ライフサイエンスコーパス: cardiac dysfunction

1 CKD frequently leads to chronic cardiac dysfunction.

2 lure where low plasma concentrations exclude cardiac dysfunction.

3 of NAD(+) prevented the mtDNA depletion and cardiac dysfunction.

4 hypertrophy of cardiac myocytes and overall cardiac dysfunction.

5 respiratory insufficiency but typically not cardiac dysfunction.

6 the life span will determine progression of cardiac dysfunction.

7 e for understanding genetic contributions to cardiac dysfunction.

8 -positive) breast cancer is dose-independent cardiac dysfunction.

9 e.Endoplasmic reticulum (ER) stress promotes cardiac dysfunction.

10 e may potentially be involved in T1D induced cardiac dysfunction.

11 d to halt or even reverse the progression of cardiac dysfunction.

12 ast activation, pathological remodeling, and cardiac dysfunction.

13 ntial target in treating diabetes-associated cardiac dysfunction.

14 has been suggested as a causative factor in cardiac dysfunction.

15 s tonically active in CHF and contributes to cardiac dysfunction.

16 ntestinal manifestations was associated with cardiac dysfunction.

17 tion of MAPKs and Akt during sepsis: role in cardiac dysfunction.

18 bitor in CLP mice reduced the development of cardiac dysfunction.

19 o the role of ncRNAs in chemotherapy-induced cardiac dysfunction.

20 rment associated with persistent subclinical cardiac dysfunction.

21 y contribute to the occurrence of later life cardiac dysfunction.

22 may be a major worldwide cause of vertebrate cardiac dysfunction.

23 erapeutic target to prevent diabetes-induced cardiac dysfunction.

24 ls, increased triglyceride accumulation, and cardiac dysfunction.

25 molecular analysis to determine the basis of cardiac dysfunction.

26 e subjected to pressure overload ameliorates cardiac dysfunction.

27 ased fibroadipogenesis in the heart and mild cardiac dysfunction.

28 an abnormal endothelial phenotype as well as cardiac dysfunction.

29 omyocyte-specific KLF5 overexpression caused cardiac dysfunction.

30 els correlate with collagen crosslinking and cardiac dysfunction.

31 sity, diminished vascular patency and severe cardiac dysfunction.

32 studied the role of ACE2 in obesity-mediated cardiac dysfunction.

33 CM) homeostasis is compromised, resulting in cardiac dysfunction.

34 everses pathological cardiac hypertrophy and cardiac dysfunction.

35 ator of doxorubicin- and trastuzumab-induced cardiac dysfunction.

36 nse to doxorubicin-induced mitochondrial and cardiac dysfunction.

37 erized as having subclinical or unrecognized cardiac dysfunction.

38 penings followed by mitochondrial damage and cardiac dysfunction.

39 also improved FA metabolism and ameliorated cardiac dysfunction.

40 ut little is known about its role in chronic cardiac dysfunction.

41 ting CVB3-induced myocarditis and preventing cardiac dysfunction.

42 nary hypertension, and reduced the degree of cardiac dysfunction.

43 the non-autonomous regulation of age-related cardiac dysfunction.

44 enovirus infection may contribute to ongoing cardiac dysfunction.

45 d-induced cardiac hypertrophy, fibrosis, and cardiac dysfunction.

46 ene (Edn1) expression is sufficient to cause cardiac dysfunction.

47 could be a potential therapy for DOX-induced cardiac dysfunction.

48 e targets in the setting of sepsis to reduce cardiac dysfunction.

49 nd provide possible mechanistic insight into cardiac dysfunction.

50 where increased NCX1 activity contributes to cardiac dysfunction.

51 ificantly reduced heart mass and ameliorated cardiac dysfunction.

52 rnitine, which correlated with the degree of cardiac dysfunction.

53 loped hypertension, cardiac hypertrophy, and cardiac dysfunction.

54 , are unusually vulnerable to stress-induced cardiac dysfunction.

55 disease severity, including hypothermia and cardiac dysfunction.

56 were protected against hyperglycemia-induced cardiac dysfunction.

57 wever, it is not clear how diabetes promotes cardiac dysfunction.

58 reactive oxygen species are key mediators of cardiac dysfunction.

59 om 10-day-old mice before the development of cardiac dysfunction.

60 er disease (NAFLD) may increase the risk for cardiac dysfunction.

61 creasing cardiac ketone delivery ameliorates cardiac dysfunction.

62 tion syndrome (OHS) has been associated with cardiac dysfunction.

63 o prevent its phosphorylation by PKB display cardiac dysfunction.

64 , increased cardiac hemorrhage, and enhanced cardiac dysfunction.

65 brogated apoptosis and prevented DOX-induced cardiac dysfunction.

66 can trigger an embryonic or fetal origin of cardiac dysfunction.

67 been correlated with glucose intolerance and cardiac dysfunction.

68 rweig et al. identified novel correlates for cardiac dysfunction.

69 ed REEP5 depletion in the mouse demonstrates cardiac dysfunction.

70 added value in identifying CCSs at risk for cardiac dysfunction.

71 iac function for studying respiratory and/or cardiac dysfunction.

72 of viral genomes in the heart tissue and by cardiac dysfunction.

73 ce of senescent cells attenuates age-related cardiac dysfunction.

74 causes of tricuspid valve, mitral valve, and cardiac dysfunction.

75 ying mild and severe influenza virus-induced cardiac dysfunction.

76 standing of how diabetic metabolism promotes cardiac dysfunction.

77 nhibited cardiac hypertrophy and ameliorated cardiac dysfunction after chronic infusion of ISO in mic

78 inhibition of IDO limits cardiac injury and cardiac dysfunction after MI.

79 otential therapeutic approach for inhibiting cardiac dysfunction after MI.

80 ocytes attenuates ventricular remodeling and cardiac dysfunction after myocardial infarction by limit

81 r initiation and progression, is linked with cardiac dysfunction, allows for the improper physiologic

82 ion of patients with cancer at high risk for cardiac dysfunction and a description of the cardiac reh

83 1 mRNA and protein expression while inducing cardiac dysfunction and action potential prolongation.

84 arcted heart, as well as its contribution to cardiac dysfunction and adverse clinical outcomes.

85 ical remodeling in the heart associated with cardiac dysfunction and adverse outcomes likely mediated

86 -1 degradation and, consequently, diminished cardiac dysfunction and adverse structural remodeling.

87 veloping strategic interventions to mitigate cardiac dysfunction and arrhythmias in DMD patients.

88 43 play a pivotal role in the progression of cardiac dysfunction and arrhythmogenesis in high-output

89 EF and if chemoreflex activation exacerbates cardiac dysfunction and autonomic imbalance.

90 These early phenotypes of diastolic cardiac dysfunction and blunted lusitropic response of c

91 Cardiac dysfunction and cardiovascular events are preval

92 Population-based estimates of cardiac dysfunction and clinical heart failure (HF) rema

93 at 6-7 weeks of age when the models display cardiac dysfunction and conduction abnormalities.

94 iotoxicity (ACT) manifesting as asymptomatic cardiac dysfunction and congestive heart failure in up t

95 C4KO mice developed modest cardiac dysfunction and dilation in response to exercise

96 ton leak as a novel mechanism of age-related cardiac dysfunction and elucidate how SS-31 can reverse

97 ythmias occurred early and in the absence of cardiac dysfunction and excess cardiac fibroadipocytes,

98 miR30d inhibition was sufficient to increase cardiac dysfunction and fibrosis after TAC.

99 Diabetes mellitus causes cardiac dysfunction and heart failure that is associated

100 nd imaging aspects of cancer therapy-related cardiac dysfunction and heart failure.

101 nd imaging aspects of cancer therapy-related cardiac dysfunction and heart failure.

102 Klotho-deficient mice exhibited cardiac dysfunction and hypertrophy before 12 weeks of a

103 s its contribution to systolic and diastolic cardiac dysfunction and impaired clinical outcomes in pa

104 flammation and fibrosis at 1 week and caused cardiac dysfunction and impaired lymphatic transport at

105 c mice (Tg) limited infarct size, attenuated cardiac dysfunction and improved cardiomyocyte survival

106 In vivo, Hrd1 knockdown exacerbated cardiac dysfunction and increased apoptosis and cardiac

107 stimulation, DKO mice are protected against cardiac dysfunction and interstitial fibrosis.

108 controls, CKD mice exhibited exacerbation of cardiac dysfunction and lung inflammation, greater incre

109 role in preventing, diagnosing, and treating cardiac dysfunction and other cardiovascular complicatio

110 F1 knockout (KO) mice were protected against cardiac dysfunction and pathological development induced

111 Myocardial scarring leads to cardiac dysfunction and poor prognosis.

112 dysinhibition, upheld(101) hearts exhibited cardiac dysfunction and remodeling comparable to that ob

113 dema, and interstitial fibrosis and prevents cardiac dysfunction and SCD.

114 MIS-C), manifested by severe abdominal pain, cardiac dysfunction and shock.

115 portunities for a more timely recognition of cardiac dysfunction and subsequent optimization of the h

116 ate that glucotoxicity by itself can trigger cardiac dysfunction and that a glucose-lowering agent ca

117 high risk for second malignant neoplasms or cardiac dysfunction and to the American Cancer Society (

118 Our prior studies suggest biventricular cardiac dysfunction and vascular impairment in baboons w

119 c dysfunction in mice, and reduced activity, cardiac dysfunction and ventricular enlargement in zebra

120 /)(-) and Npr2(+/)(-);Ldlr-/- mice developed cardiac dysfunction and ventricular fibrosis.

121 evealed that tKO hearts had left ventricular cardiac dysfunction and were hypertrophic, with a thicke

122 pproaches that alter serum S1P may attenuate cardiac dysfunction and whether S1P signaling might serv

123 disease, coronary microvascular dysfunction, cardiac dysfunction, and adverse cardiovascular outcomes

124 essure overload-induced hypertrophic growth, cardiac dysfunction, and alterations in cardiac transcri

125 iated with fatal neonatal disease, liver and cardiac dysfunction, and anemia.

126 Further, septic shock, late-onset cardiac dysfunction, and multiorgan system failure are a

127 induction of myocardial fibrosis, apoptosis, cardiac dysfunction, and premature death.

128 ed to severe myocardial fibrosis, apoptosis, cardiac dysfunction, and premature death.

129 overload manifested a defective ER response, cardiac dysfunction, and profound cell death.

130 athogenic Escherichia coli strain can induce cardiac dysfunction, and to elucidate any mechanisms inv

131 flammation, hemostasis, thrombin generation, cardiac dysfunction, and vascular stiffness and identifi

132 not confer protection against CLP-triggered cardiac dysfunction, apoptosis and inflammatory response

133 d concomitant pulmonary vascular disease and cardiac dysfunction are associated with poor prognosis.

134 tween E-selectin and ICAM-1 with subclinical cardiac dysfunction are unclear.

135 Aging-associated diseases, including cardiac dysfunction, are increasingly common in the popu

136 ent of cardiac myocytes by fibro-adipocytes, cardiac dysfunction, arrhythmias, and sudden death.

137 however, lack of Epac1 prevented subsequent cardiac dysfunction as a result of decreased cardiac myo

138 we hypothesized that rapamycin would prevent cardiac dysfunction associated with type 2 diabetes (T2D

139 ntolerance, glucose intolerance and moderate cardiac dysfunction at 6 months of age.

140 The consequences of CO poisoning include cardiac dysfunction, brain injury, and death.

141 ned according to self-report, and those with cardiac dysfunction but without clinical HF were charact

142 or life expectancy, especially in those with cardiac dysfunction, but a variety of treatment options

143 increasing cardiac FAO alone does not cause cardiac dysfunction, but protects against cardiomyopathy

144 rvivors with normal 3D LVEFs had evidence of cardiac dysfunction by global longitudinal strain (28%),

145 tic effect to prevent angiotensin II-induced cardiac dysfunction by improving cardiac lymphatic funct

146 tential roles in inflammation, fibrosis, and cardiac dysfunction: C-reactive protein (CRP); NT-pro-B-

147 nitor cell (CPC) function, and that neonatal cardiac dysfunction can be rescued by in utero injection

148 s cardiac fatty acid oxidation, and promotes cardiac dysfunction; cardiac defects can be prevented wi

149 All cardiac dysfunction categories were associated with use

150 Mice overexpressing ANGPTL2 in heart show cardiac dysfunction caused by both inactivation of AKT a

151 However, cardiac dysfunction caused by DOX limits its clinical us

152 Thus, preexisting CKD aggravates the cardiac dysfunction caused by sepsis or endotoxemia in m

153 ducible depletion of eosinophils exacerbates cardiac dysfunction, cell death, and fibrosis post-MI, w

154 logue protected against vascular, renal, and cardiac dysfunction, characterized by reduced hypertroph

155 na in cardiomyocytes in mice leads to severe cardiac dysfunction, conduction defect, ventricular arrh

156 to be central to cancer therapeutics-related cardiac dysfunction (CTRCD).

157 ncreased risk of cancer therapeutics-related cardiac dysfunction (CTRCD).

158 STZ-induced diabetic mice exhibited distinct cardiac dysfunction, dampened intracellular calcium hand

159 ion, intramyocardial bleeding, and increased cardiac dysfunction, despite equal infarct sizes.

160 Cardiac dysfunction determines prognosis in amyloid ligh

161 Cardiac dysfunction develops during sepsis in humans and

162 the effects of Abeta on atherothrombosis and cardiac dysfunction, discuss the clinical value of Alpha

163 bility transition pore (mPTP) is involved in cardiac dysfunction during chronic beta-adrenergic recep

164 ut whether IFITM3 deficiencies contribute to cardiac dysfunction during infection is unclear.

165 ost-pathogen interactions that contribute to cardiac dysfunction during invasive pneumococcal disease

166 ed mechanisms responsible for development of cardiac dysfunction during sepsis.

167 The aim of this study was to examine cardiac dysfunction during the first 2 weeks after isola

168 fective when administered before significant cardiac dysfunction, early identification of affected in

169 y 4 weeks post-I/R, wild-type mice showed no cardiac dysfunction, elevated TIMP4 levels (to baseline)

170 derlying cause of ventricular remodeling and cardiac dysfunction following myocardial infarction.

171 roponins and B-type natriuretic peptide) and cardiac dysfunction for 24-48 h after events, but what i

172 line metabolites have a primary role in this cardiac dysfunction; however, information on the molecul

173 SFN significantly prevented diabetes-induced cardiac dysfunction, hypertrophy and fibrosis.

174 acorporeal membrane oxygenation was used for cardiac dysfunction in 3,005 patients (66.5%), cardiopul

175 inhibitor-1 (I-1c) has been shown to reverse cardiac dysfunction in a model of ischemic HF.

176 al tumor suppressor activity of p53 prevents cardiac dysfunction in a mouse model induced by doxorubi

177 study sought to determine the prevalence of cardiac dysfunction in adult survivors of childhood mali

178 otential contribution of the CSAR control of cardiac dysfunction in both normal and chronic heart fai

179 hatase 1B (PTP1B) is associated with reduced cardiac dysfunction in CHF.

180 Cardiac dysfunction in CKD is characterized by aberrant

181 hibition of IkappaB kinase (IKK) reduces the cardiac dysfunction in CKD sepsis.

182 K1 (TnT-MEK1-CA) was administrated to rescue cardiac dysfunction in CM-HIPK2 knockout mice.

183 in and target the spectral manifestations of cardiac dysfunction in critical illness.

184 tered ZIP7 and ZnT7 activity, contributes to cardiac dysfunction in diabetes.

185 andidate mechanism behind the development of cardiac dysfunction in diabetes.

186 ning novel therapeutic approaches to prevent cardiac dysfunction in diabetic patients.

187 asome inhibition is also sufficient to cause cardiac dysfunction in healthy pigs, and patients using

188 herapeutic tool to reduce the progression of cardiac dysfunction in high-output heart failure.

189 It is important to note that cardiac dysfunction in HIPK2 knockout mice developed wit

190 tion of SPARC gene expression may ameliorate cardiac dysfunction in humans.

191 e the discussion regarding the potential for cardiac dysfunction in individuals in whom the risk is s

192 te the contribution of insulin signalling to cardiac dysfunction in KA hearts, we generated mice with

193 neration, leading to multiorgan fibrosis and cardiac dysfunction in mice during aging.

194 ralizes CVB3 and inhibits the development of cardiac dysfunction in mice with acute CVB3-induced myoc

195 UR2 loss-of-function causes fatigability and cardiac dysfunction in mice, and reduced activity, cardi

196 timicrobial peptide Pep2.5 may attenuate the cardiac dysfunction in murine polymicrobial sepsis throu

197 cells as integrators of perivascular CF and cardiac dysfunction in nonischemic HF.

198 ation of lipid intermediates, contributes to cardiac dysfunction in obesity and diabetes mellitus.

199 Cirrhotic cardiomyopathy (CCM) is cardiac dysfunction in patients with end-stage liver dis

200 Cardiac dysfunction in patients with liver cirrhosis is

201 g is postulated as a major driving force for cardiac dysfunction in patients with type 2 diabetes; ho

202 gh rate of myocardial fibrosis and increased cardiac dysfunction in people living with HIV.

203 examine the causes, mechanisms and impact of cardiac dysfunction in silico.

204 d here suggest an accelerated development of cardiac dysfunction in SIRT5KO mice in response to TAC,

205 mmendations for prevention and monitoring of cardiac dysfunction in survivors of adult-onset cancers.

206 ssociated with both onset and advancement of cardiac dysfunction in T1D.

207 ow that chronic rapamycin treatment prevents cardiac dysfunction in T2D mice, possibly through attenu

208 iographic parameters to identify subclinical cardiac dysfunction in the absence of overt structural a

209 esulted in severe dilated cardiomyopathy and cardiac dysfunction in the absence of stress.

210 sponsible for the impaired FA metabolism and cardiac dysfunction in the failing heart.

211 rditis with immune checkpoint inhibitors and cardiac dysfunction in the setting of cytokine release s

212 Cardiac dysfunction in the setting of isolated traumatic

213 ces likely contributes to the development of cardiac dysfunction in this setting.

214 low-twitch skeletal muscle defects accompany cardiac dysfunction in transgenic mice with a mutation i

215 ted the hypertrophic response and attenuated cardiac dysfunction in vivo.

216 myocytes in vitro, which are associated with cardiac dysfunction in vivo.

217 5-minute reperfusion) resulted in comparable cardiac dysfunction in wild-type and TIMP4(-/-) mice.

218 mic delivery of CTRP9 attenuated LPS-induced cardiac dysfunction in WT mice but not in muscle-specifi

219 icient mice, effectively correct exacerbated cardiac dysfunctions in eosinophil-deficient DeltadblGAT

220 ression, such as ventricular enlargement and cardiac dysfunction, in ARVD/C are relatively scarce.

221 ibrosis is a key antecedent to many types of cardiac dysfunction including heart failure.

222 derate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricu

223 Here we report that cardiac dysfunction induced by high-fat-diet (HFD) persi

224 TSD patients, which raises the likelihood of cardiac dysfunction induced by long-term stress exposure

225 ockout (Nrf2KO) hardly affected the onset of cardiac dysfunction induced by T1D but slowed down its p

226 bution of insulin signalling to inflammatory cardiac dysfunction induced by the activation of signall

227 rat model of "systemic inflammation-induced cardiac dysfunction" induced by intraperitoneal lipopoly

228 Cardiac dysfunction influences candidate selection for k

229 evidence suggests that echinocandin-related cardiac dysfunction is a mitochondrial drug-induced dise

230 Cardiac dysfunction is a prominent cause of mortality in

231 Purpose Cardiac dysfunction is a serious adverse effect of certa

232 By the time cardiotoxicity-associated cardiac dysfunction is detectable by echocardiography it

233 Reversible stress-induced cardiac dysfunction is frequently seen as a complication

234 Cardiac dysfunction is often associated with a shift in

235 cise mechanism by which inflammation induces cardiac dysfunction is still unclear.

236 Among Hispanics/Latinos, most cardiac dysfunction is subclinical or unrecognized, with

237 The prevailing view is that MFS-associated cardiac dysfunction is the result of aortic and/or valvu

238 eart mimicked impaired insulin signaling and cardiac dysfunction leading to HF observed after MI.

239 NA sequencing, performed before the onset of cardiac dysfunction, led to identification of 2338 diffe

240 Cardiac dysfunction may account for some of the unexplai

241 Cardiac dysfunction may be an important and underrecogni

242 st that strategies to upregulate BAG3 during cardiac dysfunction may be beneficial.

243 opose that angiogenic imbalance and residual cardiac dysfunction may exist even after recovery from P

244 Early detection of cardiac dysfunction may identify a high-risk subset of s

245 osis (T2* 6-20 milliseconds) and no signs of cardiac dysfunction (mean age, 19.8 years).

246 ]; P=0.016 for perivascular fibrosis), worse cardiac dysfunction (mean difference, -2.5 ms [95% CI, -

247 ation was impaired, scar size increased, and cardiac dysfunction more pronounced in mice with a genet

248 can result directly from the onset of a new cardiac dysfunction, most frequently an acute coronary s

249 or necrosis factor-alpha levels and improved cardiac dysfunction, myocardial inflammation, and oxidat

250 omozygous Celf1 knock-out neonates exhibited cardiac dysfunction not observed in older homozygous ani

251 g of SCN5A may contribute to a subset of the cardiac dysfunctions observed in myotonic dystrophy.

252 loss of both CM Tln1 and Tln2 and found that cardiac dysfunction occurred by 4 wk with 100% mortality

253 associated with subclinical or unrecognized cardiac dysfunction (odds ratio: 0.1; 95% confidence int

254 ent and complex cardiovascular disease where cardiac dysfunction often associates with mutations in s

255 suggesting a potential synergistic effect of cardiac dysfunction on fibrosis risk in NAFLD.

256 perspective develops cancer therapy-related cardiac dysfunction or a high-risk cardiovascular patien

257 lethal cardiac arrhythmias in the absence of cardiac dysfunction or fibroadiposis, palmoplantar kerat

258 monitoring of tissue iron sequestration and cardiac dysfunction- parameters essential for the precli

259 on by deletion of ACC2 prevented HFD-induced cardiac dysfunction, pathological remodeling, and mitoch

260 al PTP1B deficiency, is sufficient to reduce cardiac dysfunction post myocardial infarction.

261 The severity of cardiac dysfunction predicts mortality in patients with

262 Compared with those with clinical cardiac dysfunction, prevalent coronary heart disease wa

263 ts for future studies focused on the complex cardiac dysfunction processes through more efficient har

264 MAC-Mmp14 KO) resulted in attenuated post-MI cardiac dysfunction, reduced fibrosis, and preserved car

265 oved cardiac insulin sensitivity and opposed cardiac dysfunction/remodeling.

266 er weaning from bypass, she developed global cardiac dysfunction requiring veno-arterial extracorpore

267 ial-specific antioxidant before the onset of cardiac dysfunction rescues the metabolic defects.

268 modulate FA transfer to the heart and remedy cardiac dysfunction resulting from altered energy substr

269 the important role of ECC remodeling in the cardiac dysfunction secondary to chronic sympathetic act

270 96.1% of the cardiac dysfunction seen was subclinical or unrecognized

271 Hence, cardiac dysfunction should be targeted as a potentially

272 in risk factors; 7) post-ASO arrhythmias and cardiac dysfunction should raise suspicion of coronary i

273 Sepsis induced cardiac dysfunction (SIC) is a severe complication to se

274 Reversal of MF improves key measures of cardiac dysfunction, so reversal of MF represents a like

275 However, how elevated CELF1 level leads to cardiac dysfunction, such as conduction defect, DCM, and

276 ated that reduction of HIPK2 in CMs leads to cardiac dysfunction, suggesting a causal role in heart f

277 heart was an adaptive response that limited cardiac dysfunction, suggesting that manipulations that

278 ion are less prone to fibrotic remodeling or cardiac dysfunction than hearts with a lipolytic defect

279 ata suggest that polymicrobial sepsis causes cardiac dysfunction that appears to be linked to activat

280 ytes (CMs), resulting in redox imbalance and cardiac dysfunction that can be functionally measured an

281 al cell (CMC) therapy mitigates post-infarct cardiac dysfunction, the underlying mechanisms remain un

282 stablish the optimal protocol of Cfz-induced cardiac dysfunction, to investigate the underlying molec

283 otherapy are at risk for trastuzumab-related cardiac dysfunction (TRCD).

284 ptin activates mechanisms that contribute to cardiac dysfunction under physiological conditions.

285 f-function zebrafish mutants show sensitized cardiac dysfunction upon short-term verapamil treatment.

286 In addition, sepsis-induced cardiac dysfunction was attenuated in these KO mice.

287 Cardiac dysfunction was defined as left ventricular ejec

288 Post-cardiopulmonary resuscitation cardiac dysfunction was not associated with myocardial n

289 d contractile function in vitro; however, no cardiac dysfunction was observed in vivo.

290 MKIIdelta TG mice (6-8 weeks) where no overt cardiac dysfunction was present.

291 Polymicrobial sepsis-induced cardiac dysfunction was produced by cecal ligation punct

292 ys that are potentially involved in T1D with cardiac dysfunction, we sought to identify differentiall

293 Heart failure, cardiac death, and cardiac dysfunction were infrequent in both treatment gr

294 ntials were prolonged, but no arrhythmias or cardiac dysfunction were noted.

295 ce of an underlying structural or functional cardiac dysfunction (whether chronic in ADHF or undiagno

296 e mechanism involved in inflammation-induced cardiac dysfunction, which suggests that it may be a tar

297 h cardiac-specific Klf4 deficiency developed cardiac dysfunction with aging or in response to pressur

298 Previously undiagnosed cardiac dysfunction with preserved ejection fraction was

299 e demonstrated poor survival and significant cardiac dysfunction with remarkable dilation.

300 influence on offspring physiology, including cardiac dysfunction, yet many reptile embryos naturally