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

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

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

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

10 The degree of neurohormonal activation and catabolic/anabolic imbalanc

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

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

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

14 Neurohormonal activation characterizes chronic heart fai

15 Mechanical stresses and chronic neurohormonal activation conspire to propagate maladapti

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

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

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

19 Neurohormonal activation in adult congenital heart disea

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

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

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

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

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

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

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

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

28 Neurohormonal activation rapidly decreases after short-t

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

30 Neurohormonal activation was interpreted as a necessary

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

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

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

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

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

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

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

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

39 Neurohormonal activation, including aldosteronism, in HF

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

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

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

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

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

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

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

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

48 ssociated with etiopathogenic mechanisms and neurohormonal activation.

49 cular dysfunction, exercise intolerance, and neurohormonal activation.

50 heart failure are increased in patients with neurohormonal activation.

51 atic patients having evidence of significant neurohormonal activation.

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

53 monary pathology, systemic inflammation, and neurohormonal activation.

54 e levels, and hyponatremia reflected greater neurohormonal activation.

55 re phenotypes, preventing cardiac injury and neurohormonal activation.

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

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

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

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

60 We hypothesized that neurohormonal activity contributes to the initiation of

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

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

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

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

65 Camui was also activated by 4 neurohormonal agonists.

66 The neurohormonal and catabolic derangements in HF are at th

67 Examination of neurohormonal and clinical responses in patients receivi

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

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

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

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

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

73 Chronic neurohormonal and mechanical stresses are central featur

74 Beyond neurohormonal and myocyte signaling pathways, growing ev

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

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

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

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

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

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

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

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

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

84 Neurohormonal antagonism across this large and anatomica

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

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

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

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

89 [95 % CI, 0.31 to 0.94]; P=0.03) and use of neurohormonal antagonists were associated with reduced r

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

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

92 gnificantly improved with the uptitration of neurohormonal antagonists.

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

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

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

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

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

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

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

100 Proposed mechanisms include neurohormonal blockade and heart rate reduction.

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

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

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

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

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

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

107 s with heart failure treated with background neurohormonal blockade.

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

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

110 Use of neurohormonal blockers on left ventricular assist device

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

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

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

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

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

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

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

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

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

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

121 The neurohormonal control of pancreatic exocrine secretion i

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

123 Each of these neurohormonal derangements may act through increased act

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

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

126 The neurohormonal effects of irbesartan were highly variable

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

128 (0.15 and 15 mg), which produced no systemic neurohormonal effects, and (b) intranasal cocaine (2 mg/

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

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

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

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

133 ion when subjected to hemodynamic stress and neurohormonal excess.

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

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

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

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

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

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

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

141 To eliminate neurohormonal influences, neonatal rat ventricular myocy

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

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

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

145 Elevated plasma neurohormonal levels are associated with increased morta

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

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

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

149 Neurohormonal measures and visual analog self-reports of

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

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

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

153 likely involves interrelated hemodynamic and neurohormonal mechanisms.

154 ntial effects of the manipulation on unknown neurohormonal mechanisms.

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

156 sponse to increased systolic wall stress and neurohormonal mediators.

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

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

159 would primarily depend upon normalization of neurohormonal milieu.

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

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

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

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

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

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

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

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

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

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

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

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

172 ltimarker strategy targeting the natriuretic neurohormonal pathway.

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

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

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

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

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

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

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

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

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

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

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

184 Hemodynamic and neurohormonal responses to bicycle exercise, public spea

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

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

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

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

189 ve roles as neuromodulators and as classical neurohormonal roles.

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

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

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

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

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

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

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

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

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

199 ociation functional classification and their neurohormonal status before randomization.

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

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

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

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

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

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

206 We speculate that neurohormonal stimulation via this signaling cascade is

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

208 ess to likely modulate vascular responses to neurohormonal stimulation.

209 KA activities in signaling propagation under neurohormonal stimulation.

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

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

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

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

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

215 ram aimed at identifying naturally occurring neurohormonal synergies.

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

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

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

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

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

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

222 Activation of neurohormonal systems and the systemic inflammatory resp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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