Objective To observe the implementation of national food safety standard for “Iodine Concentration in Edible Salt”(GB 26878-2011) and its effectiveness on iodine nutritional status of key populations. Methods Information of iodine concentration in edible iodized salt of various provinces (autonomous regions and municipalities, including Xinjiang Production and Construction Corps) was collected using Baidu Searching Engine through the establishment of key words. Sal t samples were collected in Tianjin City and Aksu Region of Xinjiang , and the salt iodine concentration in both places was 30 mg/kg. In Tianjin, Hongqiao, Tanggu and Hangu, Beichen were selected as representatives of the downtown areas, the coastal areas and the suburbs, respectively and counties of Baodi and Ji were iodine deficiency areas in history. Sampling work was carried out from August 2012 to March 2013 in Tianjin. In Aksu, Yatuoer Township and Charqi Town in Baicheng County, Aotebeixi and Aketuohai Townships in Wushen County were chosen as iodine deficiency areas, and the survey was carried out from January to September 2013 . Random urine samples of school-age children ( 8 - 10 years old ) , pregnant women and lactating women were collected; urinary iodine was measured following the Method for Determination of Iodine in Urine by As3+-Ce4+ Catalytic Spectrophotometry(WS/T 107-2006) and iodine in edible iodized salt was measured following the General Test Method in Salt Industry Determination of Iodideion ( GB/T 13025 . 7-1999 ) . Results Fourteen of the provinces(autonomous regions and municipalities, including the Corps of Xinjiang) chose 25 mg/kg as their iodine concentration in edible iodized salt and 13 provinces chose 30 mg/kg. Besides, there were another 5 provinces providing 30 mg/kg particularly for pregnant women and lactating women while 25 mg/kg for other populations. In Tianjin, the medians of iodine concentration in edible iodized salt were ranged from 24.4 - 32.1 mg/kg in retail stores and 26.4 mg/kg at households. The household coverage rate of iodized salt and the proportion of households using adequately iodized salt were 78.5%(168/214) and 62.6%(134/214), respectively. The median ranges of urinary iodine were 178.2 - 183.9 μg/L in school children, 124.3 - 130.9 μg/L in pregnant women and 72.7 - 109.5 μg/L in lactating women. In Aksu, the medians of iodine concentration in edible iodized salt were 27.1 and 26.5 mg/kg in retail stores and households, respectively. The household coverage rate of iodized salt and the proportion of households using adequately iodized salt were 100.0% (363/363) and 98.9%(359/363), respectively. The median ranges of urinary iodine were 174.8 - 293.0, 154.9 - 230.0 and 135.8 - 239.3 μg/L among school children, pregnant women and lactating women, respectively. The median of iodine concentration in a special edible iodized salt sample reached 49.1 mg/kg, and qualified rate was 0(0/11) in Aksu. Conclusions All provinces , municipalities and autonomous regions ( including the Corps of Xingjiang ) in China have adjusted the iodine content in edible iodized salt in accordance with GB 26878-2011. However, in Tianjin the household iodine concentration in edible salt is lower than the local standards; the household coverage rate of iodized salt and the proportion of households using adequately iodized salt are lower than the national standards; pregnant women and lactating women are at risk of mild iodine deficiency.

OBJECTIVE To study the effects of yunaconitine on myocardial injury in rats and its mechanism related to mitochondrial apoptosis pathway rats. METHODS Forty SD rats were divided into normal group （normal saline）， yunaconitine high-dose and low-dose groups（0.14， 0.09 mg/kg）and aconitine group （positive control， 0.88 mg/kg） by random number method， with 10 rats in each group. They were given relevant medicine intragastrically， once a day， for consecutive 7 days. The levels of lactate dehydrogenase （LDH）， creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， superoxide dismutase （SOD） and malondialdehyde （MDA） in serum as well as the level of reactive oxygen species （ROS） in myocardial tissue were detected. The pathomorphological changes of myocardium and ultrastructural changes of myocardial mitochondria were all observed. The apoptosis of cardiomyocytes was determined. The protein relative expressions of B-cell lymphoma-2 （Bcl-2）， Bcl-2 associated X protein （Bax）， caspase-9， cleaved-caspase-9， caspase-3 and cleaved-caspase-3 were determined in myocardium of rats. RESULTS Compared with normal group， the serum levels of LDH， CK， CK-MB and MDA， the apoptotic numbers of cardiomyocytes， the level of ROS and protein expression of caspase-3 in myocardium were increased significantly in yunaconitine high-dose and low- dose groups （P＜0.05 or P＜0.01）； serum level of SOD and Bcl-2/Bax ratio in myocardium were all decreased significantly （P＜ 0.01）； the protein relative expressions of caspase-9， cleaved-caspase-9， caspase-3 and cleaved-caspase-3 in myocardium were significantly increased in yunaconitine high-dose group （P＜0.05）； some pathomorphological changes were found in 2 groups， such as myocardial fiber disorder， mitochondrial swelling. CONCLUSIONS Yunacotine could cause myocardial injury in rats. Its mechanism might be related to destroying the integrity of cardiomyocyte membrane， causing oxidative stress of cardiomyocyte， and inducing the apoptosis of myocardial cells through mitochondrial pathway.

OBJECTIVE：To study the toxicity mechanism of yunacotine-induced arrhythmia in rats. METHODS ：Totally 32 rats were randomly divided by random number table method into normal control group ，yunacotine low-dose and high-dose groups （0.09，0.14 mg/kg），aconitine group （positive control ，0.88 mg/kg），with 8 rats in each group. Administration groups were given the corresponding drugs once a day ，and normal control group was given the constant volume of normal saline ，for consecutive 7 d. After last intragastric administration ，the changes of electrocardiogram （ECG） were observed. The contents of adenosine triphosphate（ATP）in myocardial tissue and Ca 2+ in myocardial cells ，the activities of Na +-K+-ATPase and Ca 2+-Mg2+-ATPase as well as the protein expression of ranolidine receptor 2（RyR2）and Ca 2+-ATPase（SERCA2）in myocardial tissue were determined. RESULTS：Compared with normal control group ，time limit of QRS wave and QTc intervals of rats were prolonged significantly in yunaconitine low-dose group （P＜0.01）. The content of Ca 2 + in myocardial cells ， the ATP contents ， the activities of Ca2+-Mg2+-ATPase and Na +-K+-ATPase as well as the protein expression of SERCA 2 in myocardial tissue were reduced significantly （P＜0.05 or P＜0.01）. The heart rate of rats in yunaconitine high-dose group and aconitine group were increased significantly （P＜ 0.05 or P＜0.01），and time limit of QRS wave and QTc intervals were significantly prolonged （P＜0.01）；the content of Ca 2+ in myocardial cells was increased significantly （P＜0.01）；ATP content ，the activities of Ca 2+-Mg2+-ATPase and Na +-K+-ATPase，and protein expression of RyR 2 and SERCA 2 in myocardial tissue were decreased significantly （P＜0.01）. CONCLUSIONS ： Yunaconitine can induce arrhythmia in rats ，the mechanism of which may be associated with Ca 2+ overload that resulted from reducing the activities of Na +-K+-ATPase and Ca 2+-Mg2+-ATPase and down-regulating the expression of related calcium transporter RyR2 and SERCA 2.