2007 CARTILAGE BIOLOGY & PATHOLOGY GORDON RESEARCH CONFERENCE
2007 CARTILAGE BIOLOGY & PATHOLOGY GORDON RESEARCH CONFERENCE
批准号:
7386300
负责人:
HENRY M. KRONENBERG
金额:
$0.3万
依托单位国家:
美国
项目类别:
财政年份:
2006
资助国家:
美国
项目状态:
已结题
起止时间:
2006-09-15 至 2007-08-31
关键词:
AdultAgeAttentionBiochemistryBiologyBiomechanicsCartilageChondrocytesDataDegenerative polyarthritisDevelopmentDiagnosisElasticityEnsureEventEvolutionFaceGene ExpressionGenetic Predisposition to DiseaseHandHuman GeneticsHuman PathologyHypertrophyJointsLeftMechanicsMetabolicMinorityModelingMolecularMolecular and Cellular BiologyOccupationalOperative Surgical ProceduresOrganismOrthopedicsOsteoarthrosis DeformansPathogenesisPathologyPharmaceutical PreparationsPhasePrevention therapyPropertyReplacement ArthroplastyResearchRiskScientistSeminalSenior ScientistShapesSkeletal DevelopmentSkeletonStagingTimeTissue EngineeringTissuesTodayTransgenic AnimalsWomancell typeinterestprogramsskeletal disordersymposiumtissue culture
中文摘要
全世界越来越多的兴趣和魅力,其中软骨研究正在接受今天不得不做
具有软骨的两个方面:一方面,软骨是一种生物力学性能突出的永久性组织,
在成人生物体中的特性,提供关节弹性和高机械稳定性,并确保
迁移率另一方面,软骨作为一种暂时性组织在进化中进化,形成了一种模型,
骷髅骨关节炎(OA)和其他退行性关节疾病并不是随着年龄增长而不可避免的命运。
几十年的研究已经显示了大量的证据,遗传易感性和环境或
患骨关节炎的职业风险。尽管如此,在认识上仍然进展不足
OA的发病机制,包括软骨破坏和关节重塑的机制。结果是
在早期阶段,用于预防、治疗和诊断OA的药物开发进展缓慢,
关节置换手术是晚期的最终治疗方法。
由于认识到OA软骨中的变性和重塑事件反映了骨关节炎的变化,
关节软骨细胞的分化、基因表达和代谢活性,该细胞的生物学特性,
类型已经成为研究的焦点。我们在认识人类社会问题上的重大进展
骨关节炎关节中的软骨变性、肥大和重塑来自于使用
组织培养和转基因动物。强有力的证据表明,
这些事件与调节软骨细胞分化、成熟和
骨骼发育中的软骨内骨化这种调节现象的重叠是一种主要的
前两次戈登软骨生物学会议的基本原理。这两个非常成功的会议,
软骨生物学首次将骨骼发育,生物化学,
软骨生物力学,细胞和分子生物学,软骨病理学,人类遗传学,
骨骼疾病、矫形研究和组织工程。
在制定第三次会议的计划时,特别注意为年轻人提供
科学家和少数民族有机会展示和讨论他们的新数据。但也有人认为,
如果没有领导人的开创性和高度激励性的贡献,
这一领域的资深科学家,他们在塑造这一领域的形式和科学水平方面发挥了重要作用,
以前的会议。特别注意确保会议充分利用
大量女科学家担任发言人和会议主席。
英文摘要
Worldwide increasing interest and the fascination which cartilage research is receiving today has to do
with the two faces of cartilage: On the one hand, cartilage is a permanent tissue of outstanding biomechanical
properties in the adult organism, providing joints with elasticity and high mechanical stability and ensuring
mobility. On the other hand, cartilage has evolved in evolution as a transient tissue, shaping a model of the
skeleton. Osteoarthritis (OA) and other degenerative joint diseases are not an inevitable fate coming with age.
Several decades of research have shown ample evidence for genetic predisposition and for environmental or
occupational risk for developing osteoarthritis. Nevertheless, there is still insufficient progress in understanding
the pathogenesis of OA, including mechanisms of cartilage destruction and joint remodeling. As a result, there
is only slow progress in the development of medication for prevention, therapy and diagnosis of OA in early
phases, leaving joint replacement operations as the final therapy in late stages.
With the recognition that degeneration and remodeling events in OA cartilage reflect changes in
differentiation, gene expression and metabolic activities of the articular chondrocyte, the biology of this cell
type has been moving to the center of research focus. Major progress in our understanding problems of
cartilage degeneration, hypertrophy and remodeling in osteoarthritic joints has come from basic studies using
tissue culture and transgenic animals. Strong evidence shows that the molecular mechanisms responsible for
these events are very similar to mechanisms regulating chondrocyte differentiation, maturation and
endochondral ossification in skeletal development This overlap of regulatory phenomena was a major
rationale for the first two Gordon Conferences on cartilage biology. These two very successful conferences on
cartilage biology brought together, for the first time, the fields of skeletal development, biochemistry,
biomechanics, cell- and molecular biology of cartilage with the fields of cartilage pathology, human genetics of
skeletal disorders, orthopedic research and tissue engineering.
In setting up the program for the third conference, special attention is being paid to offer young
scientists and minorities the chance to present and discuss their new data. But it was also felt that the
conference would not be successful without the seminal and highly motivating contributions of the leading
senior scientists in this field who had been instrumental in shaping the format and scientific level of the
previous conferences. Special attention has been given to assure that the meeting takes full advantage of
substantial representation of woman scientists as speakers and session chairs.
期刊论文(0)
专著(0)
科研奖励(0)
会议论文
The role of osteoblast progenitors in response to bone anabolic agents
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依托单位:
PTH actions on early cells of the osteoblast lineage
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资助金额:$40.85万
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负责人:HENRY M. KRONENBERG
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依托单位:
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批准号:10451721
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项目类别:
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资助金额:$31.87万
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负责人:HENRY M. KRONENBERG
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依托单位:
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批准号:10183170
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项目类别:
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资助金额:$31.87万
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财政年份:2019
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负责人:HENRY M. KRONENBERG
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依托单位:
Administrative Core
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批准号:10626807
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项目类别:
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资助金额:$31.87万
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财政年份:2019
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负责人:HENRY M. KRONENBERG
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依托单位:
CENTER FOR SKELETAL RESEARCH
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批准号:9285601
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项目类别:
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资助金额:$69.6万
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依托单位:
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批准号:8853820
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项目类别:
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资助金额:$69.6万
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财政年份:2014
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负责人:HENRY M. KRONENBERG
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依托单位:
CENTER FOR SKELETAL RESEARCH
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批准号:8693238
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项目类别:
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资助金额:$69.6万
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财政年份:2014
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依托单位:
Genetic Analysis of Second Messengers in PTH Signaling in Bone
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批准号:7627067
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项目类别:
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依托单位:
Functions of PTH/PHTrP Receptor, PTHrP and PTH in vivo
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批准号:7432428
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项目类别:
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资助金额:$39.9万
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负责人:HENRY M. KRONENBERG
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依托单位:
Role of PLC in PTH Signaling: Mutant Receptors in Vivo
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批准号:7325709
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项目类别:
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资助金额:$30.68万
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负责人:HENRY M. KRONENBERG
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依托单位:
2007 CARTILAGE BIOLOGY & PATHOLOGY GORDON RESEARCH CONFERENCE
-
批准号:7218758
-
项目类别:
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资助金额:$1.2万
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财政年份:2006
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负责人:HENRY M. KRONENBERG
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依托单位:
Specialized Center for Cell Based Therapy
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资助金额:$210.08万
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财政年份:2005
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负责人:HENRY M. KRONENBERG
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依托单位:
Functions of PTH/PHTrP Receptor, PTHrP and PTH in vivo
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批准号:6946563
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项目类别:
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资助金额:$41.35万
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财政年份:2005
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依托单位:
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Role of PLC in PTH Signaling: Mutant Receptors in Vivo
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资助金额:$30.78万
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财政年份:2005
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依托单位:
Specialized Center for Cell Based Therapy
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批准号:7282059
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项目类别:
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资助金额:$218.94万
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财政年份:2005
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依托单位:
Role of PLC in PTH Signaling: Mutant Receptors in Vivo
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批准号:7062733
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项目类别:
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资助金额:$31.54万
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财政年份:2004
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依托单位:
Role of PLC in PTH Signaling: Mutant Receptors in Vivo
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批准号:6744652
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项目类别:
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资助金额:$31.84万
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财政年份:2003
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负责人:HENRY M. KRONENBERG
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依托单位:
OSTEOBLAST SPECIFIC ABLATION OF THE PTH/PTHRP RECEPTOR
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批准号:6660896
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项目类别:
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资助金额:$28.21万
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财政年份:2002
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负责人:HENRY M. KRONENBERG
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依托单位:
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