ライフサイエンスコーパス: cardiac function

1 ardiac fibrosis and hypertrophy and improved cardiac function.

2 rolongs SR re-uptake of calcium, and impairs cardiac function.

3 n and ICAM-1 with subclinical alterations in cardiac function.

4 anges in the intracellular redox state alter cardiac function.

5 d pulmonary vascular remodeling and improved cardiac function.

6 impact of liver inflammation and fibrosis on cardiac function.

7 ppress MI-induced granulopoiesis and improve cardiac function.

8 mitochondrial toxins resulting in a loss of cardiac function.

9 atients correlated with the infarct size and cardiac function.

10 rial hypertension but did not correlate with cardiac function.

11 earts subjected to prolonged stress maintain cardiac function.

12 es in gene expression in pathways related to cardiac function.

13 a mice suggesting that IUGT ameliorated poor cardiac function.

14 ording of multiple parameters characterizing cardiac function.

15 yocardial infarction, in each case improving cardiac function.

16 intaining cellular metabolic homeostasis and cardiac function.

17 n supplementation in HF patients may improve cardiac function.

18 duces MI-induced cardiac damage and protects cardiac function.

19 nsequently, in the inflammatory response and cardiac function.

20 ysiological effect of Tpm phosphorylation on cardiac function.

21 e cardiac myocyte hypertrophy with preserved cardiac function.

22 bFGF release system significantly increased cardiac function.

23 rdiac hypertrophy often causes impairment of cardiac function.

24 nities for intravital imaging and control of cardiac function.

25 es in left ventricular geometry and impaired cardiac function.

26 is represent promising strategies to improve cardiac function.

27 in restoration and significantly improved RV cardiac function.

28 way by recruiting NF2 to the ICD to modulate cardiac function.

29 es normalizes sympathetic drive and improves cardiac function.

30 s to myocardial fibrosis that can compromise cardiac function.

31 s can be conducted without globally altering cardiac function.

32 coupling between ketone body metabolism and cardiac function.

33 itus model) and monitored for remodeling and cardiac function.

34 on, and myocardial hypertrophy with impaired cardiac function.

35 tant mice with a GSK3beta inhibitor improves cardiac function.

36 loid cells (LysM(CRE/+)/ Hamp(f/f)) improved cardiac function.

37 d for increased beta-AR signaling to improve cardiac function.

38 on in neutrophil degranulation and preserved cardiac function.

39 l to define the roles of alphaII spectrin in cardiac function.

40 resulted in cardiac hypertrophy and impaired cardiac function.

41 echanism in the heart for maintaining normal cardiac function.

42 at identify a direct role for BAT to mediate cardiac function.

43 transverse aortic constriction and improved cardiac function.

44 atrophy induced by doxorubicin and improved cardiac function.

45 and improves diaphragm, skeletal muscle and cardiac function.

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

47 ested that traumatic brain injury may affect cardiac function.

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

49 nergic signalling in normal and pathological cardiac function.

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

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

52 the myocardium and corresponding decline in cardiac function.

53 ced adverse LV remodeling and the decline of cardiac function.

54 with crucial roles in neuronal signaling and cardiac function.

55 , and fibrosis while maintaining significant cardiac function.

56 g is the gold-standard for the assessment of cardiac function.

57 portant metric in the clinical assessment of cardiac function.

58 We aim to determine the role of ZO-1 in cardiac function.

59 ical pacing, can have deleterious effects on cardiac function.

60 ntial to mouse development, and to postnatal cardiac function.

61 r aortic pathologies and diminished baseline cardiac function.

62 t-MI) remodeling and leads to improvement in cardiac function.

63 rates in the left ventricle and deteriorated cardiac function.

64 variability, an indicator of good health and cardiac function.

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

66 including those encoding secretome; improved cardiac function; abrogated cardiac arrhythmias, fibrosi

67 usion injury potentially leading to impaired cardiac function, adverse tissue remodeling and heart fa

68 s and fibrosis that correlated with worsened cardiac function after 1 week of TAC.

69 imaging, and induce no alteration to normal cardiac function after grafting onto rat hearts.

70 othelial cells, injection of which preserved cardiac function after injury.

71 elative to controls, NaHS treatment improved cardiac function after ischaemia (mean +/- SD for area u

72 uced cardiac rupture incidence, and improved cardiac function after MI.

73 increased angiogenesis, leading to improved cardiac function after MI.

74 ure can result in significant improvement in cardiac function allowing LVAD removal; however, the rat

75 Sex disparities modulate cardiac function, although the proteins and mechanisms r

76 on in nonimmunosuppressed rats would improve cardiac function and ameliorate ventricular remodeling.

77 51(+) cells and was associated with improved cardiac function and animal survival following MI couple

78 ading tool in the discovery of mechanisms of cardiac function and arrhythmias.

79 agents new to cardiac diseases, to preserve cardiac function and attenuate fibrosis.

80 Here, we used a genetic approach to restore cardiac function and blood flow in a zebrafish model of

81 reflex activation had deleterious effects on cardiac function and cardiac autonomic control in HF rat

82 n of Ogdhl in Col4a3(-/-) mice also improved cardiac function and cardiomyocyte energy state.

83 effect of chronic kidney disease on abnormal cardiac function and cardiovascular events in those with

84 en abnormal renal function and impairment of cardiac function and cardiovascular events.

85 early sarcomere and metabolic defects alter cardiac function and contribute to the electrical instab

86 p between hybrid/complex N-glycosylation and cardiac function and disease.

87 rane protein insertion pathway in vertebrate cardiac function and disease.

88 cal shift of substrate preference, preserves cardiac function and energetics, and reduces cardiomyocy

89 further understand the relationship between cardiac function and flow, on the basis of sex, by quant

90 ased cardiac efficiency relationship between cardiac function and flow.

91 ice or chemical GSK3beta inhibition improves cardiac function and increases mice life span.

92 y artery disease (CAD) by stress CMR, beyond cardiac function and ischemia.

93 blockade led to progressive deterioration of cardiac function and left ventricle dilation.

94 ional echocardiography was used to determine cardiac function and left ventricular remodeling, and at

95 lyceride levels was associated with impaired cardiac function and maintenance of body temperature, ef

96 acute myocardial infarction led to improved cardiac function and mouse survival, and in the mdx mous

97 e aimed to investigate the interplay between cardiac function and myocardial carbohydrate metabolism

98 Cardiac function and myocardial phenotype were evaluated

99 developmental programming by MO of offspring cardiac function and predisposition to later life cardio

100 ed attention for use as scaffolds to promote cardiac function and prevent negative left ventricular (

101 using a Cx3cr1-based system led to impaired cardiac function and promoted adverse remodeling primari

102 lymphangiogenesis has been shown to improve cardiac function and reduce the progression of myocardia

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

104 d have a higher rate of haemolysis, impaired cardiac function and reduced exercise tolerance, and tha

105 Sprr3 deletion in mice showed preserved cardiac function and reduced interstitial fibrosis in vi

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

107 nal region of the WWP2 protein show improved cardiac function and reduced myocardial fibrosis in resp

108 -loaded PEG-b-PPS nanoparticles improved the cardiac function and reduced the infarct size.

109 ay represent a potential strategy to promote cardiac function and remodeling after MI.

110 ory cells, or cardiomyocytes does not affect cardiac function and remodeling in infarcted mice.

111 with the aim of inducing cardiomyopathy, and cardiac function and remodeling was assessed by echocard

112 he deleterious effects of a high-fat diet on cardiac function and remodeling, and acute injection of

113 oproteinase-2 activity, v) fibrosis, and vi) cardiac function and remodeling.

114 d to examine associations between indices of cardiac function and retinal microvasculature, adjusting

115 th the acute and chronic influence of SNs on cardiac function and structure is enacted as a result of

116 yndrome, identifying genetic determinants of cardiac function and structure may provide greater insig

117 Comparisons of the cardiac function and structure of wild-type and p38gamma

118 ings suggested a relationship between poorer cardiac function and suboptimal retinal microvascular ge

119 results in GSK3beta inhibition and improved cardiac function and survival.

120 and exerted sustained beneficial effects on cardiac function and survival.

121 , KA-PTEN mice showed significantly improved cardiac function and survival.

122 There was no recovery of cardiac function and the patient developed multiorgan fa

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

124 itney) with those volume-based parameters of cardiac function and varied between genders.

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

126 We assessed cardiac function and volume status in severe falciparum

127 eceptor (beta(1)-AR) is a major regulator of cardiac functions and is downregulated in the majority o

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

129 diac fibrosis, 2) significant improvement of cardiac function, and 3) increased total and plasma memb

130 At the same time, fibrosis impairs cardiac function, and a growing body of experimental dat

131 reased cardiomyocyte cell division, enhanced cardiac function, and improved long-term survival.

132 effector at the interface of metabolism and cardiac function, and its repression improves the outcom

133 in during MI limits cardiac damage, improves cardiac function, and mitigates remodeling to a larger e

134 R120G)-induced protein aggregation, improved cardiac function, and prolonged lifespan in vivo.

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

136 ic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce

137 ion, fibrosis, and a progressive decrease in cardiac function, are hallmarks of myocardial infarction

138 These results collectively identify cardiac function as a target for HF-FW toxicity and prov

139 ate that there are no significant changes in cardiac function as measured by echocardiography in the

140 cific deletion of IDO show an improvement of cardiac function as well as cardiomyocyte contractility

141 t year (Y) 7 (Y7) and Y15 examinations, with cardiac function assessed at Y30 after adjustment for ke

142 ce developed cardiac hypertrophy with normal cardiac function at 6 weeks of age but with a decreased

143 plex N-glycosylation contributes to aberrant cardiac function at whole-heart and myocyte levels drawi

144 PV) loops provide a wealth of information on cardiac function but are not readily available in clinic

145 AMP-PDE activity, which did not modify basal cardiac function but efficiently prevented systolic dysf

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

147 rticoid receptor) antagonists (MRAs) improve cardiac function by decreasing cardiac fibrosis.

148 o attenuate cardiac hypertrophy and preserve cardiac function by improving the expression of endothel

149 ell types, where they coordinate to regulate cardiac function by modulating critical processes such a

150 eutic potential of miR-19a/19b in protecting cardiac function by systemically delivering miR-19a/19b

151 The authors evaluated cardiac function, cardiomyocyte mechanics, and the molec

152 was accompanied by a dramatic improvement in cardiac function compared with saline-treated SRC-2-CKO

153 ere performed.Measurements and Main Results: Cardiac function data from early echocardiograms were av

154 Cardiac function declined during ESHP but was significan

155 ced cardiac myocyte hypertrophy and impaired cardiac function, demonstrating a role for ATF6 in compe

156 loss after ischemic injury improve long-term cardiac function despite a lack of durable engraftment.

157 and progression of cardiac fibrosis lead to cardiac function deterioration.

158 to cardiac dysautonomia and deterioration of cardiac function during chemoreflex activation.

159 that this new approach allows evaluation of cardiac function during specific respiratory phases.

160 B cell-specific deletion of IL-10 worsened cardiac function, exacerbated myocardial injury, and del

161 However, human assessment of cardiac function focuses on a limited sampling of cardia

162 ures may be useful for monitoring changes in cardiac function following initiation on ARNI or left ve

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

164 ine the best evaluation strategy to estimate cardiac function following transplantation.

165 chocardiography measurements correlated with cardiac function following transplantation.

166 iratory variability and better assessment of cardiac function for studying respiratory and/or cardiac

167 Conversely, Par4(-/-) mice showed impaired cardiac function, greater rates of myocardial rupture, a

168 myocardium and a high risk of deteriorating cardiac function, has a heterogeneous aetiology.

169 th dilated cardiomyopathy whose symptoms and cardiac function have recovered often ask whether their

170 About 30% of patients with impaired cardiac function have ventricular dyssynchrony and seek

171 d a subset of TOPCAT (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antag

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

173 ls: the TOPCAT trial (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antag

174 in the TOPCAT trial (Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antag

175 and TOPCAT-Americas (Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antag

176 omarkers from TOPCAT (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antag

177 We assessed cardiac function, hematopoietic response, and myeloid ph

178 esents a unique test of our understanding of cardiac function, hemodynamics, and physiological limits

179 However, despite promising improvements in cardiac function, high incidences of ventricular arrhyth

180 asures of systemic inflammation (i.e., CRP), cardiac function (i.e., NT-proBNP), and cardiac necrosis

181 mouse and study effects of this mutation on cardiac function, I(K1), and Ca(2+) handling, to determi

182 ays a critical role in neuronal development, cardiac function, immunity, and cancer.

183 This approach is used to describe cardiac function in 10 heart transplant patients, five o

184 ervation of cardiomyocyte size and long-term cardiac function in a murine infarction model followed 2

185 meliorate the cardiac remodeling and improve cardiac function in a renal artery ligated rat model (RA

186 P signaling to control heart development and cardiac function in a tissue specific manner.

187 This study evaluated cardiac function in an experimental model following expo

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

189 IL-4/IL-13 in macrophages failed to improve cardiac function in both adult and neonatal injured hear

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

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

192 ctive effects and is crucial for maintaining cardiac function in chronic hypertension.

193 ss the metabolic remodelling associated with cardiac function in diabetic db/db mice subjected to str

194 revented ceramide accumulation, and improved cardiac function in diabetic mice.

195 ial) or TOPCAT trial (Treatment of Preserved Cardiac Function in Heart Failure With an Aldosterone An

196 emic heart and in the attempts at modulating cardiac function in heart failure.

197 activation on cardiac autonomic balance and cardiac function in HF rats was abolished by ablation of

198 In contrast, ex vivo cardiac function in HFD-fed WT mice dropped ~ 50% relati

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

200 ces cardiomyocyte proliferation and improves cardiac function in infarcted hearts.

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

202 ted autoimmune heart pathology with improved cardiac function in LMP7(-/-) mice involved a changed ba

203 g cell cycle reentry that leads to augmented cardiac function in mice after myocardial infarction.

204 rtic constriction, and A61603 did not rescue cardiac function in mice with the Gq coupling-defective

205 how a modest but reproducible improvement in cardiac function in models of cardiac ischaemic injury(4

206 hils suppress granulopoiesis and may improve cardiac function in patients with acute coronary syndrom

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

208 f respiratory sinus arrhythmia would improve cardiac function in rats with heart failure.

209 t has shown to reduce remodeling and restore cardiac function in recent preclinical studies.

210 Recovery of cardiac function in response to mechanical unloading was

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

212 cardiac metabolism at baseline and impaired cardiac function in response to stress.

213 hen validated by reproducing improvements in cardiac function in the enalapril arm of SOLVD.

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

215 Identifying the causes of compromised cardiac function in this patient group may improve early

216 strate reversible, real-time photocontrol of cardiac function in translucent wildtype tadpoles.

217 the most rigorous form of imaging to assess cardiac function in vivo.

218 tion and end-inspiration measurements of the cardiac function in volunteers, incremental respiratory

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

220 velop a temporary or permanent impairment of cardiac function including acute cardiomyopathy with hem

221 injury in DM mice, as evidenced by improved cardiac function (increased LVEF and +/-Dp/dt), decrease

222 ardiography imaging was performed to measure cardiac function indices, and retinal imaging was used t

223 hey also do not correlate with biomarkers of cardiac function, inflammation, and oxidative stress.

224 atment significantly improved left ventricle cardiac function, inhibited cell apoptosis, reduced MI s

225 xynucleotides (CpG ODN) and their effects on cardiac function, injury, and a novel left ventricular (

226 cteristic of human Barth syndrome but normal cardiac function into adulthood.

227 Accurate assessment of cardiac function is crucial for the diagnosis of cardiov

228 However, when cardiac function is disrupted, OFT endocardial growth ce

229 Using echocardiography to measure cardiac function, it was revealed that tKO hearts had le

230 ne-mediated myocardial damage and decline of cardiac function, likely because of dampened activation

231 nt myocardial ischemia, leading to depressed cardiac function long term.

232 stemic and cardiac inflammation and improves cardiac function long term.

233 tion and showed a significant improvement in cardiac functions measured by intraventricular pressure-

234 perinflation, which translated into improved cardiac function, measured by left ventricular end-diast

235 s greater minute volume, as well as enhanced cardiac function mitigating the decline of fractional sh

236 Cardiac function, mitochondria function, and mitophagy a

237 Together, our results indicate that cardiac function modulates OFT morphogenesis by triggeri

238 ined with a standardized pharmacological and cardiac function monitoring protocol resulted in a high

239 time, the effect of boron supplementation on cardiac function, myocardial fibrosis, apoptosis and reg

240 Cardiac function, myocardial tissue injury, markers of i

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

242 reversing cardiac atrophy might preserve the cardiac function of cancer patients receiving anthracycl

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

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

245 nefits in old mice and SS-31 did not improve cardiac function of old mCAT mice, implicating normalizi

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

247 optimal conditions during development on the cardiac function of the offspring, independent of additi

248 All surviving recipients had normal cardiac function on echocardiogram and no evidence of ac

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

250 ated blood pressure in mice without altering cardiac function or kidney anatomy.

251 t catheterizations allowing an assessment of cardiac function over time.

252 mTORkd expression as assessed by changes in cardiac function, oxidative stress, and myocyte apoptosi

253 Cardiac function parameters, including the end-systolic

254 l MMP activation, myocardial blood flow, and cardiac function post-I/R that can be used to evaluate t

255 ssion of Adm increased lymphangiogenesis and cardiac function post-myocardial infarction while suppre

256 m6A, calcium dynamics and contractility, and cardiac function postischemia.

257 However, its relation to cardiac function, prior to clinical disease has not been

258 n myocardial repair, improved left ventricle cardiac function, reduced MI scar size, and enhanced pos

259 ower BA levels were associated with improved cardiac function, reduced myocardial damage, shock, lung

260 ients and mice with HF, however, its role in cardiac function remains poorly understood.

261 Normal cardiac function requires that intracellular Ca(2+) conc

262 Cardiac function significantly declined in T-cell-specif

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

264 R67Q(+/-) mice (n=17) showed normal cardiac function, structure, and baseline electrical act

265 dentify an endocrine role for BAT to enhance cardiac function that is mediated by regulation of calci

266 lar dysfunction, chronic RMH pacing improved cardiac function through improvements in systolic functi

267 ic CVB3-induced myocarditis and improves the cardiac function to a level equivalent to that of uninfe

268 The contribution of cardiac function to this increased disease risk is uncer

269 strain estimation can non-invasively assess cardiac functioning using subject-specific MRI.

270 ar ejection fraction (EF) is an indicator of cardiac function, usually assessed in individuals with h

271 rvous system is essential for maintenance of cardiac function via activation of post-junctional adren

272 that CM-HIPK2 is required to maintain normal cardiac function via extracellular signal-regulated kina

273 that transplantation of BAT (+BAT) improves cardiac function via the release of the lipokine 12,13-d

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

275 Cardiac function was assessed by echocardiography.

276 Cardiac function was assessed by pressure-volume loop an

277 Cardiac function was assessed in vivo, followed by histo

278 Cardiac function was assessed non-invasively using echoc

279 mice to e-cigarette vaping for 2-weeks, and cardiac function was assessed using echocardiography.

280 e effect of Klotho on lung structure, PH and cardiac function was assessed.

281 At PN80 cardiac function was evaluated by echocardiography and D

282 ity was determined by the adipose index, and cardiac function was evaluated in vivo by echocardiogram

283 5% CI 0.82-2.65) to 11.72% (3.00-24.53) when cardiac function was evaluated post-chemotherapy (p=0.01

284 The cardiac function was improved in all three global strain

285 was mixed, and assessment of posttransplant cardiac function was limited to an invasive technique (p

286 paced monotonically at a matched heart rate; cardiac function was measured using non-invasive echocar

287 Cardiac function was represented by peak exercise cardia

288 and tissue mechanical properties to overall cardiac function, we apply a multiscale biophysical biom

289 To test effects of T cell depletion on cardiac function, we gave CKD mice anti-CD3 antibody inj

290 To determine the role of BAT on cardiac function, we utilized a model of BAT transplanta

291 ular coupling, cardiac autonomic control and cardiac function were analysed in HF rats with or withou

292 LV remodeling and cardiac function were assessed by histology and echocard

293 Skeletal muscle, respiratory, and cardiac function were assessed in treated and untreated

294 analyses, and assessment of aortic valve and cardiac function were determined by echocardiography.

295 all molecules without detrimental impacts on cardiac function were identified.

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

297 flex function, cardiac autonomic control and cardiac function were studied.

298 (ECMO) artificially supports respiratory and cardiac function when conventional techniques fail.

299 Herein, we present a method to modulate cardiac function with light through a photoswitchable co

300 Dexrazoxane preserved cardiac function without compromising EFS and OS or incr