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1 sentation of light stimuli before and during hemodynamic stress.
2 imulus-evoked responses were observed during hemodynamic stress.
3 sequential protocol simulating metabolic and hemodynamic stress.
4 ardiac function in response to metabolic and hemodynamic stress.
5 egrin knockout group after acute and chronic hemodynamic stress.
6  role of calpain in the heart in response to hemodynamic stress.
7 d adaptation of the cardiovascular system to hemodynamic stress.
8 d pathway regulating the cardiac response to hemodynamic stress.
9  the risk of aortic dissection by decreasing hemodynamic stress.
10 ession of genes that condition the ER during hemodynamic stress.
11 ts undergoing hypertrophic growth induced by hemodynamic stress.
12 iomyocyte survival in mice with both age and hemodynamic stress.
13 architectural response of the vasculature to hemodynamic stress.
14 diator of cardiac hypertrophy in response to hemodynamic stress.
15 e an important cardiac signaling pathway for hemodynamic stress.
16 rently by mechanisms unique to Ang II and by hemodynamic stress.
17 ngiogenesis, inflammation and in response to hemodynamic stress.
18 efficacy when it undergoes non-physiological hemodynamic stresses.
19 rs or ivabradine, could positively influence hemodynamic stresses.
20 gestive heart failure: changes in perfusion, hemodynamic stresses, alterations in calcium metabolism,
21 pertrophy is a common response to injury and hemodynamic stress and an important harbinger of heart f
22 ckle cell disease (SCD) demonstrate cerebral hemodynamic stress and are at high risk of strokes.
23 rdiac remodeling, systemic inflammation, and hemodynamic stress and how cardiac dysfunction in turn i
24 preserved cardiac function when subjected to hemodynamic stress and neurohormonal excess.
25 pha, the heart cannot respond effectively to hemodynamic stress and rapidly fails.
26 ward S1P protecting EC from activation under hemodynamic stress and refraining coronary atheroscleros
27 yocardial phospholipid remodeling induced by hemodynamic stress and reveal novel links between this p
28             The interaction of biomarkers of hemodynamic stress and the effects of ranolazine warrant
29    We demonstrate that PO-HF is triggered by hemodynamic stress and then sets off an autoimmune-like
30 -directional velocity encoding for assessing hemodynamic stresses and corresponding blood damage inde
31 and serum biomarkers of collagen metabolism, hemodynamic stress, and myocardial injury to evaluate su
32  and serum biomarkers of collagen synthesis, hemodynamic stress, and myocardial injury were also avai
33 The complexity of the cellular interactions, hemodynamic stresses, and electrical circuitry within th
34                  Physical forces of gravity, hemodynamic stresses, and movement play a critical role
35 urin inhibition by MCIP1 under conditions of hemodynamic stress are unknown.
36 e in HFpEF but not controls, suggesting that hemodynamic stresses beyond passive stiffness and increa
37 bility of the elastic vessel wall to sustain hemodynamic stress by disrupting microfibrillar assembly
38                                       During hemodynamic stress, catecholamines and neurohumoral stim
39                                Because acute hemodynamic stress caused by intravenous infusion of sod
40  that CRF-mediated increases in LC-NE due to hemodynamic stress disrupts the transmission of informat
41                      The aorta is exposed to hemodynamic stress during exercise, but whether or not t
42                                              Hemodynamic stress during hemodialysis (HD) results in r
43 kinase expression both at baseline and after hemodynamic stress; focal adhesion kinase expression was
44 ific inhibition of SGK1 protected mice after hemodynamic stress from fibrosis, heart failure, and sod
45 ble for medial remodeling, and resolves once hemodynamic stresses have normalized without obvious int
46 tivity by physiological manipulations (i.e., hemodynamic stress, hypovolumia) remains unclear.
47 n HF through increased sympathetic activity, hemodynamic stress, hypoxemia, and oxidative stress.
48 markers of subclinical myocardial injury and hemodynamic stress identify asymptomatic individuals wit
49 tion; 3) increased mortality following acute hemodynamic stress imposed by transverse aortic constric
50 homeostatic arterial remodeling triggered by hemodynamic stress in mice and possibly in humans as wel
51 ere, we showed that NOGO-B is upregulated by hemodynamic stress in myocardial EC of ApoE(-/-) mice an
52 derlies the impact of sleep abnormalities on hemodynamic stress in patients with HF.
53 hosphorylation of Bcl-xL is also promoted by hemodynamic stress in the heart, through the H-Ras-ERK p
54 wth and cardiac functional maintenance under hemodynamic stress in vivo.
55 transverse aortic constriction as a model of hemodynamic stress in wild-type and cardiomyocyte-restri
56 or by responding to its local environment of hemodynamic stresses, in particular, shear stress.
57                 These data demonstrated that hemodynamic stress induced a protective rewiring of sphi
58                         We demonstrated that hemodynamic stress induced an early metabolic rewiring t
59                                 Hormone- and hemodynamic stress-induced GRK5 regulation may provide a
60 l that chronic upregulation of the HBP under hemodynamic stress induces pathological cardiac hypertro
61 Intima-media thickening (IMT) in response to hemodynamic stress is a physiological process that requi
62 perative management with goals of decreasing hemodynamic stress is important in patients with ischemi
63                                              Hemodynamic stress is thought to play an important role
64 sfunction, microvascular dysfunction, and/or hemodynamic stress (median [IQR] values: C-terminal proe
65 biomarkers of subclinical cardiac injury and hemodynamic stress modify the association of LVH with ad
66                     We hypothesized that the hemodynamic stress of increased arterial pressure could
67 ese individuals may be very sensitive to the hemodynamic stress of increased effective blood volume,
68                       Superimposition of the hemodynamic stress of pressure overload on G alpha q ove
69                                              Hemodynamic stress on the mammalian heart results in com
70 egulation of RAS genes is a direct effect of hemodynamic stress or is secondary to neurohumoral effec
71  have evidence of ongoing myocardial injury, hemodynamic stress, or systemic inflammation.
72 t (p 0.03) or biomarkers of inflammation and hemodynamic stress (p < 0.001) and was similar among Whi
73 sfunction, microvascular dysfunction, and/or hemodynamic stress provided modest discrimination in ear
74 at myosin heavy chain composition depends on hemodynamic stress rather than on FGF2 or hypertrophy, a
75 -CMs survival under physiologically relevant hemodynamic stress requires gradual imposition of mechan
76          Hemodialysis (HD) treatment-related hemodynamic stress results in recurrent ischemic injury
77 at protein aggregation occurs in response to hemodynamic stress, situating pressure-overload heart di
78 ndicate that calpain protects the heart from hemodynamic stresses, such as pressure overload.
79 ures with exercise as measured with invasive hemodynamic stress testing or estimated with Doppler ech
80 DM, and MR-proANP are emerging biomarkers of hemodynamic stress that have been associated with advers
81 complications, particularly with the altered hemodynamic stresses that LT patients face in the immedi
82 fferences between the RV and LV responses to hemodynamic stress, the unique stressors on the RV assoc
83      Vascular remodeling normalizes abnormal hemodynamic stresses through structural changes affectin
84                        We quantified cardiac hemodynamic stress using B-type natriuretic peptide (BNP
85                                              Hemodynamic stress via hypotensive challenge has been sh
86 ate the effects of a physiological stressor [hemodynamic stress via sodium nitroprusside (SNP) i.v.]
87                                Intradialytic hemodynamic stress was quantified using the extrema poin
88         Saphenous vein grafts are exposed to hemodynamic stress when interposed in the arterial circu
89 ta support the value of combining markers of hemodynamic stress with traditional approaches to risk a