ライフサイエンスコーパス: catecholamine

1 and other beta-AR signalling hormones (i.e. catecholamines).

2 and concentration increase of intravesicular catecholamine.

3 , increasing bioavailability of cortisol and catecholamine.

4 d the association between air pollutants and catecholamines.

5 nsient amplitude and the heart's response to catecholamines.

6 not significantly associated with any of the catecholamines.

7 beta-blockers, intra-aortic balloon pump, or catecholamines.

8 ionally little is known about the effects of catecholamines.

9 actile capacity but a diminished response to catecholamines.

10 thereby minimizing the detrimental effect of catecholamines.

11 by a drastic fall in the quantal release of catecholamines.

12 transformation overlaps with those of other catecholamines.

13 nd the need of mechanical ventilation and/or catecholamines.

14 : see text] ([Formula: see text])] and those catecholamines.

15 affin cells, altering the quantal release of catecholamines.

16 eta1-adrenergic receptors (beta1ARs) mediate catecholamine actions in cardiomyocytes by coupling to b

17 ally investigate specific glucocorticoid and catecholamine actions on the porcine immune system in th

18 molecular link that couples the coordinated catecholamine activation of the PKA pathway and of lipid

19 rthermore, a pharmacological manipulation of catecholamine activity affected learning rate following

20 Admission plasma levels of catecholamines (adrenaline, noradrenaline) and biomarker

21 Elevated catecholamines also allow for maintenance of a normal fe

22 Importantly, catecholamines also play important roles in other pathol

23 ng of insulinopenia through increased plasma catecholamine and corticosterone concentrations secondar

24 uctions in levels of glucagon, cortisol, and catecholamine and the sympathetic nerve responses to hyp

25 tion element that gives it high affinity for catecholamines and a turn-on response to norepinephrine.

26 s is associated with increased production of catecholamines and corticosteroids, decreased formation

27 ranin A (CHGA) is co-stored/co-secreted with catecholamines and crucial for secretory vesicle biogene

28 m excretion, gut microbiome, flow cytometry, catecholamines and methylation-wide changes were determi

29 ficacy and can be used in detection of other catecholamines and phenolic neurochemicals.

30 RC1 that is required for adipose browning by catecholamines and provides potential therapeutic strate

31 Glucogenic hormones, including catecholamines and vasopressin, induce frequency-modulat

32 se (TH; the first enzyme in the synthesis of catecholamines) and dopamine (DA).

33 trate buffer or reservoir to modulate lipid, catecholamine, and iron availability.

34 d sympathetic neurons synthesize and release catecholamines, and both cell types are derived from neu

35 phages do not synthesize relevant amounts of catecholamines, and hence, are not likely to have a dire

36 f adipocyte-expressed beta3 adrenoceptors by catecholamines, and identified eosinophils as a novel so

37 Reference intervals for l-DOPA, catecholamines, and metanephrines in n = 115 healthy ind

38 neous quantification of unconjugated l-DOPA, catecholamines, and metanephrines in plasma by LC-MS/MS.

39 ncluding various ways to measure heart rate, catecholamines, and sympathetic neural activity.

40 hering to the electrode and screening of the catecholamine-aptamer electrostatic interactions, allows

41 ns, and specific agonists and antagonists of catecholamines are available for the treatment of some d

42 Plasma-free metanephrines and catecholamines are essential markers in the biochemical

43 Catecholamines are known to alter GH secretion and neuro

44 Catecholamines are known to modulate the inflammatory pr

45 Catecholamines are reactive molecules that are handled t

46 ptide in resting conditions and that NPY and catecholamines are simultaneously increased during ortho

47 In this study, we describe the role of catecholamines (as mediators of the sympathetic nervous

48 tivity and revealed heterogeneous release of catecholamine at the chromaffin cell surface.

49 k electrode as a control, and the quantified catecholamines between these two techniques was the same

50 release of catecholamines, the adrenoceptors catecholamines bind to, and the cardiac and vascular res

51 in amino acid metabolism as well as GABA and catecholamine biosynthesis, indicating impairment of PLP

52 Furthermore, catecholamine levels, catecholamine biosynthetic enzymes, and sympathetic nerv

53 eased catecholamine levels and expression of catecholamine biosynthetic enzymes.

54 ing etiology is likely related to release of catecholamines, both locally in the myocardium and in th

55 VLM(RE) ), both of which contain bulbospinal catecholamine (C1) and non-C1 neurons.

56 Hindbrain catecholamine (CA) neurons are essential for elicitation

57 Catecholamines (CA) play a key role as neurotransmitters

58 c question regarding how glucocorticoids and catecholamines cause leukocyte demargination.

59 mice exhibit an impaired cardiac response to catecholamine challenge.

60 ial and attenuated ventricular arrhythmia in catecholamine-challenged Casq2(-/-) mice.

61 Lactate and catecholamine clearance were also significantly enhanced

62 blood pressure (SBP) with decreased urinary catecholamine compared to diabetic Cav2.2(+/+) mice.

63 hese vesicles contain about one tenth of the catecholamine compared with adrenal chromaffin vesicles.

64 al vesicles shows that the size and internal catecholamine concentration of vesicles varies with the

65 cells in bone marrow with increased urinary catecholamine concentrations at diagnosis.

66 We propose that sustained high catecholamine concentrations observed in the IUGR fetus

67 oxygen concentrations increase fetal plasma catecholamine concentrations, which lower fetal insulin

68 (CAPS) promotes and stabilizes the entry of catecholamine-containing vesicles of the adrenal gland i

69 ively spliced exon in CAPS leads to enhanced catecholamine content in chromaffin granules.

70 riant-dependent modulatory effect of CAPS on catecholamine content in LDCVs.SIGNIFICANCE STATEMENT Th

71 ied the mechanism of VIEC by quantifying the catecholamine content in single vesicles isolated from p

72 rter 2 and was associated with reduced renal catecholamine content.

73 These changes in catecholamines could be rescued by re-expression of DJ-1

74 d that ageing upregulates genes that control catecholamine degradation in an NLRP3 inflammasome-depen

75 The colligative properties of ATP and catecholamines demonstrated in vitro are thought to be r

76 These cellular catecholamine-dependent responses were mainly mediated b

77 hyl-paratyrosine (AMPT) over 24 h to achieve catecholamine depletion in a randomized, crossover study

78 ated with a dysregulated dopamine system and catecholamine depletion led to reward-processing deficit

79 ation in the sham condition and unrelated to catecholamine depletion.

80 peptide Y, met-enkephalin, dynorphin and the catecholamine dopamine.

81 pes (D(1-5)) are activated by the endogenous catecholamine dopamine.

82 neurotransmitter imbalance, particularly the catecholamines dopamine (DA) and noradrenaline.

83 erature argues for an important role for the catecholamines dopamine and noradrenaline in meta-learni

84 conserved precursor for the synthesis of the catecholamines dopamine and noradrenaline, in the brains

85 s the evidence implicating disruption of the catecholamines (dopamine and noradrenaline) and review t

86 ate-limiting step in the biosynthesis of the catecholamines - dopamine (DA), norepinephrine (NE), and

87 Incremental exogenous catecholamines doses may be required to counteract such

88 These findings suggest that catecholamines drive a feedforward loop, whereby upregul

89 d healing and the regulatory roles played by catecholamines during the process.

90 es an alternative source of locally produced catecholamines during the thermogenic process.

91 se of this study was to identify the role of catecholamine dysfunction and its relation to behavioral

92 Catecholamine effects on immune cell numbers were mostly

93 Our results fill this void by showing that catecholamines enhance the precision of encoding cortica

94 sed biases were altered independently by the catecholamine enhancer melthylphenidate.

95 the regulators of angiogenesis, the role of catecholamines (epinephrine, norepinephrine, and dopamin

96 omas, arising from chromaffin cells, produce catecholamines, epinephrine and norepinephrine.

97 These arrhythmias, arising from catecholamine excess rather than from a primary electrop

98 Also, we show that glucocorticoid and catecholamine exposure reorganizes cellular cortical act

99 us wounds, dopamine, the other member of the catecholamine family, has interesting and contradictory

100 stable for tens of milliseconds, as long as catecholamine flux can be detected.

101 erometry recording reveals the exocytosis of catecholamine from individual vesicles as a sequential p

102 onnectivity and advance our understanding of catecholamine function in the central nervous system.

103 ere, we tested the hypothesis that enhancing catecholamine function modulates the ability to optimise

104 At odds with common understanding of catecholamine function, we found (1) overall reduced int

105 To investigate the interaction between catecholamine functioning and behavioral, and neural res

106 1 complexes was accompanied by impairment in catecholamine homeostasis, with significant increases in

107 well-documented effect of glucocorticoid and catecholamine hormones, although the underlying mechanis

108 utic normalization of the glucocorticoid and catecholamine imbalance in SCI patients could be a strat

109 This catecholamine imbalance may contribute to the particular

110 Dopamine (DA) is the most important catecholamine in the brain, as it is the most abundant a

111 shows that chronic elevation in circulating catecholamines in IUGR fetuses persistently inhibits ins

112 (N = 32) that suggests an important role for catecholamines in learning rate regulation.

113 ntly available and can be used for measuring catecholamines in live-cell assays.

114 provides opportunity for differentiating the catecholamines in mixtures by monitoring the current at

115 an essential element in the concentration of catecholamines in secretory vesicles.

116 the rate-limiting enzyme in the synthesis of catecholamines in the brain of house crows (Corvus splen

117 Dysregulation of catecholamines in the central nervous system has previou

118 ciated with the electrochemical oxidation of catecholamines, in which DA and NE have rate constants t

119 a striking convergence and demonstrate that catecholamines increase the precision of neural represen

120 ere, we uncovered a novel mechanism by which catecholamines induce inflammation by increasing prostag

121 Catecholamines induce long-lasting proinflammatory chang

122 Pheochromocytoma is associated with catecholamine-induced cardiac toxicity, but the extent a

123 the driving force behind glucocorticoid- and catecholamine-induced demargination.

124 Here we report that, in vitro, Meto prevents catecholamine-induced down-regulation of S1PR1, a major

125 catecholoestradiol-, 17beta-oestradiol- and catecholamine-induced endothelial cell proliferation may

126 energic signalling, which leads to increased catecholamine-induced energy expenditure in the adipose

127 s is strongly related to adipose morphology, catecholamine-induced lipid mobilization (lipolysis), or

128 Deletion of NLRP3 in ageing restored catecholamine-induced lipolysis by downregulating growth

129 Catecholamine-induced lipolysis, the first step in the g

130 signalling mechanisms mediating E2 beta- and catecholamine-induced proliferation.

131 a-adrenergic signaling in TTS-iPSC-CMs under catecholamine-induced stress increased expression of the

132 repinephrine underlies optimal management in catecholamine-induced tachyarrhythmias.

133 nd to be the most common or life-threatening catecholamine-induced tachyarrhythmias.

134 renergic signaling and higher sensitivity to catecholamine-induced toxicity were identified as mechan

135 In vivo, flecainide effectively suppressed catecholamine-induced ventricular tachyarrhythmias in Ca

136 ght be implemented at a neural level through catecholamine influences on corticostriatal loops.

137 low cardiac output syndrome with need for a catecholamine infusion 48 hours after study drug initiat

138 in LVs of wildtype (WT) mice after a 1-week catecholamine infusion and a 2-week chronic pressure ove

139 njury]) who required mechanical ventilation, catecholamine infusion, or both and did not have a poten

140 ence in the composite end point of prolonged catecholamine infusion, use of left ventricular mechanic

141 r pathological conditions induced by chronic catecholamine infusions, BAY reversed both the attenuate

142 During arrhythmia provocation induced by catecholamine injections, TG animals were resistant to t

143 Finally, immunostaining revealed that catecholamine innervation of the dLGN is solely noradren

144 Overproduction of catecholamines is the biochemical hallmark of pheochromo

145 upled beta1-adrenoreceptor (beta1-AR) by the catecholamines isoprenaline (Iso) and adrenaline (Adr) i

146 I studies, we examine the effect of baseline catecholamine levels (as indexed by pupil diameter and m

147 , the impact of exercise intensity on plasma catecholamine levels among HCM patients has not been rig

148 as well as a non-linear relationship between catecholamine levels and cognitive functions.

149 ergic activity demonstrated by the increased catecholamine levels and expression of catecholamine bio

150 We pharmacologically increased synaptic catecholamine levels and measured the resulting changes

151 In Study 2 (N = 24), we manipulate catecholamine levels and neural gain using the norepinep

152 changes in conditions characterized by high catecholamine levels and propose that trained immunity u

153 ign, we pharmacologically increased synaptic catecholamine levels by administering atomoxetine, an NE

154 Exposure to high catecholamine levels is associated with inflammatory cha

155 genetic impact of peak-wise exposure to high catecholamine levels on monocytes isolated from pheochro

156 of the specific impact of these increases in catecholamine levels on perceptual encoding.

157 We show that plasma catecholamine levels remain stably low at exercise inten

158 tients with mild non-obstructive HCM, plasma catecholamine levels remain stably low at exercise inten

159 Baseline catecholamine levels tend to increase with increasing ta

160 idate and amphetamine modulate extracellular catecholamine levels through interaction with dopaminerg

161 regulation, behavioral activity, lipids, and catecholamine levels were also assessed.

162 Heart rate variability and plasma catecholamine levels were assessed as proxies of autonom

163 When assayed, urinary metanephrine and catecholamine levels were consistently elevated.

164 heart rate variability parameters nor plasma catecholamine levels were significantly different betwee

165 Urinary catecholamine levels will not be included in response as

166 ed by elevated CB neural activity and plasma catecholamine levels, and elevated reactive oxygen speci

167 and the forebrain as well, without affecting catecholamine levels, and rescued stress-induced arousal

168 Furthermore, catecholamine levels, catecholamine biosynthetic enzymes

169 methods of examining the effect of baseline catecholamine levels, our results show a striking conver

170 c systems and to provide a direct measure of catecholamine levels.

171 es with pupil diameter, an index of baseline catecholamine levels.

172 ough region-specific epigenetic activity and catecholamine levels.

173 onship between exercise intensity and plasma catecholamine levels.

174 nomenon associated with relatively increased catecholamines likely due to their suppressed degradatio

175 udy underscores the important roles that the catecholamines likely play in modulating spider vision,

176 ve exon of 40 aa is responsible for enhanced catecholamine loading of LDCVs in mouse chromaffin cells

177 A modulatory role of CAPS in catecholamine loading of vesicles has been suggested.

178 COMT modulates catecholamine metabolism, and polymorphisms within the r

179 anges in mRNA transcripts mainly involved in catecholamine metabolism.

180 which encodes a protein with homology to the catecholamine methyltransferase COMT that is linked to s

181 Catecholamines modulate the impact of motivational cues

182 y (VIEC) was used to determine the number of catecholamine molecules expelled from single vesicles on

183 aneously measure the physical size and count catecholamine molecules in individual nanometer transmit

184 vesicles and reduced the rates of release of catecholamine molecules in quanta release events.

185 y direct interaction of this domain with the catecholamine molecules that are escaping through the fu

186 A class of catecholamine neurons in SPN and SDCom neurons were also

187 However, while catecholamine neurons of the ventrolateral medulla (VLM(

188 lations in the gamma range, and modulated by catecholamine neurotransmission.

189 Catecholamine neurotransmitter levels in the synapses of

190 Dopamine (DA) is one of the most important catecholamine neurotransmitters of the human central ner

191 ssible to reduce the interference from other catecholamine neurotransmitters, including L-DOPA, epine

192 Dopamine, one of catecholamine neurotransmitters, plays an important role

193 terium Eggerthella lenta that dehydroxylates catecholamine neurotransmitters.

194 c susceptibility increases responsiveness to catecholamine neurotransmitters.

195 f four cardinal directions, and modulated by catecholamine neurotransmitters.

196 Neither catecholamines nor thyroid-stimulating hormone (TSH) are

197 Here, we assessed whether the catecholamine noradrenalin directly modulates the activi

198 nervous system, whose chief effector is the catecholamine norepinephrine (NE).

199 brain-wide neurophysiological effects of the catecholamines norepinephrine and dopamine on stimulus-e

200 A fluorescent sensor for catecholamines, NS510, is presented.

201 from diverse classes of compounds (peptides, catecholamines, nucleosides, amino acids, etc.).

202 A4(serotonin reuptake transporter), and COMT(catecholamine O-methyltransferase).

203 d by polymerization of L-DOPA and endogenous catecholamines on the electrode surface.

204 y in freely moving rats to measure real-time catecholamine overflow during acute morphine exposure an

205 tients rapidly, reducing number and doses of catecholamines (P<0.05 versus baseline) while hemodynami

206 It remains unknown whether pro-catecholamine pharmacological agents augment control-rel

207 p28 was 2.7-fold increased by removal of the catecholamine-producing adrenal glands prior to endotoxi

208 teroidogenic mesenchymal cortex and an inner catecholamine-producing medulla of neuroendocrine origin

209 o induce tyrosine hydroxylase expression and catecholamine production mediated by IL-6, factors requi

210 metabolic changes due to loss of peripheral catecholamine production.

211 Catecholamines promoted ADRB2-dependent PDAC development

212 fter 2 h of noradrenaline infusion, and both catecholamines promoted monocyte and neutrophil phagocyt

213 emical detection method for measuring plasma catecholamines (R(2) > 0.85).

214 for the first time, a mechanistic study for catecholamine redox reactions at LSGE as the electron tr

215 Thus, catecholamines reduce intrinsic correlations in a spatia

216 els of spatial organization, indicating that catecholamines reduce the strength of functional interac

217 Animal studies have demonstrated that catecholamines regulate several aspects of fear conditio

218 y inhibited nicotinic cholinergic stimulated catecholamine release from chromaffin cells.

219 xocytosis, we next amperometrically analyzed catecholamine release from PC12 cells, revealing that ch

220 physiological index of outcome-evoked phasic catecholamine release in the cortex-predicted learning r

221 association study for plasma catestatin, the catecholamine release inhibitory peptide derived from ch

222 tem activity, hemodynamics, brain perfusion, catecholamine release, and systemic inflammation after s

223 abolism, induces cell swelling and decreases catecholamine release.

224 duced mitochondrial metabolism and decreased catecholamine release.

225 d by analysis of the fractional detection of catecholamine released between electrodes and exploiting

226 l density, normal firing and the quantity of catecholamine released.

227 Catecholamines released by sympathetic nerves can activa

228 s been demonstrated as effective in reducing catecholamine requirements in patients with chronic hear

229 o dexmedetomidine resulted in a reduction of catecholamine requirements in septic shock patients.

230 s achieved common usage for the treatment of catecholamine-requiring and catecholamine-resistant shoc

231 is characterized by poor survival, a loss of catecholamine reserve and cellular structural remodeling

232 beta3ARs and Epac1 in a state we define as "catecholamine resistance."

233 the treatment of catecholamine-requiring and catecholamine-resistant shock.

234 ases mean arterial pressure in patients with catecholamine-resistant vasodilatory shock (CRVS).

235 rtisol and growth hormone responses, but not catecholamine responses to hypoglycemia.

236 tic tone and responsiveness of adipocytes to catecholamines reveals a novel role for ERbeta in contro

237 We found extensive catecholamine-rich neuronal fibers in the first- and sec

238 II receptor type 1 (AT1R), stimulates acute catecholamine secretion through coupling with the transi

239 in concentrations stimulates adrenomedullary catecholamine secretion.

240 H3S28p was increased by inhibition of the catecholamine-sensitive protein phosphatase 1 and decrea

241 Amphiphysin II (BIN1) and the restoration of catecholamine sensitivity is through reductions in G-pro

242 emia counterregulation modulates insulin and catecholamine signaling and glycogen synthase activity i

243 Dysregulated catecholamine signaling has long been implicated in drug

244 g exposure paired with withdrawal influences catecholamine signaling in vivo.

245 t target in this disorder, and modulation of catecholamine signaling may represent a viable strategy

246 ed during hyperinsulinemic hypoglycemia, and catecholamine signaling via cAMP-dependent protein kinas

247 Although catecholamine signalling in adipocytes is normal in the

248 occurs following inhibition or cessation of catecholamine signalling in IUGR fetuses.

249 Catecholamines stimulate epithelial proliferation, but t

250 energy storage and adipose expansion, while catecholamines stimulate release of adipose energy store

251 oximately 50%) was associated with abrogated catecholamine-stimulated adiponectin secretion.

252 enhancers and led to a decrease in basal and catecholamine-stimulated expression of brown fat-selecti

253 We report that during catecholamine-stimulated lipolysis, Perilipin 5 is phosp

254 In response to elevated catecholamine stimulation during development of congesti

255 beta-blockers act to block excessive catecholamine stimulation of betaARs to decrease cellula

256 Three-month-old CMs were subjected to catecholamine stimulation to simulate neurohumoral overs

257 Furthermore, under catecholamine stimulation, which also increases NO synth

258 lls, CHGA and KLKB1 proteins co-localized in catecholamine storage granules.

259 Recent studies suggest that the human catecholamine stress hormone, norepinephrine (NE), facil

260 nd in neuronal presynaptic terminals storing catecholamines such as dopamine.

261 s the rate-limiting step in the synthesis of catecholamines, such as dopamine, in dopaminergergic neu

262 e disability, myocardial injury, duration of catecholamine support, markers of shock, recurrence of v

263 This catecholamine surge leads, through multiple mechanisms,

264 ic pulmonary vasoconstriction and a profound catecholamine surge occur following WLST that result in

265 hotic drug aripiprazole and the heterocyclic catecholamine surrogates present in the beta2-adrenocept

266 rosine hydroxylase (TH), a key enzyme in the catecholamine synthesis pathway, and that this activatio

267 expression, the rate-limiting enzyme of the catecholamine synthesis, delineating a mechanism for the

268 yltransferase (PNMT) is a critical enzyme in catecholamine synthesis.

269 ydroxylase (TH), the rate-limiting enzyme in catecholamine synthesis.

270 s-evoked cortical responses suggest that the catecholamine systems are well positioned to regulate le

271 ging evidence for a causal role of the human catecholamine systems in learning-rate regulation as a f

272 As the catecholamine systems modulate these cognitive networks,

273 In adipocytes, catecholamines target the beta-adrenergic (beta-AR)/cAMP

274 Dopamine is a catecholamine that acts both as a neurotransmitter and a

275 Dopamine (DA) is a catecholamine that binds to five G protein-coupled recep

276 normal RBCs and SS-RBCs with epinephrine, a catecholamine that binds to the beta-adrenergic receptor

277 Norepinephrine (NE) is a key catecholamine that stimulates contractility by activatin

278 Understanding the synthesis and release of catecholamines, the adrenoceptors catecholamines bind to

279 me to hemodynamic stabilization, the risk of catecholamine therapy and the duration of such therapy,

280 moderate-exercise intensity until reaching a catecholamine threshold (H = 82 +/- 4 vs. C = 85 +/- 3%

281 t disease alone, supporting a direct role of catecholamine toxicity that may produce subtle but long-

282 EHM responded to chronic catecholamine toxicity with contractile dysfunction, car

283 through multiple mechanisms, that is, direct catecholamine toxicity, adrenoceptor-mediated damage, ep

284 Moreover, we investigated the role of catecholamine transmission in these changes by examining

285 s suggest that abstinence-induced changes in catecholamine transmission in visual attention areas (eg

286 MPH enhances catecholamine transmission via blockade of norepinephrin

287 isorder (ADHD), potentially due to deficient catecholamine transmission.

288 The catecholamine transporter blocker methylphenidate enhanc

289 ncreased lipid accumulation were detected in catecholamine-treated TTS-iPSC-CMs, and were confirmed b

290 y the lipid droplet protein Perilipin 5 as a catecholamine-triggered interaction partner of PGC-1alph

291 elated effects of TBZ were attenuated by the catecholamine uptake inhibitor and antidepressant buprop

292 Exogenous angiotensin II reduced catecholamine vasopressor doses and had an apparent effe

293 n arterial pressure and a rapid reduction in catecholamine vasopressor doses from 0.75 to 0.31 mcg/kg

294 ecretion was observed in patients exposed to catecholamine vasopressor infusions, but unaffected by s

295 atecholoestradiols, to 17beta-oestradiol and catecholamines, we observed that convergent MAPKs signal

296 Increased adrenal medulla-derived plasma catecholamines were necessary and sufficient to increase

297 ic signaling in MCF-7 cells, indicating that catecholamines were the responsible exercise factors.

298 Three different carbon-11-labeled catecholamines were used for positron emission tomograph

299 supports the disproportionation reaction of catecholamines, which has been previously reported, but

300 hostile outgroup, moderated by rapid-acting catecholamines, while tend-and-befriend is mainly shown