ライフサイエンスコーパス: CHF

1 CHF is caused by mutations in PKHD1, a gene encoding for

2 CHF was assessed 4 months after myocardial infarction.

3 CHF-induced endothelial dysfunction was less marked in e

4 or capsaicin from 0.27% (CHF-CA-1) to 3.03% (CHF-CA-21), oleoresin content from 2.49% (CHF-CA-5) to 9

5 3) mg GAE/g and total carotenoids from 0.09 (CHF-CA-16) to 7.72 (CHF-CA-17) mg/g dry weight.

6 Total phenolics ranged from 5.1 (CHF-CA-8) to 26.8 (CHF-CA-23) mg GAE/g and total caroten

7 in CHF-CBD animals (213 +/- 58 events h(-1) CHF, 108 +/- 48 events h(-1) CHF-CBD, P < 0.05).

8 58 events h(-1) CHF, 108 +/- 48 events h(-1) CHF-CBD, P < 0.05).

9 re were 37,441 AMI incident cases and 95,138 CHF incident cases.

10 17-109.52) in CHF-CA-6, CHF-CA-7, CHF-CA-17, CHF-CA-21, CHF-CA-22 and CHF-CA-23 genotypes.

11 mals: (1) sham CHF/sham-CBD (sham-sham); (2) CHF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD).

12 in CHF-CA-6, CHF-CA-7, CHF-CA-17, CHF-CA-21, CHF-CA-22 and CHF-CA-23 genotypes.

13 g implemented to reduce emissions of HFC-23 (CHF[Formula: see text]), a by-product during the manufac

14 esin content from 2.49% (CHF-CA-5) to 9.26% (CHF-CA-18) with high to moderate ascorbic acid.

15 d showed variation for capsaicin from 0.27% (CHF-CA-1) to 3.03% (CHF-CA-21), oleoresin content from 2

16 The antioxidant activity varied from 15.3% (CHF-CA-4) to 60.7% (CHF-CA-21).

17 -sham); (2) CHF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD).

18 1.29-1.89; MI: HR, 1.92; 95% CI, 1.57-2.34; CHF: HR, 1.90; 95% CI, 1.66-2.18, and death: HR, 1.55; 9

19 .18-1.46), MI (HR, 1.30; 95% CI, 1.15-1.46), CHF (HR, 1.29; 95% CI, 1.19-1.40), and death (HR, 1.15;

20 % (CHF-CA-21), oleoresin content from 2.49% (CHF-CA-5) to 9.26% (CHF-CA-18) with high to moderate asc

21 high ARP values (56.17-109.52) in CHF-CA-6, CHF-CA-7, CHF-CA-17, CHF-CA-21, CHF-CA-22 and CHF-CA-23

22 ivity varied from 15.3% (CHF-CA-4) to 60.7% (CHF-CA-21).

23 values (56.17-109.52) in CHF-CA-6, CHF-CA-7, CHF-CA-17, CHF-CA-21, CHF-CA-22 and CHF-CA-23 genotypes.

24 l carotenoids from 0.09 (CHF-CA-16) to 7.72 (CHF-CA-17) mg/g dry weight.

25 henolics ranged from 5.1 (CHF-CA-8) to 26.8 (CHF-CA-23) mg GAE/g and total carotenoids from 0.09 (CHF

26 1.84-3.48; MI: HR, 1.89; 95% CI, 1.26-2.83; CHF: HR, 1.96; 95% CI, 1.47-2.59; and death: HR, 1.87; 9

27 de new insights on the myopathy accompanying CHF.

28 follow-up of 9.2 years, only two additional CHF diagnoses (of 1,046 patients) occurred beyond our pr

29 llein, which we previously showed alleviates CHF in this model, attenuated these pathologic renal cha

30 Although CHF together with liver ductal plate malformations are c

31 Among admissions for AMI, CHF, and pneumonia identified in MedPAR, 29.2%, 38.0%, a

32 mission rates after hospitalization for AMI, CHF, or pneumonia for hospitals in the highest-performan

33 mission rates after hospitalization for AMI, CHF, or pneumonia for hospitals in the highest-performan

34 1.45; 95% CI: 1.40 to 1.51; p < 0.0001), and CHF (HR: 2.34; 95% CI: 2.29 to 2.39; p < 0.0001).

35 whole PLD population was CHF 23 298 046 and CHF 4298 per person.

36 dent AMI (HR = 1.07; 95% CI: 1.05, 1.08) and CHF (HR = 1.06; 95% CI: 1.05, 1.07).

37 dent AMI (HR = 1.07; 95% CI: 1.06, 1.08) and CHF (HR = 1.07; 95% CI: 1.06, 1.09).

38 HF-CA-7, CHF-CA-17, CHF-CA-21, CHF-CA-22 and CHF-CA-23 genotypes.

39 d via P,C-dimorpholinamide CHCl (6a, 6b) and CHF (7a, 7b) bisphosphonates (BPs) equipped with an (R)-

40 angiotensin II infusion, mimicking aging and CHF as reported.

41 fidence intervals (CIs) for incident AMI and CHF in relation to LAeq24 and LAeqNight using random-eff

42 s associated with elevated risks for AMI and CHF incidence.

43 s between noise and the incidence of AMI and CHF with no evidence of threshold values.

44 d traffic noise and the incidence of AMI and CHF.

45 nagement of post-procedure complications and CHF may be critical for reducing mortality rates followi

46 the link between endothelial dysfunction and CHF.

47 ave been reported for installing CH(2) F and CHF(2) groups, they are mainly limited to radical reacti

48 TS on baroreflex control both in healthy and CHF rats.

49 ohol abuse increased the risk of AF, MI, and CHF to a similar degree as other well-established risk f

50 ohol abuse diagnosis on incident AF, MI, and CHF.

51 TS on baroreflex function both in normal and CHF states is not fully understood.

52 ntrol of cardiac function in both normal and CHF states remains unknown.

53 ial effect on cardiac function in normal and CHF states.

54 t PAFs were located in ARMS2 (rs3750846) and CHF (rs570618 and rs10922109).

55 t rest and during CBC activation in sham and CHF rabbits.

56 Pathological states such as CHF, MDD, and PD are associated with an increased comple

57 dominant role on hydrodynamic instability at CHF when the height of surface structures is equal or ab

58 le wavelength on hydrodynamic instability at CHF, and the results indicate that module wavelength pla

59 e wavelength, on hydrodynamic instability at CHF.

60 as similarly increased in both MI-CHF and AV-CHF rats compared to control.

61 only in MI-CHF rats compared to Sham and AV-CHF rats.

62 uced in the CBs of MI-CHF rats but not in AV-CHF rats.

63 l (MI-CHF) and as a high output HF model (AV-CHF), respectively.

64 hypoxic ventilatory response compared to AV-CHF rats.

65 Hospital-based CHF events were only increased with sequential therapy (

66 therapy increased the risk of hospital-based CHF events.

67 lysis limited the outcomes to hospital-based CHF events.

68 th HF of a large multicenter cohort (BIOSTAT-CHF [A Systems Biology Study to Tailored Treatment in Ch

69 08 men and 402 women with HFrEF from BIOSTAT-CHF, women were older (74 [12] years vs 70 [12] years, p

70 ltivariable analysis, which included BIOSTAT-CHF risk scores, LDLR, and statin treatment as covariate

71 We did a post-hoc analysis of BIOSTAT-CHF, a prospective study in 11 European countries of pat

72 Union's Seventh Framework Programme (BIOSTAT-CHF), John and Lucille van Geest Foundation.

73 The BIOSTAT-CHF (Biology Study to Tailored Treatment in Chronic Hear

74 en added to the previously validated BIOSTAT-CHF risk scores.

75 ation of the fluorovinylidene complex [Ru(=C=CHF)(eta(5) -C5 Me5 )(dppe)][N(SO2 Ph)2 ].

76 2) CHF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD).

77 CHF/sham-CBD (sham-sham); (2) CHF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD).

78 ining fluorine in in the acetyl side chain (-CHF-CO-) bearing nucleobase uracil (5-F/5-CF3-U).

79 Metformin use in patients with moderate CKD, CHF, or CLD with hepatic impairment is associated with i

80 ed all-cause mortality in patients with CKD, CHF, or CLD with hepatic impairment, and with fewer hear

81 n the majority of the patients who developed CHF.

82 tribute to baroreflex desensitization during CHF.

83 TrkB pathway is impaired in the dmNTS during CHF provides a novel mechanism for understanding the cen

84 in BDNF-TrkB signalling in the dmNTS during CHF that contributes to sympatho-excitation and barorefl

85 ecreased TrkB expression in the dmNTS during CHF.

86 athing, RSNA and arrhythmia incidence during CHF.

87 Mainly, during CHF the CB chemosensitivity is enhanced leading to incre

88 d to the increased sympathoexcitation during CHF.

89 ic cue to modulate sympathoexcitation during CHF.

90 the boiling surface as a means of enhancing CHF has not been proposed.

91 acids and cyclopropylamines bearing CH(2)F, CHF(2), and CF(3) substituents were synthesized by diffe

92 4.06; p < 0.001), congestive heart failure (CHF) (aOR: 2.20; p = 0.011) and low AF ablation hospital

93 th the progression of chronic heart failure (CHF) and a poor prognosis.

94 xide with incident congestive heart failure (CHF) and acute myocardial infarction.

95 Patients with congestive heart failure (CHF) have impaired functional capacity and inferior qual

96 Chronic heart failure (CHF) induces endothelial dysfunction in part because of

97 Chronic heart failure (CHF) is a major public health problem.

98 farction (AMI) and congestive heart failure (CHF) is inconclusive, especially in North America.

99 ents with advanced congestive heart failure (CHF) or chronic kidney disease often have increased angi

100 nduced ischemia in congestive heart failure (CHF) patients is unknown.

101 Chronic heart failure (CHF) results in blunting of arterial baroreflex sensitiv

102 iduals have excess congestive heart failure (CHF) risk compared with uninfected people.

103 on in both normal and chronic heart failure (CHF) states remains unknown.

104 splayed [mean +/- SD; chronic heart failure (CHF) vs. Sham, respectively] a marked increase in the in

105 for incident CHD, congestive heart failure (CHF), and other causes of death.

106 art disease (IHD), congestive heart failure (CHF), and overall CVD were obtained from the national in

107 ing development of congestive heart failure (CHF), chronic activation of Gs-dependent beta1AR and Gi-

108 tes in adults with congestive heart failure (CHF), coronary artery disease (CAD), cerebrovascular acc

109 t of CKD secondary to chronic heart failure (CHF), known as cardiorenal syndrome type 2 (CRS2), clini

110 a or preeclampsia, congestive heart failure (CHF), length of stay, preterm labor, anemia complicating

111 gy and psychiatry: Congestive Heart Failure (CHF), Major Depression Disorder (MDD), Parkinson's Disea

112 and patients with congestive heart failure (CHF), matched for age, sex, and year of discharge.

113 ney disease (CKD), congestive heart failure (CHF), or chronic liver disease (CLD) with hepatic impair

114 infarction (AMI), congestive heart failure (CHF), or pneumonia and whether the lowest-performing hos

115 infarction (AMI), congestive heart failure (CHF), or pneumonia and whether the lowest-performing hos

116 ncy room visit for congestive heart failure (CHF), outpatient diagnosis of CHF, or cardiovascular dea

117 art disease (IHD), congestive heart failure (CHF), stroke, chronic kidney disease (CKD), retinopathy,

118 farction (MI), and congestive heart failure (CHF).

119 to the progression of chronic heart failure (CHF).

120 commonly observed in chronic heart failure (CHF).

121 le risk factor for congestive heart failure (CHF).

122 been described in congestive heart failure (CHF).

123 y in patients with congestive heart failure (CHF).

124 ograph features in congestive heart failure (CHF).

125 eople especially with chronic heart failure (CHF).

126 ibute to mortality in chronic heart failure (CHF).

127 l sympathetic tone in chronic heart failure (CHF).

128 onophthisis and congenital hepatic fibrosis (CHF) in the liver.

129 Congenital hepatic fibrosis (CHF) is a disease of the biliary epithelium characterize

130 ular disease were followed until their first CHF event, death, last follow-up date, or December 31, 2

131 of research on enhancing critical heat flux (CHF) has focused on altering the boiling surface propert

132 The critical heat flux (CHF) in boiling and the Leidenfrost point temperature (L

133 Enhancing the critical heat flux (CHF) of industrial boilers by surface texturing can lead

134 increase in the boiling critical heat flux (CHF) was observed.

135 he onset of pool boiling Critical Heat Flux (CHF).

136 ged from 9.5 to 12.2 for IHD, 7.7 to 9.1 for CHF, and 15.8 to 19.2 for overall CVD.

137 appearing in HEDIS, 14.4% for AMI, 18.4% for CHF, and 13.9% for pneumonia resulted in a readmission.

138 16.6% vs. 17.1% for AMI, 21.4% vs. 21.7% for CHF, and 16.3% vs. 16.4% for pneumonia).

139 Of these, 18.9% for AMI, 23.7% for CHF, and 18.3% for pneumonia resulted in a readmission t

140 years of 242.7 for IHD (P = 0.02), 271.8 for CHF (P = 0.01), and 497.2 for overall CVD (P < 0.001).

141 s may represent a modifiable risk factor for CHF and death.

142 The Central Hardwood Forest (CHF) in the United States is currently a major carbon si

143 ss-to-pay threshold of 100 000 Swiss Francs (CHF) per quality-adjusted life-year (QALY), comprehensiv

144 be important for reducing the risk of future CHF events, particularly among HIV and hepatitis C infec

145 beta,gamma-CHCl-dTTP (11a, 11b), beta,gamma-CHF (12a, 12b), and beta,gamma-CHCl (13a, 13b) dATP dias

146 3b), beta,gamma-CHCl- (34a, 34b), beta,gamma-CHF-dCTP (35a, 35b) were obtained.

147 as also independently associated with higher CHF incidence (HRIQR = 1.04, 95% CI: 1.03, 1.06).

148 ant murine model of nonischemic hypertrophic CHF, transverse aortic constriction (TAC).

149 g/mg DPPH, high ARP values (56.17-109.52) in CHF-CA-6, CHF-CA-7, CHF-CA-17, CHF-CA-21, CHF-CA-22 and

150 al perfusion and neurohormonal activation in CHF patients with reduced left-ventricular function usin

151 icating that the CSAR is tonically active in CHF and contributes to cardiac dysfunction.

152 pheral (renal) sympathetic nerve activity in CHF rats but not in sham rats.

153 central chemoreflex function are altered in CHF and that they contribute to autonomic imbalance and

154 Interestingly, BK application in CHF rats increased cardiac systolic and diastolic volume

155 our patients, most of those mutations are in CHF.

156 hese responses were significantly blunted in CHF rats.

157 ransfection of KLF2 to the carotid bodies in CHF rabbits restored KLF2 expression, and reduced AHI (7

158 agonism had little effect on reducing BRS in CHF animals, which is corroborated by the observation of

159 neration, likely contributing to cachexia in CHF and chronic kidney disease.

160 sing and lowering HR on exercise capacity in CHF as assessed by symptom-limited treadmill exercise te

161 y the role of the HR on exercise capacity in CHF.

162 contributes to impaired exercise capacity in CHF.

163 ionship between HRR and exercise capacity in CHF; and 2) the effect of increasing and lowering HR on

164 cardiac and peripheral responses to CSAR in CHF animals compared to sham-operated controls.

165 R, LVSP, dp/dt, LVEDP and ESPVR decreased in CHF rats whereas lidocaine had little effect in sham rat

166 significant myocardial perfusion defects in CHF patients.

167 tion in their function has been described in CHF.

168 The baroreflex desensitization in CHF is at least partly the result of central neuronal ne

169 flexes to augmented sympathetic discharge in CHF could help in developing new therapeutic approaches

170 a causal role for endothelial dysfunction in CHF development.

171 sociated with reduced cardiac dysfunction in CHF.

172 am rats, whereas it had less of an effect in CHF rats.

173 Importantly, sympatho-excitation in CHF exacerbates its progression and is strongly related

174 cardiac contractility to a greater extent in CHF rats than sham rats.

175 wever, the mechanisms leading to fibrosis in CHF remain elusive.

176 Arrhythmia incidence was increased in CHF-sham and reduced in CHF-CBD animals (213 +/- 58 even

177 cardiac cachexia and exercise intolerance in CHF.

178 The decreased preload by lidocaine in CHF rats may be due to a reduction in peripheral vascula

179 Here we report on the existence of maxima in CHF enhancement at intermediate texture density using me

180 entricular end-diastolic volume (preload) in CHF rats, which was not observed in sham rats.

181 creased LV end-diastolic volume (preload) in CHF rats, which was not observed in sham rats.

182 th less effect on systolic blood pressure in CHF rats.

183 sympathoexcitatory responses from the PVN in CHF.

184 nce was increased in CHF-sham and reduced in CHF-CBD animals (213 +/- 58 events h(-1) CHF, 108 +/- 48

185 KLF2), mediates increased CBC sensitivity in CHF and contributes to associated autonomic, respiratory

186 Alterations to NTS signalling in CHF remain particularly undefined.

187 286/+690 enhancer activity was suppressed in CHF mouse skeletal muscle, suggesting that AT2R expressi

188 esting that AT2R expression is suppressed in CHF via inhibition of AT2R intronic enhancer activity, l

189 of NMDA-NR1 to mediate sympathoexcitation in CHF.

190 ausally related to the sympathoexcitation in CHF.

191 (INcrease Of VAgal TonE in CHF [INOVATE-HF]; NCT01303718).

192 iven that beta2AR expression is unaltered in CHF, a beta-arrestin-biased agonist that operates throug

193 Incident CHF, atrial arrhythmias, ventricular arrhythmias, and ma

194 3 participants over 6.9 years, 3844 incident CHF events occurred.

195 between stage of liver fibrosis and incident CHF is modified by HIV/HCV status.

196 of advanced fibrosis/cirrhosis and incident CHF persisted regardless of HIV/HCV status.

197 Participants were followed for incident CHF and death.

198 The population-level risk for incident CHF attributed to PVCs was 8.1% (95% CI: 1.2% to 14.9%).

199 e relationship among PVC frequency, incident CHF, and mortality in the general population remains unk

200 a decrease in LVEF, an increase in incident CHF, and increased mortality.

201 ntricular ejection fraction (LVEF), incident CHF, and death in a population-based cohort.

202 p = 0.005), a 48% increased risk of incident CHF (HR: 1.48; 95% CI: 1.08 to 2.04; p = 0.02), and a 31

203 ere associated with greater odds of incident CHF.

204 is is independently associated with incident CHF and 2) the association between stage of liver fibros

205 California, CHD was associated with incident CHF, atrial arrhythmias, and fetal growth restriction an

206 y rats with coronary artery ligation-induced CHF and sham operated controls and recorded blood pressu

207 nternational Congestive Heart Failure (INTER-CHF) study, we aimed to measure mortality at 1 year in p

208 average willingness to pay per household is CHF 100 (US$ 73) annually for reducing the potential env

209 thin the PVN of left coronary artery-ligated CHF rats.

210 iltration rate less than 60 mL/min/1.73 m2), CHF, or CLD with hepatic impairment; 2) compared diabete

211 A maximum CHF of 1.8 kW/cm(2) was achieved on a copper structure w

212 res ultimately limits the CHF; and a maximum CHF of 7-8 kW/cm(2) may be achieved using diamond surfac

213 s and the 5-year risk of first-time CVA, MI, CHF, and all-cause mortality was investigated using mult

214 ntly associated with future risk of CVA, MI, CHF, and death, with higher degrees of retinopathy appea

215 MI-CHF rats exhibited a significantly enhanced hypoxic vent

216 incidence was similarly increased in both MI-CHF and AV-CHF rats compared to control.

217 ly to the CB region was decreased only in MI-CHF rats compared to Sham and AV-CHF rats.

218 rats were used as a low output HF model (MI-CHF) and as a high output HF model (AV-CHF), respectivel

219 ription factor, was reduced in the CBs of MI-CHF rats but not in AV-CHF rats.

220 eric arteries showed that in wild-type mice, CHF markedly impaired NO-dependent flow-mediated dilatat

221 n endothelial dysfunction and aggravation of CHF is not directly established.

222 ife may contribute to the ischemic burden of CHF patients with coronary artery disease.

223 the limitation of which is characteristic of CHF.

224 heart failure (CHF), outpatient diagnosis of CHF, or cardiovascular death.

225 els of TrkB protein and mRNA in the dmNTS of CHF rats.

226 ighted conventional radiographic features of CHF as reasons for an elevated BNP prediction more frequ

227 ndly assessed by two experts for features of CHF.

228 n-ischemic cardiomyopathy without history of CHF were studied with cardiovascular magnetic resonance

229 and who had a normal LVEF and no history of CHF.

230 e was associated with increased incidence of CHF (hazard ratio for an interquartile-range increase (H

231 riuretic peptide [BNP] result as a marker of CHF) and unlabeled data set (without BNP result).

232 s At a cutoff BNP of 100 ng/L as a marker of CHF, the correctly trained model achieved an AUC of 0.82

233 n chronic diseases, we used a mouse model of CHF and found that muscle regeneration was markedly redu

234 1(del4/del4)) mouse, which is orthologous of CHF, we show that Pkhd1(del4/del4) cholangiocytes are ch

235 nd revealed new details about the physics of CHF.

236 hes intended to attenuate the progression of CHF.

237 te to autonomic imbalance and progression of CHF.

238 case incremental cost-effectiveness ratio of CHF 14 312 per QALY.

239 niformly was associated with greater risk of CHF events across subgroups stratified by eGFR, proteinu

240 The specificity for the 15-year risk of CHF exceeded 90% when PVCs included at least 0.7% of ven

241 sis are associated with an increased risk of CHF.

242 erapy in Congestive Heart Failure (SECRET of CHF) trials.

243 ith Challenging Volume Management [SECRET of CHF]; NCT01584557).

244 ve are considered markers of the severity of CHF.

245 mated annual costs for upgrading 123 STPs of CHF 133 million (US$ 97 million) or CHF 86 (US$ 63) per

246 e heat transfer area, and liquid pressure on CHF is precisely quantified.

247 failure readmissions in patients with CKD or CHF.

248 ee of AMI (referred to as the AMI cohort) or CHF (the CHF cohort) at baseline.

249 STPs of CHF 133 million (US$ 97 million) or CHF 86 (US$ 63) per household connected to these STPs.

250 oint [95% CI, 0.1 to 0.5 percentage point]), CHF (21.7% vs. 21.4%; difference, 0.3 percentage point [

251 selectively lowered diastolic blood pressure CHF rats.

252 The RECEDE-CHF trial (SGLT2 Inhibition in Combination With Diuretic

253 n that endothelial protection per se reduces CHF and further suggest a causal role for endothelial dy

254 coupled thermal-hydraulic model that relates CHF enhancement to rewetting of a hot dry spot on the bo

255 Severe CHF was the same for 2-year and 1-year trastuzumab.

256 se capacity and HRR is much weaker in severe CHF compared to normal left ventricular function; 2) inc

257 easured in three groups of animals: (1) sham CHF/sham-CBD (sham-sham); (2) CHF/sham-CBD (CHF-sham); a

258 Compared to sham, CHF rats exhibit a reduced increase in the slope of the

259 of the photoresist was treated with a short CHF(3) reactive ion etch to ensure consistent hydrophobi

260 rior studies on boiling crisis indicate that CHF monotonically increases with increasing texture dens

261 etics and with the ipsocentric method at the CHF/6-31G** level to calculate current-density maps.

262 (referred to as the AMI cohort) or CHF (the CHF cohort) at baseline.

263 how that, when rewetting is facilitated, the CHF increases linearly with the effective surface heat t

264 current carbon sink will persist and if the CHF will eventually become a carbon source.

265 atho-inhibition of BDNF was withdrawn in the CHF state, thus contributing to the increased sympatheti

266 rkB signalling is impaired in the NTS in the CHF state.

267 aggerated peripheral vasoconstriction in the CHF state.

268 whether liver fibrosis stage influences the CHF risk or if HIV or hepatitis C virus (HCV) infection

269 the surface structures ultimately limits the CHF; and a maximum CHF of 7-8 kW/cm(2) may be achieved u

270 rch reports a substantial enhancement of the CHF by 112% and an increase of the LPT by 40 K using an

271 nvestigate aboveground carbon density of the CHF from 2010 to 2300 under current climate.

272 ermediate demographic approach predicted the CHF would become a carbon source between 2110 and 2260,

273 rs and the trans head-head isomer, where the CHF group is defined as the TrFE "head".

274 e Pharmacogenomic Registry (n=247), the TIME-CHF (Trial of Intensified Versus Standard Medical Therap

275 s after TAC, mice developed CKD secondary to CHF associated with elevated renal GPCR-Gbetagamma signa

276 the mechanism governing the hitherto unknown CHF enhancement maxima.

277 f freedom has enabled reaching unprecedented CHF levels and revealed new details about the physics of

278 rsely affect exercise capacity in unselected CHF patients.

279 s CBC responses to hypoxia (all P < 0.05 vs. CHF empty virus).

280 it of screening the whole PLD population was CHF 23 298 046 and CHF 4298 per person.

281 ced fibrosis/cirrhosis) were associated with CHF (hazard ratio [95% confidence interval], 1.17 [1.07-

282 e increased sympathetic tone associated with CHF.

283 The largest effects occurred with CHF (incidence rate ratio [IRR] range, 4.84-13.4 across

284 ients with cirrhosis (41%) and patients with CHF (44%).

285 rrhosis (from 2.6% to 2.1%) or patients with CHF (from 2.5% to 1.4%) (P < .01).

286 or patients without CHF versus patients with CHF (from 55% to 73.5%, P < .001).

287 ications for rehabilitation of patients with CHF and provide new insights on the myopathy accompanyin

288 apacity and quality of life in patients with CHF and stimulate skeletal muscle myofibrillar and mitoc

289 C activation has been shown in patients with CHF as well as in animal models.

290 xed-rate pacing) in unselected patients with CHF does not improve peak exercise capacity; and 3) acut

291 of peak oxygen consumption in patients with CHF due to left ventricular systolic dysfunction.

292 We randomized 36 patients with CHF to BFRRE, RIC, or nontreatment control.

293 udied 50 patients with CRC, 51 patients with CHF, and 51 control subjects.

294 ith and without cirrhosis, and patients with CHF, decreased over time.

295 utflow is commonly observed in patients with CHF.

296 minative power for identifying patients with CHF.

297 croinjection of NMDA in the PVN of rats with CHF.

298 ted FGF-23 was associated more strongly with CHF than with atherosclerotic events (P=0.02), and unifo

299 ase patients (mean age+/-SD, 62+/-10 y) with CHF longer than 3 mo and ejection fraction less than 40%

300 riminative power of RFs for patients without CHF versus patients with CHF (from 55% to 73.5%, P < .00