ライフサイエンスコーパス: high-energy phosphate

1 ls convert energy stored in ketone bodies to high energy phosphates.

2 hogluconate) and the associated reduction in high-energy phosphates.

3 reatine phosphate (PCr) are prime myocardial high-energy phosphates.

4 The high-energy phosphates adenosine triphosphate (ATP) and

5 ess the impact of sex and menopause on brain high-energy phosphates [adenosine triphosphate (ATP), ph

6 ing ischemia and enhanced the resynthesis of high-energy phosphates after reperfusion.

7 P turnover was determined from the change in high energy phosphates and lactate production, the latte

8 izing the ischemic area, plus the changes in high-energy phosphate and the total adenine nucleotide p

9 ve and absolute concentrations of myocardial high-energy phosphates and ATP flux through CK in the fa

10 cing myocardial infarct size, and preserving high-energy phosphates and cardiac function.

11 ma2N488I hearts had normal resting levels of high-energy phosphates and could improve cardiac perform

12 e preischemia group to total preservation of high-energy phosphates and glutathione status in reperfu

13 eks after tendon release, when the levels of high-energy phosphates and glycerophospholipids were low

14 scopy was used to quantify concentrations of high-energy phosphates and pH in the knee extensors of s

15 early, rapid exercise-induced declines in SM high-energy phosphates and reduced oxidative capacity co

16 mb skeletal muscle, to noninvasively measure high-energy phosphates and the effect of magnetization t

17 ely affect the intracellular availability of high-energy phosphates and ultimately, cellular metaboli

18 d the quantitative relationship between NAA, high-energy phosphates, and ADP levels in the hippocampu

19 13.8% placebo at 30 minutes), yet myocardial high-energy phosphates ATP and ADP reduced by ischemia i

20 animal models implicate impaired myocardial high-energy phosphate availability in HF.

21 across mitochondrial membranes can transfer high energy phosphate between the cytosol and mitochondr

22 Ks), catalyzes the reversible transfer of a "high-energy" phosphate between ATP and a phosphoguanidin

23 t require intracellular compounds containing high-energy phosphate bonds and was not affected by anal

24 acids, costs of synthesis vary from 12 to 74 high-energy phosphate bonds per molecule.

25 ganic polyphosphate (poly P), a reservoir of high-energy phosphate bonds with multiple roles.

26 With its high-energy phosphate bonds, adenosine triphosphate (ATP

27 bon, requires approximately 20 to 60 billion high-energy phosphate bonds.

28 These findings implicate roles for PCr as a high-energy phosphate buffer in the fusion of multiple c

29 s independently cause reductions in cerebral high-energy phosphates, CBF, and cortical ADC values.

30 rct size, and a greatly improved recovery of high energy phosphates compared with that in nontransgen

31 Concentrations of high energy phosphate compounds, inorganic phosphate and

32 ring ischemia and diminished regeneration of high-energy phosphate compounds on reperfusion.

33 MRS by determining the concentrations of the high-energy phosphate compounds, ATP and phosphocreatine

34 METHODS AND Resting SM high-energy phosphate concentrations and ATP flux rates

35 (XO) inhibitor allopurinol improves cardiac high-energy phosphate concentrations in human heart fail

36 ctions observed at MR spectroscopy, although high-energy phosphate concentrations were lower at biops

37 e mechanistic in vivo relationships among SM high-energy phosphate concentrations, mitochondrial func

38 lar pH and steady-state metabolite ratios of high-energy phosphate-containing compounds (phosphocreat

39 osphates (PP-IPs) represent a novel class of high-energy phosphate-containing messengers which contro

40 allenge resulted in progressive depletion of high-energy phosphate content and failure to sustain hig

41 Abnormalities in high-energy phosphate content and limitations in adenosi

42 is during ischemia, and improved recovery of high-energy phosphate content in old GLUT1-TG hearts (P<

43 ansgenic hearts during reperfusion despite a high-energy phosphate content similar to that in nontran

44 Changes in high-energy phosphate content suggest that an energy-req

45 eductions in contractility, vascularization, high-energy phosphate content, and lactate production.

46 not associated with changes in either pHi or high-energy phosphate content, as assessed by 31P nuclea

47 Rapid exercise-induced high-energy phosphate decline and lower ATP at fatigue w

48 inversely related to rapid exercise-induced high-energy phosphate decline and worse SM energetic pro

49 gnificantly faster rates of exercise-induced high-energy phosphate decline than did HFrEF patients wi

50 I, less calf muscle, faster exercise-induced high-energy phosphate decline, and worse SM energetics a

51 A rigor force, possibly resulting from high-energy phosphate depletion and/or an increase in AD

52 exhibited severe EI, the most rapid rates of high-energy phosphate depletion during exercise, and imp

53 onomic tone, atrial stretch, or depletion of high-energy phosphates do not contribute significantly t

54 d slice extracts to ask: 1) if FBP preserves high energy phosphates during HI; and 2) if exogenous [1

55 4) Glucose and insulin, which increase high-energy phosphates during ischemia, reduced increase

56 amate uptake into synaptic vesicles by other high-energy phosphates has not been described.

57 n, phosphocreatine (PCr) acts a reservoir of high-energy phosphate (HEP) bonds, and creatine kinases

58 is associated with reductions in myocardial high-energy phosphate (HEP) levels, which are more sever

59 onship between the alterations in myocardial high-energy phosphate (HEP) metabolism and protein expre

60 lyzed for citrulline (determinant of NO) and high-energy phosphates (HEP) and their metabolites using

61 ence of chronic alteration in homeostasis of high energy phosphates in HD models in the earliest stag

62 Both IP and TP protocols increased levels of high energy phosphates in the pre-ischaemic heart.

63 invasive technique that can directly measure high-energy phosphates in the myocardium and identify me

64 or acetyl kinase, two enzymes that generate high-energy phosphate intermediates.

65 elates to limited ATP synthesis capacity and high energy phosphate kinetic abnormalities previously d

66 FBP did not improve high energy phosphate levels or change (1)H metabolite p

67 Changes in myocardial high-energy phosphate levels and pH were studied by 31P

68 ertrophied hearts, alterations in myocardial high-energy phosphate levels do not induce abnormal mech

69 an reduced acidification and preservation of high-energy phosphate levels during ischemia contribute

70 hether modulation of intracellular pH and/or high-energy phosphate levels during ischemia contributed

71 n of intracellular pH and/or preservation of high-energy phosphate levels during ischemia contributed

72 No difference in intracellular pH or high-energy phosphate levels was found between the beta-

73 d Somah solution demonstrated an increase in high-energy phosphate levels, protection of cardiac myoc

74 Controls maintained high-energy phosphate levels, unlike THY, which demonstr

75 P NMR) spectroscopy to noninvasively measure high-energy phosphate levels; mitochondrial aconitase ac

76 ition of aldose reductase activity preserves high-energy phosphates, maintains a lower cytosolic NADH

77 nt in skeletal muscle that has a key role in high energy phosphate metabolism.

78 fore and after 20 h of hypoxic exposure, and high-energy phosphate metabolism [measured as the phosph

79 This finding suggests alterations in high-energy phosphate metabolism and regulation of oxida

80 tic resonance spectroscopy to measure muscle high-energy phosphate metabolism during plantar flexion

81 s, 31P NMR spectroscopy was used to evaluate high-energy phosphate metabolism in isolated rat hearts

82 osphate is consistent with an abnormality of high-energy phosphate metabolism in the basal ganglia of

83 ormobaric hypoxia causes a rapid decrease in high-energy phosphate metabolism in the human cardiac le

84 ectroscopy (MRS) studies link alterations of high-energy phosphate metabolism in valvular disease and

85 They suggest that impaired high-energy phosphate metabolism is a marker of hypertro

86 We postulated that changes in cardiac high-energy phosphate metabolism may underlie the myocar

87 nuclear magnetic resonance spectroscopy and high-energy phosphate metabolism using 31P nuclear magne

88 rsus high workload contractile function) and high-energy phosphate metabolism.

89 status nor IV iron significantly influenced high-energy phosphate metabolism.

90 phosphorylation, which are key components of high-energy phosphate metabolism.

91 c decompensation manifested by a decrease in high energy phosphate metabolites (ATP, ADP, and phospho

92 ectroscopy is a noninvasive method to detect high-energy phosphate metabolites, such as ATP.

93 c metabolic flux depends on the diffusion of high-energy phosphate molecules (e.g., ATP and phosphocr

94 be poised to provide bursts of site-specific high-energy phosphate necessary for efficient receptor s

95 annose, UDP-derivatives), energy metabolism (high-energy phosphates, nicotinic coenzymes, oxypurines)

96 raction, online desalting, separation of the high-energy phosphates on a C18 reversed-phase column us

97 ations of both calcium-activated tension and high-energy phosphates on increased DCS.

98 Although local burn injury does not alter high-energy phosphates or pH, apart from PCr reduction,

99 re no known efficient prebiotic synthesis of high-energy phosphates or phosphate esters.

100 e, but did not prevent the level decrease in high-energy phosphates or protein constituents of mitoch

101 cation of bioenergetic molecules, containing high-energy phosphates, over the whole brain as well as

102 etermine the relationship between myocardial high-energy phosphates, phosphocreatine, and ADP and oxy

103 in vivo assessment of changes in the brain's high-energy phosphates-phosphocreatine (PCr), inorganic

104 anic phosphate (relative to the exchangeable high-energy phosphate pool) were measured serially in an

105 alone, also produces significant recovery of high-energy phosphate pools.

106 release, reduced malondialdehyde formation, high-energy phosphate preservation, and improved call mo

107 tored continuously (porphyrinic sensor), and high-energy phosphates, reduced and oxidized glutathione

108 This is coupled to preservation of high-energy phosphates, reducing subsequent reactive oxy

109 phosphorylation demonstrating a lack of any high energy phosphate shuttle.

110 Hemodynamics, transmural blood flow, and high-energy phosphates (spatially localized 31P-nuclear

111 late PFK-1 activity in concert with cellular high energy phosphate status.

112 se animals demonstrated enhanced recovery of high energy phosphate stores and correction of metabolic

113 hen, to assess the contribution of decreased high-energy phosphate supply, hearts received 5) glucose

114 kinase expression falls, possibly impairing high-energy phosphate transfer from the mitochondria to

115 ylate kinase 2 (AK2), an enzyme critical for high-energy phosphate transfer from the mitochondria, as

116 rest as well as improving the efficiency of high-energy phosphate transfer.

117 tutes an alternative means for mitochondrial high-energy phosphate transport, these results indicate

118 come more "energetically costly" in terms of high-energy phosphate use, accumulation of ADP, and decr

119 n a neurodegenerative model, brain levels of high energy phosphates using microwave fixation, which i

120 reperfusion, during which time we monitored high-energy phosphates using 31P-NMR and left-ventricula

121 High energy phosphates were significantly lower (P<0.05)

122 tion, cellular Na and Ca, myocardial pH, and high-energy phosphates were examined in perfused hearts

123 Myocardial high-energy phosphates were measured by using magnetic r

124 Myocardial high-energy phosphates were measured with 31P-NMR spectr