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6 tnatal Wt1(Cre);Alk3(fl/fl) specimens showed myxomatous changes in the leaflets of the mitral valve.
7 lapse of the anterior leaflet, the degree of myxomatous changes in the MV, lack of mitral annuloplast
9 ovel, genetically engineered murine model of myxomatous changes of the mitral valve and provide criti
11 and more extensible than normal valves, and myxomatous chordae are more mechanically compromised tha
13 Fibro-elastic deficiency (FED) and diffuse myxomatous degeneration (DMD) are phenotypes of degenera
16 mediate extracellular matrix degradation in myxomatous degeneration by excessive secretion of catabo
17 titial cells in 14 mitral valves removed for myxomatous degeneration from patients with mitral regurg
18 ibited morphological changes consistent with myxomatous degeneration in the walls of knockout hearts.
21 Little is known about the pathophysiology of myxomatous degeneration of the mitral valve, the patholo
22 c examination of excised allografts revealed myxomatous degeneration without immunologic reaction.
25 show that FED and DMD, although both labeled myxomatous, display considerable physiological phenotypi
26 nts, myxomatous in 19, combined ischemic and myxomatous in 16, rheumatic in 5, infective in 3, and un
27 the MV disease was ischemic in 33 patients, myxomatous in 19, combined ischemic and myxomatous in 16
30 ral valve prolapse (MVP) is characterized by myxomatous leaflets and left ventricular (LV) fibrosis o
31 United States and Europe, and progression of myxomatous mitral prolapse is the most common cause of m
32 itral regurgitation (9.98 +/- 155 cm(2)) and myxomatous mitral regurgitation annuli (13.29 +/- 3.05 c
35 4 years; 67% men) with grade III+ or greater myxomatous mitral regurgitation who underwent exercise e
36 In both ischemic mitral regurgitation and myxomatous mitral regurgitation, annular dynamics and an
42 o define the cellular mechanisms involved in myxomatous mitral valve disease and calcific aortic valv
43 ls undergo dramatic changes in the course of myxomatous mitral valve disease in both dogs and humans.
48 receptor, and osteocalcin were increased in myxomatous mitral valves by protein and gene expression
49 rganization in healthy and lesional areas of myxomatous mitral valves of dogs, using synchrotron smal
50 acellular matrix of normal mitral valves and myxomatous mitral valves with either unileaflet prolapse
56 ted soft tissue (including edema, mucin, and myxomatous tissue) have typical MR imaging properties, a
57 itral valve was acquired in 32 patients with myxomatous valve disease (MVD) and moderate to severe re
58 cumulation of proteoglycans is a hallmark of myxomatous valve disease, based on these data we hypothe
63 tin, but not alpha-actin or desmin, cells in myxomatous valves contained both vimentin and alpha-acti
68 that glycosaminoglycans (GAGs) accumulate in myxomatous valves, previous biochemical analyses have no
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