ライフサイエンスコーパス: cardiac function

1 increased expression of proteins involved in cardiac function.

2 concentration of ISO (1 x 10(-5) M) rescued cardiac function.

3 etic variants in different key regulators of cardiac function.

4 cardiac hypertrophy and fibrosis and rescued cardiac function.

5 ardiac hypertrophy and fibrosis and improves cardiac function.

6 P and HEY2) and others with as yet undefined cardiac function.

7 and improves diaphragm, skeletal muscle and cardiac function.

8 studying the genetics underpinning mammalian cardiac function.

9 erexpression delayed and limited the loss of cardiac function.

10 in Hsd11b2(-/-) fetuses, suggesting impaired cardiac function.

11 ed stem cells compromises the improvement in cardiac function.

12 d highlights the importance of enhancers for cardiac function.

13 imal models we have found adverse effects on cardiac function.

14 xpression), less cardiac fibrosis and better cardiac function.

15 ration and leads to a sustained reduction of cardiac function.

16 ompanied by a rapid, progressive decrease in cardiac function.

17 s abnormality by gene transfer might improve cardiac function.

18 CCN1-infected control subjects, and improved cardiac function.

19 nd downstream effectors essential for proper cardiac function.

20 r neuron output that is necessary for proper cardiac function.

21 ions of baroreflex dysfunction and preserved cardiac function.

22 ricular systolic function post-MI, restoring cardiac function.

23 p < 0.01), and was associated with impaired cardiac function.

24 lation of collagen fibers with impairment of cardiac function.

25 n peri-infarct ventricular tissue, improving cardiac function.

26 plete resolution of symptoms and recovery of cardiac function.

27 ested that traumatic brain injury may affect cardiac function.

28 ceptor kinase 2, a key negative regulator of cardiac function.

29 gonist liraglutide exhibited preservation of cardiac function.

30 resultant dyspnea, independent of markers of cardiac function.

31 asmic, Omi/HtrA2 on myocardial apoptosis and cardiac function.

32 n of CTGF/CCN2 to mediate fibrosis and alter cardiac function.

33 e that is critical for learning, memory, and cardiac function.

34 e, body mass index, major comorbidities, and cardiac function.

35 , emphasising the importance of this gene in cardiac function.

36 ormin had no effect on systolic or diastolic cardiac function.

37 t adverse transgenerational effects on adult cardiac function.

38 recipient mouse heart, but led to diminished cardiac function.

39 nergic signalling in normal and pathological cardiac function.

40 tored impaired calcium balance and recovered cardiac function.

41 ine (SPARC), a protein involved in mammalian cardiac function.

42 o optimize neuronal coordination of regional cardiac function.

43 biosynthesis, and consequently, beta-AR and cardiac function.

44 air myocardial damage and completely recover cardiac function.

45 namic changes correspond with restored fetal cardiac function.

46 etermines the severity with which it affects cardiac function.

47 eficial effects of FoxO4 deletion on post-MI cardiac function.

48 hether reprogramming leads to improvement of cardiac function.

49 effective iron homeostasis is important for cardiac function.

50 arge animal models of heart failure restores cardiac function.

51 ic signaling pathways mediate key aspects of cardiac function.

52 transverse aortic constriction and improved cardiac function.

53 n of infarct size and persistent recovery of cardiac function.

54 g to a highly undeveloped ventricle and poor cardiac function.

55 ion of cardiac hypertrophy and protection of cardiac function.

56 atrophy induced by doxorubicin and improved cardiac function.

57 stimulate cardiac repair and restoration of cardiac function.

58 pertrophy is adaptive, resulting in improved cardiac function.

59 toring patient-reported changes that reflect cardiac function.

60 od flow (MBF) is the critical determinant of cardiac function.

61 ies of the effects of mutations and drugs on cardiac function.

62 ces stroke risk, and can preserve or improve cardiac function.

63 nt tau at 24 hours, hyperoxia did not affect cardiac function.

64 attenuated ventricular dilation and improved cardiac function.

65 eversed these changes together with improved cardiac functions.

66 lated changes in cutaneous microvascular and cardiac functions.

67 60%, respectively, while sparing immune and cardiac functions.

68 h dobutamine provoked distinctive effects on cardiac function: 1) optimized cardiac energy-dependent

69 thelial progenitor cell colony outgrowth and cardiac function after AMI.

70 romote adult CM proliferation and to improve cardiac function after MI was examined.

71 ne origin, we addressed the impact of MCs on cardiac function after MI, using the c-Kit-independent M

72 gnificantly decreased infarct size, improved cardiac function after myocardial I/R and modulated memb

73 plantation markedly improved vascularity and cardiac function after myocardial infarction without any

74 Moreover, TG demonstrated improved cardiac function after myocardial infarction.

75 epresents a potential approach for restoring cardiac function after myocardial injury, but the techni

76 n and relaxation are important parameters of cardiac function altered in many heart pathologies.

77 ces of extracellular volume (ECV) changes on cardiac function and adverse events, understand its incr

78 role for myeloid-derived VEGFA in improving cardiac function and angiogenesis.

79 t defects, as well as periodic assessment of cardiac function and arrhythmia monitoring, is essential

80 I, hearts from Nod1(-/-)-PMI mice had better cardiac function and attenuated structural remodeling.

81 Cardiac architecture is fundamental to cardiac function and can be assessed non-invasively with

82 ng); traditional methods were used to assess cardiac function and cardiovascular disease.

83 al stem cells (MSCs) transplanted to improve cardiac function and cells of the recipient.

84 chaemia-reperfusion (IR), restores depressed cardiac function and contraction, reduces infarct sizes,

85 in MBL2 KI mice revealed that 3F8 preserved cardiac function and decreased infarct size and fibrin d

86 asma concentrations associated with improved cardiac function and decreased ventricular diameter.

87 MC deficiency led to reduced postischemic cardiac function and depressed cardiomyocyte contractili

88 and mitochondria are inextricably linked to cardiac function and dysfunction.

89 Crude oil disrupts cardiac function and has been associated with heart malf

90 lism, often contributing to the worsening of cardiac function and health outcomes.

91 However, objective measures of cardiac function and health-related quality of life are

92 cruitment, along with improvements in global cardiac function and hemodynamics.

93 al dysfunction has been linked to decline in cardiac function and increased risk of cardiovascular di

94 th reexpression of fetal genes and decreased cardiac function and is often a precursor to heart failu

95 nance imaging, which was performed to assess cardiac function and late gadolinium enhancement, and T1

96 Cardiac function and left ventricular structure were mon

97 l ischemia, Trem-1 blockade also ameliorates cardiac function and limits ventricular remodeling as as

98 hypertrophy in addition to deterioration of cardiac function and massive cardiac fibrosis, all featu

99 We quantified effects on cardiac function and morphogenesis, characterized novel

100 Changes in cardiac function and morphology are recognizable at an a

101 Cardiac function and morphology were measured 6 weeks af

102 familial dilated cardiomyopathy and improve cardiac function and morphology.

103 dministration into infarcted hearts restored cardiac function and morphology.

104 nts with sepsis, which, in turn, may improve cardiac function and outcome in these patients.

105 f baroreflex dysfunction with intraoperative cardiac function and outcomes were assessed.

106 Cardiac function and pathological changes (hypertrophy,

107 C L48Q after the MI therapeutically enhances cardiac function and performance, without compromising s

108 pression of TnC L48Q before the MI preserves cardiac function and performance.

109 calcium and CaMKII homeostasis, and improved cardiac function and postarrest outcome in vivo.

110 x deposition that contributes to compromised cardiac function and potentially heart failure.

111 nsistent beneficial and plausible effects on cardiac function and pulmonary vasculature that may cont

112 alleviated Dox-cardiotoxicity with improved cardiac function and reduced cardiomyocyte apoptosis.

113 Moreover, SeV-GMT improved cardiac function and reduced fibrosis after myocardial i

114 Exosomes from hypoxic CPCs improved cardiac function and reduced fibrosis.

115 reconditioned with cardiotrophin-1 preserved cardiac function and reduced infarct size, parallel to t

116 g showed that ZYZ-168 substantially improved cardiac function and reduced interstitial fibrosis.

117 protective effect following TAC, normalizing cardiac function and reducing arrhythmogeneity at the ce

118 e8(-/-) mice displayed greater alteration in cardiac function and remodeling.

119 assessed the pharmacokinetics and effects on cardiac function and structure of the cardiac myosin act

120 The effects of neurological injury on cardiac function and structure will be summarized, and f

121 Moreover, this method significantly enhances cardiac function and survival of animals after myocardia

122 fibrosis, reduced hypertrophy, and improved cardiac function and survival.

123 ing breathing variability, chemoreflex gain, cardiac function and sympatho-vagal balance, and arrhyth

124 raction; uncompensated changes in pHi impair cardiac function and trigger arrhythmia.

125 in plasma (primary endpoint) and changes in cardiac function and ventricular diameters.

126 ive reference standard for the evaluation of cardiac function and viability.

127 Assessment of cardiac function and volume assessment is becoming an es

128 lication of ultrasound to assess a patient's cardiac function and volume status is becoming commonpla

129 ross a wide range of clinical conditions and cardiac functions and was shown to affect patients' outc

130 effects on motor, central nervous system and cardiac function, and alternative more selective treatme

131 ed modest cardiac hypertrophy, impairment of cardiac function, and dysregulated expression of genes a

132 me on agalsidase, determination of renal and cardiac function, and evaluation of FD-related symptoms.

133 his correspondence is a reply to Galectin-3, Cardiac Function, and Fibrosis by Wouter C. Meijers et a

134 oral stimulation and monitored for survival, cardiac function, and fibrotic remodeling.

135 Glyco(Lo) mice had larger myocytes, enhanced cardiac function, and higher capillary-to-myocyte ratios

136 CM after MI significantly improved survival, cardiac function, and infarct size 4 weeks after MI.

137 rvous system regulates all aspects of normal cardiac function, and is recognized to play a critical r

138 protein C (cMyBP-C)] is essential for normal cardiac function, and mutations in cMyBP-C cause cardiac

139 -aortic constriction significantly preserves cardiac function, and reduces interstitial fibrosis but

140 liorated left ventricular dilation, improved cardiac function, and tended to reduce fibrosis.

141 fluid-regulatory hormones, the vasculature, cardiac function, and the autonomic nervous system.

142 uction of toxic lipids as a means to improve cardiac function are suggested.

143 ly restored t-tubule structure and preserved cardiac function as measured by invasive hemodynamics, w

144 s autonomic nAChRs leading to disruptions of cardiac function as well as systemic and uterine hemodyn

145 All patients underwent comprehensive cardiac function assessment, including tissue Doppler im

146 nique can provide striking new insights into cardiac function at the whole heart level during health

147 BP increased to approximately 130 mm Hg, and cardiac function became markedly impaired.

148 types in the infarct border zone can improve cardiac function but are limited by systemic side effect

149 hways, since not only do adipokines regulate cardiac function, but also the heart affects EpAT biolog

150 Genetic absence of Mmp9 also improved cardiac function, but increased superoxide remained.

151 Women often recover cardiac function, but long-lasting morbidity and mortali

152 ypertrophic response and decreases sustained cardiac function, but the cardiomyocyte-specific effects

153 cle function as early as 7 weeks and reduced cardiac function by 28 weeks, suggesting that the diseas

154 ng maladaptive signaling, but also improving cardiac function by altering the myofilament-Ca(2)(+) re

155 rect activation or inhibition of the CSAR on cardiac function by pressure-volume (P-V) loop analysis

156 to significant improvements of survival and cardiac function by suppressing infiltration of multiple

157 ocytic pericardial nephrocytes that modulate cardiac function by uncharacterized mechanisms.

158 We evaluated blood pressure, cardiac function (by echocardiography), fibrosis (with M

159 fect of a non-hypertensive dose of leptin on cardiac function, [Ca(2+) ]i handling and cellular elect

160 e analysed the effect of leptin treatment on cardiac function, [Ca(2+) ]i handling and cellular elect

161 an important determinant of QOL, and because cardiac function can influence exercise performance, it

162 py does not result in long-term worsening of cardiac function, cardiac symptoms, or health-related qu

163 deling post-MI leads to progressive impaired cardiac function caused by a disarray of several process

164 emia, obesity, and normal blood pressure and cardiac function compared with C57BLKS/J mice at 6 to 8

165 ted post-infarction remodeling, and improved cardiac function compared with control subjects.

166 wed significantly improved reprogramming and cardiac function compared with those exposed to only GMT

167 ia, and child hypoxia significantly improved cardiac function compared with those from saline-treated

168 Cardiac function decreased following TAC in WT mice, but

169 erturbations in these pathways can result in cardiac function deficits and heart failure.

170 OCK partially rescued the in vivo Snrk cmcKO cardiac function deficits.

171 performance status of 2 or less, have normal cardiac function (defined by ejection fraction above 50%

172 ed by the heart to augment mitochondrial and cardiac function during a normal physiological stress, s

173 s work has identified new targets to improve cardiac function during aging.

174 y represses collagen expression and improves cardiac function during hypertrophy.

175 r diastolic dysfunction and worsening global cardiac function evidenced by elevated E/A ratios and my

176 ium, induce cardiomyocyte death, and disrupt cardiac function following bacteremia, but it is unknown

177 iR combo in vivo is associated with improved cardiac function following myocardial infarction.

178 es represents a potential means of restoring cardiac function following myocardial injury.

179 ntiated into CMs, ECs, and SMCs and improved cardiac function for up to 12 weeks after transplantatio

180 f HF impacts virtually all aspects of normal cardiac function - from structure and mechanics to metab

181 While the relevance of Ca(2+) homeostasis in cardiac function has been extensively investigated, the

182 de synthase 1 (NOS1) as a major modulator of cardiac function has been extensively studied in experim

183 this approach on Duchenne muscular dystrophy cardiac function has yet to be evaluated.

184 ndary analyses of the Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antag

185 HFpEF enrolled in the Treatment Of Preserved Cardiac Function Heart Failure With an Aldosterone Antag

186 45%, were enrolled in Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antag

187 of the TOPCAT trial (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antag

188 ing can characterize different parameters of cardiac function; however, despite previously published

189 improved hypertrophy, resulting in improved cardiac function; however, mechanisms for normoxic neona

190 onductance catheterization revealed impaired cardiac function in 2-month-old male transgenic (Tg) mic

191 to reduce ventricular remodeling and improve cardiac function in a murine myocardial infarction (MI)

192 We sought to assess cardiac function in a pelagic fish species, the cobia (R

193 ) in embryonic heart and results in impaired cardiac function in adulthood.

194 MSC therapy improves cardiac function in animal models of both AMI and chroni

195 Indeed, IL-4c administration enhanced cardiac function in association with reduced infarct siz

196 rct size and improved coronary flow rate and cardiac function in both C57BLKS/J and db/db mice.

197 mpact of NAD(+) precursor supplementation on cardiac function in both mouse models.

198 tion of the cardio-cardiac reflex control of cardiac function in both normal and CHF states remains u

199 e left ventricular remodeling and decline in cardiac function in both small and large animal models.

200 although leptin treatment was deleterious on cardiac function in control animals, leptin had a cardio

201 study deepens our understanding of impaired cardiac function in diabetes, identifies GCH1 as a modul

202 mpression-resistant elements that may impair cardiac function in disease.

203 e SPARC in the noncell autonomous control of cardiac function in Drosophila and suggest that modulati

204 gical mechanisms underlying deterioration of cardiac function in HFpEF are poorly understood.

205 ressed chemoreflex function or its effect on cardiac function in HFpEF.

206 n imaging and analysis toolset for measuring cardiac function in intact, unanesthetized Drosophila me

207 nergistically reduces scar size and improves cardiac function in ischemic cardiomyopathy.

208 ts ischemia/reperfusion injury, and improves cardiac function in ischemic rat hearts.

209 genome editing on dystrophin expression and cardiac function in mdx/Utr(+/-) mice after a single sys

210 nvestigated the effect of preexisting CKD on cardiac function in mice with sepsis and whether inhibit

211 l environment alter metabolic parameters and cardiac function in mice.

212 markers in the serum and heart and restores cardiac function in mice.

213 thesized that physiological perturbations in cardiac function in microgravity may be a consequence of

214 Ameliorated cardiac function in Nod1(-/-)-PMI mice was associated wi

215 gests that CSAR has a differential effect on cardiac function in normal and CHF states.

216 T release, and led to marked preservation of cardiac function in our study.

217 An accurate evaluation of cardiac function in patients with cirrhosis remains a ch

218 Cardiac output (CO) is a key indicator of cardiac function in patients with heart failure.

219 ated increase in AKT activation improved the cardiac function in pressure overloaded Hras null hearts

220 , cardiac arrhythmogenesis and impairment in cardiac function in rats with HFpEF.

221 Recovery of cardiac function in response to mechanical unloading was

222 TNC deficiency further impaired cardiac function in response to pressure overload and ex

223 lation and cardiac hypertrophy, and improved cardiac function in responses to stresses.

224 Preservation of cardiac function in sepsis by Pep2.5 is associated with

225 although leptin treatment was deleterious on cardiac function in sham, leptin had a cardioprotective

226 rogressive, life-threatening collapse of the cardiac function in spite of treatment with venous-arter

227 nd alteration of this homeostasis influences cardiac function in the adult heart.

228 Understanding the mechanisms that support cardiac function in the early phase post MI and identify

229 to be beneficial in maintaining cellular and cardiac function in the face of multiple proteotoxic ins

230 cells have been effectively used to promote cardiac function in the pathological heart.

231 e LIM protein ratio, is also correlated with cardiac function in the transition to failure in a guine

232 d slow-twitch myofiber proteins, and rescued cardiac function in Trbp(cKO) mice.

233 owever, how its hyperphosphorylation affects cardiac function in vivo remains unknown.

234 n to have significantly different effects on cardiac function in vivo.

235 Embryonic exposure to caffeine altered cardiac functions in offspring.

236 irst review the key role of Ca(2+) in normal cardiac function-in particular, excitation-contraction c

237 decreased metabolic efficiency and disrupted cardiac function including prolonged QT interval duratio

238 Several processes that affect cardiac function, including ischemia, obesity, diabetes

239 CPC exosomes derived from neonates improved cardiac function independent of culture oxygen levels, w

240 duced myocardial infarction, measurements of cardiac function, infarct size, apoptosis, both vascular

241 An impairment of cardiac function is a key feature of the cardiovascular

242 ll types via viral fusogens to determine how cardiac function is impacted.

243 VNS control over cardiac function is maintained during chronic therapy.

244 oxide synthase 1 (NOS1), major modulator of cardiac function, is the cofactor tetrahydrobiopterin (B

245 lated changes in cutaneous microvascular and cardiac functions limit the extent of cutaneous vasodila

246 associated with a significant improvement in cardiac function (LV ejection fraction +6.07% [95% confi

247 T-cell purinergic signaling, cytokines, and cardiac function (magnetic resonance tomography at 9.4 T

248 ese age-related changes in microvascular and cardiac functions maximally restrain the levels of cutan

249 MR protocol allowed for the determination of cardiac function, myocardial inflammation, myocardial fi

250 for embryonic development, iron acquisition, cardiac function, neuropeptide biogenesis, and other cri

251 ement, increased infarct size, and depressed cardiac function, newly implicating MerTK in cardiac rep

252 This improved cardiac function occurred despite persisting indications

253 R1 degradation and Ca(2+) signaling, but the cardiac function of Herpud1 remains unknown.

254 y, normalized fetal weight, and improved the cardiac function of Hsd11b2(-/-) fetuses.

255 However, the in vivo cardiac function of IF1 and the potential therapeutic ap

256 may serve as a promising tool for monitoring cardiac function of patients in clinical settings.

257 Our method can measure the cardiac function of single micropatterned hiPSC-CMs and

258 ts and mechanisms of myricitrin (Myr) on the cardiac function of streptozotosin-induced diabetic mice

259 evidence for positive adhesiotropy as a new cardiac function of sympathetic signaling.

260 e heart and provide an integrated picture of cardiac functions of the SUMO system under physiologic o

261 strated that Cas9 expression does not affect cardiac function or gene expression.

262 expression differences at baseline influence cardiac function, particularly through the protein kinas

263 Cardiac function, peak oxygen uptake (o2peak), lipid sta

264 Impaired cardiac function persists in the era of effective human

265 o explore the role of phosphodiesterase 2 in cardiac function, propensity to arrhythmia, and myocardi

266 was more potent than metoprolol in improving cardiac function, pulmonary vascular remodeling, and inf

267 left ventricular volume without compromising cardiac function, reduced the expression of genes associ

268 educes ventricular dyssynchrony and improves cardiac function relative to right ventricular apex (RVA

269 athology and inflammation, and also worsened cardiac function, relative to age-matched mdx mice.

270 Cardiac function requires continuous high levels of ener

271 The severe depression of cardiac function responded promptly to interleukin-1 inh

272 The decrease in cardiac function seen with MSC-VSVG treatment versus MSC

273 Cardiac function significantly declined in T-cell-specif

274 ion of viable myocardium and augmentation of cardiac functions similar to cardiac stem cell therapy.

275 some benefits over surgery alone in terms of cardiac function, somatic growth, and quality of life.

276 TCM, or nCPC-derived exosomes in recovering cardiac function, stimulating neovascularization, and pr

277 an ischemic cause of heart failure and worse cardiac function, than those in whom sudden death did no

278 n in beta-adrenergic-mediated enhancement of cardiac function, transgenic (TG) mice expressing non-ph

279 e end of the treatment protocol, we assessed cardiac function using echocardiography, the myofilament

280 al processes such as lymphocyte trafficking, cardiac function, vascular development, and inflammation

281 PH, cardiac function, vascular remodeling, and valve structu

282 iveness of this delivery system in improving cardiac function, ventricular wall thickness, angiogenes

283 eceived anthracyclines and were screened for cardiac function via echocardiograms.

284 Cardiac function was assessed after reperfused or nonrep

285 Vascular and cardiac function was assessed at 8, 16, and 24 weeks of

286 Cardiac function was assessed by left ventricular ejecti

287 rior descending coronary artery ligation and cardiac function was assessed using echocardiography for

288 Defective cardiac function was associated with altered protein lev

289 Cardiac function was evaluated by magnetic resonance ima

290 Cardiac function was evaluated with echocardiography.

291 Impaired diastolic and systolic cardiac function was observed in IUGR offspring with dif

292 Cardiac function was represented by peak exercise cardia

293 temperature per se is a major determinant of cardiac function, we characterized the effects of hypert

294 Consistent with this decreased cardiac function, we show that elevated serum bile acids

295 ell phenotypes, cell functions, and post-AMI cardiac function were determined.

296 Cardiac hypertrophy, fibrosis, and cardiac function were examined in these mice.

297 ta-regression revealed that infarct size and cardiac function were influenced independently by choice

298 variables, volume shifts, fluid balance, and cardiac function were monitored during hemorrhage and re

299 ease BP significantly and to markedly impair cardiac function, with effects mediated by NO produced b

300 displayed severe cardiomyopathy and loss of cardiac function, with elevation of several markers of h