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1 l calcium required for myocyte apoptosis and myocardial failure.
2 ular hypertrophy followed by a transition to myocardial failure.
3 N apoptosis may serve as biologic markers of myocardial failure.
4 rity, and rescue animals from sepsis-induced myocardial failure.
5 ons for the pathophysiology and treatment of myocardial failure.
6 as been implicated in the pathophysiology of myocardial failure.
7 yocytes may contribute to the progression of myocardial failure.
8  were independent risk factors for death and myocardial failure.
9 ons of segmental function that precede overt myocardial failure.
10  significantly increased in individuals with myocardial failure, a condition associated with increase
11 mmunodeficiency virus infection, septicemia, myocardial failure, atherosclerosis, metabolic disorders
12 ase (CAD) who died suddenly, 32% who died of myocardial failure, but in non-CAD patients, they were p
13 a may contribute to ventricular dilation and myocardial failure by promoting the remodeling of inters
14                                              Myocardial failure caused 66 of 107 complication-related
15 nts) with SD and 40% (6 of 15 patients) with myocardial failure did not have the MI diagnosed during
16 MI was classified as "sudden unexpected" or "myocardial failure" from clinical information only, the
17                                              Myocardial failure has a central role in the complex pat
18                                              Myocardial failure has been considered to be an irrevers
19                    Specific treatment of the myocardial failure has been hampered by the lack of unde
20 he mechanisms by which interleukin 6 induces myocardial failure in meningococcal sepsis and to identi
21                                              Myocardial failure is an important problem after heart t
22                                              Myocardial failure is associated with adverse remodeling
23                                              Myocardial failure is influenced by an altered myeloid c
24 n from compensatory concentric remodeling to myocardial failure is not completely understood in human
25                                              Myocardial failure, leading to inotrope-unresponsive sho
26 e overloading may eventually decompensate to myocardial failure, mechanisms responsible for this tran
27  involved children who died from intractable myocardial failure preceded by a metabolic acidosis, lip
28                                           In myocardial failure this alteration in gene expression of
29 AR function contribute to the development of myocardial failure, transgenic mice with cardiac-restric
30                                        Early myocardial failure was a potential contributor to the co
31 t in the intrinsic defect(s) responsible for myocardial failure will likely translate into important