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应用钙
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     Methods The fluorescent Ca2+ indicator Fluo-3 was used to observe and quantitate the calcium signal directly in activated RBL-2H3 mast cells by a flow cytometer and a confocal fluorescence microscope with laser.
     方法应用钙离子荧光指示剂Fluo-3,通过流式细胞仪和激光共聚焦荧光显微镜分析肥大细胞RBL-2H3活化时细胞内钙离子浓度([Ca2+]i)的变化和细胞外钙离子浓度对释放组胺的影响,观察钙离子信号与肥大细胞活化的关系。
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     Methods:Angiotensin Ⅱ(AngⅡ,10 -7 mol/L), ryanodine (RY, 10 -7 mol/L),inositol (1,4,5) trisphosphate (IP 3, 10 -7 mol/L) were applied to stimulate the [Ca 2+ ]i,CaN activity and protein expression were measured in primary cultured cardiomyocytes from wistar rat. [Ca 2+ ]i was measured using Fura 2/AM fluorescent technique.
     方法 :以原代培养的乳鼠心肌细胞为模型 ,血管紧张素Ⅱ(AngⅡ)、雷尼丁 (RY)和三磷酸肌醇 (IP3 ) (浓度均为 10 - 7mol/L)激活心肌细胞 [Ca2 + ]i,应用钙荧光指剂Fura 2 /AM动态观测心肌细胞 [Ca2 + ]i浓度 ,同时检测心肌细胞CaN活性及蛋白表达。
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     METHOD: The concentration of [Ca 2+ ]i was determined by using spectrofluorometer and fluorescent Ca 2+ probe fura-2 /Am.
     方法 :采用荧光分光光度法 ,应用钙离子探针 (Fura - 2 /AM) ,检测 [Ca2 +]i浓度。
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     Parthenogenetic activation of calcium ionophore A23187 and 6-dimethylaminopurine on human oocytes
     应用钙离子载体A23187及6-甲基嘌呤对人卵母细胞进行孤雌激活
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     Methods The intracellular Ca~(2+) level was investigated by using Fura-2/AM (fluorescence indicator).
     方法:应用钙荧光指示剂Fura-2/AM检测细胞内钙离子浓度([Ca~(2+)]i);
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     Applications of the value-added calcium source
     源的比较和应用
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     (D) applications;
     D. 应用;
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     Applying .
     应用.
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     The Clinical Use of Calcium Antagonists
     拮抗剂的临床应用
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46 cases of hypertension were treated with nifedipine from September, 1983 to January, 1984, The efiect of decreasing blood pressure was available. All the eases were primary hypertension, including those treated with or without antihypertensive drags, 30~40mg daily, and for certain individuals 120my. divided into3~4 times daily by oral administration. One course of treatment needed one month. In 46 cases the drug was effective-for 86.95%; available for 13.04% and ineffective for none. No difference of effects...

46 cases of hypertension were treated with nifedipine from September, 1983 to January, 1984, The efiect of decreasing blood pressure was available. All the eases were primary hypertension, including those treated with or without antihypertensive drags, 30~40mg daily, and for certain individuals 120my. divided into3~4 times daily by oral administration. One course of treatment needed one month. In 46 cases the drug was effective-for 86.95%; available for 13.04% and ineffective for none. No difference of effects of decreased blood pssure was noted among the various stages of hypertension. The sam was true of various forms, age groups and onset and duration of the disease (p>0.05) It was also always available to increase the dosage or add Inderal or/and Dihydroehlorothiazide for some base in which the effect was unavailable, and for renal and troublesome hypertension. The effect of nifedipine was rapid and its side-effects was low. In emergeucy cases of hypertension it was usually used.

本文应用钙离子拮抗剂——硝苯吡啶对46例高血压进行临床疗效观察,结果显示硝苯吡啶对各类、各期以及不同年龄组、不同年限的高血压患者均有效,显效率可达86.95%,作用迅速、无副作用。配合β受体阻滞剂或/和双氢克尿塞则疗效更显,尤适用于肾性及难治性高血压。部分产生耐受性者可加量或加用β阻滞剂。

The importance of intracellular calcium ion in macrophage (Mφ) activation for tumor tcytolysis (MMTC) was investigated by using calcium channel blockers, nifedipine verapamil and intracellular calcium ion antagonists. nicardipine and ruthenium red. Nifedipine or verapamil did not suppress but significantly enhance Mφ activation by macrophageactivating factor (MAF) . However, nicardipine and ruthenium red bothinhibited Mφ activation by MAF and calcium ionophore A 23187. Activation of Mφ by lipopolysaccharide...

The importance of intracellular calcium ion in macrophage (Mφ) activation for tumor tcytolysis (MMTC) was investigated by using calcium channel blockers, nifedipine verapamil and intracellular calcium ion antagonists. nicardipine and ruthenium red. Nifedipine or verapamil did not suppress but significantly enhance Mφ activation by macrophageactivating factor (MAF) . However, nicardipine and ruthenium red bothinhibited Mφ activation by MAF and calcium ionophore A 23187. Activation of Mφ by lipopolysaccharide (LPS) was Likewise inhibited. These results suggest that extracellular catcium may not be involved in Mφ activation by MAF and Mφ activation by MAF, A23187, or LPS is intracellular calcium (?)on dependent.

应用钙离子通道阻断剂nifedipine和verapamil以及胞内钙离子拮抗剂nicardipilie和ruthenium red,观察了胞内钙离子在Mφ活化杀伤肿瘤细胞的重要性。nifedipine和verapamil不抑制而强烈的增强MAF诱导的Mφ活化,nicardipine和ruthenium red均抑制MAF和钙离子载体A_(23187)诱导的Mφ活化,LPS活化Mφ的作用同样受到抑制。这些结果提示,胞外钙离子可能不参与MAF诱导的Mφ活化,MAF、A_(23187)、LPS活化Mφ的作用是胞内钙离子依赖的。

Ca~(2+)-selective microelectrode technique was used to study the effect of somatostatin on HCl-induced change in extracellular Ca~(2+) activity of toad gastric smooth muscle in vitro. Following decline in pH of the perfusate from 7. 4 to 5. 4. a rapid decrease in extracellular Ca~(2) activity with a latent period of 30 s was observed. Within 5 min after decline in pH. the mean Ca~(2+) activity was 85. 7% of the control value (n=9). Pretreatment of the smooth muscle with somatostatin significantly inhibited the...

Ca~(2+)-selective microelectrode technique was used to study the effect of somatostatin on HCl-induced change in extracellular Ca~(2+) activity of toad gastric smooth muscle in vitro. Following decline in pH of the perfusate from 7. 4 to 5. 4. a rapid decrease in extracellular Ca~(2) activity with a latent period of 30 s was observed. Within 5 min after decline in pH. the mean Ca~(2+) activity was 85. 7% of the control value (n=9). Pretreatment of the smooth muscle with somatostatin significantly inhibited the decrease in Ca~(2+) activity induced by HC1. Within 5 min after decline in pH.the Ca~(2+) activity was decreased on average to 92. 6% of the control value(n=10). The amplitude of decrease in Ca~(2+) activity was significantly lower than that of HC1 group. The results suggest that somatostatin inhibits the HC1induced decrease in extracellular Ca~(2+) activity of gastric smooth muscle.

应用钙离子选择微电极技术测定了蜍离体胃平滑肌细胞受盐酸刺激时细胞外Ca~(2+)活度的变化及生长抑素对它的影响.结果发现,当流液的pH由7.4降至5.4时.约经30s.Ca~(2+)活度迅速下降,2min后达最低值,5min内平均降到对照值的85.7%(n=9).若事先用生长抑素处量平滑肌条,盐酸降低Ca~(2+)活度的效应受到明显抑制,在pH降到5.4后5min内Ca~(2+)活度平均降到对照值的92.6%(n=10),与单纯的盐酸效应相比有明显的差异(P<0.01)。结果提示,生长抑素可抑制盐酸降低平滑肌细胞外Ca~(2+)活度的效应.

 
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