ライフサイエンスコーパス: Krebs

1 Krebs cycle enzyme activity in Bacillus subtilis was exa

2 Krebs cycle flux was also stimulated by CGP37157 when gl

3 Krebs cycle intermediates such as succinate, citrate, an

4 Krebs cycle substrates (KCS) can stabilise the colour of

5 Krebs von den Lungen (KL)-6 is pathophysiological biomar

6 helate magnesium and to inhibit aconitase, a Krebs cycle enzyme.

7 such as the molecular chaperone Hsp60p and a Krebs cycle protein, Kgd2p.

8 required to allow the use of glutamine as a Krebs cycle substrate in T cells.

9 ranslation and RNA synthesis activities in a Krebs-2-derived in vitro system that supported complete,

10 al carcinoma, is caused by inactivation of a Krebs cycle enzyme due to mutation.

11 This work outlines the use of a Krebs cycle metabolon catalyst obtained through the in s

12 Succinate, a Krebs cycle intermediate, increases after dysregulated e

13 al. (2016) identify a mechanism that uses a Krebs cycle protein to control local activation of a ubi

14 v.) and nondiabetic rats and perfused with a Krebs-albumin-red cell solution (K2RBC, Hct 20%).

15 c switch to aerobic glycolysis, accumulating Krebs' cycle intermediates that alter transcription of i

16 s a key component of the tricarboxylic acid (Krebs) cycle.

17 LECA later acquired the fully aerobic Krebs cycle-oxidative phosphorylation-mitochondrial meta

18 howed hypoglycemia, lactic acidosis, altered Krebs cycle function and dysregulated fatty acid oxidati

19 Interestingly, among Krebs cycle intermediates, only succinic acid monomethyl

20 ite concentrations (glycolytic, anaplerotic, Krebs cycle intermediates).

21 32.2]), angiopoietin-2 (6.4 [1.3-30.4]), and Krebs von den Lungen-6 (5.1 [3.0-12.2]).

22 nt of electron transport chain complexes and Krebs cycle enzymes revealed that alpha-ketoglutarate de

23 th increased cellular ATP (1.7-3.0-fold) and Krebs cycle intermediates, including citrate, isocitrate

24 ling to the glycolysis, gluconeogenesis, and Krebs cycle (n = 48) and an exploration by the next-gene

25 female mouse kidneys towards glycolysis and Krebs cycle activity.

26 dinated set of enzymes of the glycolytic and Krebs cycle pathways, which we propose may antagonize Tr

27 extensive catabolism via the glycolytic and Krebs cycle pathways.

28 articularly at the amino acid metabolism and Krebs cycle level.

29 s, ATP machinery, fatty acid metabolism, and Krebs cycle, which further decreased in expression durin

30 mulation is dependent on calcium release and Krebs cycle activity.

31 NaDC-1, couples the transport of sodium and Krebs cycle intermediates, such as succinate and citrate

32 of mitochondrial reactive oxygen species and Krebs' cycle intermediates, and increased resistance to

33 red rat hepatocytes were incubated in anoxic Krebs-Ringer-HEPES buffer at pH 6.2 for 4 hours and reox

34 In wheat germ and mouse ascites Krebs-2 in vitro translation systems, PCI6 inhibited tra

35 onsequently, the mitochondrial products ATP, Krebs cycle intermediates, glutamate, and acetoacetate w

36 '-cyclic monophosphate (1 uM) to the bathing Krebs-Henseleit solutions.

37 utely alkaline loaded by replacing bilateral Krebs bicarbonate Ringer (KBR) with Hepes-buffered Ringe

38 guinea pigs and kept alive in oxygen bubbled Krebs' solution.

39 Decreased (13)C-Krebs cycle intermediates suggested that PM(2.5) exposur

40 -) mice had diminished levels of circulating Krebs Von Den Lungen 6 (alveolar epithelial injury marke

41 trode in an airtight stirred bath containing Krebs solution buffered with HEPES at 37 degrees C (pH 7

42 its were suspended in organ baths containing Krebs solution; isometric tension was then measured.

43 ich persisted in TTX (0.5 microM)-containing Krebs solution, were reduced by 70% in a low-Na+ (26 mM)

44 perfused mouse liver model with deoxygenated Krebs-Henseleit buffer followed by oxygenated buffer.

45 Five of seven detected Krebs cycle metabolites were depleted in mdx urine, with

46 sted even in perfusions of zero calcium-EGTA Krebs solution suggesting that the calcium oscillation i

47 Eight Krebs cycle enzyme components were isolated upon chemica

48 our drainage period, animals received either Krebs Ringer Henseleit (the bile-depleted group), or sod

49 ally before and after incubation with either Krebs solution alone or with the NO-inhibitor, NG-monome

50 zed arrest, hearts were arrested with either Krebs-Henseleit (KH) buffer (control), KH buffer contain

51 was compared in hearts protected with either Krebs-Henseleit solution (K-H), pinacidil (50 micromol/L

52 The nuclear-encoded Krebs cycle enzymes, fumarate hydratase (FH) and succina

53 e carbon into glucose via glutamine entering Krebs cycle at alpha-ketoglutarate or 2) through simple

54 ger than those elicited by other (equimolar) Krebs cycle intermediates.

55 [2-(13)C]pyruvate was also used to evaluate Krebs cycle metabolism and demonstrated a unique marker

56 odelling indicates altered metabolic fluxes (Krebs cycle, fatty acid, carbohydrate, amino acid metabo

57 In Ca2+-free Krebs-Ringer bicarbonate buffer containing 2.8 mmol/l gl

58 This current was inhibited in chloride-free Krebs solution or by inhibiting basolateral chloride upt

59 involved in basic metabolic processes (e.g. Krebs cycle), (iii) genes required to survive oxidative

60 of central carbon metabolic pathways (e.g., Krebs cycle enzymes), as well as transporters and enzyme

61 evidence of profoundly dampened glycolysis, Krebs cycle, fatty acid beta oxidation and amino acid me

62 y and inhibition by catalytic products, Hans Krebs first demonstrated the existence of multiple gluta

63 In Escherichia coli, the homodimeric Krebs cycle enzyme isocitrate dehydrogenase (EcIDH) is r

64 In Krebs extracts, dipyridamole specifically inhibited vira

65 on periods of 60 min each at 37 degrees C in Krebs Ringers Henseleit (KRH) solution in an atmosphere

66 The in vivo decrease in Krebs cycle activity in the 6-week post-MI heart may rep

67 ni were isolated by collagenase digestion in Krebs-Ringer bicarbonate (KRB) buffer at 37 degrees C.

68 longus muscles were preincubated for 4 h in Krebs-Henseleit solution containing glucose or glucose +

69 Dopamine was incubated in Krebs bicarbonate medium and its rate of chemical degrad

70 Vessels were incubated in Krebs buffer at 37 degrees C.O(2)(-) was measured by luc

71 s (human, rabbit, and rat) were incubated in Krebs solution containing [3H]-norepinephrine ([3H]NE) f

72 Intact porcine lenses were incubated in Krebs solution.

73 Sphincter muscle was incubated in Krebs-Ringer bicarbonate buffer in the absence and prese

74 After 10 minutes' incubation in Krebs bicarbonate medium, the dopamine concentration dec

75 (0.2 uM), then reperfused for 45 minutes in Krebs solution, when functional recovery was assessed.

76 re isolated, cultured, and then perifused in Krebs-Ringer bicarbonate buffer with 2 mmol/l glutamine

77 alterations after MI in which reductions in Krebs cycle activity precede a reduction in pyruvate deh

78 After storage, the cells were rewarmed in Krebs-Henseleit buffer with air at 37 degrees C for 1 hr

79 teries without endothelium were suspended in Krebs-Ringer bicarbonate solution for isometric tension

80 everal previous studies, our method included Krebs cycle intermediates (m/z <200), which we found to

81 rmined to be significantly altered including Krebs cycle intermediates, amino acids that have not bee

82 ized energy production components, including Krebs cycle and electron transport genes, decreased by 4

83 to supply sufficient pyruvate for increased Krebs cycle flux when glucose is limiting.

84 ally improves glucose homeostasis, increases Krebs cycle activity, and reduces the levels of acylcarn

85 Using an isolated, Krebs solution-perfused rat heart we measured the change

86 tial shifted to -90 mV in a low-Na+, high-K+ Krebs solution.

87 cterial growth; depressed activities of many Krebs cycle enzymes, including pyruvate:ferredoxin oxido

88 In this study, we measured Krebs cycle flux in real time in perfused rat hearts usi

89 and AD patients included energy metabolism, Krebs cycle, mitochondrial function, neurotransmitter an

90 ative phosphorylation, glutamine metabolism, Krebs cycle, and fatty acid oxidation.

91 as glucose, amino acid and lipid metabolism, Krebs cycle, and immune responses and those hitherto unk

92 completely abolished by low Ca2+, high Mg2+ Krebs solution or Krebs solution containing Co2+ (2 mM)

93 Low Ca2+/high Mg2+ Krebs solution or TTX did not change the resting membran

94 either a high-K+ (7 mM) or Cd2+ (100 microM) Krebs solution.

95 eased substrate supply for the mitochondrial Krebs cycle compared with APAP alone.

96 d diminished production of the mitochondrial Krebs cycle substrate citrate, a precursor to cellular l

97 In addition, the mitochondrial Krebs cycle was modulated to increase synthesis of malic

98 the substrate flux through the mitochondrial Krebs cycle, it was observed that the reduced liver inju

99 a rate-limiting enzyme in the mitochondrial Krebs cycle.

100 At 6 weeks after MI, in vivo mitochondrial Krebs cycle activity was impaired, with decreased (13)C-

101 mol (5 x 10(5) cpm/ micromol) of HNE in 2 mL Krebs-Hansleit buffer for 1 hour at 37 degrees C.

102 on, were reduced by 70% in a low-Na+ (26 mM) Krebs solution, indicating the involvement of Na+ ions.

103 nstant flow of 10 mL/min by using a modified Krebs-Henseleit solution equilibrated with 95% oxygen an

104 tant flow rate of 10 mL/min using a modified Krebs-Henseleit solution equilibrated with 95% oxygen an

105 eys were isolated and perfused with modified Krebs-Henseleit buffer.

106 oved from the rat and perfused with modified Krebs-Henseleit buffers containing 7.5 or 2.5 g/dL bovin

107 trogenic, sodium-dependent transport of most Krebs cycle intermediates (Km = 20-60 microM), including

108 strate that in cell-free extracts from mouse Krebs-2 ascites, microRNA-mediated translational repress

109 uscles were isolated and incubated in normal Krebs-Henseleit buffer (pH 7.4).

110 ; Roe, 0.36 (P < 0.001); Collins, 0.82 (ns); Krebs, 0.14 (P < 0.01).

111 ollins usage occurred in the SE; and 100% of Krebs and 46% of Stanford usage occurred in the W.

112 of mitochondrial stress and accumulation of Krebs cycle intermediates in adipose tissue in diabetes

113 ve stress, antioxidant enzyme, activities of Krebs cycle and respiratory chain enzymes, mitochondrial

114 ly consumes O2, rendering standard assays of Krebs cycle turnover unusable.

115 er at constant flow; perfusates consisted of Krebs-Henseleit buffer or buffer plus washed RBCs at a H

116 Cardioplegia consisted of Krebs-Henseleit solution either alone (control) or with

117 ocytes results in a global downregulation of Krebs cycle and OXPHOS gene expression, defective mitoch

118 Therefore, CcpA controls expression of Krebs cycle genes directly by regulating transcription o

119 Langendorff method under a constant flow of Krebs-Henseleit buffer containing (18)F-FDG with a rate

120 and tandem mass spectrometry measurement of Krebs cycle intermediates revealed a negative impact of

121 molecule: malate dehydrogenase, a member of Krebs cycle, and adenosine triphosphate synthase.

122 The metabolism of Krebs cycle intermediates is of fundamental importance f

123 neoplasms, displays genetic modifications of Krebs cycle components as well as electron transport cha

124 horylation and Ca2+ -dependent regulation of Krebs cycle dehydrogenases, illustrating how the model c

125 ements and balances the bioenergetic role of Krebs cycle-derived electron donors.

126 Accordingly, Ca(2+)-induced stimulation of Krebs cycle dehydrogenases during beta-adrenergic stimul

127 t), involved in the transport and storage of Krebs cycle intermediates in tissues important in fly me

128 yze the Na(+)-driven concentrative uptake of Krebs cycle intermediates and sulfate into cells; disrup

129 ting sequence appended restored viability on Krebs cycle substrates and ATP synthesis capabilities bu

130 We did not detect glycolysis or Krebs-cycle-related defects in the iar4 mutant, and a T-

131 hed by low Ca2+, high Mg2+ Krebs solution or Krebs solution containing Co2+ (2 mM) and Cd2+ (400 micr

132 r effects on HIF-1 are not mimicked by other Krebs cycle intermediates, including succinate and fumar

133 the periphery and immersed in an oxygenated Krebs-Ringer buffer.

134 slices were first equilibrated in oxygenated Krebs buffer (KRB) (120 min) then superfused for 10 min

135 were harvested and maintained in oxygenated Krebs solution in an organ bath at 37 degrees C.

136 fused alternately with a modified oxygenated Krebs-Henseleit buffer and with buffer containing varied

137 minutes via the portal vein with oxygenated Krebs-Henseleit bicarbonate buffer solution at a pressur

138 mitochondrial metabolism, including partial Krebs' cycle activation and significant accumulation of

139 owth inhibition was accompanied by perturbed Krebs cycle activity, inhibition of lipid and nucleotide

140 s, nicotinamides, tryptophan, phospholipids, Krebs and urea cycles, and revealed kidney dysfunction b

141 - 0.8 ml min-1 in hearts perfused with plain Krebs solution, by 3.8 +/- 0.8 ml min-1 in hearts to whi

142 re randomly assigned to perfusion with plain Krebs solution, or with Krebs solution to which L-NAME a

143 found to be primarily the result of reduced Krebs cycle gene transcription.

144 pyruvate concentrations coupled with reduced Krebs cycle intermediates and short-chain acylcarnitines

145 proceed in the same sequence as the reverse Krebs cycle, resembling a protometabolic pathway, with g

146 larographic chamber containing air-saturated Krebs-Henseleit buffer plus 20 mM glucose, PO2 being mon

147 These experiments use the sequential Krebs TCA cycle enzymes from yeast mitochondrial malate

148 Elevated levels of serum Krebs von den Lungen-6 and C-reactive protein are both a

149 orrelated well with GSIS, in particular some Krebs cycle intermediates, malonyl-CoA, and lower ADP le

150 tilization and in the activities of specific Krebs cycle enzymes alpha-ketoglutarate dehydrogenase (K

151 ion, extracellular matrix structure, sugars, Krebs cycle intermediates, microbe-derived metabolites a

152 amino acids, fumarate and malate, suggesting Krebs cycle up-regulation.

153 intermediate in the tricarboxylic acid (TCA, Krebs) cycle and a promising therapeutic agent in its ow

154 ciated with mdx disease progression and that Krebs cycle deficiencies are a downstream consequence of

155 We first demonstrate that Krebs cycle intermediates, such as fumaric acid esters,

156 h that of other metabolites, indicating that Krebs cycle flux can be measured directly.

157 The Krebs cycle plays a fundamental role in cardiac energy p

158 The Krebs tricarboxylic acid cycle (TCA) is central to metab

159 mming, enhancing glycolysis and altering the Krebs cycle.

160 se (PNPase), a DEAD-box RNA helicase and the Krebs cycle enzyme aconitase.

161 Lysine metabolism in plasma and the Krebs cycle in CSF were significantly affected in MCI vs

162 s by phosphoenolpyruvate carboxylase and the Krebs cycle were measured by 13C incorporation from [1-1

163 in glycogen metabolism, glycolysis, and the Krebs cycle, but the levels of pentose phosphate pathway

164 intermediates succinate and citrate, and the Krebs cycle-derived metabolite itaconate.

165 formation of acetyl CoA from glucose and the Krebs cycle.

166 production of 2-methylcitrate (2-MC) by the Krebs cycle enzyme citrate synthase (GltA).

167 of chemical modification of proteins by the Krebs cycle intermediate, fumarate, is significantly inc

168 previously been shown to be modulated by the Krebs cycle metabolite citrate in Escherichia coli.

169 ynthesis requires precursors supplied by the Krebs cycle, which in turn requires anaplerosis to reple

170 ntal occurrence of P3N, which shuts down the Krebs cycle by inactivating succinate dehydrogenase and

171 is generated internally in humans during the Krebs cycle, is an attractive alternative to these thera

172 Mutations in the gene encoding the Krebs cycle enzyme fumarate hydratase (FH) predispose to

173 tance not only for flux of fuel entering the Krebs cycle but for overall energy homeostasis.

174 also use mitochondrial respiration, feed the Krebs cycle with glutamine, and favor the accumulation o

175 at pyruvate, the precursor substrate for the Krebs cycle, regulates I(crac) to prolong Ca(2+) influx

176 A key bioenergetic target for the Krebs cycle, the electron transport chain, also becomes

177 n uptake for cellular function, e.g. for the Krebs cycle.

178 Removal of CaCl2 from the Krebs solution, disruption of the endothelium, and admin

179 )C enrichment in products of glycolysis, the Krebs cycle, the pentose phosphate pathway, nucleobases,

180 Perhaps surprisingly for immunologists, the Krebs cycle has emerged as the central immunometabolic h

181 mplex (OGDHc), a rate-limiting enzyme in the Krebs (citric acid) cycle.

182 t PM(2.5) exposure led to a reduction in the Krebs cycle capacity.

183 ural evidence of substrate channeling in the Krebs cycle metabolon.

184 s transported to mitochondria for use in the Krebs cycle to generate ATP.

185 e oxidation of respiratory substrates in the Krebs cycle to generate NADH and flavin adenine dinucleo

186 erent as fuel procurement, catabolism in the Krebs cycle, and stepwise oxidation of reducing equivale

187 and fumarate, its immediate precursor in the Krebs cycle, in affected subjects' fibroblasts.

188 genase (IDH), a key regulatory enzyme in the Krebs cycle, is a multi-tetrameric enzyme.

189 esults in the inhibition of aconitase in the Krebs cycle, resulting in the accumulation of citrate an

190 -rehydration of citrate to isocitrate in the Krebs cycle.

191 genase (OGDH), a rate-limiting enzyme in the Krebs cycle.

192 eroxisomal citrate synthases involved in the Krebs tricarboxylic acid (TCA) cycle and glyoxylate path

193 trate synthase are sequential enzymes in the Krebs tricarboxylic acid cycle.

194 ve decarboxylation of alpha-ketoacids in the Krebs' cycle.

195 m normal rats were incubated for 1 hr in the Krebs-Henseleit buffer media containing normal rat sera,

196 m normal rats were incubated for 1 hr in the Krebs-Henseleit buffer media containing zymosan-activate

197 itive [4Fe-4S] (de)hydratases, including the Krebs cycle aconitase and the Entner-Doudoroff pathway 6

198 ese concentrations nitric oxide inhibits the Krebs enzyme aconitase and complex IV of the electron tr

199 enzyme A (CoA) species incorporated into the Krebs cycle, whereas the myocardial concentration of ace

200 and decrease the entry of pyruvate into the Krebs cycle-without compromising the consumption of oxyg

201 mplex for enhanced flux of pyruvate into the Krebs cycle.

202 ottlenecks of carbon substrate flux into the Krebs cycle.

203 This process links the Krebs cycle to oxidative phosphorylation and ATP synthes

204 rial membrane protein complex that links the Krebs cycle to the electron transport system.

205 ires gluconeogenesis, valine metabolism, the Krebs cycle, the GABA shunt, the glyoxylate shunt and th

206 ubtilis encodes aconitase, the enzyme of the Krebs citric acid cycle, which is responsible for the in

207 ymes of the tricarboxylic acid branch of the Krebs citric acid cycle.

208 le in cellular energetics as a member of the Krebs cycle and as complex II of the aerobic respiratory

209 ydratase-1 resulted in the inhibition of the Krebs cycle and enhanced pyruvate shunting toward the gl

210 is the only membrane-bound component of the Krebs cycle and in addition functions as a member of the

211 drogenase (PDH) is the main regulator of the Krebs cycle and is located upstream of the electron tran

212 ndria, the expression of key elements of the Krebs cycle and oxidative phosphorylation (OXPHOS).

213 xidizes succinate to fumarate as part of the Krebs cycle and reduces ubiquinone in the electron trans

214 ct of H(2)S required a basal activity of the Krebs cycle and was most pronounced at intermediate conc

215 ible glutathionylation and inhibition of the Krebs cycle enzyme alpha-ketoglutarate dehydrogenase.

216 ts showed that the control and fluxes of the Krebs cycle in heart disease can be studied using hyperp

217 d isocitrate dehydrogenase activities of the Krebs cycle increased at 2, 3, 12, and/or 14 h, and thes

218 hortage and a reduction in the levels of the Krebs cycle intermediate alpha-ketoglutarate (alpha-KG).

219 )cysteine (2SC) is formed by reaction of the Krebs cycle intermediate fumarate with cysteine residues

220 formed by a Michael addition reaction of the Krebs cycle intermediate, fumarate, with cysteine residu

221 activation, there is an accumulation of the Krebs cycle intermediates succinate and citrate, and the

222 s apoptosis was preceded by depletion of the Krebs cycle intermediates, was prevented by two Krebs cy

223 Disruption of the Krebs cycle is a hallmark of cancer, and MDH2 has been r

224 d for eliciting the anaplerotic shift of the Krebs cycle observed in cancer cells.

225 zyme of the tricarboxylic acid branch of the Krebs cycle, exhibited reduced growth yield in broth med

226 zyme of the tricarboxylic acid branch of the Krebs cycle, had a greatly reduced ability to sporulate.

227 wo components of the oxidative branch of the Krebs cycle, IDH and citrate synthase.

228 fumA genes, encoding key constituents of the Krebs cycle, proved to be repressed by the loss of both

229 zyme of the tricarboxylic acid branch of the Krebs cycle, was shown to be required for de novo synthe

230 ymes of the tricarboxylic acid branch of the Krebs cycle.

231 lectron transport chain and aconitase of the Krebs cycle.

232 ate as part of the proper functioning of the Krebs cycle.

233 rganic acids, including intermediates of the Krebs cycle.

234 er experimental work on the structure of the Krebs TCA cycle metabolon.

235 To understand the many roles of the Krebs tricarboxylic acid (TCA) cycle in cell function, w

236 The enzymes of the Krebs tricarboxylic acid cycle in mitochondria are propo

237 atase, one of the constituent enzymes of the Krebs tricarboxylic acid cycle.

238 ion of genes involved in beta-oxidation, the Krebs cycle, and the electron transport chain concomitan

239 y acid carbons substantially replenished the Krebs cycle, and were incorporated into aspartate (a nuc

240 Finally, we show that supplementing the Krebs cycle in an ex vivo fatigue/recovery assay signifi

241 nd showed reduced substrate flux through the Krebs cycle compared with GSH.

242 Besides being oxidized through the Krebs cycle, proline is used to make citrate via reducti

243 to which indomethacin had been added to the Krebs buffer.

244 tanoin, which provides key substrates to the Krebs cycle in the brain, we wished to assess its therap

245 DH and alpha-ketoglutarate (alpha-KG) to the Krebs cycle, hence increasing the beta-cell ATP-to-ADP r

246 carbon metabolism linking glycolysis to the Krebs cycle.

247 Our forward genetic selection unearthed the Krebs cycle enzyme citrate synthase (CitA) as a checkpoi

248 n may reflect an inability to upregulate the Krebs cycle following exercise.

249 nitate, which is further catabolized via the Krebs cycle.

250 Aconitase activity associated with the Krebs cycle is also reduced in the striatum of PINK1(-/-

251 estigation of enzyme organization within the Krebs cycle metabolon was accomplished by in vivo cross-

252 These data suggest a common origin for these Krebs cycle enzymes in mitochondria and CFB group bacter

253 We show that this Krebs-cycle enzyme is essential for mtDNA maintenance in

254 mulation and (ii) energy deprivation through Krebs cycle disruption associated with branched-chain ke

255 tanedioic acid, which is likely converted to Krebs cycle intermediates by BbdG.

256 d in the perfusate from rat liver exposed to Krebs-Ringer bicarbonate buffer only, 0-1mM [3,4-(13)C(2

257 odium-independent mechanism for transporting Krebs and citric acid cycle intermediates through the ep

258 ansporter-a membrane protein that transports Krebs cycle intermediates.

259 bs cycle intermediates, was prevented by two Krebs cycle substrates, but was unrelated to ATP synthes

260 Kidney proximal tubule cells take up Krebs cycle intermediates for metabolic purposes and for

261 ncentrations and decreased levels of urinary Krebs cycle metabolites when compared to controls, sugge

262 rations were inversely correlated with urine Krebs cycle metabolite concentrations.

263 (PV-HA) perfused rat liver (n = 6-10) using Krebs bicarbonate buffer at constant PV (12 ml min-1) an

264 Three groups were studied using Krebs-Henseleit buffer (KH): controls (12 mL/min, n = 6)

265 A critical distinguishing pathway was Krebs cycle metabolite depletion in mdx urine.

266 the at-risk population, when increased, were Krebs von den Lungen-6 (odds ratio [95% CI], 6.1 [3.0-12

267 = 77) later and placed in a tissue bath with Krebs-Henseleit buffer.

268 were initially perfused at 37 degrees C with Krebs-Ringer's (KR) solution (in mmol/L: Ca(2+) 2.5, K(+

269 were perfused (40 mL/min, 37 degrees C) with Krebs' solution in a recirculating system.

270 ere perfused as follows: seven controls with Krebs-Henseleit (KH) buffer (Group 1), five hearts with

271 We perfused isolated working rat hearts with Krebs-Henseleit buffer containing [2-3H]glucose (5 mmol/

272 rat hearts were reperfused for 30 mins with Krebs-Henseleit solution alone (control, n = 8), or with

273 Hearts were labeled for 40 minutes with Krebs-Henseleit buffer containing [35S]methionine, and t

274 e hearts were reperfused for 30 minutes with Krebs-Henseleit buffer.

275 fused initially by the Langendorff mode with Krebs-Henseleit buffer (KHB) for 15 minutes in the absen

276 used for 10 min in the Langendorff-mode with Krebs-Henseleit buffer in the absence or presence of bri

277 ts and perfused in the Langendorff mode with Krebs-Henseleit solution under the following conditions:

278 ant myocardial washout of (99m)TcN-NOET with Krebs-Henseleit buffer.

279 perfusion with plain Krebs solution, or with Krebs solution to which L-NAME and/or indomethacin had b

280 king Sprague-Dawley rat hearts perfused with Krebs buffer and glucose, or glucose plus insulin or bet

281 abbit hearts were isolated and perfused with Krebs buffer.

282 In hearts perfused with Krebs solution alone, nitric oxide (NO) release into the

283 s with intact endothelium were perfused with Krebs solution containing phenylephrine.

284 ast in agarose gel threads and perfused with Krebs-Henseleit bicarbonate buffer.

285 Rat hindlimbs were perfused with Krebs-Henseleit bicarbonate containing 4% bovine serum a

286 abbit hearts were retrogradely perfused with Krebs-Henseleit buffer (KHB).

287 (six groups, each n = 6/group) perfused with Krebs-Henseleit buffer alone or with propofol (10 uM).

288 ir wild-type littermates, were perfused with Krebs-Henseleit buffer and subjected to 20 minutes of is

289 Hearts were perfused with Krebs-Henseleit buffer at 85 mm Hg.

290 olated working rat hearts were perfused with Krebs-Henseleit buffer containing only glucose 5 mmol/L

291 Rabbit hearts were perfused with Krebs-Henseleit buffer on a Langendorff apparatus.

292 ere mounted onto an organ bath perfused with Krebs-Henseleit buffer.

293 Rat hearts were perfused with Krebs-Henseleit solution containing glucose and either n

294 lated canine atria (n=20) were perfused with Krebs-Henseleit solution.

295 d storage (SCS), livers were reperfused with Krebs-Henseleit buffer solution at 37 degree C for 30 mi

296 cally exposed and continuously suffused with Krebs Ringer bicarbonate warmed to 37 degrees C.

297 transducer and a motor arm, superfused with Krebs-Henseleit (K-H) solution (pH 7.4, room temperature

298 0.01 vs. control mesenteries superfused with Krebs-Henseleit buffer).

299 e measured in rat trabeculae superfused with Krebs-Henseleit solution, with or without propofol or is

300 ts was perfused at physiologic workload with Krebs-Henseleit buffer containing 10 mmol/L glucose; a s