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991.
Giles S. Porter 《The Western journal of medicine》1931,34(5):391-407
992.
Giles S. Porter 《The Western journal of medicine》1931,34(4):319-334
993.
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996.
Giles S. Porter 《The Western journal of medicine》1932,36(5):373-374
997.
George M. Giles 《BMJ (Clinical research ed.)》1900,1(2043):485-487
998.
Mulligan C Rochford J Denyer G Stephens R Yeo G Freeman T Siddle K O'Rahilly S 《The Journal of biological chemistry》2002,277(45):42480-42487
999.
Kelvin KL Wong Pongpat Thavornpattanapong Sherman CP Cheung Zhonghua Sun Jiyuan Tu 《BMC cardiovascular disorders》2012,12(1):1-18
Background
This study characterizes the distribution and components of plaque structure by presenting a three-dimensional blood-vessel modelling with the aim of determining mechanical properties due to the effect of lipid core and calcification within a plaque. Numerical simulation has been used to answer how cap thickness and calcium distribution in lipids influence the biomechanical stress on the plaque.Method
Modelling atherosclerotic plaque based on structural analysis confirms the rationale for plaque mechanical examination and the feasibility of our simulation model. Meaningful validation of predictions from modelled atherosclerotic plaque model typically requires examination of bona fide atherosclerotic lesions. To analyze a more accurate plaque rupture, fluid-structure interaction is applied to three-dimensional blood-vessel carotid bifurcation modelling. A patient-specific pressure variation is applied onto the plaque to influence its vulnerability.Results
Modelling of the human atherosclerotic artery with varying degrees of lipid core elasticity, fibrous cap thickness and calcification gap, which is defined as the distance between the fibrous cap and calcification agglomerate, form the basis of our rupture analysis. Finite element analysis shows that the calcification gap should be conservatively smaller than its threshold to maintain plaque stability. The results add new mechanistic insights and methodologically sound data to investigate plaque rupture mechanics.Conclusion
Structural analysis using a three-dimensional calcified model represents a more realistic simulation of late-stage atherosclerotic plaque. We also demonstrate that increases of calcium content that is coupled with a decrease in lipid core volume can stabilize plaque structurally. 相似文献1000.
Pyruvate kinase is one of the enzymes which can be phosphorylated by stimulation of the cell with either glucagon or Ca2+-linked hormones. Whether these two classes of hormones phosphorylate the same site on the enzyme is unclear. Our results demonstrate that isolation of [32P]phosphorylated type-L pyruvate kinase from glucagon-treated hepatocytes followed by aspartyl-prolyl cleavage yields a [32P]phosphorylated peptide of Mr 17,000. This fragment is also phosphorylated in response to the Ca2+-mediated agonist phenylephrine. 相似文献