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1 a) and viability (insulin-stimulated (18)F-2-deoxyglucose).
2 n the presence of the glycolysis inhibitor 2-deoxyglucose.
3  coupled with tracer radioactively labeled 2-deoxyglucose.
4 s if glucose is replaced with nonmetabolized deoxyglucose.
5 ravenous injection of the glucopenic agent 2-deoxyglucose.
6 reased in Arabidopsis cells in response to 2-deoxyglucose.
7 e a functional isoform with low affinity for deoxyglucose.
8 e of metabolic inhibition with cyanide and 2-deoxyglucose.
9 ly different sensitivities to lysozyme and 2-deoxyglucose.
10           We also compared uptake of FLT and deoxyglucose.
11 RNAs inhibits insulin-stimulated uptake of 2-deoxyglucose.
12 e as a function of growth than did uptake of deoxyglucose.
13 S42, UW479 and RES186) using metformin and 2-deoxyglucose.
14 5Y neuroblastoma cells with sodium azide and deoxyglucose.
15       Glucose uptake was measured using (3)H-deoxyglucose.
16 se that converts UDP-glucose to UDP-4-keto-6-deoxyglucose.
17  glucose analogs alpha-methyl glucoside or 2-deoxyglucose.
18 th of these UOK257 cells by treatment with 2-deoxyglucose.
19 eoxyglucose (5 and 6) > compounds with 2,3,6-deoxyglucose (10).
20  imaging with fluorine-18-labeled 2-fluoro-2-deoxyglucose ((18)FDG) ligand with kinetic analysis demo
21 13)N-ammonia and of the glucose tracer (18)F-deoxyglucose ((18)FDG) was graded on a five-point scale
22  tomography with (11)C-acetate, (18)F-fluoro-deoxyglucose ((18)FDG), and (18)F-fluoro-thiaheptadecano
23 m(-2)), using [(15)O]H(2)O and [(18)F]fluoro-deoxyglucose ([(18)F]FDG) to quantify tissue perfusion a
24 e accumulation of two cytotoxic compounds, 2-deoxyglucose (2-DG) and copper(II)diacetyl-bis(N(4)-meth
25 chment learning and its neural correlates [2-deoxyglucose (2-DG) autoradiography].
26      Treatment with the glycolytic blocker 2-deoxyglucose (2-DG) decreases association of the redox s
27 gher uptake of radio-labeled [14C]2-fluoro-2-deoxyglucose (2-DG) in the preoptic area (25%) and signi
28 ats show fourth ventricular application of 2-deoxyglucose (2-DG) inhibits NST neurons and activates d
29                                   Although 2-deoxyglucose (2-DG) is well characterized as a glycolyti
30 e assessed based on LCGU using the [(14)C]-2-deoxyglucose (2-DG) method.
31 ucose utilization (LCGU) using the [(14)C]-2-deoxyglucose (2-DG) method.
32 male, Sprague-Dawley rats using the [(14)C]2-deoxyglucose (2-DG) method.
33 ing the quantitative autoradiographic 2-[14C]deoxyglucose (2-DG) method.
34  glucose utilization (LCGU) using the [14C]2-deoxyglucose (2-DG) method.
35 ponses to glycemic challenges [intravenous 2-deoxyglucose (2-DG) or insulin].
36 , we show that the hexose kinase inhibitor 2-deoxyglucose (2-dG) preferentially kills cancer cells wi
37                Significant differences for 2-deoxyglucose (2-DG) relative recovery at 1.0 microL/min
38 n and does not respond to either Ca(2+) or 2-deoxyglucose (2-DG) stimulation.
39                                Patterns of 2-deoxyglucose (2-DG) uptake in the glomerular layer of th
40    The study objective was to determine if 2-deoxyglucose (2-DG), a glucose analogue that blocks its
41 al MAN perfusion of the glucoprivic agent, 2-deoxyglucose (2-DG), under normal and hypoglycemic condi
42 emission maximum 794 nm, was conjugated to 2-deoxyglucose (2-DG).
43  in the nucleus in response to glucose and 2-deoxyglucose (2-DG).
44 ion of an inhibitor of glucose metabolism, 2-deoxyglucose (2-DG).
45  abilities upon glycolysis inhibition with 2-deoxyglucose (2-DG).
46 thoxyphenylhydrazone (FCCP, 50 nmol/L) and 2-deoxyglucose (2-DG, 10 mmol/L), there was a decrease in
47 ficacy of F1,6BP was compared with that of 2-deoxyglucose (2-DG; an inhibitor of glucose uptake and g
48 s is reciprocally regulated by glucose and 2-deoxyglucose (2-DG; inhibitor of cellular glucose metabo
49                         The glucose analog 2-deoxyglucose (2-DOG) reduced ROS to levels found in non-
50 059; and (c) effects of AICAR on aPKCs and 2-deoxyglucose (2-DOG) uptake were inhibited by genistein,
51 was assessed via measurement of zero-trans 2-deoxyglucose (2-DOG) uptake.
52 hlearis muscles were incubated with [(3)H]-2-deoxyglucose (2DG) +/- 100 microU/ml insulin.
53 iple brain structures during neglect using 2-deoxyglucose (2DG) as a metabolic marker of neural activ
54                                Conversely, 2-deoxyglucose (2DG) blocked glycolysis and partially inhi
55 owing exposure using uptake of 14C-labeled 2-deoxyglucose (2DG) in quiet.
56                         The glucose analog 2-deoxyglucose (2DG) inhibits the growth of Saccharomyces
57               After 15 min, the quantified 2-deoxyglucose (2DG) method was carried out in freely beha
58                       Then, we used [(14)C]2-deoxyglucose (2DG) uptake and single-neuron recording to
59 ons of primary visual cortex and measuring 2-deoxyglucose (2DG) uptake to assess neural activity in s
60                            Rates of muscle 2-deoxyglucose (2DG) uptake were determined by measuring a
61 teral neuronal and hemodynamic changes and 2-deoxyglucose (2DG) uptake, as measured by autoradiograph
62 the impact of glycolysis inhibition, using 2-deoxyglucose (2DG), in combination with cytotoxic agents
63  metabolism with the glycolysis inhibitor, 2-deoxyglucose (2DG), is a viable therapeutic strategy, bu
64  withdrawal or glycolytic inhibition using 2-deoxyglucose (2DG).
65       These effects were mimicked by 8 g/l 2-deoxyglucose (2DOG) (transported, phosphorylated but not
66                                  We used a 2-deoxyglucose (2DOG) energy clamp to set DeltaPsi at fixe
67 , we used pharmacological agents (insulin, 2-deoxyglucose, 3-nitropropionic acid, and kainic acid) to
68 ond gene encodes a bifunctional UDP-4-keto-6-deoxyglucose-3,5-epimerase/-4-reductase that converts UD
69 elated positively with in vitro assays of 3H-deoxyglucose (3H-DG) uptake in cells harvested via bronc
70 -deoxyglucose (8 and 9) > compounds with 2,6-deoxyglucose (5 and 6) > compounds with 2,3,6-deoxygluco
71 cose analogues 3-O-methylglucose (3OMG) or 6-deoxyglucose (6DOG) has been cited as evidence for metab
72             The activity of compounds with 2-deoxyglucose (8 and 9) > compounds with 2,6-deoxyglucose
73        Similarly, in cancer cells OLIG and 2-deoxyglucose, a glycolytic inhibitor, depolarized mitoch
74                                   In turn, 2-deoxyglucose, a non-metabolizable glucose analogue, elic
75                   RESULTS- We show that 1) 2-deoxyglucose, a nonmetabolizable glucose analog, mimics
76  degrees of overlap in their monomolecular 2-deoxyglucose activation patterns to test the theory in a
77 ly enter torpor in response to fasting and 2-deoxyglucose administration.
78 ose analogs such as 3-O-methyl-glucose and 2-deoxyglucose also caused an induction, suggesting that s
79         The cells were highly sensitive to 2-deoxyglucose, an inhibitor of glycolysis and proposed an
80 sing two-photon imaging of a near-infrared 2-deoxyglucose analogue (2DG-IR), that glucose is taken up
81 h glucose deprivation combined with 0.5 mm 2-deoxyglucose and 5 mm azide ("chemical ischemia") to mod
82                          Previously, we used deoxyglucose and chilling treatments to implicate Nup170
83 lidinedione-derived ERMA, CG-12, vis-a-vis 2-deoxyglucose and glucose deprivation, we obtain evidence
84 rences in the insulin-stimulated uptake of 2-deoxyglucose and in the activity of carnitine palmitoyl
85 re decreased by the glucose antimetabolite 2-deoxyglucose and increased by high blood glucose concent
86                 Secretion was inhibited by 2-deoxyglucose and iodoacetate, confirming active secretio
87 ll death in response to the combination of 2-deoxyglucose and metformin.
88  is observed under metabolic inhibition with deoxyglucose and oligomycin, indicating an energy-indepe
89 lls are 10 and 4.9 times more sensitive to 2-deoxyglucose and oxamate, respectively, than wt cells.
90       Moreover, the glycolysis inhibitors, 2-deoxyglucose and oxamate, selectively inhibited the grow
91 ound that ABT-263 increased sensitivity to 2-deoxyglucose and promoted rapid and extensive cell death
92                                  In vitro, 2-deoxyglucose and radiation synergistically up-regulated
93 n the presence of the glycolysis inhibitor 2-deoxyglucose and radiation treatment followed by PBMC ch
94 e synergy between the glycolytic inhibitor 2-deoxyglucose and rapamycin in decreasing cell viability.
95  be mimicked with the glycolytic inhibitor 2-deoxyglucose and reversed with a pyruvate analogue.
96 rocess, because cells depleted of ATP with 2-deoxyglucose and sodium azide were unable to properly re
97         Using this knowledge we identified 2-deoxyglucose and temsirolimus as agents that can be adde
98                                  Uptake of 2-deoxyglucose and various indexes of oxidative and glycol
99 lar layer was measured as uptake of [(14)C]2-deoxyglucose and was mapped into anatomically standardiz
100 patterns were measured as uptake of [(14)C]2-deoxyglucose and were mapped into standardized data matr
101 ty (euglycemic-hyperinsulinemic clamp with 2-deoxyglucose) and fat utilization during 1 h of exercise
102 creases in permeability, aliphatic alcohols, deoxyglucose, and chilling trigger the reversible dissoc
103          In HeLa and A549 cells, mannitol, 2-deoxyglucose, and ionomycin, but not 5-aminoimidazole-4-
104 mannosamine, Glc, GlcNAc, GalNAc, mannose, 2-deoxyglucose, and oligosaccharides of chitosan.
105                               Furthermore, 2-deoxyglucose- and ionomycin-stimulated AMPK activity, al
106                                    We used 2-deoxyglucose autoradiographic mapping of neural activity
107 min; n = 6) was comparable to that for (14)C-deoxyglucose autoradiographic methods.
108 sing c-Fos early gene expression and (14)C 2-deoxyglucose autoradiography during mother-to-infant fea
109                                          14C-deoxyglucose autoradiography was performed 45 min after
110 tumors had similar uptake of [(18)F]fluoro-2-deoxyglucose before and after 2 weeks of 2-DG treatment
111              Inhibition of hexokinase with 2-deoxyglucose blocked the transforming activity of CBL mu
112 lucosensors detect mannose, d-glucose, and 2-deoxyglucose but not galactose, l-glucose, alpha-methyl-
113    Hydralazine activated more neurons than 2-deoxyglucose but similar numbers of catecholaminergic ne
114  by the non-metabolizable glucose analogue 2-deoxyglucose, but not by stimulating intracellular ATP p
115 uated by fructose, galactose, mannose, and 2-deoxyglucose, but not by the non-metabolizable glucose a
116 bles that of cortical metabolism seen with 2-deoxyglucose, but the increase in vascular density prece
117 erregulatory responses to hypoglycemia and 2-deoxyglucose, but the mechanisms that mediate these resp
118 of conversion of dTDP-6FGlc to dTDP-4-keto-6-deoxyglucose by each Asp135 variant was identical to tha
119 onversion of dTDP-glucose into dTDP-4-keto-6-deoxyglucose by Escherichia coli dTDP-glucose 4,6-dehydr
120 neurons shortly after vascular insulin and 2-deoxyglucose challenges.
121 7-nitrobenz-2-oxa-1, 3-diazol-4-yl) amino)-2 deoxyglucose compared with those from HIV(-) controls.
122 ing intact Mpi(-/-) fibroblasts with 2-[(3)H]deoxyglucose confirmed mannose-dependent hexokinase inhi
123 low uptake activity for the glucose analog 2-deoxyglucose, consistent with a role in the transport of
124                 Systemic administration of 2-deoxyglucose depleted ADR content in control rats, and C
125 al, we have measured the uptake of tritiated deoxyglucose (DG) in neutrophils isolated from human per
126 ulin-stimulated glucose uptake ((18)F-fluoro-deoxyglucose) during euglycemic (5.6 mmol/l), physiologi
127 he presence of an inhibitor of glycolysis, 2-deoxyglucose, enhanced the generation of memory cells an
128 quantitatively by measuring uptake of [14C]2-deoxyglucose evoked by each odorant.
129 pare the neuronal populations activated by 2-deoxyglucose evoked glucoprivation.
130                              [18F]2-fluoro-2-deoxyglucose (FDG) -positron emission tomography (PET) h
131 heterogeneity in the uptake of [(18)F]fluoro-deoxyglucose (FDG) in single cells, which was found cons
132 emission tomography (PET) imaging with (18)F deoxyglucose (FDG) is a molecular imaging modality that
133 ism was assessed with (18)F-labeled fluoro-2-deoxyglucose (FDG) positron emission tomography in 236 y
134 nd response monitoring by using (18)F-fluoro-deoxyglucose (FDG) positron emission tomography.
135 ositron emission tomography with fluorine-18-deoxyglucose (FDG-PET) detects active lymphoid tissues d
136  by positron emission tomography using (18)F-deoxyglucose (FDG-PET) has not been established after sa
137 n vitro work and confirms the selectivity of deoxyglucose for viable cells over necrotic regions and
138 sures derived from the comparison of [14C]-2-deoxyglucose glomerular activity pattern data yielded a
139 ia and knob can incorporate and accumulate 2-deoxyglucose (glucose analog), but not when blocking GLU
140 sitivity to radiation with or without 25mM 2-deoxyglucose (glycolytic inhibitor) was evaluated in clo
141 diopharmaceutical used in PET imaging - [18F]deoxyglucose - has a limited role in diagnosing primary
142       SF188 cells were highly sensitive to 2-deoxyglucose however, combination of metformin with 2-de
143 rceptual similarity and comparability with 2-deoxyglucose imaging data from the olfactory bulb are de
144        C-fos immunohistochemistry and [14C]2-deoxyglucose imaging identified brain structures involve
145  conversion of CDP-D-glucose to CDP-4-keto-6-deoxyglucose in an NAD(+)-dependent manner.
146 of excised plaques confirmed accumulation of deoxyglucose in macrophage-rich areas of the plaque.
147                              The uptake of 2-deoxyglucose in MIN6 cells was similarly inhibited (IC(5
148 tic agents (ERMAs) such as resveratrol and 2-deoxyglucose in suppressing carcinogenesis in animal mod
149  catalyzes C-3 deoxygenation of CDP-4-keto-6-deoxyglucose in the biosynthesis of 3,6-dideoxyhexoses,
150               The tumor microdistribution of deoxyglucose in viable, hypoxic, and necrotic regions sh
151                           Uptake of 2-[(14)C]deoxyglucose in vivo was reduced by a high-fat diet in a
152                               Injection of 2-deoxyglucose induced a very rapid sympathoadrenal respon
153      In contrast, the glycolytic inhibitor 2-deoxyglucose induced prosurvival autophagy.
154                                Addition of 2-deoxyglucose inhibited seed germination, but did so less
155 re layer was assessed by mapping uptake of 2-deoxyglucose into anatomically standardized data matrice
156 ation of AMPK in response to ionomycin and 2-deoxyglucose is not impaired in LKB1(-/-) murine embryo
157 animals studied using the metabolic marker 2-deoxyglucose, layer 4 was 25% denser than the other laye
158 ng p53, we showed that CR mimetics such as 2-deoxyglucose led to a decrease in Mcl-1 expression and s
159 nd pdk1, lung fluorine-18-labeled 2-fluoro-2-deoxyglucose ligand uptake was significantly increased i
160 nthesis (oligomycin, 2,4-dinitrophenol, or 2-deoxyglucose) made them more susceptible to cell death b
161 sults fail to confirm predictions based on 2-deoxyglucose maps of bulbar activity that enantiomers of
162                                    [(14)C] 2-deoxyglucose maps to investigate patterns of glucose uti
163 e distinguishable functionally, we used [14C]deoxyglucose metabolic mapping in the rat and tested whe
164 avioral abnormalities, we applied the [(14)C]deoxyglucose method for the determination of cerebral me
165              To this end, we used the [14C]2-deoxyglucose method to determine glomerular responses to
166 uctures in this system, we used the [(14)C]2-deoxyglucose method to determine glomerular responses to
167 sured in the same monkeys using the 2-[(14)C]deoxyglucose method.
168 cocaine self-administration using the 2-[14C]deoxyglucose method.
169  and glycolysis (as measured by (18)fluoro-2-deoxyglucose microPET) of glioblastoma xenografts engine
170 ffects of metabolic blockade (cyanide plus 2-deoxyglucose) on Ca2+ release from the sarcoplasmic reti
171                         Compounds, such as 2-deoxyglucose or 6-aminonicotinamide, that reduced the fr
172 directly inhibited glycolysis using either 2-deoxyglucose or iodoacetic acid.
173 aspase-dependent cell death in response to 2-deoxyglucose or its combination with metformin.
174 s, Thr49 was phosphorylated in response to 2-deoxyglucose or phenformin, stimuli that activate the AM
175        This increase was blocked by either 2-deoxyglucose or the protein phosphatase inhibitor, calyc
176 ysis brought about by glucose deprivation, 2-deoxyglucose, or Akt inhibition.
177  were exposed to the glycolytic inhibitor, 2-deoxyglucose, or fatty acid synthase inhibitors to pertu
178 cell lines, 5 small-molecule perturbagens (2-deoxyglucose, oxamate, oligomycin, rapamycin, and wortma
179  between increased normalized (18)F fluoro-2-deoxyglucose PET SUVmax, outcome, and EMT in NSCLC.
180 glucose metabolism (imaged with [(18)F]fluro-deoxyglucose PET), and structural atrophy (imaged by MRI
181 static lesions in both tumor types with [18F]deoxyglucose PET, as compared with previous studies.
182 urrent prostate cancer than (18)F-2-fluoro-D-deoxyglucose-PET and monoclonal antibody imaging with th
183 lity, validity and reproducibility of fluoro-deoxyglucose-PET/CT for imaging of atherosclerotic plaqu
184                                       Fluoro-deoxyglucose-PET/CT imaging is currently used to improve
185                                       Fluoro-deoxyglucose-PET/CT imaging is demonstrated to have the
186                                    18-Fluoro-deoxyglucose positron emission tomography (FDG-PET) is a
187    We retrospectively evaluated (18)fluoro-2-deoxyglucose positron emission tomography (FDG-PET) scan
188                                        [18F]-deoxyglucose positron emission tomography (PET) and matc
189  that contained fluorine 18 ((18)F) fluoro-2-deoxyglucose positron emission tomography (PET) and mess
190 iew addresses technical improvements in [18F]deoxyglucose positron emission tomography (PET) and new
191 al blood to clinical outcomes and (18)fluoro-deoxyglucose positron emission tomography combined with
192 icient rationale given the utility of fluoro-deoxyglucose positron emission tomography in diagnostic
193 cs, magnetic resonance imaging and 18-fluoro-deoxyglucose positron emission tomography results, and n
194 lizing on the diagnostic utility of 18fluoro-deoxyglucose positron emission tomography that relies on
195  on magnetic resonance imaging and 18-fluoro-deoxyglucose positron emission tomography.
196               High-resolution (18)F-labelled deoxyglucose positron-emission tomography (FDG-PET) was
197                      Using 18FDG (18fluoro-2-deoxyglucose) positron emission tomography, we found tha
198 n brain glucose metabolism (measured by [18F]deoxyglucose-positron emission tomography) and on its re
199 ular responses relative to resveratrol and 2-deoxyglucose, respectively.
200    In addition, treatment of NOD mice with 2-deoxyglucose resulted in improved beta cell granularity.
201 tudies using intrinsic optical imaging and 2-deoxyglucose) resulted in increased detection thresholds
202                             Regionally, F-18 deoxyglucose score was highest in segments with late gad
203 ose however, combination of metformin with 2-deoxyglucose significantly reduced cell proliferation co
204 ndent manner, whereas oxidative stress and 2-deoxyglucose stimulated phosphorylation at this site via
205                                            2-deoxyglucose stimulated Thr49 phosphorylation of endogen
206 is, functional magnetic resonance imaging, 2-deoxyglucose studies, and induction of gene expression h
207 results are consistent with a previous (14)C-deoxyglucose study of the isoflurane-anesthetized rat.
208 of pyruvate or alpha-ketocaproate, but not 2-deoxyglucose, suggesting that mitochondrial metabolism w
209      We demonstrate that the parthenolide, 2-deoxyglucose, temsirolimus (termed PDT) regimen is a pot
210  determined by NMR spectroscopy, including 2-deoxyglucose, the glucose analogue used for tumor detect
211 as little change in the microdistribution of deoxyglucose throughout this time course.
212 hen prediabetic NOD mice were treated with 2-deoxyglucose to block aerobic glycolysis, there was a re
213 of ATP by the addition of sodium azide and 2-deoxyglucose to block ATP production by oxidative phosph
214 positron emission tomography (PET) and [18F] deoxyglucose to compare the brain metabolic responses (m
215 er, we used the quantitative method of (14)C-deoxyglucose to reveal changes in activity, in the corte
216 rase/-4-reductase that converts UDP-4-keto-6-deoxyglucose to UDP-rhamnose.
217 e, we show that low doses of verapamil and 2-deoxyglucose, to accentuate the cost of resistance and t
218 ies examining the LC values for radiolabeled deoxyglucose tracers used to estimate the glucose metabo
219 dipocytes also attenuated insulin-stimulated deoxyglucose transport and Myc-GLUT4-EGFP translocation
220 pha (GSK-3alpha) phosphorylation, as well as deoxyglucose transport in 3T3-L1 adipocytes.
221 onse relationship for insulin stimulation of deoxyglucose transport in primary adipocytes derived fro
222  was screened for their ability to inhibit 2-deoxyglucose transport in primary rat adipocytes.
223                                              Deoxyglucose transport mediated by GLUT9 was not inhibit
224 cells failed to attenuate insulin-stimulated deoxyglucose transport or Myc-tagged GLUT4-GFP transloca
225 HLDB2 failed to attenuate insulin-stimulated deoxyglucose transport.
226 me- and concentration-dependent decline in 2-deoxyglucose transport.
227 on preconditioning (1 h of antimycin A and 2-deoxyglucose treatment followed by 1 h of recovery), ade
228 g p38 vectors reduced apoptosis induced by 2-deoxyglucose treatment, whereas overexpression of wild-t
229 [(14)C]glucose into glycogen (60%) and [(3)H]deoxyglucose uptake (40%) but did not inhibit phosphoryl
230 ose incorporation into glycogen (60%), [(3)H]deoxyglucose uptake (60%), and protein kinase B phosphor
231  We therefore examined the effects of HGF on deoxyglucose uptake (DOGU), glucose utilization, and fat
232 assessments of cold-induced changes in BAT 2-deoxyglucose uptake (increased 2.7-fold), BAT lipogenesi
233 lted in increased glycolysis and increased 2-deoxyglucose uptake (P < 0.05).
234 ice, caCaMKKalpha increased in vivo [(3)H]-2-deoxyglucose uptake 2.5-fold and AMPKalpha1 and -alpha2
235 ocytes, and their membrane concentrations, 2-deoxyglucose uptake activities, and sensitivities to pCM
236 s N terminus suppressed insulin-stimulated 2-deoxyglucose uptake and Glut4 translocation to roughly t
237 n insulin signaling and insulin-stimulated 2-deoxyglucose uptake and glycogen synthesis.
238 bitor LY-294002 display a decrease in both 2-deoxyglucose uptake and hexokinase activity as compared
239 , is required for insulin-stimulated 2-[(3)H]deoxyglucose uptake and metabolism.
240  significant correlation between posterior 2-deoxyglucose uptake and molecular properties associated
241 is manifested as improved insulin-mediated 2-deoxyglucose uptake and suppression of lipolysis.
242 aCaMKKalpha increased basal in vivo [(3)H]-2-deoxyglucose uptake approximately twofold, insulin incre
243 t with DMOG or DHB reverses the decline in 2-deoxyglucose uptake caused by NGF withdrawal and suppres
244 ron emission tomography of 2-[(18)F]fluoro-2-deoxyglucose uptake combined with computed tomography.
245  Cip4-null mice exhibited increased [(14)C]2-deoxyglucose uptake compared with cells from wild-type m
246 by individual odorant chemicals, we mapped 2-deoxyglucose uptake during exposures to vapors arising f
247 les with the greatest UBX-Cter expression, 2-deoxyglucose uptake during fasting was similar to that i
248 nfusion rate and 90% greater muscle [(3)H]-2-deoxyglucose uptake during hyperinsulinemic-euglycemic c
249 evious studies, we mapped glomerular layer 2-deoxyglucose uptake evoked by hundreds of both systemati
250         In past studies in which we mapped 2-deoxyglucose uptake evoked by systematically different o
251 d with c-Fos immunohistochemistry and [14C]2-deoxyglucose uptake implicate a prominent involvement of
252 nduced PPAR gamma-dependent adipogenesis and deoxyglucose uptake in 3T3-L1 preadipocytes at a potency
253 on of [(14)C]glucose into glycogen and [(3)H]deoxyglucose uptake in L-CPT I-transduced, palmitate-tre
254 rogressive but similar levels of increased 2-deoxyglucose uptake in macrophages that reached up to si
255  first investigated glomerular patterns of 2-deoxyglucose uptake in response to aromatic compounds th
256 ent with the 2.5- to threefold increase in 2-deoxyglucose uptake in skeletal muscle, heart, and white
257 ytokine, increases macrophage glycolysis and deoxyglucose uptake in vitro and acutely enhances (18)F-
258 ke in transfected muscles, we measured [3H]2-deoxyglucose uptake in vivo following intravenous glucos
259 tified activity patterns by mapping [(14)C]2-deoxyglucose uptake into anatomically standardized data
260                    In vivo 2-[(18)F]fluoro-2-deoxyglucose uptake into brown adipose tissue (BAT) was
261 glucose infusion rate and markedly reduced 2-deoxyglucose uptake into skeletal muscle (85-90%) and wh
262 tive to WL5, submaximal insulin-stimulated 2-deoxyglucose uptake into the epitrochlearis muscle was l
263 rug triester 70 did induce enhancements in 2-deoxyglucose uptake into two different cell lines with c
264 e together with impaired exercise-mediated 2-deoxyglucose uptake into white but not red muscles.
265  robust and surprisingly focal patterns of 2-deoxyglucose uptake involving clusters of neighboring gl
266 Ischemia stimulated a 2.5-fold increase in 2-deoxyglucose uptake over base line in WT, whereas the in
267 ozygote matings exhibited reduction of the 2-deoxyglucose uptake rate: one by 50% (presumed heterozyg
268 ly active cdc42 (CA-cdc42; V12) stimulated 2-deoxyglucose uptake to 56% of the maximal insulin respon
269                                     Muscle 2-deoxyglucose uptake was similarly reduced under these co
270 activity of the alpha2 isoform of AMPK and 2-deoxyglucose uptake were assessed in incubated rat exten
271 no significant changes in AMPK activity or 2-deoxyglucose uptake were detected.
272 q), and CA-cdc42 on GLUT4 translocation or 2-deoxyglucose uptake were inhibited by microinjection of
273 entiated adipocytes and insulin-stimulated 2-deoxyglucose uptake were slightly lower than in adipocyt
274 osely with decreases in glucose transport (2-deoxyglucose uptake), measured during a subsequent 20-mi
275 testing, measurement of in vivo myocardial 2-deoxyglucose uptake, and echocardiography were performed
276                     FosB immunoreactivity, 2-deoxyglucose uptake, and firing activity of LHb were stu
277 ipocytes, we analyzed Akt phosphorylation, 2-deoxyglucose uptake, and Glut4 translocation by immunofl
278 ults in decreased insulin-stimulated 2-[(3)H]deoxyglucose uptake.
279 ng a hyperinsulinemic-euglycemic clamp and 2-deoxyglucose uptake.
280 porter-4 accumulation, and enhanced [(3)H]-2-deoxyglucose uptake.
281 dose-response curve for insulin stimulated 2-deoxyglucose uptake.
282 adiponectin secretion and insulin-stimulated deoxyglucose uptake.
283 correlation between tumor blood flow and 18F-deoxyglucose uptake.
284 -stimulated GLUT4 translocation as well as 2-deoxyglucose uptake.
285 ion, gACRP30 caused a 1.5-fold increase in 2-deoxyglucose uptake.
286 M2), resulted in a 2.5-fold increase in (3)H-deoxyglucose uptake.
287 tory activation and uptake of radiolabeled 2-deoxyglucose was assessed before and after GM-CSF exposu
288 Rather, IRF3 activation by tunicamycin and 2-deoxyglucose was inhibited by 4-(2-aminoethyl)-benzenesu
289                                        2[14C]deoxyglucose was used to assess MGU.
290  depletion, equivalent ATP loss induced by 2-deoxyglucose was without toxicity, arguing that bioenerg
291 cancer cells to ERMAs, including CG-12 and 2-deoxyglucose, we demonstrated that this beta-TrCP accumu
292 7-nitrobenz-2-oxa-1, 3-diazol-4-yl) amino)-2 deoxyglucose were analyzed by flow cytometry on monocyte
293           Glycogen synthesis and uptake of 2-deoxyglucose were reduced in skeletal muscle, suggesting
294 ked by the energy poisons sodium azide and 2-deoxyglucose, whereas staining of the nucleus (nucleolus
295 rated by using an inhibitor of glycolysis, 2-deoxyglucose, which almost totally abolished low-dose ar
296 lucose-inhibited neurons were activated by 2-deoxyglucose, which also activates counterregulatory res
297  form glucose, the nonmetabolizable sugars 2-deoxyglucose, which is still converted to G-6-P as well
298 adiotracer for oncologic PET is (18)F-fluoro-deoxyglucose, which measures glucose accumulation as a s
299 radiation response after administration of 2-deoxyglucose, which significantly (p<0.05) potentiated e
300                                   Using F-18 deoxyglucose with heparin pretreatment, metabolic rate o

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