ライフサイエンスコーパス: RVH

1 RVH also increased myocardial expression of inflammatory

2 RVH and RVH+S had similarly increased arterial pressure

3 RVH was defined using sex-specific normative equations b

4 RVH was induced by pulmonary artery constriction for 36

5 gs were studied after 12 wk: normal (n = 7), RVH (n = 7), or RVH+simvastatin (RVH+S; 80 mg/d; n = 6).

6 s maladaptive RVH is imprecise, but adaptive RVH is associated with better functional capacity and su

7 load and mass some patients develop adaptive RVH (concentric with retained RV function), while others

8 rgic signaling, and metabolism than adaptive RVH, and these derangements often involve the left ventr

9 hese findings indicate that the EF hands and RVH domain act as a functional unit during Ca(2+)-induce

10 this agent did not protect the EF hands and RVH domain from trypsin cleavage.

11 he development of pulmonary hypertension and RVH, and promotes regression of pulmonary arterial neoin

12 oped pulmonary artery medial hypertrophy and RVH, which was normalized by administration of AP-Cav.

13 Neointimal lesions and RVH were similar whether injury preceded pneumonectomy o

14 ssion could affect the development of PH and RVH remains unknown.

15 pulmonary artery medial hypertrophy, PH, and RVH.

16 natal rhIGF-1/BP3 treatment restored RAC and RVH to normal values when compared with placebo injectio

17 RVH and RVH+S had similarly increased arterial pressure and seru

18 me-series analysis was undertaken to compare RVH pre- and post-vaccine introduction using rotavirus-n

19 d antenatal sFlt-1 reduced RAC and decreased RVH in infant rats.

20 r blockade decreased PAP in utero, decreased RVH and distal muscularization of small pulmonary arteri

21 cose oxidation is beneficial in experimental RVH and can be achieved by inhibition of pyruvate dehydr

22 r remodeling and hypertrophy in experimental RVH independent of lipid lowering.

23 (62.9 MBq +/- 40.7) baseline acquisition for RVH and a high activity (303.4 MBq +/- 48.1) acquisition

24 The recommended ECG screening criteria for RVH are not sufficiently sensitive or specific for scree

25 The ECG screening criteria for RVH from the 2009 American Heart Association Recommendat

26 Current ECG criteria for RVH were based on cadaveric dissection in small studies.

27 ific (many >95%) but had low sensitivity for RVH by cMRI.

28 of NMDAR-DeltaCa(2+) signalling in MNCs from RVH rats, partly due to blunted endoplasmic reticulum Ca

29 arger and prolonged DeltaCa(2+) in MNCs from RVH rats.

30 4) had higher mPAP (40 +/- 9 mm Hg), greater RVH, and more severe pulmonary arterial neointimal forma

31 A total of 6% had RVH, which was generally mild.

32 on of images in patients suspected of having RVH or obstruction compared with administration of lower

33 o contains an N-terminal recoverin homology (RVH) domain that is related to the N termini of the reco

34 spected of having renovascular hypertension (RVH) were randomly selected from archived databases and

35 tructure in swine renovascular hypertension (RVH) would be improved by simvastatin treatment.

36 MNCs in sham and renovascular hypertensive (RVH) rats.

37 y cells (MNCs) in renovascular hypertensive (RVH) rats.

38 not in MNCs from renovascular hypertensive (RVH) rats.

39 MNCs of sham and renovascular hypertensive (RVH) rats.

40 ng in right ventricular failure/hypertrophy (RVH) are poorly understood.

41 he ET axis is upregulated in RV hypertrophy (RVH) and that ERAs have direct effects on the RV myocard

42 RV hypertrophy (RVH) triggered by pressure overload is initially compens

43 el density, and right ventricle hypertrophy (RVH).Measurements and Main Results: Antenatal PHi therap

44 rom rats with right ventricular hypertrophy (RVH) and control rats.

45 ficantly less right ventricular hypertrophy (RVH) and pulmonary arterial neointimal formation.

46 changes, and right ventricular hypertrophy (RVH) caused by prolonged closure of the ductus arteriosu

47 criteria for right ventricular hypertrophy (RVH) measured by cardiac magnetic resonance imaging (cMR

48 eloped severe right ventricular hypertrophy (RVH) whereas animals with a medial hypertrophy pattern o

49 density, and right ventricular hypertrophy (RVH).

50 evelop PH and right ventricular hypertrophy (RVH).

51 ibuting in turn to higher firing activity in RVH rats.

52 ed also to higher ongoing firing activity in RVH rats.

53 expression of NMDAR subunits were altered in RVH rats.

54 R1-NR2A-D subunit expression were altered in RVH rats.

55 an upregulation of the myocardial ET axis in RVH.

56 GRK2 interactions has therapeutic benefit in RVH.

57 rats, but this effect was largely blunted in RVH rats.

58 els/cm(2); P < 0.05), which was decreased in RVH+S (72.5 +/- 14.9 vessels/cm(2)), whereas capillary d

59 ition of IA and enhanced MNC excitability in RVH rats.

60 e-1-receptor signaling, which is impaired in RVH.

61 -positive, PVN-RVLM (OT-PVN-RVLM) neurons in RVH rats.

62 ltaCa(2+) responses in sham rats, but not in RVH rats.

63 f sham rats, but this effect was occluded in RVH rats, thus equalizing the magnitude and time course

64 Acute inotropic support in RVH is best accomplished by dobutamine, reflecting its b

65 The enhanced endogenous glutamate tone in RVH rats was not due to blunted glutamate transporter ac

66 ine) versus pulmonary artery banding-induced RVH (PAB-RVH).

67 Maladaptive RVH shares metabolic abnormalities with cancer including

68 Clinically, maladaptive RVH is characterized by increased N-terminal pro-brain n

69 function), while others develop maladaptive RVH, characterized by dilatation, fibrosis, and RV failu

70 In maladaptive RVH there is reduced inotrope responsiveness because of

71 At the molecular level, maladaptive RVH displays greater impairment of angiogenesis, adrener

72 fferentiation of adaptive versus maladaptive RVH is imprecise, but adaptive RVH is associated with be

73 sensitive or specific for screening for mild RVH in adults without clinical cardiovascular disease.

74 of remodeling (MCT only) developed moderate RVH compared with control animals.

75 Compared with normal, RVH showed increased spatial density of microvessels (16

76 and positively correlated with the degree of RVH (RV thickness/body surface area; r(2)=0.838 and r(2)

77 Q 123 treatment prevented the development of RVH as determined by the ratio of the right ventricle/le

78 bated NMDAR-DeltaCa(2+) responses in MNCs of RVH rats affected both somatic and dendritic compartment

79 e in somatodendritic compartments of MNCs of RVH rats, and (2) that a blunted ER Ca(2+) buffering cap

80 s sharply increased in compensating phase of RVH tissues but was lost in decompensation phase of RVH.

81 ng the transition from compensating phase of RVH toward decompensation phase of RVH.

82 sues but was lost in decompensation phase of RVH.

83 phase of RVH toward decompensation phase of RVH.

84 after 12 wk: normal (n = 7), RVH (n = 7), or RVH+simvastatin (RVH+S; 80 mg/d; n = 6).

85 suspected of having obstruction (P = .80) or RVH (P = .24).

86 us pulmonary artery banding-induced RVH (PAB-RVH).

87 In PAH-RVH versus PAB-RVH there was greater downregulation of beta1-, alpha1-

88 m; P<0.001) were lower in PAH-RVH versus PAB-RVH.

89 or downregulation also occurred in human PAH-RVH.

90 ed with pulmonary arterial hypertension (PAH-RVH; SU5416+chronic-hypoxia or Monocrotaline) versus pul

91 In PAH-RVH versus PAB-RVH there was greater downregulation of b

92 s 244.1+/-12.4 m; P<0.001) were lower in PAH-RVH versus PAB-RVH.

93 c receptors impairs inotropic reserve in PAH-RVH.

94 also preserved lung structure and prevented RVH after postnatal hyperoxia.

95 tment preserved lung structure and prevented RVH in antenatal and postnatal BPD models.

96 scular growth and lung function and prevents RVH after intrauterine ETX exposure.

97 proves lung structure and function, prevents RVH, and improves placental structure following antenata

98 function in renovascular hypertensive rats (RVH).

99 drenergic remodeling were compared in rodent RVH associated with pulmonary arterial hypertension (PAH

100 Neointimal lesions and severe RVH developed in these animals but were not seen in anim

101 Despite similar RVH, cardiac output (58.3+/-4.9 versus 82.9+/-4.8 mL/min

102 al (n = 7), RVH (n = 7), or RVH+simvastatin (RVH+S; 80 mg/d; n = 6).

103 Confocal immunohistochemistry showed that RVH myocardial ET type A (but not type B) receptor and E

104 the EF hands protected sites within both the RVH domain and EF hands from trypsin cleavage and increa

105 nt DGK alpha fragment that included both the RVH domain and EF hands.

106 ship (Hill coefficient) was decreased in the RVH group at SL = 2.0 microns (4.3 +/- 0.4 versus 3.1 +/

107 Maximal force was increased in the RVH group: 1.20 +/- 0.10 versus 1.62 +/- 0.13 mg at SL =

108 half-maximal activation was increased in the RVH group: 2.64 +/- 0.13 versus 3.47 +/- 0.22 mumol/L at

109 Maximal tension, however, was reduced in the RVH group: 24.3 +/- 1.91 versus 37.5 +/- 2.92 mN/mm2 at

110 Deletion of the RVH domain resulted in loss of Ca(2+)-dependent activati

111 As with Ca(2+), this activation required the RVH domain.

112 samples, and from rats with normal RV versus RVH attributable to PAH.

113 e effects of ERAs on the RV in patients with RVH and PAH.

114 RV myocardial samples from 34 patients with RVH were compared with 16 nonhypertrophied RV samples, a