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 lular levels of creatine and its derivatives phosphocreatine and creatinine and suppressed proliferat

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

27 Phosphocreatine and inorganic phosphate (Pi) varied in o

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

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

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

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

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

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

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

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

36 tyl compounds, glutamate+glutamine, creatine+phosphocreatine, and choline compounds in 78 children an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 %, P=0.04), driven primarily by reduction in phosphocreatine/ATP (by 17%, P<0.001), with CK k(f) unch

55 )P magnetic resonance spectroscopy to assess phosphocreatine/ATP and CK kinetics, at rest and during

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

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

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

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

60 , P = .03), and was accompanied by a fall in phosphocreatine/ATP ratio by 0.4 (2.2 +/- 0.4 to 1.8 +/-

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

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

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

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

65 At rest, although myocardial phosphocreatine/ATP was 14% lower in obesity (1.9+/-0.3

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

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

68 ed, compensating for depleted energy stores (phosphocreatine/ATP), but potentially limiting greater A

69 ty and myocardial levels of phosphocreatine, phosphocreatine/ATP, and ATP/ADP to normalize in debandi

70 ed, maintaining ATP delivery despite reduced phosphocreatine/ATP.

71 , 38.4+/-7.4, debanding, 35.6+/-8.7, P=0.71; phosphocreatine/ATP: sham, 1.22+/-0.23 debanding, 1.11+/

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

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

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

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

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

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

78 rtrophic hearts and normalized energy state (phosphocreatine:ATP) and consequently, AMP activated pro

79 uring exercise as a consequence of increased phosphocreatine availability.

80 Phosphocreatine/beta-nucleoside triphosphate ratios usin

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

82 110% peak aerobic power reduced VO2, muscle phosphocreatine breakdown and muscle acidification, elim

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

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

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

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

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

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

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

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

91 ATP and phosphocreatine concentrations were inversely correlated

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

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

94 ctions in the intramuscular ATPAMP ratio and phosphocreatine concentrations.

95 ad abnormally high gray matter creatine plus phosphocreatine concentrations.

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

97 Right forearm muscle phosphocreatine content and intracellular pH were assess

98 phosphogluconate and subsequent reduction in phosphocreatine correlated with significant potentiation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 Phosphocreatine/creatine and citrate were identified at

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 Phosphocreatine in brainstem correlated with respiratory

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

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

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

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

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

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

143 Fatiguing exercise causes hydrolysis of phosphocreatine, increasing the intracellular concentrat

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

145 meter estimates were derived including: ATP, phosphocreatine, inorganic phosphate, adenosine diphosph

146 Brain phosphocreatine/inorganic phosphate and NTP/exchangeable

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 ATP content, phosphocreatine, nicotinamide adenine dinucleotide and i

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

165 tyl compounds, glutamate+glutamine, creatine+phosphocreatine, or choline compounds measured by proton

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 PArg and phosphocreatine (PCr) concentrations were calculated to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 Phosphocreatine (PCr) plays a vital role in neuron and m

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

197 cle oxidative capacity was measured from the phosphocreatine (PCr) recovery kinetics following a 24 s

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

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

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

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

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

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

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

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

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

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

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

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

210 tify intracellular inorganic phosphate (Pi), phosphocreatine (PCr), and betaATP.

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

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

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

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

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

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

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

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

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

220 gy in the form of adenosine triphosphate and phosphocreatine (PCr).

221 1.7 mM the smallest detectable difference in phosphocreatine (PCr).

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

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

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

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

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

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

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

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

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

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

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

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

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

235 reduce its activity and myocardial levels of phosphocreatine, phosphocreatine/ATP, and ATP/ADP to nor

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

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

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

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

240 ng possible reduced utilization of the brain phosphocreatine pool.

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

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

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

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

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

246 1 (-6.8, -1.1), p = 0.011; and post-exercise phosphocreatine recovery rate constant -0.34 min-1 (-0.5

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

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

249 esonance spectroscopy demonstrates prolonged phosphocreatine recovery time constant after exercise in

250 e in magnetic resonance spectroscopy-derived phosphocreatine recovery time was not detected (P=0.199)

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

252 A phosphocreatine resonance was detected in livers of mice

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

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

255 normalize in debanding towards sham values (phosphocreatine: sham, 38.4+/-7.4, debanding, 35.6+/-8.7

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

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

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

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

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

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

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

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

264 Myocardial ratio of phosphocreatine to adenosine triphosphate, an establishe

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

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

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

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

269 The phosphocreatine to ATP ratio, inorganic phosphate to ATP

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

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

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

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

274 -18% [IQR, -17% to -19%], P=0.002; ratio of phosphocreatine to ATP, 1.81+/-0.35 versus 2.05+/-0.29,

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

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

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

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

279 as resting DeltaGATP, magnesium, and dynamic phosphocreatine to inorganic phosphate recovery were dec

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

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

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

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

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

285 31P-MRS at rest showed a reduced phosphocreatine-to-inorganic phosphate ratio in the symp

286 +/- 0.1, p = 0.015) were increased, but the phosphocreatine-to-Pi ratio (2.1 +/- 0.6 versus 3.2 +/-

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

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

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

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

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

292 31P NMR data showed that phosphocreatine was significantly depleted in cells expo

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

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

295 etected in the brainstem where DeltaGATP and phosphocreatine were reduced.

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

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

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

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

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