组织构建与生物活性因子

组织构建与生物活性因子的相关文献在2013年到2016年内共计53篇,主要集中在基础医学 等领域,其中期刊论文53篇、专利文献555907篇;相关期刊1种,包括中国组织工程研究等; 组织构建与生物活性因子的相关文献由142位作者贡献,包括王哲、乔世斌、乔岩等。

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组织构建与生物活性因子—发文趋势图

组织构建与生物活性因子

-研究学者

  • 王哲
  • 乔世斌
  • 乔岩
  • 于芳芳
  • 付月
  • 侯传举
  • 冯永强
  • 冯璋
  • 刘佩佩
  • 刘宇鹏

组织构建与生物活性因子

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    • 李稚; 洪平; 吴瑛; 张亮; 李端英
    • 摘要: BACKGROUND:Due to the differences of sport events and individual metabolic characteristics of athletes, it is difficult to establish uniform biological indexes for training monitoring. Current individual evaluation is a longitudinal analysis relying on experience or numerical variation width, which is less objective.OBJECTIVE: To explore the individual function assessment and monitoring by monitoring blood biochemical indexes and brain function indexes in elite gymnasts, in order to accurately reflect the body changes resulting from training loads. METHODS:Thirty gymnasts from the Chinese national gymnastics team preparing for London Olympic Games were enroled in this study and monitored from the last winter training until the London Olympic Games. The blood biochemical indicators and brain function indicators were measured and assessed individually according to according to the principle of quality control (alert value=mean±SD, and controled variable=mean±2SD). RESULTS AND CONCLUSION:Under the relatively uniform test conditions, it is feasible to individualy assess the blood biochemical and brain function indexes of elite gymnasts in accordance with the principle of quality control, which is more accurate and objective to reflect the body changes under training load and the current state of athletes. In addition, the combined monitoring of blood biochemical indexes and brain function indexes is more comprehensive to evaluate the body function and status of elite gymnasts.%背景:由于运动项目特点的差异及运动员个体代谢特征的差异,难以建立统一的生物学指标训练监控标准,其个体化评估目前仍停留在依靠经验、依据数值变化幅度的个体纵向分析及评定,缺乏更客观性个体化评估方法。目的:探讨血液生化、脑功能监测个体化机能评定与监控的评估方法,在优秀体操运动员训练过程中,精准反映训练负荷带来人体变化的方法。方法:以国家体操队备战伦敦奥运30名集训队员为研究对象,以伦敦奥运会前最后一个冬训至奥运赛前为监控周期,进行系统的血液生化、脑功能监测,依质量控制原理(警戒值=均值±标准差,控制值=均值±2标准差),对优秀体操运动员的血液生化和脑功能指标进行个体化评估。结果与结论:在保证测试条件相对统一的前提下,依质量控制原理对优秀体操运动员的血液生化和脑功能指标进行个体化评估是可行的,可以更精准、客观地反映出训练负荷所带来的人体变化及运动员的现实状态。且血液生化和脑功能指标联合监测评估,可以更全面地评价运动员的身体机能和状态。
    • 李稚12; 洪平3; 吴瑛1; 张亮2; 李端英2
    • 摘要: 背景:由于运动项目特点的差异及运动员个体代谢特征的差异,难以建立统一的生物学指标训练监控标准,其个体化评估目前仍停留在依靠经验、依据数值变化幅度的个体纵向分析及评定,缺乏更客观性个体化评估方法。目的:探讨血液生化、脑功能监测个体化机能评定与监控的评估方法,在优秀体操运动员训练过程中,精准反映训练负荷带来人体变化的方法。方法:以国家体操队备战伦敦奥运30名集训队员为研究对象,以伦敦奥运会前最后一个冬训至奥运赛前为监控周期,进行系统的血液生化、脑功能监测,依质量控制原理(警戒值=均值±标准差,控制值=均值±2标准差),对优秀体操运动员的血液生化和脑功能指标进行个体化评估。结果与结论:在保证测试条件相对统一的前提下,依质量控制原理对优秀体操运动员的血液生化和脑功能指标进行个体化评估是可行的,可以更精准、客观地反映出训练负荷所带来的人体变化及运动员的现实状态。且血液生化和脑功能指标联合监测评估,可以更全面地评价运动员的身体机能和状态。
    • 刘宇鹏; 赵德伟; 王卫明; 张耀; 李放; 刘振刚
    • 摘要: 背景:骨折愈合过程十分复杂,需要多种细胞因子的参与.目前研究较多的细胞因子有骨形态发生蛋白、成纤维细胞生长因子、转化生长因子β、血管内皮细胞生长因子和胰岛素样生长因子,但神经生长因子在骨折愈合过程中对血管内皮细胞生长因子的作用尚不明确.目的:观察神经生长因子对兔骨折愈合中血管内皮生长因子表达的影响.方法:实验建立标准兔桡骨骨折模型,分别用神经生长因子、神经生长因子单克隆抗体和生理盐水进行干预,即应用神经生长因子组、拮抗神经生长因子组和对照组.结果与结论:损伤后24,48 h和损伤后1,3,6,8周Western blot检测骨折端组织血管内皮生长因子蛋白的表达分析结果显示,3组各时间点血管内皮生长因子表达的关系为:应用神经生长因子组>对照组>拮抗神经生长因子组(P<0.05).结果证实,在骨折愈合过程当中,应用神经生长因子可以促进血管内皮生长因子表达.
    • 刘宇鹏; 赵德伟; 王卫明; 张耀; 李放; 刘振刚
    • 摘要: 背景:骨折愈合过程十分复杂,需要多种细胞因子的参与.目前研究较多的细胞因子有骨形态发生蛋白、成纤维细胞生长因子、转化生长因子β、血管内皮细胞生长因子和胰岛素样生长因子,但神经生长因子在骨折愈合过程中对血管内皮细胞生长因子的作用尚不明确.目的:观察神经生长因子对兔骨折愈合中血管内皮生长因子表达的影响.方法:实验建立标准兔桡骨骨折模型,分别用神经生长因子、神经生长因子单克隆抗体和生理盐水进行干预,即应用神经生长因子组、拮抗神经生长因子组和对照组.结果与结论:损伤后24,48 h和损伤后1,3,6,8周Western blot检测骨折端组织血管内皮生长因子蛋白的表达分析结果显示,3组各时间点血管内皮生长因子表达的关系为:应用神经生长因子组>对照组>拮抗神经生长因子组(P<0.05).结果证实,在骨折愈合过程当中,应用神经生长因子可以促进血管内皮生长因子表达.
    • 韩海燕; 张逸驰; 季淑琼; 梁奇明; 朱遂强; 薛峥
    • 摘要: 背景:抑制小鼠海马脑片整合素活动后,虽然不会影响长时程增强的诱导,但却带来快速的长时程增强衰减,证明整合素对于诱导后长时程增强的维持和稳定起到关键的作用。目的:通过在体电生理技术阐明整合素的β1亚基在活体大鼠的海马 CA1区中β淀粉样蛋白抑制长时程增强的过程中所起到的作用。方法:将15只 SD 大鼠等分为对照组、β淀粉样蛋白组和β1整合素拮抗剂组,分别给予生理盐水,β淀粉样蛋白和β1整合素的选择性拮抗剂,记录自给予β淀粉样蛋白前10 min 至高频强直刺激后3 h时的兴奋性突触后电位。结果与结论:给予对照组大鼠高频强刺激后兴奋性突触后电位明显增强,增幅在30%以上。β淀粉样蛋白组大鼠给予高频强刺激后兴奋性突触后电位在3 h 中被显著抑制,没有出现明显的变化。而β1整合素拮抗剂组大鼠给予高频强刺激后兴奋性突触后电位又出现明显的增强。推测β1整合素在活体大鼠的海马 CA1区中β淀粉样蛋白抑制长时程增强的过程中可能起着重要的介导作用,而其特异性的拮抗剂或抗体可以阻断这种介导作用。%BACKGROUND: Inhibition of integrin activity in the hippocampal slices of mice cannot influence the induction of long-term potentiation, but bring rapid long-term potentiation attenuation, proving integrin plays a key role in maintaining and stabilizing the long-term potentiation after induction. OBJECTIVE: To explain the influence of integrin beta-1 subunit during the inhibition of long-term potentiation induced by amyloid beta-protein in rat hippocampus CA1 in vivo using electrophysiological technology. METHODS: Fifteen Sprague-Dawley rats were equal y randomized into control group treated with normal saline, amyloid beta-protein group treated with amyloid beta-protein, and integrin beta-1 subunit inhibitor group treated with selective antagonist for integrin beta-1 subunit. Excitatory postsynaptic potentials were recorded from 10 minutes before amyloid beta-protein administration til 3 hours after high-frequency tetanic stimulation. RESULTS AND CONCLUSION: In the control group, excitatory postsynaptic potentials were enhanced significantly with an increment of 30%. In the amyloid beta-protein group, excitatory postsynaptic potentials were obviously restraint within 3 hours after high-frequency tetanic stimulation and had no remarkable increase. It can be speculated by the results that integrin beta-1 subunit may be important to the long-term potentiation inhibited by amyloid beta-protein in the rat hippocampal CA1 region in vivo. The special inhibitor or antibody of integrin beta-1 subunit has the ability to stop the mediation.
    • 林喜秀; 周桔; 罗自强; 瞿树林; 赵用强; 邱继旺
    • 摘要: 背景:低氧训练时,机体既要承受运动负荷,同时处于外界的低氧环境,此时,心组织将如何适应其变化?其机制研究国内外较少。目的:观察低氧与低氧训练对大鼠心肌细胞凋亡及Bax及Bcl-2表达的影响。方法:SD大鼠共60只随机分为6组,常氧组、低氧8h组、低氧12h组、常氧训练组、低氧8h训练组和低氧12h训练组,每组10只。后3组大鼠每天在坡度为0的动物跑台上以25m/min的速度训练1h。训练完后,将低氧8h组、低氧8h训练组和低氧12h组、低氧12h训练组放入氧体积分数为12.5%(相当于海拔4000m)的低氧舱内8h和12h。实验期为4周,5d/周。最后1次实验结束后24h,大鼠均实施速眠新II腹腔麻醉后取材,采用苏木精-伊红染色、原位末端脱氧核糖核苷酸转移酶介导的dUTP缺口末端标记法及蛋白免疫组织化学法检测各组大鼠心肌细胞凋亡和Bcl-2、Bax蛋白表达。结果与结论:①与常氧组相比,低氧12h组、常氧训练组、低氧训练组心肌细胞凋亡指数均显著增加(P〈0.05);低氧12h训练组心肌细胞凋亡指数显著多于常氧训练组和低氧8h训练组(P〈0.05)。②与常氧组比较,其他各组Bcl-2、Bax、Bcl-2/Bax均显著性增高(P〈0.05):常氧训练组Bcl-2、Bax、Bcl-2/Bax表达显著高于低氧8h组,显著低于低氧12h训练组(P〈0.05);低氧12h训练组Bcl-2、Bax、Bcl-2/Bax表达比低氧12h组、低氧8h训练组显著增加(P〈0.05)。提示低氧、低氧训练可诱导大鼠心肌细胞Bcl-2、Bax蛋白表达,运动时低氧刺激与细胞凋亡率、凋亡指数及病理损伤有关,其中以低氧12h后运动训练组最明显,心肌细胞的凋亡调控与Bcl-2和Bax相关。
    • 林喜秀; 周桔; 罗自强; 瞿树林; 赵用强; 邱继旺
    • 摘要: BACKGROUND: During hypoxia training, the body should bear the motor load and stay in the hypoxic environment outside. OBJECTIVE: To observe the effect of hypoxia and hypoxia training on myocardial apoptosis and the expression of Bax and Bcl-2 in rats. METHODS: Sixty Sprague-Dawley rats were randomly divided into six groups: normoxia group, 8 hours hypoxia group, 12 hours hypoxia group, normoxia training group, 8 hours hypoxia training group and 12 hours hypoxia training group, 10 rats in each group. The rats of normoxia training group, 8 hours hypoxia training group and 12 hours hypoxia training group were introduced to treadmil running on an incline of 0° at 25 m/min for 1 hour. After training, the rats of group 8 hours hypoxia group, 8 hours hypoxia training group, 12 hours hypoxia group and 12 hours hypoxia training group were exposed to hypoxic chamber with 12.5% volume fraction of oxygen (equal to altitude 4000 m) for 8 hours and 12 hours every day respectively. The course of the experiment was 4 weeks, 5 days every week. At 24 hours after the final experiment, the rats were treated with intraperitoneal anesthesia of sumianxin Ⅱ to obtain the samples, then hematoxylin-eosin staining, in situ terminal deoxyribonucleotide transferase-mediated dUTP nick end labeling method and protein immunohistochemistry methods were used to detect the myocardial apoptosis and the expression of Bax and Bcl-2 in rats. RESULTS AND CONCLUSION: Compared with the normoxia group, the myocardial apoptosis index was significantly increased in the 24 hours hypoxia group, normoxia training group and hypoxia training group (P <0.05); the myocardial apoptosis index in the 12 hours hypoxia training group was significantly higher than that in the normoxia training group and 8 hours hypoxia training group (P < 0.05). Compared with normoxia group, the expressions of Bcl-2, Bax and Bcl-2/Bax in the other five groups were significantly increased (P < 0.05); the expressions of Bcl-2, Bax and Bcl-2/Bax in normoxia training group were significantly higher than those in the 8 hours hypoxia group, and significantly lower than those in the 12 hours hypoxia group (P < 0.05); the expressions of Bcl-2, Bax and Bcl-2/Bax in the 12 hours hypoxia training group were significantly higher than those in the 12 hours hypoxia group and the 8 hours hypoxia training group (P < 0.05). Hypoxia and hypoxia training could induce the protein expressions of Bcl-2 and Bax in myocardial tissue. Hypoxia training was related with apoptosis rate and apoptotic index and pathological damage, especial y the 12 hours hypoxia training. Bcl-2 and Bax participated in regulating the myocardial apoptosis.%  背景:低氧训练时,机体既要承受运动负荷,同时处于外界的低氧环境,此时,心组织将如何适应其变化?其机制研究国内外较少。目的:观察低氧与低氧训练对大鼠心肌细胞凋亡及 Bax 及 Bcl-2表达的影响。方法:SD 大鼠共60只随机分为6组,常氧组、低氧8 h 组、低氧12 h 组、常氧训练组、低氧8 h 训练组和低氧12 h 训练组,每组10只。后3组大鼠每天在坡度为0的动物跑台上以25 m/min 的速度训练1 h。训练完后,将低氧8 h 组、低氧8 h 训练组和低氧12 h 组、低氧12 h 训练组放入氧体积分数为12.5%(相当于海拔4000 m)的低氧舱内8 h 和12 h。实验期为4周,5 d/周。最后1次实验结束后24 h,大鼠均实施速眠新Ⅱ腹腔麻醉后取材,采用苏木精-伊红染色、原位末端脱氧核糖核苷酸转移酶介导的dUTP 缺口末端标记法及蛋白免疫组织化学法检测各组大鼠心肌细胞凋亡和 Bcl-2、Bax 蛋白表达。结果与结论:①与常氧组相比,低氧12h 组、常氧训练组、低氧训练组心肌细胞凋亡指数均显著增加(P <0.05);低氧12 h 训练组心肌细胞凋亡指数显著多于常氧训练组和低氧8h 训练组(P <0.05)。②与常氧组比较,其他各组 Bcl-2、Bax、Bcl-2/Bax 均显著性增高(P <0.05);常氧训练组 Bcl-2、Bax、Bcl-2/Bax 表达显著高于低氧8 h 组,显著低于低氧12 h 训练组(P <0.05);低氧12 h 训练组 Bcl-2、Bax、Bcl-2/Bax 表达比低氧12 h 组、低氧8 h 训练组显著增加(P <0.05)。提示低氧、低氧训练可诱导大鼠心肌细胞 Bcl-2、Bax 蛋白表达,运动时低氧刺激与细胞凋亡率、凋亡指数及病理损伤有关,其中以低氧12 h 后运动训练组最明显,心肌细胞的凋亡调控与 Bcl-2和 Bax 相关。
    • 韩海燕; 张逸驰; 季淑琼; 梁奇明; 朱遂强; 薛峥
    • 摘要: 背景:抑制小鼠海马脑片整合素活动后,虽然不会影响长时程增强的诱导,但却带来快速的长时程增强衰减,证明整合素对于诱导后长时程增强的维持和稳定起到关键的作用。目的:通过在体电生理技术阐明整合素的β1亚基在活体大鼠的海马CA1区中β淀粉样蛋白抑制长时程增强的过程中所起到的作用。方法:将15只SD大鼠等分为对照组、G淀粉样蛋白组和β1整合素拮抗剂组,分别给予生理盐水,β淀粉样蛋白和β1整合素的选择性拮抗剂,记录自给予β淀粉样蛋白前10min至高频强直刺激后3h时的兴奋性突触后电位。结果与结论:给予对照组大鼠高频强刺激后兴奋性突触后电位明显增强,增幅在30%以上。β淀粉样蛋白组大鼠给予高频强刺激后兴奋性突触后电位在3h中被显著抑制,没有出现明显的变化。而β1整合索拈抗剂组大鼠给予高频强刺激后兴奋性突触后电位又出现明显的增强。推测β1整合素在活体大鼠的海马CA1区中β淀粉样蛋白抑制长时程增强的过程中可能起着重要的介导作用,而其特异性的拮抗剂或抗体可以阻断这种介导作用。
    • 赵亦兵; 黄晓峰
    • 摘要: 背景:小鼠的下颌下腺是研究唾液腺的发育的良好模型,转化生长因子β是器官发育和疾病中重要的生长因子,但是在下颌下腺中转化生长因子β受体的表达以及作用机制至今并不明确。目的:观察胚胎小鼠下颌下腺发育过程中转化生长因子βⅠ型受体和Ⅱ型受体以及p-ERK1/2的表达,揭示转化生长因子β在小鼠涎腺发育中的作用。方法:取C57BL/6J小鼠胚胎期第14.5天的标本,使用转化生长因子βⅠ型受体和Ⅱ型受体以及p-ERK1/2抗体,对小鼠的下颌下腺进行免疫组化染色。取新生小鼠标本,大体观察下颌下腺,并且使用苏木精-伊红染色观察其形态。结果与结论:①小鼠出生时,下颌下腺位于下颌骨下方;苏木精-伊红染色发现小鼠下颌下腺的腺泡、导管和闰管细胞也已经分化完成。②在胚胎期第14.5天,转化生长因子βⅠ型和Ⅱ型受体在腺泡上皮和导管上皮内高表达,而腺体上皮细胞外的间充质没有表达。③p-ERK1/2主要也是表达在下颌下腺的上皮细胞中,与转化生长因子βⅠ型受体和Ⅱ型受体在下颌下腺中的表达基本一致。说明在小鼠下颌下腺的发育过程中,转化生长因子β蛋白可能通过与上皮细胞表面的受体结合,激活ERK信号通路来调节涎腺腺泡和导管的发育。
    • 刘翠芸; 张伟; 刘佩佩; 叶长根; 易珍; 孙水林
    • 摘要: 背景:干扰素α-2a 改善肝纤维化的机制直到目前仍尚未阐明。目的:进一步验证干扰素α-2a 对 CCl4诱导大鼠肝纤维化模型中肝星状细胞凋亡的影响。方法:建立 CCl4诱导肝纤维化模型,健康 SD 雌性大鼠50只,采用随机对照原则将 SD 大鼠分成5组,即生理盐水对照组、纤维化模型组、6×104 U/kg 干扰素α-2a 干预组、12×104 U/kg 干扰素α-2a 干预组及6×104 U/kg 干扰素α-2a 对照组。造模8周时取肝组织标本,分别进行肝纤维化指标检测;RT-PCR分析肝组织 bcl-2、bax 的表达;免疫组织化学染色用 a 平滑肌肌动蛋白对活化的肝星状细胞进行标记。结果与结论:肝组织病理形态显示 CCl4诱导肝纤维化成功建立,表现为纤维化模型组汇管区周围纤维化明显,有芒状纤维和纤维间隔形成,各干扰素α-2a 干预组肝纤维化有不同程度缓解。纤维化模型组有大量 a 平滑肌肌动蛋白阳性表达,6×104 U/kg 干扰素α-2a 干预组 a 平滑肌肌动蛋白阳性表达较纤维化模型组减少,12×104 U/kg 干扰素α-2a 干预组更少,6×104 U/kg 干扰素α-2a 对照组未见 a 平滑肌肌动蛋白阳性表达。结果提示干扰素α-2a 能下调 CCl4诱导肝纤维化 bcl-2的表达,及上调 bax 的表达。提示干扰素α-2a 阻断 CCl4诱导肝纤维化机制存在通过调节 bcl-2、bax 的表达,诱导肝星状细胞凋亡途径,该调节作用可能与干扰素α-2a 剂量相关。%BACKGROUND: Up to now, the mechanism underlying interferon alpha 2a to improve hepatic fibrosis has not been clarified. OBJECTIVE: To investigate the effect of interferon alpha 2a on hepatic stel ate cells apoptosis in the CCl4-induced hepatic fibrosis rat model. METHODS: We established the CCl4-induced hepatic fibrosis models in rats. Fifty healthy female Sprague-Dawley rats were equal y and randomly divided into five groups, certainly each group included 10. Five groups were saline control group, hepatic fibrosis model group (model group), 6×104 U/kg interferon alpha 2a intervention group, 12×104 U/kg interferon alpha 2a intervention group and 6×104 U/kg interferon alpha 2a control group. At 8 weeks after modeling, blood and liver tissues were col ected to detect the indicators of hepatic fibrosis; the expression of bcl-2 and bax in the liver tissue was analyzed with semi-quantitative reverse transcription-PCR; and immunohistochemical staining was used to mark a-smooth muscle actin in activated hepatic stel ate cells. RESULTS AND CONCLUSION: Pathological morphology of the liver tissue demonstrated that the hepatic fibrosis model was successful y established. The model group had fibrosis significantly around the portal area; in addition, Mans-like fibers and fibrous septa formed. Different interferon alpha 2a intervention groups had fibrosis relief to different extent. a-smooth muscle actin had a great amount of positive expression in the model group, while the positive expression of a-smooth muscle actin was lower in the interferon alpha 2a intervention groups, especial y in the 12×104 U/kg interferon alpha 2a intervention group as compared the model group. In addition, there was no expression of a-smooth muscle actin in the 6×104 U/kg interferon alpha 2a control group. Interferon alpha 2a could down-regulate bcl-2 expression and up-regulate bax expression in CCl4-induced hepatic fibrosis models. These findings indicate that the mechanism of interferon alpha 2a blocking CCl4-induced hepatic fibrosis is mainly present by regulating the expression of bcl-2 and bax to induce apoptosis of hepatic stel ate cells, and this regulatory role is possibly related to interferon alpha 2a dose.
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