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Methods: To observe the protective effects of EAB extraction on anoxia model in normal mice.

对小鼠常压耐缺氧作用的实验研究,以观察鬼箭羽提取物对小鼠常压下抗耐缺氧的能力。

Hypoxia: Condition in which tissues are starved of oxygen. The extreme is anoxia.

低氧:身体组织缺氧的状态,最严重的情况是缺氧。

Prior administration of "Styrax Pill for Coronary Disease" proper (6 components viz., styrax liquidus, Borneolum, Lignum santali, Aristolochia, Olibanum and Cinnabaris) or the mixture of Styrax liquidus, Borneolum, Lignum Santali and Olibanum to mice prolonged the survival time of the animals subjected to low pressure hypoxia. Styrax liquidus and Borneolum administered separately showed the same effect, whereas none of the other four components showed significant protection.

用小鼠耐缺氧试验和麻醉狗冠状窦血流量及心脏动-静脉血氧差(MA-VO_2)的实验研究冠心苏合丸及其成分的作用,发现:(1)冠心苏合丸能延长小鼠耐缺氧的时间;(2)冠心苏合丸能使心肌梗塞狗的CSF回升,减少心率和MA-VO_2,对非心肌梗塞狗不能提高CSF但亦能减少心率和MA-VO_2;(3)在本实验条件下,苏合香脂和冰片似为冠心苏合丸中起作用的两个成分,其余成分如檀香、青木香、乳香或其油均未能证实其效果。

VEGF protein was induced by hypoxia in rat cerebral microvascular endothelial cells, and NYA could upregulate the expression of VEGF protein, which may be one of the protection mechanisms for cerebral microvascular endothelial cells.

缺氧可诱导脑微血管内皮细胞VEGF蛋白的表达;脑溢安可以上调VECF蛋白的表达,这可能是脑溢安对缺氧的脑微血管内皮细胞的保护作用机制之一。

SW480 and SW620 cells were also used to study the gene regulation with high carbohydrate intake, where it was shown that during glycolysis eight genes, HK1 (nuclear gene encoding mitochondrial protein, transcript variant 1), GPI, GAPD (glyceraldehyde-3-phosphate dehydrogenase), PGK1 (phosphoglycerate kinase 1), PGK2 (phosphoglycerate kinase 2), ENO2 (enolase 2), PKM2 (pyruvate kinase, muscle, transcript variant 2) and GLUT1 (facilitated glucose transporter, member 1) are over-expressed. In our study, we also found that during hypoxia of cancer tissues the resulting up-regulation of HIF-2α(hypoxia-inducible factor 2, alpha subunit) would in turn up-regulate the GLU1 gene, further activating glycolysis.

另一方面,在高碳水化合物的调控研究上,吾人也利用SW480和SW620细胞株分析证实醣解水解活化过程中,其六碳醣激酶-1(HK1)、葡萄糖磷酸异构酶、3-磷酸甘油醛脱氢酶、磷酸甘油酸激酶-1(PGK1)、磷酸甘油酸激酶-2(PGK2)、烯醇酶-2(ENO2)、丙酮酸激酶-2(PKM2)以及葡萄糖输送蛋白-1(GLUT1)等共有8个基因是连续上升的过度表现;此外,吾人也发现当癌细胞在缺氧的组织中,其缺氧转录子-2α基因(HIF-2α)表现上升后,会活化GLU1基因上升,进一步活化醣解代谢的进行。

By superfusion of ET-1, the hypoxiainduced decrease in RPF was remarkably potentiated (from 136±9 to 48±27 bpm) and the occurrence of pacemaker arrest was shifted to 20±6 min.

缺氧的条件下持续灌流ET-1(1 nmol/L)20 min时,可显著加重缺氧所致的RPF降低,使起搏细胞的RPF由对照的136±9 bpm降至48±27 bpm(p.01),起搏细胞的停跳时间前移至20±6 min。

But the effluent ammonium in the anoxic reactor, where enough NO2 were present, was equal to the blank system, and no ammonium was converted to such nitrogen compounds as NO2- and N2 by Nitrosomonas eutropha using NO2 as electron acceptor, which maybe caused by lack of the function bacteria. There were two ANAMMOX reaction pathways in the one-stage autotrophic nitrogen removal system. One way was that after part of NH4+ was oxidized to NH2OH under aerobic conditions, NH2OH and NO2- were converted to N2O under anaerobic conditions, at last N2O was further converted to N2 which realized the nitrogen removal; Another way was that at first NO2- was reduced to NH2OH, NH2OH reacted with NH4+ to form N2H4, which was further converted to N2 subsequently, realizing the nitrogen removal.

结果表明:单级自养脱氮系统内6.72%的氨氮是通过吹脱等物化作用去除的,不超过6.02%的氨氮是通过传统硝化反硝化途径去除的,87.26%左右的氨氮是由自养脱氮途径去除的,自养脱氮反应起主要脱氮作用;在足够NO2存在且缺氧的条件下,单级自养脱氮系统内的出水氨氮浓度与空白反应器相当,NH4+并没有被亚硝化单胞菌以NO2为电子受体氧化为NO2-和N2等化合物而得以去除,可能是因为系统内不存在该代谢功能的亚硝化功能菌;单级自养脱氮系统内存在两条ANAMMOX反应途径:其中一条途径即NH4+在好氧条件下被氧化为NH2OH后,生成的NH2OH与系统内的NO2-在缺氧条件下被转化为N2O,N2O则进一步被转化为N2而实现氮的去除;另外一条途径即NO2-首先被还原为NH2OH,生成的NH2OH则与系统内的NH4+反应生成N2H4,N2H4继续被转化为N2而实现氮的去除。

That because dyoxygen induced trophocyte proliferation and hCG secretion, at that moment, hPL level is not high, which is consistent with hPL level in placenta dysfunction, What this study show that hCG increase being not promote hPL secretion significantly may explain the phenomenon.

而在一些妊娠晚期子宫胎盘局部缺氧的病例,往往表现为hCG水平高于正常相同孕周妊娠者,这是因为缺氧诱发了滋养细胞的增生,hCG大量分泌,但此时hPL水平不高,是与胎盘功能不良时hPL水平往往不高相一致,本研究结果显示的hCG增高并不明显促进hPL的分泌可能可以解释这一现象。

Studies of the Weddell seal in the laboratory have described the physiological mechanisms that allow the seals to cope with the extreme oxygen deprivation that occurs during its longest dives, which can extend 500 meters below the ocean's surface and last for over 70 minutes.

威德尔海豹长时间潜水时,可以潜到水下500米深处,待上70多分钟,这时候会出现极度缺氧情况,而人们在实验室里对威德尔海豹的研究却表明,它们有一种特殊的生理机制来适应这种极度缺氧的情况。

Massive clinical practices proof,when breathes to the palpitation stops and its the serious oxygen deficit breath failure patient,the single track dependence nose drive pipe attracts the oxygen,the face guard attracts the oxygen or the mouth suitable breath is impossible to correct the oxygen deficit condition,must promptly carry on in the trachea to insert a tube,after the mouth or the nose trachea establishment artificial respiration channel,is the effective method.

大量的临床实践证明,对于心跳呼吸停止及其严重缺氧的呼吸衰竭患者,单纯依靠鼻导管吸氧,面罩吸氧或口对口呼吸不可能纠正缺氧状态,必须及时进行气管内插管,经口或鼻气管建立人工呼吸通道,才是行之有效的方法。

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