Experimental Study on Fatigue Phenomenon of the Anterior Cruciate Ligament by Excessive Exercise

过度运动引起前十字韧带疲劳现象的实验研究

基本信息

  • 批准号:
    03670707
  • 负责人:
  • 金额:
    $ 1.47万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
  • 财政年份:
    1991
  • 资助国家:
    日本
  • 起止时间:
    1991 至 1993
  • 项目状态:
    已结题

项目摘要

1.The effect of enforced exercise on biomechanical properties and morphological characteristis of the anterior cruciate ligament(ACL) of bipedal rats was examined. The bipedal rats were forced to run on a motor-driven treadmill at 20 degrees decline and at a speed of 20 m/min for 30 min on each of six consecutive days during the four-week period. Strength results for bipedal rats with exercise (E(+)G) were significantly lower than those for bipedal rats without exercise(E(-)G)at the loading rates 8.3mm/sec and 1*10^3 mm/sec. A load relaxation test showed a larger load-relaxation phenomenon in E(-)G than in E(+)G.The viscosity of the ACL was higher in E(+)G than in E(-)G.In E(+)G,eighty-one percent of the fibroblasts in the ACL were spindle-shaped with indented nucleus. There was an increased number of rough surfaced endoplasmic reticula and lysosomal vesicles in the fibroblasts of E(+)G.The collagen fibril diameters of E(+)G varied in size from 20 to 120 nm. The mean collagen fibril diameter of E(+)G was significantly lower than that of E(-)G.2.The effect of basic Fibroblast Growth Factor(bFGF) on the repair of full-thickness articular cartilage defects was studied. The smaller full-thickness defects(* 3 mm in diameter in adolescent rabbits) are repaired spontaneously, but the larger defects cannot be repaired with cartilage. The administration of bFGF (0.05ng/h) for two weeks elicited the differentiation from mesenchymal cells to chondrocytes in the 5 mm full-thickness defects in the femoral trochlea of adolescent rabbits. Within eight weeks, the defects showed almost complete recovery of epiphyseal morphology. On the other hand, the administration of neutralizing antibody to bFGF (50 ng/h) for two weeks inhibited chondrogenic differentiation in the center of the 3 mm full-thickness defects.
1.研究了强运动对双足大鼠前交叉韧带(ACL)生物力学特性和形态特征的影响。在4周内连续6天,强迫双足大鼠在电机驱动的跑步机上以20度下倾、20米/分钟的速度跑步30分钟。在8.3mm/sec和1*10^3 mm/sec加载速率下,运动两足大鼠的强度结果(E(+)G)显著低于未运动两足大鼠(E(-)G)。载荷松弛试验表明,E(-)G的载荷松弛现象大于E(+)G。E(+)G时ACL的黏度高于E(-)G时。在E(+)G中,81%的前交叉韧带成纤维细胞呈梭形,细胞核凹陷。E(+)G成纤维细胞表面粗糙的内质网和溶酶体囊泡增多。E(+)G的胶原原纤维直径在20 ~ 120nm之间。E(+)G的平均胶原纤维直径显著低于E(-)G。研究碱性成纤维细胞生长因子(bFGF)在全层关节软骨缺损修复中的作用。小的全层缺损(青春期家兔直径* 3mm)可自行修复,大的缺损不能用软骨修复。bFGF (0.05ng/h)连续2周诱导青春期兔股滑车5 mm全层缺损从间充质细胞向软骨细胞分化。在8周内,缺损的骨骺形态几乎完全恢复。另一方面,给予bFGF中和抗体(50 ng/h)两周,可抑制3 mm全层缺损中心的软骨分化。

项目成果

期刊论文数量(5)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Katsuhiko Sakuma, Hiroshi Mizuta, Katsumasa Takagi and Kazuki Takashima: "Effects of Enforced Exercise on Biomechanical Properties of the Anterior Cruciate Ligament of Bipedal Rats" The Journal of the Japanese Orthopaedic Association. 66-11. 1146-1155 (19
Katsuhiko Sakuma、Hiroshi Mizuta、Katsumasa Takagi 和 Kazuki Takashima:“强制运动对双足大鼠前十字韧带生物力学特性的影响”日本骨科协会杂志。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Katsuhiko Sakuma, Hiroshi Mizuta, and Katsumasa Takagi: "Ultrastructural Changes of Collagen Fibers in the Anterior Cruciate Ligament of Bipedal Rats after Enforced Rnning" The Journal of the Japanese Orthopaedic Association. 67-7. 655-661 (1993)
Katsuhiko Sakuma、Hiroshi Mizuta 和 Katsumasa Takagi:“强制跑步后双足大鼠前十字韧带胶原纤维的超微结构变化”日本骨科协会杂志。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Katsuhiko Sakuma.Hiroshi Mizuta,Katsumasa Takagi and Kazuki Takashima: "Effects of Enforced Exercise on Biomechanical Properties of the Anterior Cruciate Ligament of Bipedal Rats" The Journal of the Japanese Orthopaedi Association. 66. 1146-1155 (1992)
Katsuhiko Sakuma.Hiroshi Mizuta、Katsumasa Takagi 和 Kazuki Takashima:“强制运动对双足大鼠前十字韧带生物力学特性的影响”日本骨科协会杂志。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Katsuhiko Sakuma.Hiroshi Mizuta and Katsumasa Takagi: "Ultrastructural Changes of Collagen Fibers in the Anterior Cruciate Ligament of Bipedal Rats after Enforced Running" The Journal of Japanese Orthopaedic Association. 67. 655-661 (1993)
Katsuhiko Sakuma.Hiroshi Mizuta 和 Katsumasa Takagi:“强制跑步后双足大鼠前十字韧带胶原纤维的超微结构变化”日本骨科协会杂志。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Katsuhiko Sakuma: "Effects of Enforced Exercise on Biomechanical Properties of the Arterior Cruciate digament of Bipedal Rats" Journal of the Japanese Orthopaedic Association. 66. 1146-1155 (1992)
Katsuhiko Sakuma:“强制运动对双足大鼠前十字韧带生物力学特性的影响”日本骨科协会杂志。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ monograph.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ sciAawards.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ conferencePapers.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ patent.updateTime }}

MIZUTA Hiroshi其他文献

MIZUTA Hiroshi的其他文献

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

{{ truncateString('MIZUTA Hiroshi', 18)}}的其他基金

Development of a novel therapy targeting the unfolded protein response in osteoarthritis
开发针对骨关节炎中未折叠蛋白反应的新疗法
  • 批准号:
    17K11013
  • 财政年份:
    2017
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Functional analysis of endoplasmic reticulum stress in the progression of cartilage degeneration
内质网应激在软骨退变进展中的功能分析
  • 批准号:
    23592219
  • 财政年份:
    2011
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Development of atom-scale design and characterization technique towards single-dopant controlled silicon nanoelectronics
单掺杂控制硅纳米电子学的原子级设计和表征技术的发展
  • 批准号:
    22310085
  • 财政年份:
    2010
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Pathogenesis and pathological role of endoplasmic reticulum stress in cartilage degeneration
内质网应激在软骨退变中的发病机制及病理作用
  • 批准号:
    20591784
  • 财政年份:
    2008
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Highly-functional hybrid silicon single-electron devices inccoporating nanoelectromechanical structures
结合纳米机电结构的高功能杂化硅单电子器件
  • 批准号:
    18310097
  • 财政年份:
    2006
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Analyses of induction of autophagic response related to the chondrocyte cell-death in osteroarthritis.
与骨关节炎软骨细胞死亡相关的自噬反应诱导分析。
  • 批准号:
    18591667
  • 财政年份:
    2006
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Multi-scale design and analysis for developing 1-nm-scale neosilicon quantum information devices
开发1纳米级新硅量子信息器件的多尺度设计与分析
  • 批准号:
    16310097
  • 财政年份:
    2004
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
An investigation on the effect of FGF-2 for the induction of chondrogenesis in full-thickness articular cartilage defects.
FGF-2 对全层关节软骨缺损诱导软骨形成作用的研究。
  • 批准号:
    12671426
  • 财政年份:
    2000
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Elucidation of the mechanism of TGF-βsignaling in the repair process of full-thickness defects of rat articular cartilage.
阐明TGF-β信号在大鼠关节软骨全层缺损修复过程中的作用机制。
  • 批准号:
    10671368
  • 财政年份:
    1998
  • 资助金额:
    $ 1.47万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了