In a survey on the Yellow Sea and the East China Sea on August 20-30 of 1999,we found a hypoxic zone(<2 mg/L)of 13700 km2 with an average thickness of 20m at the bottom of the Changjiang(Yangtze River)Estuary,with ...In a survey on the Yellow Sea and the East China Sea on August 20-30 of 1999,we found a hypoxic zone(<2 mg/L)of 13700 km2 with an average thickness of 20m at the bottom of the Changjiang(Yangtze River)Estuary,with an oxygen minimum value of 1 mg/L.The extension of the dissolved oxygen deficiency extended to the 100m isobath in a southeastward direction along the bottom of the continental shelf of the East China Sea.During the last two decades,the minimum dissolved oxygen values in the low oxygen region of the Changjiang Estuary have decreased from 2.85 mg/L to 1 mg/L.In the hypoxic zone,the apparent oxygen utilization(AOU)was 5.8 mg/L and the total oxygen depletion approximately 1.59×10^(6) t.The strong halocline above the hypoxic zone,as a result of affluent water from the Changjiang,Taiwan Warm Current(TWC),and the high concentrations of particle organic carbon(POC)and nitrogen(PON)are the major factors causing the formation of the hypoxic zone.The POC:PON ratios and nutrient concentration distributions in the hypoxic zone suggest that the oxygen deficiency in the bottom water during the summer in the East China Sea off the Changjiang is the result of organic carbon production enhanced by nutrients from the Changjiang and fluvial organic matter input,followed by a shift in regeneration of nutrients in the East China Sea.展开更多
Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury.Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to i...Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury.Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to investigate whether intermittent hypoxia could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. Adult male Sprague-Dawley rats were exposed to hypoxia simulated 5000 m in a hypobaric chamber for 6 h/day, lasting 42 days. Normoxia group rats were kept under normoxic conditions. Isolated perfused hearts from both groups were subjected to 30 min of global ischemia followed by 60 min reperfusion.Incidence of apoptosis in cardiac myocytes was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and DNA agarose gel electrophoresis. Expressions of apoptosis related proteins,Bax and Bcl-2, in cytosolic and membrane fraction were detected by Western Blotting. After ischemia/reperfusion,enhanced recovery of cardiac function was observed in intermittent hypoxia hearts compared with normoxia group.Ischemia/reperfusion-induced apoptosis, as evidenced by TUNEL-positive nuclei and DNA fragmentation, was significantly reduced in intermittent hypoxia group compared with normoxia group. After ischemia/reperfusion,expression of Bax in both cytosolic and membrane fractions was decreased in intermittent hypoxia hearts compared with normoxia group. Although ischemia/reperfusion did not induce changes in the level of Bcl-2 expression in cytosolic fraction between intermittent hypoxia and normoxia groups, the expression of Bcl-2 in membrane fraction was upregulated in intermittent hypoxia group compared with normoxia group. These results indicated that the cardioprotection of intermittent hypoxia against ischemia/reperfusion injury appears to be in part due to reduce myocardial apoptosis. Intermittent hypoxia attenuated ischemia/reperfusion-induced apoptosis via increasing the ratio of Bcl-2/Bax, especially in membrane fraction.展开更多
基金This study was made under the auspices of the National Key Basic Research Program of the Ministry of Science and Technology,P.R.China(Grant No.G1999043705)and the Shanghai Priority Academic Discipline.
文摘In a survey on the Yellow Sea and the East China Sea on August 20-30 of 1999,we found a hypoxic zone(<2 mg/L)of 13700 km2 with an average thickness of 20m at the bottom of the Changjiang(Yangtze River)Estuary,with an oxygen minimum value of 1 mg/L.The extension of the dissolved oxygen deficiency extended to the 100m isobath in a southeastward direction along the bottom of the continental shelf of the East China Sea.During the last two decades,the minimum dissolved oxygen values in the low oxygen region of the Changjiang Estuary have decreased from 2.85 mg/L to 1 mg/L.In the hypoxic zone,the apparent oxygen utilization(AOU)was 5.8 mg/L and the total oxygen depletion approximately 1.59×10^(6) t.The strong halocline above the hypoxic zone,as a result of affluent water from the Changjiang,Taiwan Warm Current(TWC),and the high concentrations of particle organic carbon(POC)and nitrogen(PON)are the major factors causing the formation of the hypoxic zone.The POC:PON ratios and nutrient concentration distributions in the hypoxic zone suggest that the oxygen deficiency in the bottom water during the summer in the East China Sea off the Changjiang is the result of organic carbon production enhanced by nutrients from the Changjiang and fluvial organic matter input,followed by a shift in regeneration of nutrients in the East China Sea.
基金The study was supported by grants from National Natural Science Foundation of Chinathe Science and Technology committee of Shanghai Municipality(02JC14038).
文摘Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury.Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to investigate whether intermittent hypoxia could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. Adult male Sprague-Dawley rats were exposed to hypoxia simulated 5000 m in a hypobaric chamber for 6 h/day, lasting 42 days. Normoxia group rats were kept under normoxic conditions. Isolated perfused hearts from both groups were subjected to 30 min of global ischemia followed by 60 min reperfusion.Incidence of apoptosis in cardiac myocytes was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and DNA agarose gel electrophoresis. Expressions of apoptosis related proteins,Bax and Bcl-2, in cytosolic and membrane fraction were detected by Western Blotting. After ischemia/reperfusion,enhanced recovery of cardiac function was observed in intermittent hypoxia hearts compared with normoxia group.Ischemia/reperfusion-induced apoptosis, as evidenced by TUNEL-positive nuclei and DNA fragmentation, was significantly reduced in intermittent hypoxia group compared with normoxia group. After ischemia/reperfusion,expression of Bax in both cytosolic and membrane fractions was decreased in intermittent hypoxia hearts compared with normoxia group. Although ischemia/reperfusion did not induce changes in the level of Bcl-2 expression in cytosolic fraction between intermittent hypoxia and normoxia groups, the expression of Bcl-2 in membrane fraction was upregulated in intermittent hypoxia group compared with normoxia group. These results indicated that the cardioprotection of intermittent hypoxia against ischemia/reperfusion injury appears to be in part due to reduce myocardial apoptosis. Intermittent hypoxia attenuated ischemia/reperfusion-induced apoptosis via increasing the ratio of Bcl-2/Bax, especially in membrane fraction.
