ライフサイエンスコーパス: neurohormonal

1 acterized by acute nocturnal hemodynamic and neurohormonal abnormalities that may increase the risk o

2 t could be made for attempting to also treat neurohormonal abnormalities.

3 strong predictor of higher urine output, but neurohormonal activation (as evidenced by blood urea nit

4 mmation (C-reactive protein and fibrinogen), neurohormonal activation (B-type natriuretic peptide [BN

5 ogen and plasminogen activator inhibitor-1), neurohormonal activation (B-type natriuretic peptide), a

6 olinium enhancement with proteins reflecting neurohormonal activation (NT-proBNP [N-terminal pro-B-ty

7 oop diuretic efficiency [P 0.33 for all]) or neurohormonal activation (plasma or urine renin [P 0.36

8 deling in CKD are multifactorial and include neurohormonal activation (with increased activation of t

9 to more complex models that have implicated neurohormonal activation and adverse cardiac remodeling

10 nered significant interest as a biomarker of neurohormonal activation and appears to yield independen

11 by hemodynamic abnormalities that result in neurohormonal activation and autonomic imbalance with in

12 have non-lipid-lowering effects that impact neurohormonal activation and cardiac remodeling.

13 The degree of neurohormonal activation and catabolic/anabolic imbalanc

14 Hypochloremia is associated with neurohormonal activation and diuretic resistance with ch

15 part of both established pathways, including neurohormonal activation and fibrosis, and less familiar

16 n heart failure; however, these agents cause neurohormonal activation and have been associated with w

17 ty and visceral adiposity are accompanied by neurohormonal activation and imbalances in adipokine sec

18 in the torsemide group was offset by greater neurohormonal activation and kidney dysfunction.

19 emodeling is influenced by hemodynamic load, neurohormonal activation and other factors still under i

20 as not, however, associated with evidence of neurohormonal activation because the change in norepinep

21 Neurohormonal activation characterizes chronic heart fai

22 Mechanical stresses and chronic neurohormonal activation conspire to propagate maladapti

23 een proposed that ventricular dilatation and neurohormonal activation during heart failure lead to up

24 It is not known whether a similar pattern of neurohormonal activation exists in adults with congenita

25 Despite its description some 25 years ago, neurohormonal activation has long been neglected as an i

26 Neurohormonal activation in adult congenital heart disea

27 istance, and mitigate the effects of adverse neurohormonal activation in AHF.

28 -induced changes in myocardial perfusion and neurohormonal activation in CHF patients with reduced le

29 When homeostasis is perturbed by neurohormonal activation in heart failure, levels of NPs

30 These data suggest a role for neurohormonal activation in loop diuretic-associated mor

31 onal studies and trials suggest compensatory neurohormonal activation in patients treated with renin-

32 Serum soluble ST2 is a novel biomarker for neurohormonal activation in patients with heart failure.

33 ven the important role of cardiac injury and neurohormonal activation in the pathways leading from hy

34 in decompensated heart failure (HF), reduces neurohormonal activation in the short term.

35 This finding suggests that cardiac neurohormonal activation may be a unifying feature among

36 fficient to cause cardiac impairment through neurohormonal activation of (nicotinamide adenine dinucl

37 Neurohormonal activation rapidly decreases after short-t

38 Therapy designed to address neurohormonal activation should include therapy to impro

39 Neurohormonal activation was interpreted as a necessary

40 electrolyte wasting, renal dysfunction, and neurohormonal activation were not observed.

41 This study suggests improvements in neurohormonal activation with this treatment.

42 ant reduction in LV mass, LV dilatation, and neurohormonal activation, and it preserved LV geometry.

43 Chloride plays a role in renal salt sensing, neurohormonal activation, and regulation of diuretic tar

44 with clinical and cardiac status, reflected neurohormonal activation, and was associated with cardia

45 cognized limitations of diuretic resistance, neurohormonal activation, and worsening renal function.

46 mbination of potential mechanisms, including neurohormonal activation, apoptosis, and the inflammator

47 to investigate whether a surrogate for renal neurohormonal activation, blood urea nitrogen (BUN), cou

48 as sodium avidity, diuretic resistance, and neurohormonal activation, but this has not been conclusi

49 retics such as furosemide induce substantial neurohormonal activation, contributing to the limited im

50 es of CSA, including altered blood gases and neurohormonal activation, could result in further left v

51 In the heart and kidneys, shared pathways of neurohormonal activation, hypertension, and vascular and

52 changes leading to venous renal congestion, neurohormonal activation, hypothalamic-pituitary stress

53 Neurohormonal activation, including aldosteronism, in HF

54 res of worse heart failure and biomarkers of neurohormonal activation, inflammation, myocyte injury,

55 iuretic peptides are released in response to neurohormonal activation, myocardial stretch, and wall t

56 gan injury is the consequence of maladaptive neurohormonal activation, oxidative stress, abnormal imm

57 fusion and congestion as well as maladaptive neurohormonal activation, oxidative stress, hormonal imb

58 portant regulators of sodium homeostasis and neurohormonal activation, raising the possibility that o

59 ncerns that some diuretics may cause harm by neurohormonal activation, these agents continue to be th

60 Vascular rigidity, neurohormonal activation, tissue hypoxia, and abnormal i

61 out a 24-h period and were associated with a neurohormonal activation, ventricular arrhythmic burden,

62 Episodes of CA were associated with neurohormonal activation, ventricular arrhythmic burden,

63 cular dysfunction, exercise intolerance, and neurohormonal activation.

64 graphy-derived strains) was improved, as was neurohormonal activation.

65 incidence driven by hemodynamic changes and neurohormonal activation.

66 heart failure are increased in patients with neurohormonal activation.

67 atic patients having evidence of significant neurohormonal activation.

68 l regional flow conditions, and cytokine and neurohormonal activation.

69 monary pathology, systemic inflammation, and neurohormonal activation.

70 associated with markers of inflammation and neurohormonal activation.

71 ssociated with etiopathogenic mechanisms and neurohormonal activation.

72 e levels, and hyponatremia reflected greater neurohormonal activation.

73 re phenotypes, preventing cardiac injury and neurohormonal activation.

74 e stepwise availability of drugs that target neurohormonal activation: beta-adrenergic receptor block

75 sminogen activator inhibitor-1, fibrinogen), neurohormonal activity (aldosterone, renin, B-type natri

76 imer and plasminogen activator inhibitor-1), neurohormonal activity (aldosterone-to-renin ratio, B-ty

77 Therefore, inhibitors of neurohormonal activity (like beta-blockers or angiotensi

78 ations in cardiac output, functional status, neurohormonal activity and transcriptional profiles but

79 We hypothesized that neurohormonal activity contributes to the initiation of

80 rongly related to mortality, and blockade of neurohormonal activity in experimental PAH improved surv

81 novel insights shed new light on the role of neurohormonal activity in PAH.

82 sure and heart rate, carbohydrate tolerance, neurohormonal activity).

83 rized by systemic inflammation and increased neurohormonal activity, even in the absence of obesity.

84 lipid-lowering therapy (LDL-C <1.4 mmol/L), neurohormonal agents, and lifestyle modification, are cr

85 Camui was also activated by 4 neurohormonal agonists.

86 sic renal disease, but are likely related to neurohormonal and adipokine-mediated pathways that are d

87 The neurohormonal and catabolic derangements in HF are at th

88 Examination of neurohormonal and clinical responses in patients receivi

89 pnea is highly prevalent and associated with neurohormonal and electrophysiological abnormalities tha

90 of body wasting is strongly correlated with neurohormonal and immune abnormalities.

91 The tumor, through the release of these neurohormonal and immune mediators, can control the main

92 e, initiating the cycle of vasoconstriction, neurohormonal and inflammatory activation, and adverse v

93 nts with cancer experience marked changes in neurohormonal and inflammatory processes in the year aft

94 year after diagnosis and tracked changes in neurohormonal and inflammatory processes.

95 Chronic neurohormonal and mechanical stresses are central featur

96 Beyond neurohormonal and myocyte signaling pathways, growing ev

97 suggests that renal dysfunction, along with neurohormonal and proinflammatory cytokine activation in

98 here was no significance correlation between neurohormonal and proinflammatory cytokine levels.

99 s studies have shown beneficial hemodynamic, neurohormonal and renal effects of bolus dose and 6-h in

100 The authors evaluated the neurohormonal and subjective mood response of children w

101 several trials have studied the hemodynamic, neurohormonal, and clinical effects of digoxin, providin

102 depressive symptom domains and inflammatory, neurohormonal, and coagulation markers is unknown.

103 veloping CHF produced favorable hemodynamic, neurohormonal, and contractile effects in the setting of

104 Worsening signs and symptoms, neurohormonal, and renal abnormalities occurring soon af

105 Given the hemodynamic, neurohormonal, and renal effects of natriuretic peptides

106 Neurohormonal antagonism across this large and anatomica

107 remodeling and a decrease in LV volumes (eg, neurohormonal antagonists and LV assist devices), but th

108 e whether SBP reduction or titration of oral neurohormonal antagonists during acute decompensated hea

109 clinical status following the withdrawal of neurohormonal antagonists largely consists of observatio

110 Uptitration of neurohormonal antagonists occurred in >50% of admissions

111 ardiomyopathy is largely limited to the same neurohormonal antagonists used in other forms of cardiom

112 Furthermore, titration of oral neurohormonal antagonists was actually associated with i

113 [95 % CI, 0.31 to 0.94]; P=0.03) and use of neurohormonal antagonists were associated with reduced r

114 ndard current evidence-based LVSD therapies (neurohormonal antagonists, diuretics and cardiac resynch

115 hock is associated with medical therapy with neurohormonal antagonists, female gender, and New York H

116 leads to interruption and discontinuation of neurohormonal antagonists, which may worsen heart failur

117 gnificantly improved with the uptitration of neurohormonal antagonists.

118 briefly discuss what the future landscape of neurohormonal anti-obesity combinations may hold.

119 -induced obesity, suggesting that integrated neurohormonal approaches to obesity pharmacotherapy may

120 In the failing heart, long-term neurohormonal/autocrine-paracrine activation results in

121 ion in the harmful long-term consequences of neurohormonal/autocrine-paracrine effects and retard the

122 r pharmacological intervention have targeted neurohormonal axes and hemodynamic disturbances in HF.

123 Chronic stimulation of the beta-adrenergic neurohormonal axis contributes to the progression of hea

124 Yet the role of the individual's neurohormonal background in these processes remains unde

125 of HF after CRT may include up-titration of neurohormonal blockade and an exercise prescription thro

126 Proposed mechanisms include neurohormonal blockade and heart rate reduction.

127 es have been observed wherein the benefit of neurohormonal blockade appears to extend to a higher eje

128 yses of the 1050 A-HeFT patients on standard neurohormonal blockade demonstrated that FDC I/H produce

129 ances in pharmacological treatments aimed at neurohormonal blockade for heart failure in the setting

130 The advent of neurohormonal blockade in heart failure (HF) has been an

131 studies suggest that further pharmacological neurohormonal blockade may not be safe or effective, whi

132 ity care (HIC) arm with fast up-titration of neurohormonal blockade or to usual care (UC).

133 Comprehensive uptitration of neurohormonal blockade targets fundamental mechanisms un

134 In STRONG-HF, intensive uptitration of neurohormonal blockade was associated with more efficien

135 ne, (6) no previous attempt at comprehensive neurohormonal blockade, and (7) no structured cardiac tr

136 In addition to the established benefits of neurohormonal blockade, new mechanical and electrical th

137 s with heart failure treated with background neurohormonal blockade.

138 With the discovery of neurohormonal blockers capable of reducing mortality in

139 standard therapy for heart failure including neurohormonal blockers is efficacious and increases surv

140 Use of neurohormonal blockers on left ventricular assist device

141 s with moderate to severe HF who were taking neurohormonal blockers produced early and sustained sign

142 othalamic-pituitary axis, a highly conserved neurohormonal cascade that culminates in systemic secret

143 ch was accompanied by a normalization of the neurohormonal (catecholamines and aldosterone) status of

144 on of these latter inputs occurs at upstream neurohormonal cells and at the insulin signaling cascade

145 not only to gastric restriction but also to neurohormonal changes.

146 xercise, LV stroke volume remained lower and neurohormonal concentrations remained higher in the paci

147 alterations in circulating cytokines, unique neurohormonal constellations, endotoxin-lipoprotein inte

148 ity of interaction within the context of the neurohormonal construct.

149 nd topology of this signaling network permit neurohormonal control of excitation-contraction coupling

150 al new information has been published on the neurohormonal control of pancreatic exocrine function.

151 The neurohormonal control of pancreatic exocrine secretion i

152 ars to be a critical mechanistic link within neurohormonal crosstalk governing cardiac contractile si

153 Each of these neurohormonal derangements may act through increased act

154 pharmacotherapies targeting primarily global neurohormonal dysregulation, heart failure (HF) is a gro

155 sk related to subclinical myocardial damage, neurohormonal dysregulation, inflammation associated wit

156 reast cancer cell colonization of bone via a neurohormonal effect on the host bone marrow stroma.

157 ined the hemodynamic, echocardiographic, and neurohormonal effects of intravenous istaroxime in patie

158 The neurohormonal effects of irbesartan were highly variable

159 n to reverse the deleterious hemodynamic and neurohormonal effects that occur after myocardial infarc

160 (0.15 and 15 mg), which produced no systemic neurohormonal effects, and (b) intranasal cocaine (2 mg/

161 Despite favorable hemodynamic and neurohormonal effects, endothelin receptor antagonists h

162 an SG, likely related to its more pronounced neurohormonal effects.

163 te myocardial infarction in the Eplerenone's Neurohormonal Efficacy and Survival Study, a multicenter

164 after LVAD support suggest a primary role of neurohormonal environment in determining reverse remodel

165 caused by changes in the local and systemic neurohormonal environment.

166 ion when subjected to hemodynamic stress and neurohormonal excess.

167 of ionic channels, cellular energy balance, neurohormonal expression, inflammatory response, and phy

168 The possible role of several neurohormonal factors in pathogenesis of hypertension ha

169 owth is triggered by autocrine and paracrine neurohormonal factors released during biomechanical stre

170 s do not preclude a possible primary role of neurohormonal factors underlying other facets of reverse

171 represented by abnormal circulating or local neurohormonal factors, mechanical stress, intracellular

172 n of substrate stiffness, and treatment with neurohormonal factors.

173 on or a primary "defect" related to specific neurohormonal immune phenotype(s).

174 lear export provides a key mechanism for the neurohormonal induction of such activity.

175 To eliminate neurohormonal influences, neonatal rat ventricular myocy

176 mens, including anticoagulants, statins, and neurohormonal inhibition, were found to further reduce m

177 rbidity end point in those receiving neither neurohormonal inhibitor and an adverse trend in those tr

178 Body weight is regulated by complex neurohormonal interactions between endocrine signals of

179 ed from the gut through hormone-hormonal and neurohormonal interactions.

180 Elevated plasma neurohormonal levels are associated with increased morta

181 ent of symptoms as demonstrated by increased neurohormonal levels in patients with asymptomatic left

182 activity and monthly pre- and post-enalapril neurohormonal levels were compared.

183 The increases in other neurohormonal levels were not useful in predicting the s

184 ys and vice versa, as well as alterations in neurohormonal markers and inflammatory molecular signatu

185 Neurohormonal measures and visual analog self-reports of

186 ctive once mated and identify the underlying neurohormonal mechanism.

187 scular tone is regulated by the interplay of neurohormonal mechanisms and endothelial-dependent facto

188 Perhaps the most prominent among these neurohormonal mechanisms is the adrenergic (or sympathet

189 lter gut microbiota; however, the underlying neurohormonal mechanisms of satiety remain poorly unders

190 racterized by a complex interplay of several neurohormonal mechanisms that become activated in the sy

191 likely involves interrelated hemodynamic and neurohormonal mechanisms.

192 ntial effects of the manipulation on unknown neurohormonal mechanisms.

193 biomarkers can be categorized empirically as neurohormonal mediators, markers of myocyte injury and r

194 sponse to increased systolic wall stress and neurohormonal mediators.

195 events, consistent with their likely role as neurohormonal messengers.

196 d to the left ventricle [LV]) and normalized neurohormonal milieu (provided to LV and right ventricle

197 would primarily depend upon normalization of neurohormonal milieu.

198 Recently, clinicians have begun to adopt a neurohormonal model in which heart failure progresses be

199 This has lead us to question whether the neurohormonal model of HF can be sustained by simply sta

200 navigating the multifaceted labyrinth of the neurohormonal model that has led to the current imbrogli

201 Neurohormonal modulation and afterload reduction are key

202 sistent with the hypothesis that substantial neurohormonal modulation of ECL cell function exists.

203 nging cue responsiveness across insects; the neurohormonal modulation of olfactory neurons uncovered

204 scusses remodeling, initial therapy based on neurohormonal modulation, and treatment of decompensated

205 levated left ventricular pressure as well as neurohormonal modulation, we hypothesized that BNP might

206 Moreover, it is also a neurohormonal modulator at low doses.

207 this hypothesis, we measured stress-related neurohormonal modulators and sex hormones in male and fe

208 other receptor sites include neurokinin and neurohormonal modulators, chloride channels and opioid r

209 d novel agents to improve systolic function, neurohormonal modulators, heart rhythm and synchronizati

210 lected biomarkers from 4 biological domains: neurohormonal (N-terminal pro-atrial natriuretic peptide

211 s, there are data showing the involvement of neurohormonal, nutritional, and inflammatory mechanisms

212 can be sustained by simply stacking multiple neurohormonal or cytokine blockers together as treatment

213 ls perturb the fly's hemolymph, activating a neurohormonal pathway linking clock neurons to juvenile

214 BBB serving as a molecular gatekeeper for a neurohormonal pathway that regulates social behavior.

215 ltimarker strategy targeting the natriuretic neurohormonal pathway.

216 in 14 candidate genes selected a priori from neurohormonal pathways for their potential role in exerc

217 The renal and neurohormonal pathways of obesity and hypertension are i

218 ith the use of agents that block maladaptive neurohormonal pathways.

219 gma is observed in guideline-directed use of neurohormonal pharmacotherapies as a standard of care in

220 ad a less severe hemodynamic, biomarker, and neurohormonal profile, and it was treated with a more in

221 e, a less severe hemodynamic, biomarker, and neurohormonal profile, and who are treated with a more i

222 e point for signaling of multiple Gq-coupled neurohormonal receptors.

223 (high-sensitivity troponin T (hs-cTnT)); (b) neurohormonal regulation (N-terminal pro-Brain-natriuret

224 des are critical secondary messengers in the neurohormonal regulation in the cardiovascular system.

225 New therapies show great promise for the neurohormonal regulation of heart failure and the abilit

226 ghts the recent advances in knowledge of the neurohormonal regulation of pancreatic exocrine secretio

227 The results support the novel concept that neurohormonal regulation of the innate immune system pla

228 volved in cold-related energy metabolism and neurohormonal regulation.

229 Other clusters were composed of neurohormonal regulators of mineral metabolism, intermed

230 ting the structural myocardial proteins, the neurohormonal regulatory proteins, the vascular proteins

231 nine vasopressin (AVP) is a component of the neurohormonal response to congestive heart failure (CHF)

232 h in experimental VO is mostly driven by the neurohormonal response, with an initial increase in myoc

233 We sought to compare the neurohormonal responses and clinical effects of long-ter

234 Hemodynamic and neurohormonal responses to bicycle exercise, public spea

235 athways include reflexive and uncontrollable neurohormonal responses to food images, cues, and smells

236 cose homeostasis, which reduces symptoms and neurohormonal responses to hypoglycemia.

237 lean control subjects, indicating attenuated neurohormonal responses to stress in obesity.

238 ventricle, triggers an array of compensatory neurohormonal responses, and induces a distinctive ventr

239 , and neuropil, suggesting both synaptic and neurohormonal roles.

240 ve roles as neuromodulators and as classical neurohormonal roles.

241 Both cardiac and vascular aging involve neurohormonal signaling (eg, renin-angiotensin, adrenerg

242 n part as a result of a normalization of the neurohormonal signaling axis.

243 t heart responds to biomechanical stress and neurohormonal signaling by hypertrophic growth, accompan

244 nd endothelin (ET) receptors, after elevated neurohormonal signaling of the sympathetic nervous syste

245 s from increased hemodynamic load or altered neurohormonal signaling remains controversial.

246 ent learning and memory mechanisms translate neurohormonal signals of energy balance into adaptive be

247 Blood-borne neurohormonal signals reflect the intermittent burst-lik

248 Thus, these groups may form a neurohormonal spectrum reflecting different stages of hy

249 nctional abnormalities, and abnormalities in neurohormonal status (e.g., elevated natriuretic peptide

250 ociation functional classification and their neurohormonal status before randomization.

251 r (LV) pump function, systemic hemodynamics, neurohormonal status, and regional blood flow distributi

252 , a strategy that also improves symptoms and neurohormonal status.

253 ed by cardiac-LC proteins was independent of neurohormonal stimulants, vascular factors, or extracell

254 ne but inhibits the hypertrophic response to neurohormonal stimulation in vivo and in vitro, through

255 ion represents a key signaling mechanism for neurohormonal stimulation of diversified physiological p

256 s in cardiac energy metabolism downstream of neurohormonal stimulation play a crucial role in the pat

257 via transverse aorta constriction or chronic neurohormonal stimulation via Angiotensin II infusion.

258 We speculate that neurohormonal stimulation via this signaling cascade is

259 res, calcium handling, responses to hypoxia, neurohormonal stimulation, and electric pacing, and are

260 with the CIP4 compartment were increased by neurohormonal stimulation, but minimally by pacing.

261 sors were induced by pacing and minimally by neurohormonal stimulation, providing functional evidence

262 KA activities in signaling propagation under neurohormonal stimulation.

263 ess to likely modulate vascular responses to neurohormonal stimulation.

264 egration of signaling initiated by different neurohormonal stimuli, as well as long-term effects of c

265 ypertrophic response to pressure overload or neurohormonal stimuli, miR-133a down-regulation permitte

266 secretory epithelial cells, independent from neurohormonal stimuli.

267 biomarkers reflecting myocardial injury and neurohormonal stress (malignant LVH) is associated with

268 tance to cell death, cellular proliferation, neurohormonal stress, angiogenesis, and genomic instabil

269 infected to express beta3AR and subjected to neurohormonal stress.

270 rhythmias given the metabolic, ischemic, and neurohormonal stressors present in the intensive care un

271 tional classes I to III who were enrolled in neurohormonal substudies of the SOLVD trial; age-matched

272 ement through balanced vasodilatory effects, neurohormonal suppression and enhanced natriuresis and d

273 ram aimed at identifying naturally occurring neurohormonal synergies.

274 sociated with left ventricular (LV) failure, neurohormonal system activation, and diminished exercise

275 entricular (LV) function, contractility, and neurohormonal system activity in a model of congestive h

276 e on LV function, systemic hemodynamics, and neurohormonal system activity in a model of congestive h

277 cluded the effects of LV loading conditions, neurohormonal system activity, and myocardial contractil

278 However, the central effect of this neurohormonal system in neural control of cardiovascular

279 istic features of heart failure; conversely, neurohormonal systems activated in heart failure (norepi

280 Activation of neurohormonal systems and the systemic inflammatory resp

281 ide unique benefits for LV pump function and neurohormonal systems in the setting of CHF.

282 egulation by the complex interaction between neurohormonal systems involved in sodium and water homeo

283 s variation in the structure and function of neurohormonal systems originally adapted to motivate par

284 To compensate, neurohormonal systems such as the renin-angiotensin-aldo

285 ilure is characterized by activation of many neurohormonal systems with vasoconstrictor and vasodilat

286 ar that complex interactions of environment, neurohormonal systems, and transgenerational effects dir

287 characterized by activation of many of these neurohormonal systems, few studies have evaluated plasma

288 aluate a possible relationship between these neurohormonal systems, we studied the effects of chronic

289 heart failure has focused on the blockade of neurohormonal systems.

290 evidence points to a ceiling effect as newer neurohormonal targets are exploited in an incremental ma

291 ortant synergy of addressing hemodynamic and neurohormonal targets of HF therapy.

292 road in HF and begin to fervently pursue non-neurohormonal therapeutic targets, we must also direct a

293 elines, with emphasis on titration of proven neurohormonal therapies for HF.

294 ntally improve prognosis beyond foundational neurohormonal therapies.

295 me between the first NT-proBNP elevation and neurohormonal therapy prescription of 1 day (IQR, 0.5-9

296 ion triggered the initiation or titration of neurohormonal therapy.

297 ese findings may indicate suppression of the neurohormonal triggers for VA by current heart failure t

298 Hemodynamic derangements and maladaptive neurohormonal upregulations contribute to fluctuations i

299 New discoveries of the interactions between neurohormonal, vascular, and coagulation systems are beg

300 critical to study to consider oxytocin as a neurohormonal weight loss treatment.