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acute ischemic brain injury
相关语句
  急性缺血性脑损伤
     1,3,6 ,24 hours after ischemia,rats were killed and c-fos protein(FOS)and HSP70 immune positive cells of cortex tissue in ischemic region were determined by immunohistochemistry assay to observe the influence on anti-apoptosis gene expression at early stages of acute ischemic brain injury.
     分别于缺血后的1、3、6、24h处死 ,进行免疫组织化学染色 ,检测缺血区皮层脑组织c-fos蛋白 (FOS)及HSP70蛋白免疫阳性细胞 ,以观察井穴放血法对急性缺血性脑损伤后早期抑凋亡基因表达的影响。
短句来源
     NITRIC OXIDE DERIVED FROM PERIPHERAL BLOOD MONONUCLEAR CELLS AND ACUTE ISCHEMIC BRAIN INJURY
     单个核细胞源性一氧化氮与急性缺血性脑损伤
短句来源
     Rats were divided into sham operation group,cerebral ischemia group and treatment group. Acute ischemic brain injury was made by middle cerebral artery obstruction(MCAO). Well acupoints blood-letting therapy ,one drip each time ,was given in rats in treatment group immediately after cerebral ischemia.
     [方法]将实验大鼠分为假手术组、脑缺血组和脑缺血 +井穴放血治疗组 ,一侧大脑中动脉阻塞致急性缺血性脑损伤模型 (MCAO) ,治疗组在脑缺血后即刻给予井穴放血治疗 ,出血量为每穴1滴。
短句来源
     OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2. DESIGN: A completely randomized controlled trial.
     目的:探讨尼莫地平对磷脂酶A2激活致急性缺血性脑损伤中的保护作用。 设计:完全随机对照实验。
短句来源
  “acute ischemic brain injury”译为未确定词的双语例句
     s: To observe the protective function of well acupoints blood-letting method against acute ischemic brain injury.
     [目的]观察井穴放血法对急性缺血性脑损伤的脑保护作用。
短句来源
  相似匹配句对
     Oligodendrocytes and Ischemic Brain Injury
     少突胶质细胞与缺血性脑损伤
短句来源
     Significance of somatostatin in acute brain injury
     生长抑素在急性颅脑损伤中的意义
短句来源
     Pathogenesis of acute focal ischemic cerebral injury
     急性局灶性脑缺血性脑损伤发生机制
短句来源
     Acute traumatic diffuse brain injury (ATDBI)
     急性外伤性弥漫性脑损伤
短句来源
     Establishment and evaluation of acute closed brain injury
     急性闭合性脑损伤模型的建立与评估
短句来源
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By radioimmunoassay,on the model of four-vessel occlusion in the rat,the changes of Leu-enkelphin(LEK),β-Endorphin(β-EP),DynorphinA1-13(DynA1-13)in cortex(Cor), hypothalamus(Hyp.)and striatum(Str.)were observed at in tervals of 10,30 and 60 minutes after cerebral isehemia. The results showed the three kinds of opioid peptides changed differently after ischemia. This probably indicated that they played different roles in acute ischemic brain injury.

本文应用四血管关闭大鼠全脑缺血模型,借助放射免疫分析法观察了大鼠脑缺血后10min、30min、60min三个时程点皮层(COr)、下丘脑(Hyp)和纹状体(Str)内的亮脑啡肽(LEK)、β-内啡肽(β-EP)、强啡肽A_(1~13)(DynA_(1~13))等三种内源性阿片肽含量的改变,结果发现大鼠脑缺血后三种阿片肽含量的变化规律有所不同,提示它们在缺血性脑损伤中的作用可能有异。

s: To observe the protective function of well acupoints blood-letting method against acute ischemic brain injury. Rats were divided into sham operation group,cerebral ischemia group and treatment group. Acute ischemic brain injury was made by middle cerebral artery obstruction(MCAO). Well acupoints blood-letting therapy ,one drip each time ,was given in rats in treatment group immediately after cerebral ischemia. 1,3,6 ,24 hours after ischemia,rats were killed and c-fos protein(FOS)and HSP70 immune...

s: To observe the protective function of well acupoints blood-letting method against acute ischemic brain injury. Rats were divided into sham operation group,cerebral ischemia group and treatment group. Acute ischemic brain injury was made by middle cerebral artery obstruction(MCAO). Well acupoints blood-letting therapy ,one drip each time ,was given in rats in treatment group immediately after cerebral ischemia. 1,3,6 ,24 hours after ischemia,rats were killed and c-fos protein(FOS)and HSP70 immune positive cells of cortex tissue in ischemic region were determined by immunohistochemistry assay to observe the influence on anti-apoptosis gene expression at early stages of acute ischemic brain injury. Increased expression of c-fos protein and HSP70 protein in cortex tissue of ischemic region was observed with no expression of HSP70 1 hour after ischemia,while the expression of FOS was increased. Expression of FOS and HSP70 tended to increase with the time elapsed during the following 3,6,24 hours. The count of c-fos and HSP70 immune positive cells in treatment group was all higher than that in model group during the same period of time with statistical significance.[Conclusion] Well acupoints blood-letting therapy can obviously enhance the expression of c-fos and HSP70 protein in ischemic region,increase the ability against apoptosis and the tolerance and adaptation ability of nerve cell to hypoxia and ischemia ,and enhance the neuron compliance after ischemia,thus further influencing the expression of objective gene at late stages,resisting the development of apoptosis,enhancing the repairing ability of brain. It is suggested that well acupoints blood-letting therapy has certain protective action against early stroke.

[目的]观察井穴放血法对急性缺血性脑损伤的脑保护作用。[方法]将实验大鼠分为假手术组、脑缺血组和脑缺血 +井穴放血治疗组 ,一侧大脑中动脉阻塞致急性缺血性脑损伤模型 (MCAO) ,治疗组在脑缺血后即刻给予井穴放血治疗 ,出血量为每穴1滴。分别于缺血后的1、3、6、24h处死 ,进行免疫组织化学染色 ,检测缺血区皮层脑组织c-fos蛋白 (FOS)及HSP70蛋白免疫阳性细胞 ,以观察井穴放血法对急性缺血性脑损伤后早期抑凋亡基因表达的影响。[结果]c-fos蛋白和HSP70蛋白在缺血区皮层脑组织表达增加 ,缺血后1hHSP70无表达 ,FOS表达增加 ,在随后观察的3、6、24h时程内HSP70和FOS均有随缺血时间延长表达增多的趋势。井穴放血治疗组在以上各时程c-fos及HSP70免疫阳性细胞数均高于同时段的缺血病模组 ,有统计学意义。[结论]急性脑缺血后应用井穴放血干预治疗可明显增强缺血区脑组织对抗神经细胞凋亡的即刻早期基因c-fos蛋白和抗应激HSP70蛋白的表达 ,从而提高了缺血后神经细胞对缺血、缺氧的耐受和适应能力 ,提高了缺血后神经元的可塑性 ,进而可影响晚期目的基因的表达 ,抵抗细胞凋亡的发展 ...

[目的]观察井穴放血法对急性缺血性脑损伤的脑保护作用。[方法]将实验大鼠分为假手术组、脑缺血组和脑缺血 +井穴放血治疗组 ,一侧大脑中动脉阻塞致急性缺血性脑损伤模型 (MCAO) ,治疗组在脑缺血后即刻给予井穴放血治疗 ,出血量为每穴1滴。分别于缺血后的1、3、6、24h处死 ,进行免疫组织化学染色 ,检测缺血区皮层脑组织c-fos蛋白 (FOS)及HSP70蛋白免疫阳性细胞 ,以观察井穴放血法对急性缺血性脑损伤后早期抑凋亡基因表达的影响。[结果]c-fos蛋白和HSP70蛋白在缺血区皮层脑组织表达增加 ,缺血后1hHSP70无表达 ,FOS表达增加 ,在随后观察的3、6、24h时程内HSP70和FOS均有随缺血时间延长表达增多的趋势。井穴放血治疗组在以上各时程c-fos及HSP70免疫阳性细胞数均高于同时段的缺血病模组 ,有统计学意义。[结论]急性脑缺血后应用井穴放血干预治疗可明显增强缺血区脑组织对抗神经细胞凋亡的即刻早期基因c-fos蛋白和抗应激HSP70蛋白的表达 ,从而提高了缺血后神经细胞对缺血、缺氧的耐受和适应能力 ,提高了缺血后神经元的可塑性 ,进而可影响晚期目的基因的表达 ,抵抗细胞凋亡的发展 ,增强脑修复能力。表明井穴放血法对中风初期有一定的脑保护作用

BACKGROUND: Activated by Ca2+, phospholipase A2 will aggravate the influx of Ca2+ or the release of intracellular Ca2+, and then forms a vicious circle, which results in a continuous increase in free calcium level and leads to server injury in neural cells. OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2. DESIGN: A completely randomized controlled trial. SETTING: Intensive Care Unit (ICU) of Children's Hospital, Chongqing...

BACKGROUND: Activated by Ca2+, phospholipase A2 will aggravate the influx of Ca2+ or the release of intracellular Ca2+, and then forms a vicious circle, which results in a continuous increase in free calcium level and leads to server injury in neural cells. OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2. DESIGN: A completely randomized controlled trial. SETTING: Intensive Care Unit (ICU) of Children's Hospital, Chongqing Medical University. MATERIALS: From January 2001 to October 2003, it was completed at the ICU of Children's Hospital, Chongqing Medical University. Thirty male rats were selected and divided into sham operation group, ischemia group and nimodipine treated group randomly, with 10 rats in each group. METHODS: In sham operation group, the right common carotid artery was identified by blunt dissection without ligation under anesthesia in rats. In ischemia group, at 30 minutes before cerebral ischemia, 2 mL saline was injected intraperitoneally. In nimodipine treated group, at 30 minutes before cerebral ischemia, 0.2 g/L nimodipine (2 mg/kg) was injected intraperitoneally. In all the three groups, the duration between ischemia and decollation was 120 minutes. Rats were decollated under anesthesia and their brains were taken out to assess the activity of phospholipase A2, the free calcium level in brain cells, the brain water content and the changes in mRNA levels of type Ⅱ phospholipase A2 (secretive phospholipase A2) and type Ⅳ phospholipase A2 (cytoplasmic phospholipase A2) in brain tissue. MAIN OUTCOME MEASURES: ① The activity of phospholipase A2 in brain tissue; ② the free calcium levels in brain cells; ③ the brain water content; ④ the mRNA levels of type Ⅱ phospholipase A2 (secretive phospholipase A2) and type Ⅱ phospholipase A2 (cytoplasmic phospholipase A2) in brain tissue were measured in rats in all the groups. RESULTS: All of the 30 rats entered the statistical analysis. ① The activity of phospholipase A2 in brain tissue: In ischemia group and nimodipine treated group, the activity of phospholipase A2 were higher than that in sham operation group (57.8±7.2), (42.5±6.1), (17.1±5.3)%, P < 0.05-0.01, and it was a litter lower in nimodipine treated group than that in ischemia group (P < 0.05). ②The free calcium levels in brain cells: It was higher in nimodipine treated group and ischemia group than that in sham operation group (775.8±105.5), (497.2±45.9), (103.8±10.3) μmol/L, P < 0.05-0.01, and it was lower in nimodipine group than in ischemia group (P < 0.01). ③ The brain water content: It was higher in nimodipine group and ischemia group than that in sham operation group (82.9±0.5), (80.0±1.1), (72.1±0.01)%, P < 0.05-0.01, and it was lower in nimodipine treated group than that in ischemia group (P < 0.05). ④ In sham operation group, no significant mRNA of type Ⅱ phospholipase A2 could be detected in brain tissue. And the mRNA level of type Ⅱ phospholipase A2 in brain tissue was very low. At 120 minutes after ischemia, mRNA of type Ⅱ phospholipase A2 was detectable and the expression of type Ⅱ phospholipase A2 was increased. Compared to ischemia group, the expression of type Ⅱ phospholipase A2 was not decreased in nimodipine treated group while the expression of type Ⅱ phospholipase A2 was decreased. CONCLUSION: Nimodipine is capable of decreasing the free calcium level in brain cells, the activity of phospholipase A2 in brain tissue and the brain water content after ischemia. However, it cannot significantly inhibit the expressions of type Ⅱ phospholipase A2 and type Ⅱ phospholipase A2 after cerebral ischemia.

背景:磷脂酶A2能被Ca2+激活,而被激活的磷脂酶A2又能使Ca2+内流或细胞内Ca2+释放,形成恶性循环,使神经细胞游离Ca2+浓度持续增加,导致神经细胞严重损伤。目的:探讨尼莫地平对磷脂酶A2激活致急性缺血性脑损伤中的保护作用。设计:完全随机对照实验。单位:重庆医科大学儿童医院ICU。材料:实验于2001-01/2003-10在重庆医科大学儿科研究所完成,选择30只雄性Wistar大鼠,随机分为假手术组、缺血组、尼莫地平干预组,每组10只。方法:假手术组:大鼠仅在麻醉状态下分离右侧颈总动脉,不予阻断血流。缺血组:脑缺血前30min,每只大鼠腹腔注射2mL生理盐水。尼莫地平干预组:脑缺血前30min,每只大鼠腹腔注射0.2g/L的尼莫地平2mg/kg。3组大鼠自缺血开始至处死的时间均为120min。大鼠在麻醉状态下断头处死,取脑组织检测磷脂酶A2活性、脑细胞游离Ca2+浓度、脑组织水含量及检测脑组织中Ⅱ类A型分泌型磷脂酶A2和Ⅳ类胞浆型磷脂酶A2mRNA表达的改变。主要观察指标:①各组大鼠脑组织磷脂酶A2活性。②各组大鼠脑细胞游离Ca2+浓度。③各组大鼠脑含水量。④各组大鼠脑组织中Ⅱ类A型分泌型磷脂酶A2和...

背景:磷脂酶A2能被Ca2+激活,而被激活的磷脂酶A2又能使Ca2+内流或细胞内Ca2+释放,形成恶性循环,使神经细胞游离Ca2+浓度持续增加,导致神经细胞严重损伤。目的:探讨尼莫地平对磷脂酶A2激活致急性缺血性脑损伤中的保护作用。设计:完全随机对照实验。单位:重庆医科大学儿童医院ICU。材料:实验于2001-01/2003-10在重庆医科大学儿科研究所完成,选择30只雄性Wistar大鼠,随机分为假手术组、缺血组、尼莫地平干预组,每组10只。方法:假手术组:大鼠仅在麻醉状态下分离右侧颈总动脉,不予阻断血流。缺血组:脑缺血前30min,每只大鼠腹腔注射2mL生理盐水。尼莫地平干预组:脑缺血前30min,每只大鼠腹腔注射0.2g/L的尼莫地平2mg/kg。3组大鼠自缺血开始至处死的时间均为120min。大鼠在麻醉状态下断头处死,取脑组织检测磷脂酶A2活性、脑细胞游离Ca2+浓度、脑组织水含量及检测脑组织中Ⅱ类A型分泌型磷脂酶A2和Ⅳ类胞浆型磷脂酶A2mRNA表达的改变。主要观察指标:①各组大鼠脑组织磷脂酶A2活性。②各组大鼠脑细胞游离Ca2+浓度。③各组大鼠脑含水量。④各组大鼠脑组织中Ⅱ类A型分泌型磷脂酶A2和胞浆型磷脂酶A2表达情况。结果:30只大鼠均进入结果分析。①各组大鼠脑组织磷脂酶A2活性:缺血组、尼莫地平干预组均高于假手术组([57.8±7.2),(42.5±6.1),(17.1±5.3)%,P<0.05~0.01],尼莫地平干预组低于缺血组(P<0.05)。②各组大鼠脑细胞游离Ca2+浓度:缺血组、尼莫地平干预组均高于假手术组([775.8±105.5),(497.2±45.9),(103.8±10.3)μmol/L,P<0.05~0.01],尼莫地平干预组低于缺血组(P<0.01)。③各组大鼠脑含水量:缺血组、尼莫地平干预组均高于假手术组([82.9±0.5),(80.0±1.1),(72.1±0.01)%,P<0.05~0.01],尼莫地平干预组低于缺血组(P<0.05)。④假手术组脑组织中无明显Ⅱ类A型分泌型磷脂酶A2mRNA表达,胞浆型磷脂酶A2mRNA表达水平很低。缺血后120min后脑组织中出现Ⅱ类A型分泌型磷脂酶A2mRNA表达,胞浆型磷脂酶A2mRNA表达水平明显增强。尼莫地平干预组与缺血组比较,Ⅱ类A型分泌型磷脂酶A2mRNA表达水平无明显降低,胞浆型磷脂酶A2mRNA表达水平有所降低。结论:尼莫地平可降低缺血后脑细胞游离Ca2+浓度,脑组织中磷脂酶A2的活性和脑含水量,但不能明显抑制脑缺血后Ⅱ类A型分泌型磷脂酶A2mRNA及胞浆型磷脂酶A2mRNA的表达。

 
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