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

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

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

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

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

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

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

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

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

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

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

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

14 13.8% placebo at 30 minutes), yet myocardial high-energy phosphates ATP and ADP reduced by ischemia i

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

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

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

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

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

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

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

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

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

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

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

26 Concentrations of high energy phosphate compounds, inorganic phosphate and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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