ライフサイエンスコーパス: phosphocreatine

1 gnificant relationship NAA and either ATP or phosphocreatine.

2 , some 30% of this in phosphorylated form as phosphocreatine.

3 ically by decreased tissue levels of ATP and phosphocreatine.

4 recoveries of contractile function, ATP, and phosphocreatine.

5 arts were able to hydrolyze and resynthesize phosphocreatine.

6 ellular ATP through generation and import of phosphocreatine.

7 rylates the metabolite creatine, to generate phosphocreatine.

8 e of taurine, glucose, lactate, and creatine/phosphocreatine.

9 rom controls for N-acetyl-aspartate:creatine/phosphocreatine (11% lower, P < 0.001), N-acetyl-asparta

10 lower, P < 0.001), and myo-inositol:creatine/phosphocreatine (17% higher, P < 0.001).

11 -fold) and a decrease in HEP (ATP 45-51% and phosphocreatine 45-58%) 2 h after KA injection in brain

12 Exogenous creatine kinase (500 to 4000 IU/L, phosphocreatine 5 mM) added to human plasma induced a do

13 ) had stress-induced reduction in myocardial phosphocreatine-adenosine triphosphate ratio by phosphor

14 djusting for CAD and cardiac risk factors, a phosphocreatine-adenosine triphosphate ratio decrease of

15 t negative correlation between T1 values and phosphocreatine/adenosine triphosphate ratios (r=-0.59,

16 In both groups of patients, the phosphocreatine and adenosine diphosphate recovery half-

17 high-energy phosphate-containing compounds (phosphocreatine and adenosine triphosphate [ATP]), inorg

18 reversible conversion of creatine and ATP to phosphocreatine and ADP, thereby helping maintain energy

19 Phosphocreatine and ATP levels fell abruptly, and lactat

20 he concentrations of inorganic phosphate and phosphocreatine and calculating the ratio of inorganic p

21 tate, and the predominantly glial creatine + phosphocreatine and choline compounds.

22 ontrols and higher gray matter creatine plus phosphocreatine and choline concentrations in patients w

23 g N-acetyl-aspartate, myo-inositol, creatine/phosphocreatine and choline-containing compounds, which

24 of an ATP-regenerating system consisting of phosphocreatine and creatine kinase, suggesting that the

25 ne conditions alphaMHC403/+ hearts had lower phosphocreatine and increased inorganic phosphate conten

26 Phosphocreatine and inorganic phosphate (Pi) varied in o

27 zopolrestat hearts during ischemia, as were phosphocreatine and left ventricular-developed pressure

28 versible conversion of creatine and MgATP to phosphocreatine and MgADP.

29 her anterior cingulate myo-inositol/creatine-phosphocreatine and myo-inositol (mmol/liter) levels tha

30 inhibition decreased resting levels of ATP, phosphocreatine and myoglobin, suggesting that sildenafi

31 complexes was required to simulate measured phosphocreatine and OXPHOS responses to both moderate an

32 nhibits PGTF binding, but in the presence of phosphocreatine and phosphocreatine kinase, this capacit

33 roducts utilization as a source of anserine, phosphocreatine and taurine was discussed.

34 p between myocardial high-energy phosphates, phosphocreatine, and ADP and oxygen consumption (MVO(2))

35 aining compounds, Cr represents creatine and phosphocreatine, and Cit represents citrate.

36 The result is depletion of myocardial ATP, phosphocreatine, and creatine kinase with decreased effi

37 well maintained by addition of oligomycin A, phosphocreatine, and creatine phosphokinase.

38 -Acetylaspartate, choline moieties, creatine-phosphocreatine, and glutamate-glutamine metabolite leve

39 romised muscle fuel status as judged by ATP, phosphocreatine, and glycogen content.

40 tate, choline-containing compounds, creatine/phosphocreatine, and lactate signal intensities from fou

41 atine, choline-containing compounds:creatine/phosphocreatine, and myo-inositol:creatine/phosphocreati

42 erse relaxation times for Cho, creatine plus phosphocreatine, and NAA expressed relative to control s

43 ls were expressed as ratios to creatine plus phosphocreatine, and NAAG was expressed as a ratio to N-

44 We present methods to measure ATP, phosphocreatine, and total creatine (the sum of creatine

45 ture, and concentrations of muscle creatine, phosphocreatine, and total creatine did not differ signi

46 ter and on luminometric measurements of ATP, phosphocreatine, and total creatine.

47 ng the product of the CK enzymatic reaction, phosphocreatine, as an indicator of transfection.

48 ecoveries of the energy metabolites, ATP and phosphocreatine, as measured by 31P nuclear magnetic res

49 K+ stimulation produced responses of phosphocreatine, ATP and lactate levels and of GPR simil

50 ociated with faster postischemic recovery of phosphocreatine, ATP, and pH as assessed by (31)P nuclea

51 es, with a marked decrease in subendocardial phosphocreatine/ATP (31P magnetic resonance spectroscopy

52 , which demonstrated significantly decreased phosphocreatine/ATP and increased cytosolic ADP despite

53 During stress, a further reduction in phosphocreatine/ATP occurred in obese (from 1.73+/-0.40

54 on of SERCA2a in failing hearts improved the phosphocreatine/ATP ratio (1.23+/-0.28).

55 peak filling rate (P<0.001) and a 15% lower phosphocreatine/ATP ratio (1.73+/-0.40 versus 2.03+/-0.2

56 icular mass, leptin, waist-to-hip ratio, and phosphocreatine/ATP ratio.

57 time curve analysis) and cardiac energetics (phosphocreatine/ATP ratio; (31)P-magnetic resonance spec

58 Myocardial phosphocreatine/ATP ratios and the CK forward flux rates

59 allogeneic pMultistem cells (subendocardial phosphocreatine/ATP to 1.34+/-0.29; n=7; P<0.05).

60 On multivariable analysis, phosphocreatine/ATP was the only independent predictor o

61 ummit of Everest, cardiac energetic reserve (phosphocreatine/ATP) falls, but skeletal muscle energeti

62 line in diastolic function (P<0.01), cardiac phosphocreatine:ATP ratio (P<0.01), peak exercise cardia

63 Older high-active women demonstrated a phosphocreatine:ATP ratio and relative peak O2 consumpti

64 ly significant stenosis had decreases in the phosphocreatine:ATP ratio during exercise that were more

65 However, TAT-HK2 also decreased the phosphocreatine:ATP ratio that correlated with reduced r

66 ts correlated with a better energetic state (phosphocreatine:ATP ratio) when subjected to increasing

67 and 26% higher than older low-active women (phosphocreatine:ATP ratio, 1.9+/-0.2 versus 1.4+/-0.1; P

68 uring exercise as a consequence of increased phosphocreatine availability.

69 Phosphocreatine/beta-nucleoside triphosphate ratios usin

70 In contrast, oxidative resynthesis of phosphocreatine between intermittent contractions and in

71 110% peak aerobic power reduced VO2, muscle phosphocreatine breakdown and muscle acidification, elim

72 ptake, higher concentrations of glycogen and phosphocreatine, but delayed recovery after ischemia.

73 osphocreatine (NAA/Cr), choline-creatine and phosphocreatine (Cho/Cr), and choline-N-acetylaspartate

74 etabolite ratios N-acetyl-aspartate:creatine/phosphocreatine, choline-containing compounds:creatine/p

75 estimated from the initial rate of change of phosphocreatine concentration ([PCr]) using 31P-magnetic

76 cle respiratory capacity, ii) resting muscle phosphocreatine concentration ([PCr]) would negatively c

77 say, ATP concentration was decreased by 23%, phosphocreatine concentration by 42%, CK enzyme activity

78 sphate (ATP) concentration decreased by 10%, phosphocreatine concentration decreased by 30%, and tota

79 chondrial respiration (and in particular the phosphocreatine concentration, [PCr]) show similar non-l

80 ATP and phosphocreatine concentrations were inversely correlated

81 ange in muscle energy status because ATP and phosphocreatine concentrations were lower after metformi

82 (F = 4.692, p = .036), whereas brain ATP and phosphocreatine concentrations, as well as brain parench

83 ctions in the intramuscular ATPAMP ratio and phosphocreatine concentrations.

84 ad abnormally high gray matter creatine plus phosphocreatine concentrations.

85 atine kinase and its substrates creatine and phosphocreatine constitute an intricate cellular energy

86 Right forearm muscle phosphocreatine content and intracellular pH were assess

87 phosphogluconate and subsequent reduction in phosphocreatine correlated with significant potentiation

88 ios of N-acetylaspartate (NAA), creatine and phosphocreatine (Cr + PCr), and choline (Cho).

89 -containing compounds (Ch) and creatine plus phosphocreatine (CR) (NAA/[Cr + Ch]) in the anterior as

90 ne-containing compounds (Cho), creatine plus phosphocreatine (Cr) and myo-Inositol (m-Ins), were quan

91 Average N-acetylaspartate (NAA)/creatine-phosphocreatine (Cr) and NAA/choline-containing compound

92 zed in each patient, and the NAA to creatine-phosphocreatine (Cr) plus choline-containing compounds (

93 line-containing compounds (Cho) and creatine/phosphocreatine (Cr) to citrate (Cit) (ie, [Cho + Cr]/Ci

94 -acetyl aspartyl glutamate (NAA), creatine + phosphocreatine (Cr), choline-containing compounds (Cho)

95 ns of N-acetyl-aspartate, total creatine and phosphocreatine (Cr), choline-containing compounds, glut

96 ine-containing compounds (Cho); creatine and phosphocreatine (Cr); myo-inositol (Ins); N-acetyl-aspar

97 laspartate [NAA], choline [Ch], creatine and phosphocreatine [Cr]) were obtained in the occipital gra

98 cetylaspartate (NA), choline (Cho), creatine-phosphocreatine (Cre) and lactate, from four 15-mm slice

99 ontaining compounds (CHO), and creatine plus phosphocreatine (CRE) from multiple whole-brain slices c

100 ine-containing compounds (CHO), and creatine/phosphocreatine (CRE) signal intensities from multiple w

101 gamma-aminobutyric acid (Glx); creatine and phosphocreatine (Cre); choline-containing compounds (Cho

102 lic enzymes for rapid ATP generation via the phosphocreatine-creatine kinase (PCr/CK) system, as a un

103 Phosphocreatine/creatine and citrate were identified at

104 Thus, the ratio of phosphocreatine/creatine decreased to one third of contr

105 d number of mitochondrial profiles, a higher phosphocreatine/creatine ratio, elevated glutamate level

106 ethod, as well as phosphocreatine levels and phosphocreatine/creatine ratios, were decreased in diabe

107 e was inversely related to the intracellular phosphocreatine:creatine ratio suggesting that the eleva

108 osolic energy reserves (mm: ATP 5, ADP 0.01, phosphocreatine (CrP) 10) fructose-1,6-bisphosphate (FBP

109 duction occurred in muscle acidification and phosphocreatine depletion during ipsilateral forearm exe

110 e, H(+) , adenosine diphosphate, lactate and phosphocreatine depletion was 55 +/- 30, 62 +/- 18, 129

111 ring the second high Ca2+ challenge, whereas phosphocreatine did not differ from controls, suggesting

112 To determine phosphocreatine, endogenous ATP is first destroyed, and

113 sphate/exchangeable phosphate pool (EPP) and phosphocreatine/EPP (both p < 0.05); for lactate/N-acety

114 Analysis of the recovery kinetics for phosphocreatine following exercise provides evidence for

115 gh-energy phosphate molecules (e.g., ATP and phosphocreatine) from the mitochondria to cellular ATPas

116 rease in the ratio of inorganic phosphate to phosphocreatine, from 0.23 +/- 0.1 to 1.0 +/- 0.7 (p < .

117 001), and impaired cardiac energetic status (phosphocreatine/gamma-adenosine triphosphate ratio, 1.3+

118 Compared with healthy control subjects, the phosphocreatine/gamma-ATP ratio was reduced significantl

119 The phosphocreatine/gamma-ATP ratio was similar in newly dia

120 sis, there was no significant correlation of phosphocreatine/gamma-ATP ratio with myocardial perfusio

121 ine-containing compounds (Cho), creatine and phosphocreatine, glutamine and glutamate, N-acetylaspart

122 of the sarcoplasmic reticulum is suggested (Phosphocreatine+Glycogen+H(+)Creatine+Glycogen(n)(-1)+Gl

123 rmine the rates of ATP(OX), ATP(GLY) and net phosphocreatine hydrolysis in vivo during maximal muscle

124 a high rate of anaerobic ATP production from phosphocreatine hydrolysis.

125 g compounds, myo-inositol, and creatine plus phosphocreatine in frontal lobe gray matter and white ma

126 Increased creatine and phosphocreatine in R6/2 mice was associated with decreas

127 metabolic alterations consisted of increased phosphocreatine in the frontal cortex and increased the

128 by the donor cells led to the production of phosphocreatine in the host liver, permitting (31)P magn

129 It plays an analogous role to that of phosphocreatine in vertebrates.

130 and total creatine (the sum of creatine and phosphocreatine) in alkaline cell extracts.

131 Muscle adenosine triphosphate/(phosphocreatine + inorganic phosphate) at rest was signi

132 Regressions for pH(i) versus VO2, phosphocreatine/inorganic phosphate ratio (PCr/Pi) versu

133 A significant reduction in the phosphocreatine: inorganic phosphate ratio was observed

134 tine, endogenous ATP is first destroyed, and phosphocreatine is then quantitatively reacted with exog

135 , but in the presence of phosphocreatine and phosphocreatine kinase, this capacity is lost, presumabl

136 ging of perfusion, and (31)P-spectroscopy of phosphocreatine kinetics.

137 resonance studies demonstrated decreases in phosphocreatine levels and increases in ADP and AMP leve

138 d by metabolite indicator method, as well as phosphocreatine levels and phosphocreatine/creatine rati

139 show normal adenosine triphosphate (ATP) and phosphocreatine levels at rest but cannot maintain norma

140 s had normal ATP and only slightly decreased phosphocreatine levels by (31)P NMR spectroscopy, and th

141 exert neuroprotective effects by increasing phosphocreatine levels or by stabilizing the mitochondri

142 ain energy (i.e., adenosine triphosphate and phosphocreatine levels).

143 tion and enhanced post- ischemic recovery of phosphocreatine levels, both of which were blocked by co

144 icant decline in N-acetyl-aspartate:creatine/phosphocreatine (mean: 2.2%/year; 95% confidence interva

145 have higher cingulate myo-inositol/creatine-phosphocreatine measurements than patients with intermit

146 production, an effect that was abrogated by phosphocreatine-mediated reactivation of the arginine-cr

147 y measures of N-acetylaspartate-creatine and phosphocreatine (NAA/Cr), choline-creatine and phosphocr

148 ges in the tissue contents of ATP, ADP, AMP, phosphocreatine or creatine.

149 centrations of Cho (P < .001), creatine plus phosphocreatine (P = .02), NAA (P = .02), and mI (P = .0

150 ges in the ratios of inorganic phosphate and phosphocreatine, particularly during exercise provide in

151 In the brain, phosphocreatine (PCr) acts a reservoir of high-energy ph

152 s from a single chamber phantom containing a phosphocreatine (PCr) and ATP solution.

153 contraction may arise primarily from muscle phosphocreatine (PCr) and glycogen breakdown, circulatin

154 Significant changes in ATP, phosphocreatine (PCr) and inorganic phosphate (Pi) occur

155 P-NMR spectroscopy was performed to quantify phosphocreatine (PCr) and inorganic phosphate (Pi) withi

156 hesis were calculated from the evolutions of phosphocreatine (PCr) and pH.

157 from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling.

158 phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) are reduced in human myocardial in

159 Here, we demonstrate a novel role for phosphocreatine (PCr) as a spatiotemporal energy buffer

160 However, the intramuscular phosphocreatine (PCr) component of ATP generation was gr

161 CK velocity decreased by 64%; ATP and phosphocreatine (PCr) concentrations decreased by 51% an

162 ydrate (CHO) ingestion on changes in ATP and phosphocreatine (PCr) concentrations in different muscle

163 PArg and phosphocreatine (PCr) concentrations were calculated to

164 P production (evidenced by unchanged ATP and phosphocreatine (PCr) concentrations) or to PDC inhibiti

165 As expected, ATP was maintained as phosphocreatine (PCr) content briefly dropped and then r

166 by we could measure changes in ATP, ADP, and phosphocreatine (PCr) during stimulation of the sarcopla

167 The role of the creatine kinase (CK)/phosphocreatine (PCr) energy buffer and transport system

168 ntact cells adapting an in vivo technique of phosphocreatine (PCr) formation following energy interru

169 vity, COx subunit IV mRNA abundance, ATP and phosphocreatine (PCr) levels in amygdala, hippocampus an

170 ATP and phosphocreatine (PCr) levels were measured as an index o

171 of inspired oxygen (FiO2) to achieve varying phosphocreatine (PCr) levels.

172 e hypoxia was confirmed by measuring ATP and phosphocreatine (PCr) levels.

173 ysis and by Adenosine Triphosphate (ATP) and Phosphocreatine (PCr) levels.

174 oenergetic abnormalities including decreased phosphocreatine (PCr) normalized to ATP.

175 The effects of phosphocreatine (PCr) on sarcoplasmic reticulum (SR) Ca(

176 tic resonance spectroscopy was used to study phosphocreatine (PCr) onset kinetics in exercising human

177 for the enzyme creatine kinase, may increase phosphocreatine (PCr) or phosphocyclocreatine (PCCr) lev

178 d calculated adenosine diphosphate (ADP) and phosphocreatine (PCr) recoveries after exercise, consist

179 In this study we intend to characterize phosphocreatine (PCr) recovery kinetics with phosphorus-

180 Brief transient phosphocreatine (PCr) recovery overshoot (measured absol

181 phodiesters (PDEs), alpha-ATP, gamma-ATP and phosphocreatine (PCr) relative to beta-ATP were measured

182 n transfer on inorganic phosphate (P(i)) and phosphocreatine (PCr) resonances during saturation of ga

183 n of steady state energy balance to decrease phosphocreatine (PCr) reversibly and to measure the rate

184 Results The phosphocreatine (PCr) signal-to-noise ratio increased 2.

185 s of the CK reaction, and the unidirectional phosphocreatine (PCr) to adenosine triphosphate (ATP) me

186 Thirty minutes of ischemia caused phosphocreatine (PCr) to fall and P(i) to rise while pH

187 onstrate that hearts lacking M-CK have lower phosphocreatine (PCr) turnover but increased glucose-6-p

188 ctate accumulation as well as muscle ATP and phosphocreatine (PCr) utilisation based on analysis of m

189 n a single protocol to noninvasively measure phosphocreatine (PCr), adenosine triphosphate (ATP), and

190 etermine the relationship between changes in phosphocreatine (PCr), adenosine triphosphate (ATP), int

191 concentrations of inorganic phosphate (Pi), phosphocreatine (PCr), ATP, and phosphodiesters during r

192 There is low phosphocreatine (PCr), low CK reaction rates, and high m

193 magnetic resonance spectroscopy followed the phosphocreatine (PCr), Pi and pH dynamics at 6-9 s inter

194 the high-energy phosphate compounds, ATP and phosphocreatine (PCr), ratios of inorganic phosphate (Pi

195 In this paper, we examine the stimulation of phosphocreatine (PCr)-induced glutamate uptake and deter

196 ed biochemically by tissue levels of ATP and phosphocreatine (PCr).

197 hypoxia was documented by levels of ATP and phosphocreatine (PCr).

198 y a decrease in the tissue levels of ATP and phosphocreatine (PCr).

199 only by glycogenolysis and net splitting of phosphocreatine (PCr).

200 1.7 mM the smallest detectable difference in phosphocreatine (PCr).

201 energy phosphate metabolism [measured as the phosphocreatine (PCr)/ATP ratio] was measured using (3)(

202 Phosphocreatine (PCr)/ATP was determined with 31P NMR an

203 MR) spectroscopy was used to measure cardiac phosphocreatine (PCr)/ATP, and MR imaging and echocardio

204 cognitive tests were used to assess cardiac phosphocreatine (PCr)/ATP, cardiac function, and cogniti

205 ites including ATP/inorganic phosphate (Pi), phosphocreatine (PCr)/Pi, N-acetyl aspartate (NAA)/creat

206 exercise, there was a significant sparing of phosphocreatine (PCr, approximately 25 %, P < 0.05) and

207 etabolites (ATP to inorganic phosphate [Pi], phosphocreatine [PCr] to Pi, N-acetyl aspartate [NAA] to

208 erate exercise, an association of Vm,O2 and [phosphocreatine] ([PCr]) kinetics is a necessary consequ

209 Muscle [phosphocreatine] ([PCr]) responses to exercise, however,

210 re determined the dynamics of intramuscular [phosphocreatine] ([PCr]) simultaneously with those of .V

211 y protons was required to reproduce observed phosphocreatine, pH and vOX kinetics during exercise.

212 puts with experimental human data, including phosphocreatine, pH, pulmonary oxygen uptake and fluxes

213 In patients, the phosphocreatine/phosphate (PCr/Pi) ratio decreased signi

214 culating the ratio of inorganic phosphate to phosphocreatine (Pi/PCr).

215 The higher phosphocreatine:Pi and ATP:Pi ratios after 1,3-bis(2-chl

216 ATP:Pi ratio, 186 +/- 69% (P < 0.05) higher phosphocreatine:Pi ratio, and 0.17 +/- 0.06 pH units (P

217 ment of the kinetics of replenishment of the phosphocreatine pool after exercise using (31)P magnetic

218 ng possible reduced utilization of the brain phosphocreatine pool.

219 phocreatine, present as early as 4 weeks for phosphocreatine, preceding motor system deficits and dec

220 e found significantly increased creatine and phosphocreatine, present as early as 4 weeks for phospho

221 This enabled the local assessment of phosphocreatine recovery kinetics following a plantar fl

222 ition, slow decay of ESA was required to fit phosphocreatine recovery kinetics, and the time constant

223 rcise (ml.kg-1.min-1), and the post-exercise phosphocreatine recovery rate constant (min-1), a measur

224 1 (-6.8, -1.1), p = 0.011; and post-exercise phosphocreatine recovery rate constant -0.34 min-1 (-0.5

225 nced MRI calf muscle perfusion and (31)P MRS phosphocreatine recovery time constant (PCr) were measur

226 al capacity was assessed as the postexercise phosphocreatine recovery time constant (tauPCr) by (31)P

227 eft-ventricular developed pressure, improved phosphocreatine recovery, and reduced Na+ overload.

228 A phosphocreatine resonance was detected in livers of mice

229 ss, neither creatine uptake nor an effect on phosphocreatine resynthesis or performance was found aft

230 hange in the ratio of inorganic phosphate to phosphocreatine seen.

231 The first involves the phosphocreatine shuttle, where flagellar creatine kinase

232 at the expense of mitochondrial ATP via the phosphocreatine shuttle.

233 s a low energetic state of tissues using the phosphocreatine shuttle.

234 strated a greater consumption of high-energy phosphocreatine stores than did the other groups (contro

235 s of native substrates such as ADP, ATP, and phosphocreatine substantially reduce [alpha32P]ATP nucle

236 ased lactate content by 4-fold and decreased phosphocreatine to 60% of control.

237 Perhexiline improved myocardial ratios of phosphocreatine to adenosine triphosphate (from 1.27+/-0

238 Our aim was to measure the cardiac phosphocreatine to adenosine triphosphate ratio (PCr/ATP

239 Myocardial ratio of phosphocreatine to adenosine triphosphate, an establishe

240 (31)P NMR analysis showed a reduced ratio of phosphocreatine to ATP content in failing+Ad.betagal-GFP

241 We measured the change in the ratio of phosphocreatine to ATP during exercise.

242 rast, TG-AAC mice maintained LV function and phosphocreatine to ATP ratio and had <10% mortality.

243 panied by ventricular dilation and decreased phosphocreatine to ATP ratio and reached a mortality rat

244 The phosphocreatine to ATP ratio, inorganic phosphate to ATP

245 The similar phosphocreatine to ATP ratios in SZ and healthy controls

246 sting calf muscle the concentration ratio of phosphocreatine to ATP was reduced, and the resting intr

247 The ratio of phosphocreatine to ATP was unaffected by heart rhythm du

248 y evaluated ventricular energetics (ratio of phosphocreatine to ATP).

249 -18% [IQR, -17% to -19%], P=0.002; ratio of phosphocreatine to ATP, 1.81+/-0.35 versus 2.05+/-0.29,

250 concomitant with a reduction in the ratio of phosphocreatine to ATP.

251 ATP derived from the conversion of phosphocreatine to creatine by creatine kinase provides

252 roof of principle, we show the conversion of phosphocreatine to creatine by spatiotemporal mapping of

253 y demonstrated a significant decrease in the phosphocreatine to inorganic phosphate ratio in resting

254 ine kinase, the enzyme that utilizes ADP and phosphocreatine to rapidly regenerate ATP, may modulate

255 where flagellar creatine kinase (Sp-CK) uses phosphocreatine to rephosphorylate ADP.

256 The apical phosphocreatine-to-ATP ratio (PCr/ATP) was lower in seve

257 impaired cardiac energetics (indexed by the phosphocreatine-to-ATP ratio measured by (31)P magnetic

258 or myocardial triglyceride content (MTG) and phosphocreatine-to-ATP ratio, respectively.

259 31P-MRS at rest showed a reduced phosphocreatine-to-inorganic phosphate ratio in the symp

260 +/- 0.1, p = 0.015) were increased, but the phosphocreatine-to-Pi ratio (2.1 +/- 0.6 versus 3.2 +/-

261 rgy flows from these central mitochondria as phosphocreatine toward the photoreceptor's synaptic term

262 Because ATP is replenished from phosphocreatine via the creatine kinase reaction, we hav

263 d pressure was depressed by 20%, and cardiac phosphocreatine was depleted by 65.5% +/- 14% (P < 0.05

264 f muscle and flexor digitorum superficialis, phosphocreatine was depleted more rapidly in patients th

265 ased approximately 10-fold, but the K(m) for phosphocreatine was relatively unaffected.

266 31P NMR data showed that phosphocreatine was significantly depleted in cells expo

267 Recoveries of function, ATP, and phosphocreatine were higher in TGbetaARK1 hearts than in

268 e/phosphocreatine, and myo-inositol:creatine/phosphocreatine were measured using online software (PRO

269 model of brain energy deficit, both ATP and phosphocreatine were significantly reduced.

270 n the pipette but not at 10 mM ATP and 10 mM phosphocreatine when IK-ATP was always blocked.

271 hepatic hypoxia and catalyzes production of phosphocreatine, which is imported through the SLC6A8 tr

272 after quantitative conversion of creatine to phosphocreatine with a large excess of exogenous ATP, co

273 ion of all ATP to ADP, and final reaction of phosphocreatine with ADP to form ATP.