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冷损伤    
相关语句
  cold injury
    Results When the vessels were exposed to cold for 1,2,4 min respectively,LDH activity in the cultured medium increased and SOD activity in the vessels decreased at different level,indicating varying degree of vessel injury:slight ,moderate and severe cold injury.
    结果 当血管暴露于- 20 ℃环境1 、2 、4 分钟后,血管培养液中LDH 活力的增强幅度和血管SOD 活力的降低程度均逐步增大,表明血管分别相应受到轻、中、重度冷损伤
短句来源
    Conclusion The decrease of NOS activity may lead to the disorder in vascular circulation of cold injury,SOD and Vit C could prevent from or alleviate cold injury by increasing NOS activity.
    结论 血管NOS 活力降低是导致冷损伤组织血液循环障碍发生的重要原因; SOD 及Vit C 可通过调节提高血管NOS 活力,防止或减缓机体冷?
短句来源
  cold injury
    Results When the vessels were exposed to cold for 1,2,4 min respectively,LDH activity in the cultured medium increased and SOD activity in the vessels decreased at different level,indicating varying degree of vessel injury:slight ,moderate and severe cold injury.
    结果 当血管暴露于- 20 ℃环境1 、2 、4 分钟后,血管培养液中LDH 活力的增强幅度和血管SOD 活力的降低程度均逐步增大,表明血管分别相应受到轻、中、重度冷损伤
短句来源
    Conclusion The decrease of NOS activity may lead to the disorder in vascular circulation of cold injury,SOD and Vit C could prevent from or alleviate cold injury by increasing NOS activity.
    结论 血管NOS 活力降低是导致冷损伤组织血液循环障碍发生的重要原因; SOD 及Vit C 可通过调节提高血管NOS 活力,防止或减缓机体冷?
短句来源
  cold injured
    Changes of NO synthase activity in the cold injured blood vessels and its biological significance
    冷损伤血管NO合成酶活力的变化及其生物学意义
短句来源
    Objective To explore the new therapy by observing the changes of NO synthase(NOS) activity in the cold injured blood vessels and by studying the effects of SOD and Vit C on the changes of NOS activity.
    目的 观察不同程度冷损伤血管NO 合成酶( NOS) 活力的变化,并研究超氧化物歧化酶(SOD) 和Vit C 对这种变化的影响。
短句来源
    Changes of lipid peroxidation(LPO) in cold injured blood vessels
    冷损伤血管脂质过氧化水平的变化及其意义
短句来源
  cold injury
    Results When the vessels were exposed to cold for 1,2,4 min respectively,LDH activity in the cultured medium increased and SOD activity in the vessels decreased at different level,indicating varying degree of vessel injury:slight ,moderate and severe cold injury.
    结果 当血管暴露于- 20 ℃环境1 、2 、4 分钟后,血管培养液中LDH 活力的增强幅度和血管SOD 活力的降低程度均逐步增大,表明血管分别相应受到轻、中、重度冷损伤
短句来源
    Conclusion The decrease of NOS activity may lead to the disorder in vascular circulation of cold injury,SOD and Vit C could prevent from or alleviate cold injury by increasing NOS activity.
    结论 血管NOS 活力降低是导致冷损伤组织血液循环障碍发生的重要原因; SOD 及Vit C 可通过调节提高血管NOS 活力,防止或减缓机体冷?
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  cold injury
Myofibroblasts in subepicardium after local cold injury
      
Bioluminescence imaging of ATP, glucose, and lactate was performed in serial tissue sections at 4 h (n=4), 12 h (n=4) and 24 h (n=4) after cold injury or sham surgery.
      
Experiments also demonstrated that mortality of the larvae maintained in an extended supercooled state at -23°C was due to cold injury rather than freezing.
      
The metacarpal phalangeal joints and wrists were spared in all patients, and fingers which had been protected from the initial cold injury were similarly not affected.
      
A brief (2-h) exposure to 0°C elicits a protective response against subsequent cold injury at-10°C in the temperate flies and in B.
      
更多          
  cold injury
Myofibroblasts in subepicardium after local cold injury
      
Bioluminescence imaging of ATP, glucose, and lactate was performed in serial tissue sections at 4 h (n=4), 12 h (n=4) and 24 h (n=4) after cold injury or sham surgery.
      
Experiments also demonstrated that mortality of the larvae maintained in an extended supercooled state at -23°C was due to cold injury rather than freezing.
      
The metacarpal phalangeal joints and wrists were spared in all patients, and fingers which had been protected from the initial cold injury were similarly not affected.
      
A brief (2-h) exposure to 0°C elicits a protective response against subsequent cold injury at-10°C in the temperate flies and in B.
      
更多          
  cold injury
Myofibroblasts in subepicardium after local cold injury
      
Bioluminescence imaging of ATP, glucose, and lactate was performed in serial tissue sections at 4 h (n=4), 12 h (n=4) and 24 h (n=4) after cold injury or sham surgery.
      
Experiments also demonstrated that mortality of the larvae maintained in an extended supercooled state at -23°C was due to cold injury rather than freezing.
      
The metacarpal phalangeal joints and wrists were spared in all patients, and fingers which had been protected from the initial cold injury were similarly not affected.
      
A brief (2-h) exposure to 0°C elicits a protective response against subsequent cold injury at-10°C in the temperate flies and in B.
      
更多          


The effects of frostbite during hypoxia at 6 000 m simulated altitude on serum angiotensin Ⅰ converting enzyme (ACE) activity in rats were investigated. Before freezing, the serum ACE activity in rats of frostbite during hypoxia after high altitude acclimation (FHAC) group and frostbite during acute hypoxia (FAH) group was 50.0±5.8 U and 60.0±6.7 U respectively, and much lower than that of frostbite at normoxia (FN) group(78.1±4.0 U, P<0.05). At 4 hours after frostbite, ACE activities of FN and FAH groups all...

The effects of frostbite during hypoxia at 6 000 m simulated altitude on serum angiotensin Ⅰ converting enzyme (ACE) activity in rats were investigated. Before freezing, the serum ACE activity in rats of frostbite during hypoxia after high altitude acclimation (FHAC) group and frostbite during acute hypoxia (FAH) group was 50.0±5.8 U and 60.0±6.7 U respectively, and much lower than that of frostbite at normoxia (FN) group(78.1±4.0 U, P<0.05). At 4 hours after frostbite, ACE activities of FN and FAH groups all tended to increase. At 24 hours after frostbite, the ACE activity of FAH group recovered, but the activity of FHAC group detected at 72 hours after frostbite was still higher than that before freezing. The results showed that exposure to hypoxia alone could decrease the serum ACE activity in rats. Combination of exposure to hypoxia and cold could make the ACE activity tend to increase, suggesting that there might be damage of vascular endothelial cells, and that the damage in rats of FHAC group might be much severe.

实验观察了在模拟海拔6000m缺氧冻伤对大鼠血清血管紧张素Ⅰ转换酶(ACE)活性的影响。大鼠血清ACE活性以U(nmol·ml-1·min1)表示。致冻前,缺氧习服缺氧冻伤(FHAC)组和急性缺氧冻伤(FAH)组大鼠血清ACE活性分别为50.0±5.8和60.0±6.7U(P>0.05)明显低于平原冻伤(FN)组的78.1±4.0U(P<0.01和P<0.05);冻后4h,FAH组和FHAC组大鼠血清ACE活性均呈现较冻前增高趋势;冻后24h,FAH组与冻前无差异,而FHAC组冻后72h仍呈增长趋势。结果表明:单纯缺氧暴露可使大鼠血清ACE活性降低,而缺氧复合冷损伤则使大鼠血清ACE活性呈现增高趋势,提示可能有内皮细胞损伤,缺氧习服缺氧冻伤后内皮细胞损伤可能较重

Objective To explore the new therapy by observing the changes of NO synthase(NOS) activity in the cold injured blood vessels and by studying the effects of SOD and Vit C on the changes of NOS activity.Methods The aortic artery was isolated from Wistar rats and cultured in PBS medium for 1 h,then exposed to -20 ℃ cold environment.LDH activity was measured using Biochemistry Automatic Analysis Meter,NOS and SOD activities in blood vessels were analysed respectively by Griess assay and adrenalin autooxidation...

Objective To explore the new therapy by observing the changes of NO synthase(NOS) activity in the cold injured blood vessels and by studying the effects of SOD and Vit C on the changes of NOS activity.Methods The aortic artery was isolated from Wistar rats and cultured in PBS medium for 1 h,then exposed to -20 ℃ cold environment.LDH activity was measured using Biochemistry Automatic Analysis Meter,NOS and SOD activities in blood vessels were analysed respectively by Griess assay and adrenalin autooxidation method. Results When the vessels were exposed to cold for 1,2,4 min respectively,LDH activity in the cultured medium increased and SOD activity in the vessels decreased at different level,indicating varying degree of vessel injury:slight ,moderate and severe cold injury.After 4 h of cold exposure,NOS activity in the slight ,moderate and severe injured vessels increased by 15.3%,and decreased by 17.9%,29.6% respectively as compared with control.The changes of the NOS activity was time dependent.Treating with SOD(200 U/ml) or Vit C(50 mg/ml) immediatly after cold exposure made NOS and SOD activity in the vessels significantly increase and LDH in the medium decrease. Conclusion The decrease of NOS activity may lead to the disorder in vascular circulation of cold injury,SOD and Vit C could prevent from or alleviate cold injury by increasing NOS activity.

目的 观察不同程度冷损伤血管NO 合成酶( NOS) 活力的变化,并研究超氧化物歧化酶(SOD) 和Vit C 对这种变化的影响。方法 分离Wistar 大鼠主动脉,并在PBS 培育液中培养1 小时,然后使其暴露于- 20 ℃环境。以全自动生化分析仪测定血管培养液中乳酸脱氢酶(LDH) 活力,以Griess化学法观测血管NOS 活力,以肾上腺素自氧化法测定血管SOD 活力。结果 当血管暴露于- 20 ℃环境1 、2 、4 分钟后,血管培养液中LDH 活力的增强幅度和血管SOD 活力的降低程度均逐步增大,表明血管分别相应受到轻、中、重度冷损伤冷损伤后4 小时,轻度冷损伤血管NOS 活力较未冷冻血管增加15 .3 % ,中、重度冷损伤血管NOS 活力则显著下降,分别达17 .9 % 、29 .6 % 。血管冷冻后立即给予SOD(200 U/ ml) 或Vit C(50 mg/ml) ,可使冷损伤血管NOS 活力分别较未经SOD 或Vit C 处理者显著升高,并降低了冷损伤血管培养液中LDH 活力,使血管SOD 活力回升。结论 血...

目的 观察不同程度冷损伤血管NO 合成酶( NOS) 活力的变化,并研究超氧化物歧化酶(SOD) 和Vit C 对这种变化的影响。方法 分离Wistar 大鼠主动脉,并在PBS 培育液中培养1 小时,然后使其暴露于- 20 ℃环境。以全自动生化分析仪测定血管培养液中乳酸脱氢酶(LDH) 活力,以Griess化学法观测血管NOS 活力,以肾上腺素自氧化法测定血管SOD 活力。结果 当血管暴露于- 20 ℃环境1 、2 、4 分钟后,血管培养液中LDH 活力的增强幅度和血管SOD 活力的降低程度均逐步增大,表明血管分别相应受到轻、中、重度冷损伤冷损伤后4 小时,轻度冷损伤血管NOS 活力较未冷冻血管增加15 .3 % ,中、重度冷损伤血管NOS 活力则显著下降,分别达17 .9 % 、29 .6 % 。血管冷冻后立即给予SOD(200 U/ ml) 或Vit C(50 mg/ml) ,可使冷损伤血管NOS 活力分别较未经SOD 或Vit C 处理者显著升高,并降低了冷损伤血管培养液中LDH 活力,使血管SOD 活力回升。结论 血管NOS 活力降低是导致冷损伤组织血液循环障碍发生的重要原因;SOD 及Vit C 可通过调节提高血管NOS 活力,防止或减缓机体冷?

 
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