of the circulation in heart failure. This review and our recent studies suggest that: (1) baroreceptor reflex is blunted in heart failure; (2) central angiotensin II and reactive oxygen species play an important role in blunted baroreceptor reflex; (3) cardiac sympathetic afferent stimulation and chemoreceptor reflex inhibit baroreceptor reflex; and (4) exercise training normalizes abnormal reflexes in the heart failure state.