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Objective To investigate the current situation of iodine deficiency disorders and the effect of control measures in Sanmenxia city of Henan province, and to formulate targeted control measures for iodine deficiency disorders. Methods In 2008, five villages(offices) were selected according to the east, west, south,north and center position in each county in 6 counties(cities, districts) of Lingbao, Shan, Hubin, Yima, Mianchi,and Lushi in Sanmenxia city. One primary school was selected in each village(office), fifty students aged 8 - 10 in each primary school were randomly selected to check thyroid and their urine and edible salt were collected to detect iodine. Thirty 5th-grade students in each school were selected to carry out the questionnaire survey of health education about iodine deficiency disorders. According to the east, west, south, north and center position, five potable water samples were selected to detect iodine in the village where the primary school was in. Questionnaire survey was also carried out among ten housewives in the village. Thyroid was examined by palpation;ammonium persulfate digestion-arsenic cerium catalytic spectrophotometry(WS/T 107-2006) was used to detect urinary iodine;direct titration(GB/T 13025-1999 ) was used to detect salt iodine;arsenic cerium catalytic spectrophotometry (GB/T 5750.5-2006) was used to detect water iodine. Results One thousand and five hundreds children aged 8 - 10 were analyzed in 6 counties(cities, districts), the rate of goiter was 3.30%(50/1500), the median of urinary iodine was 273.15 μg/L. One thousand and five hundreds salt samples were detected, the coverage rate of iodized salt was 99.93% (1499/1500), the qualified rate of iodized salt was 98.00% (1469/1499), the edible rate of qualified iodized salt was 97.93% (1469/1500), the coverage rate of non-iodized salt was 0.07% (1/1500), the median of salt iodine was 28.9 mg/kg. One hundred and fifty water samples were collected, the median of water iodine was 2.76 μg/L. The pass rate of the questionnaire survey of health education about iodine deficiency disorders was 97.11% (874/900) in students and 98.67% (296/300) in housewives, respectively. Conclusions The prevention and control of iodine deficiency disorders has achieved significant results and the monitoring indicators have reached the national standard for eliminating iodine deficiency disorders in Sanmenxia city.

6.Effect of hypoxia combined with exercise training on mitochondrial con-tent in skeletal muscle of rats

Hai BO ; Peng PENG ; Yongsheng QIN ; Yong ZHANG

Chinese Journal of Pathophysiology 2014;(8):1461-1466

[ABSTRACT]AIM:Toinvestigatetheeffectofhypoxiacombinedwithexercisetrainingonmitochondrialcon-tent, and the role of mitochondrial biogenesis and mitophagy in this process .METHODS:Male Sprague-Dawley rats were randomly divided into 4 groups:normoxia control (NC) group, normoxia+training (NT) group, hypoxia+control (HC) group, and hypoxia+training (HT) group.The hypoxic animals were housed in normobaric hypoxic tent (11.3 % oxy-gen) for consecutive 4 weeks.The exercise training animals were exercised on a motor-driven rodent treadmill (5°) at a speed of 15 m/min, 60 min/d, 5 d/week for 4 weeks.Mitochondrial membrane potential was determined using JC-1 fluo-rescent probe .ATP synthesis capacity was determined using a bioluminescence technique .The protein expression of cyto-chrome C oxidase IV (COXIV), voltage-dependent anion channel-1 (VDAC-1), peroxisome proliferator-activated receptor gamma cofactor 1 alpha (PGC-1α), mitochondrial transcription factor A (Tfam),Bcl-2/adenovirus E1B 19 kD-interacting protein 3 (Bnip3) and beclin-1 in the muscles was detected by Western blotting .RESULTS:Compared with NC group, hypoxia attenuated mitochondrial membrane potential , ATP synthesis capacity , and the expression of COXIV , VDAC-1, PGC-1αand Tfam.Furthermore, hypoxia increased the expression of Bnip 3 and beclin-1.Compared with HC group , the exercise training elevated mitochondrial membrane potential , ATP synthesis capacity , and the expression of COXIV , VDAC-1, PGC-1α, Tfam, Bnip3 and beclin-1.CONCLUSION:A combination of reduced mitochondrial biogenesis and increased mitophagy seems to be responsible for the decrease in mitochondrial content after hypoxia .Exercise training with hypoxia elevates mitochondrial content and function in hypoxia , which may be mediated by appropriate increase and co-reg-ulation of mitochondrial biogenesis and mitophagy .