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 n CHF-sham animals (sham-sham 0.49 +/- 0.05; CHF-sham 0.79 +/- 0.06), and was attenuated in CHF-CBD a

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

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

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

9 58 events h(-1) CHF, 108 +/- 48 events h(-1) CHF-CBD, P < 0.05).

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

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

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

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

17 % (CHF-CA-21), oleoresin content from 2.49% (CHF-CA-5) to 9.26% (CHF-CA-18) with high to moderate asc

18 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

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

20 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.

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

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

23 beta-blockers (OR, 1.0 [95% CI, 0.57-1.9]); CHF with use of ACE inhibitor (OR, 0.98 [95% CI, 0.61-1.

24 nges in patients with AF and/or CHF and in a CHF-related AF animal model and assessed its potential r

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

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

27 d EcSOD expression significantly ameliorated CHF-induced oxidative stress, MAFbx/Atrogin-1 mRNA expre

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

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

30 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).

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

32 ascular perturbations are present in CRC and CHF.

33 the link between endothelial dysfunction and CHF.

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

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

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

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

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

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

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

41 rapeutic target in wasting disorders such as CHF and CKD.

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

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

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

45 e wavelength, on hydrodynamic instability at CHF.

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

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

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

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

50 hypoxic ventilatory response compared to AV-CHF rats.

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

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

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

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

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

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

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

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

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

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

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

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

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

64 n the majority of the patients who developed CHF.

65 ents with LGE had greater risk of developing CHF than patients without LGE (hazard ratio, 5.23 [2.61-

66 tribute to baroreflex desensitization during CHF.

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

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

69 ecreased TrkB expression in the dmNTS during CHF.

70 athing, RSNA and arrhythmia incidence during CHF.

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

72 d to the increased sympathoexcitation during CHF.

73 ic cue to modulate sympathoexcitation during CHF.

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

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

76 isk of adjudicated congestive heart failure (CHF) and atherosclerotic events (myocardial infarction,

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

78 Congestive heart failure (CHF) is a leading cause of morbidity and mortality, and

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

80 ents with advanced congestive heart failure (CHF) or chronic kidney disease (CKD) often have increase

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

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

83 ntially attenuated in chronic heart failure (CHF) patients.

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

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

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

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

88 of beta-blockers; congestive heart failure (CHF) with use of angiotensin-converting enzyme (ACE) inh

89 diac death, severe congestive heart failure (CHF), and confirmed significant LVEF decrease remained l

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

91 In congestive heart failure (CHF), carotid body (CB) chemoreceptor activity is enhanc

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

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

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

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

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

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

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

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

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

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

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

103 commonly observed in chronic heart failure (CHF).

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

105 been described in congestive heart failure (CHF).

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

107 toms in patients with chronic heart failure (CHF).

108 without history of congestive heart failure (CHF).

109 cardial infarction or chronic heart failure (CHF).

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

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

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

113 function causes congenital hepatic fibrosis (CHF), Caroli disease (CD), and autosomal recessive polyc

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

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

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

117 approximately two times critical heat flux (CHF) increase compared to that of a plain surface.

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

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

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

121 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.

122 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).

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

124 ears, 360 participants were hospitalized for CHF (27 events/1000 person-years) and 287 had an atheros

125 e echocardiography reduced lifetime risk for CHF by 2.3% (with assessment every 10 years) to 8.7% (an

126 ment effectiveness, absolute excess risk for CHF, and asymptomatic left ventricular dysfunction asymp

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

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

129 e resolution of the corresponding beta,gamma-CHF-dGTP spectra, stating further that 1 decomposed unde

130 amma-fluoromethylenetriphosphate (beta,gamma-CHF-UTP, 1) by (19)F NMR under conditions we previously

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

132 +/- 2% reduction from pre-pace, P < 0.05) in CHF-CBD compared to CHF-sham rabbits.

133 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

134 were augmented in CHF-sham and abolished in CHF-CBD animals.

135 eat stress evoked similar SSNA activation in CHF patients (Delta891+/-110 U/min) and the control subj

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

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

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

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

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

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

142 F-sham 0.79 +/- 0.06), and was attenuated in CHF-CBD animals (0.59 +/- 0.05) (P < 0.05 for all compar

143 nd VE responses to hypoxia were augmented in CHF-sham and abolished in CHF-CBD animals.

144 hese responses were significantly blunted in CHF rats.

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

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

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

148 ntributing to the development of cachexia in CHF and CKD.

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

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

151 contributes to impaired exercise capacity in CHF.

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

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

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

155 significant myocardial perfusion defects in CHF patients.

156 tion in their function has been described in CHF.

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

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

159 a causal role for endothelial dysfunction in CHF development.

160 sociated with reduced cardiac dysfunction in CHF.

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

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

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

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

165 < 0.05), and this increase was not found in CHF-CBD animals (25 +/- 1% max, P < 0.05 vs. CHF-sham).

166 Resting RSNA was greater in CHF-sham compared to sham-sham animals (43 +/- 5% max vs

167 variability ratio was similarly increased in CHF and reduced by CBD (P < 0.05).

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

169 SRC (peak coherence) was increased in CHF-sham animals (sham-sham 0.49 +/- 0.05; CHF-sham 0.79

170 and apnoea-hypopnoea index were increased in CHF-sham animals and reduced in CHF-CBD animals (P < 0.0

171 cardiac cachexia and exercise intolerance in CHF.

172 cardiac cachexia and exercise intolerance in CHF.

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

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

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

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

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

178 sympathoexcitatory responses from the PVN in CHF.

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

180 increased in CHF-sham animals and reduced in CHF-CBD animals (P < 0.05).

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

182 Alterations to NTS signalling in CHF remain particularly undefined.

183 286/+690 enhancer activity was suppressed in CHF mouse skeletal muscle, suggesting that AT2R expressi

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

185 of NMDA-NR1 to mediate sympathoexcitation in CHF.

186 ausally related to the sympathoexcitation in CHF.

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

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

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

190 3 participants over 6.9 years, 3844 incident CHF events occurred.

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

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

193 Participants were followed for incident CHF and death.

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

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

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

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

198 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

199 ere associated with greater odds of incident CHF.

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

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

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

203 prove ventricular function in pacing-induced CHF rabbits.

204 ility and cardiac function in pacing-induced CHF rabbits.

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

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

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

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

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

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

211 MI-CHF rats exhibited a significantly enhanced hypoxic vent

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

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

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

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

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

217 We isolated neonatal CHF/Hey2-knockout (KO) cardiac myocytes and measured act

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

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

220 the limitation of which is characteristic of CHF.

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

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

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

224 n-ischemic cardiomyopathy without history of CHF, myocardial fibrosis is a strong and independent pre

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

226 when crossbred into a mouse genetic model of CHF (alpha-myosin heavy chain-calsequestrin), MCK-EcSOD

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

228 ssification improvement, 29.6%) and onset of CHF (net reclassification improvement, 25.4%; both P<0.0

229 t was a composite of cardiac death, onset of CHF, and aborted sudden cardiac death.

230 1(del4/del4)) mouse, which is orthologous of CHF, we show that Pkhd1(del4/del4) cholangiocytes are ch

231 nd revealed new details about the physics of CHF.

232 hes intended to attenuate the progression of CHF.

233 te to autonomic imbalance and progression of CHF.

234 independently associated with graded risk of CHF (hazard ratio [HR], 1.45 per doubling [95% confidenc

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

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

237 sis are associated with an increased risk of CHF.

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

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

240 ve are considered markers of the severity of CHF.

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

242 d, generate a total annual economic value of CHF 155 million (US$ 113 million).

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

244 ed miR29b changes in patients with AF and/or CHF and in a CHF-related AF animal model and assessed it

245 failure readmissions in patients with CKD or CHF.

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

247 risk of cardiovascular events, particularly CHF, in patients with CKD stages 2-4.

248 selectively lowered diastolic blood pressure CHF rats.

249 mendations for cardiac assessment may reduce CHF incidence, but less frequent assessment may be prefe

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

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

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

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

254 CoQ(1)(0)/d and in patients with less severe CHF.

255 The incidence of severe CHF (0.8%, 0.8%, and 0.0%, respectively) and confirmed s

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

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

258 The lifetime risk for systolic CHF among 5-year childhood cancer survivors aged 15 year

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

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

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

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

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

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

265 aggerated peripheral vasoconstriction in the CHF state.

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

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

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

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

270 %) phenotypes, or in the distribution of the CHF risk allele (P = .7) between the reticular pseudodru

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

272 uidity are the main causes for promoting the CHF increase.

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

274 nges were observed longitudinally within the CHF-CBD group before and after CBD.

275 rheology of nanoparticles could attribute to CHF enhancement phenomena.

276 m pre-pace, P < 0.05) in CHF-CBD compared to CHF-sham rabbits.

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

278 the mechanism governing the hitherto unknown CHF enhancement maxima.

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

280 rsely affect exercise capacity in unselected CHF patients.

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

282 CHF-CBD animals (25 +/- 1% max, P < 0.05 vs. CHF-sham).

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

284 e increased sympathetic tone associated with CHF.

285 patients (age, 53+/-12 years; 86% men) with CHF were studied.

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

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

288 study of consecutive ambulant patients with CHF (New York Heart Association class III/IV) referred f

289 stics and clinical outcomes of patients with CHF and Kussmaul physiology have not been studied.

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

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

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

293 ssmaul physiology is common in patients with CHF referred for heart transplantation and is associated

294 aneous vascular conductance in patients with CHF was significantly lower than that in healthy control

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

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

297 utflow is commonly observed in patients with CHF.

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

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

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