排序方式: 共有4条查询结果,搜索用时 0 毫秒
1
1.
Mechanical and physiological processes contribute to joint tissue adaptations during growth and exercise and after injury. Those adaptations are often in response to the mechanotransductive stimuli linked to the transmission of forces across these load-bearing structures. Muscle-tendon interactions have been explored during skeletal loading and describe the relation of sarcomere shortening at the expense of tendon lengthening(1,2). The effects of load transmission through the bone-tendon and bone-ligament complexes, however, have not been studied as extensively, although both disuse and exercise will alter the stiffness of these significant structures. Recently, however, renewed interest has emerged about the pathogenesis underlying enthesopathies and enthesitis, and investigators are beginning to reveal the intricacies of bone-tendon and bone-ligament complexes(3,4,5). Here, we summarize the structure and function of the types of entheses between bone-tendon and bone-ligament, and relate how mechanical loading leads to functional adaptation, and at times, entheseal pathophysiology. 相似文献
2.
Zhuo Li Gengshu Wu Roger B. Sher Zohreh Khavandgar Martin Hermansson Gregory A. Cox Michael R. Doschak Monzur Murshed Frank Beier Dennis E. Vance 《Biochimica et Biophysica Acta (BBA)/General Subjects》2014
Background
Choline kinase has three isoforms encoded by the genes Chka and Chkb. Inactivation of Chka in mice results in embryonic lethality, whereas Chkb−/− mice display neonatal forelimb bone deformations.Methods
To understand the mechanisms underlying the bone deformations, we compared the biology and biochemistry of bone formation from embryonic to young adult wild-type (WT) and Chkb−/− mice.Results
The deformations are specific to the radius and ulna during the late embryonic stage. The radius and ulna of Chkb−/− mice display expanded hypertrophic zones, unorganized proliferative columns in their growth plates, and delayed formation of primary ossification centers. The differentiation of chondrocytes of Chkb−/− mice was impaired, as was chondrocyte proliferation and expression of matrix metalloproteinases 9 and 13. In chondrocytes from Chkb−/− mice, phosphatidylcholine was slightly lower than in WT mice whereas the amount of phosphocholine was decreased by approximately 75%. In addition, the radius and ulna from Chkb−/− mice contained fewer osteoclasts along the cartilage/bone interface.Conclusions
Chkb has a critical role in the normal embryogenic formation of the radius and ulna in mice.General Significance
Our data indicate that choline kinase beta plays an important role in endochondral bone formation by modulating growth plate physiology. 相似文献3.
Remesz Ross Khurelbaatar Tsolmonbaatar Grotski Miranda Popowics Tracy Rafferty Katherine Herring Susan W. Addison Owen Doschak Michael R. Romanyk Dan L. 《Biomechanics and modeling in mechanobiology》2022,21(4):1251-1265
Biomechanics and Modeling in Mechanobiology - Cranial sutures are complex soft tissue structures whose mechanics are often studied due to their link with bone growth in the skull. Researchers will... 相似文献
4.
Pan W Borovac J Spicer Z Hoenderop JG Bindels RJ Shull GE Doschak MR Cordat E Alexander RT 《American journal of physiology. Renal physiology》2012,302(8):F943-F956
Passive paracellular proximal tubular (PT) and intestinal calcium (Ca(2+)) fluxes have been linked to active sodium (re)absorption. Although the epithelial sodium/proton exchanger, NHE3, mediates apical sodium entry at both these sites, its role in Ca(2+) homeostasis remains unclear. We, therefore, set out to determine whether NHE3 is necessary for Ca(2+) (re)absorption from these epithelia by comparing Ca(2+) handling between wild-type and NHE3(-/-) mice. Serum Ca(2+) and plasma parathyroid hormone levels were not different between groups. However, NHE3(-/-) mice had increased serum 1,25-dihydroxyvitamin D(3). The fractional excretion of Ca(2+) was also elevated in NHE3(-/-) mice. Paracellular Ca(2+) flux across confluent monolayers of a PT cell culture model was increased by an osmotic gradient equivalent to that generated by NHE3 across the PT in vivo and by overexpression of NHE3.( 45)Ca(2+) uptake after oral gavage and flux studies in Ussing chambers across duodenum of wild-type and NHE3(-/-) mice confirmed decreased Ca(2+) absorption in NHE3(-/-) mice compared with wild-type mice. Consistent with this, intestinal calbindin-D(9K), claudin-2, and claudin-15 mRNA expression was decreased. Microcomputed tomography analysis revealed a perturbation in bone mineralization. NHE3(-/-) mice had both decreased cortical bone mineral density and trabecular bone mass. Our results demonstrate significant alterations of Ca(2+) homeostasis in NHE3(-/-) mice and provide a molecular link between Na(+) and Ca(2+) (re)absorption. 相似文献
1