ライフサイエンスコーパス: 11C

1 11C HED retention indexes (RIs), which reflect nerve den

2 11C-(+)-PHNO PET before and after oral amphetamine was u

3 11C-(R)-PK11195 positron emission tomography reveals inc

4 11C-(R)-Rolipram binding in the brain was measured using

5 11C-(R)-Rolipram brain positron emission tomography scan

6 11C-dLop may be superior to 11C-loperamide in measuring

7 11C-Loperamide is an avid substrate for P-glycoprotein (

8 11C-PBB3 binding capacity in the white matter segment co

9 11C-PBR28 PET can detect the 18-kDa translocator protein

10 11C-PiB PET and 18F-flortaucipir uptake was quantified i

11 11C-Pittsburgh compound B and 11C-(R)-PK11195 positron e

12 [11C]-(+)-PHNO binding in SN was related to self-reported

13 [11C]CUMI-101 is the first selective serotonin receptor (

14 [11C]DPN VD did not undergo systematic changes between ti

15 [11C]FLB 457 binding potential, specific compared to nond

16 [11C]GV1-57 additionally measured rates of neuron regener

17 [11C]GV1-57 monitored native OSN population dynamics in r

18 [11C]LY2795050 volume of distribution values in amygdala-

19 [11C]LY2795050 volume of distribution values in an amygda

20 [11C]MeDAS-PET is a promising imaging marker for monitori

21 [11C]PIB distribution volume ratios were calculated using

22 [11C]PiB PET could be valuable in imaging amyloid deposit

23 [11C]PiB PET was used to image amyloid deposition in 11 c

24 [11C]PiB shows increased binding following TBI.

25 [11C]UCB-J binding potential (BP(ND)) was estimated using

26 to the SEPT6 and SEPT7 groups (SEPT6C/8C/10C/11C and SEPT7C, respectively) and provide clear evidence

27 omer [d(G 1A 2T 3A 4 G 5 C 6 G 7 C 8T 9A 10T 11C 12)] 2 are studied by using deuterium solid-state NM

28 omer [d(G 1A 2T 3A 4 G 5 C 6 G 7 C 8T 9A 10T 11C 12)] 2 are studied using deuterium solid-state NMR (

29 raphic (PET) imaging study using carbon 11 ([11C])-labeled PBR28 in patients with temporal lobe epile

30 the complete structures of the serotype 11B, 11C, and 11F polysaccharides and a revision to the serot

31 esis and evaluation of 3-[3,5-dimethyl-4-(4-[11C]methylpiperazinecarbonyl)-1H-pyrrol-2-ylmethylene]-2

32 ci in patients with TLE ([11C]PBR28: 2%-6%; [11C]DPA-713: 4%-9%).

33 tests, and associations between 18F-MK-6240, 11C-PiB, and age.

34 ved in 10 steps with a total yield of 9.7%, [11C]14 was obtained through radiomethylation in a range

35 All subjects underwent a 11C-PIB scan and structural MRI.

36 injection of 11C-methylaminoisobutyric acid (11C-MeAIB).

37 We acquired [11C]DASB PET images for 26 additional patients with SAD

38 Neuroinflammation did not affect [11C]MeDAS uptake in the brain as long as the myelin shea

39 drug of abuse underwent PET scanning after [11C]-(+)-PHNO.

40 nd synthesized our GSM-based imaging agent, [11C]SGSM-15606.

41 Although 11C-PIB accumulation is greater in patients with AD than

42 ent 3 T magnetic resonance imaging, amyloid (11C-PiB) positron emission tomography and tau (18F-AV-14

43 le; has as much alphaGlcNAc as 11F, 11B, and 11C CPS do; and may represent a new serotype.

44 ), 28 of whom underwent both 18F-AV-1451 and 11C-PK-11195 PET, and matched control subjects (14 for 1

45 mes, and regional binding of 18F-AV-1451 and 11C-PK11195 were derived from 15 temporo-parietal region

46 Autopsy and 11C-PiB positron emission tomography.

47 11C-Pittsburgh compound B and 11C-(R)-PK11195 positron emission tomography was used to

48 of the combined 11C-dihydrotetrabenazine and 11C-Pittsburgh compound-B results.

49 to evaluate serotonin terminal function and 11C-raclopride PET to evaluate dopamine release.

50 ng for the assessment of tract integrity and 11C-raclopride positron emission tomography to measure c

51 rrelation between levels of amyloid load and 11C-(R)-PK11195 binding potentials at a voxel level with

52 correlation was found between psychosis and 11C-PBB3 binding capacity in the white matter.

53 ssed as standardized uptake value ratio, and 11C-PiB were given as distribution volume ratio.

54 AD, including CERAD score, Braak score, and 11C-PiB retention, with serum markers of glucose homeost

55 d by initial loss of cardiac MIBG signal and 11C-colonic donepezil signal followed by loss of putamin

56 a secondary loss of cardiac MIBG signal and 11C-donepezil signal.

57 e cortical distribution maps of 18F-T807 and 11C-PiB.

58 triatal vesicular monoamine transporters and 11C-Pittsburgh compound-B positron emission tomography i

59 torage was performed with [13N]-ammonia and [11C]-epinephrine 4 to 12 weeks later.

60 To test this hypothesis, amphetamine and [11C]FLB 457 positron emission tomography were used to me

61 re of serotonin synthesis rate capacity and [11C]DASB binding potential as an index of serotonin tran

62 tes [123I]-m-iodobenzylguanidine (MIBG) and [11C]-m-hydroxyephedrine (HED) are used as markers of car

63 ipsilateral to contralateral [11C]PBR28 and [11C]DPA-713 standardized uptake values from temporal reg

64 Relative [11C]PBR28 and [11C]DPA-713 uptakes were higher ipsilateral than contral

65 e (dopamine D2/D3 receptor radioligand) and [11C]cocaine (dopamine transporter radioligand).

66 re of presynaptic vesicular DA storage, and [11C]raclopride (RAC), an indicator of D2/D3 receptor ava

67 ects using positron emission tomography and [11C]raclopride (dopamine D2/D3 receptor radioligand) and

68 eory using fast-scan cyclic voltammetry and [11C]raclopride PET in mice during chemogenetic activatio

69 tomography imaging with the D2/D3 antagonist 11C-raclopride, we analysed striatal D2/D3 availability

70 ing in the brain was measured using arterial 11C-(R)-rolipram levels to correct for the influence of

71 Amyloid-positivity was defined as 11C-Pittsburgh compound B target-to-cerebellar ratio abo

72 henyl)-6-hydroxybenzothiazole (also known as 11C-6-OH-BTA-1 or 11C-PIB) binds to amyloid-beta (Abeta)

73 and carbon 11-labeled Pittsburgh Compound B (11C-PiB) positron emission tomographic (PET) imaging.

74 variants using [11C]-Pittsburgh compound B ([11C]PIB) and [18F]-labeled fluorodeoxyglucose positron e

75 n, carbon 11-labeled Pittsburgh Compound B ([11C]PiB) PET imaging to measure amyloid burden, and stru

76 th carbon 11-labeled Pittsburgh Compound B ([11C]PiB) positron emission tomography (PET).

77 Because [11C]raclopride competes with endogenous dopamine for bin

78 laminomethyl-phenylsulfanyl)- benzonitrile ([11C]DASB), a serotonin transporter radioligand.

79 re was a strong positive correlation between 11C-PK-11195 and 18F-AV-1451 uptake in all disease group

80 ly, we found an inverse relationship between 11C-PIB BPND and rCBF MR imaging in the voxel-based anal

81 Both 11C-loperamide and its putative radiometabolite 11C-dLop

82 Amyloid load assessed by both 11C-PIB PET and amyloid histology was highest in the fro

83 tidepressant pharmacotherapy completed both [11C]WAY-100635 PET scans with a metabolite-corrected art

84 who had 2 or more OGTTs and underwent brain 11C-PiB positron emission tomography.

85 n resistance were also correlated with brain 11C-PiB retention in an additional 53 living subjects fr

86 conventional clinical evaluation followed by 11C-dihydrotetrabenazine positron emission tomography im

87 AV-1451 PET), neuroinflammation (measured by 11C-PK11195 PET) and brain atrophy (derived from structu

88 variants in four women: missense mutation c.11C --> A (p.A4E) was found in two women; deletion c.

89 n of tau burden in TBI brains, we calculated 11C-PBB3 binding capacity (cm3), which is a summed voxel

90 PET with [methyl-(11)C]-choline (11C-choline) can be useful for detecting well-differenti

91 diastinum ratios (P < 10-5, ANOVA) and colon 11C-donepezil standard uptake values (P = 0.008, ANOVA).

92 ith Lewy bodies on the basis of the combined 11C-dihydrotetrabenazine and 11C-Pittsburgh compound-B r

93 To confirm 11C-PBB3 binding to tau deposits in TBI brains, we condu

94 t the depth of neocortical sulci, confirming 11C-PBB3 binding to tau lesions.

95 s the ratio of ipsilateral to contralateral [11C]PBR28 and [11C]DPA-713 standardized uptake values fr

96 5%), followed by the temporoparietal cortex (11C-PIB BPND: 0.75+/-0.08; amyloid histology: 13.9%+/-0.

97 ts with Lewy body disease with low cortical [11C]PiB retention.

98 not rule out the possibility that decreased [11C]raclopride binding reflects decreases in receptor le

99 l)-4-methyl-1,2,4-triaz ine-3,5(2H,4H)dione (11C-MMP), a 5-HT1AR agonist.

100 The distomer, [11C](+)-12a, failed to give a sustained CB1 receptor-spe

101 healthy controls was reflected by elevated [11C]DASB binding potential in the raphe nuclei region, c

102 We evaluated 11C-loperamide as a PET radiotracer to measure P-gp func

103 baseline PETs using 6-[18F]fluorodopa (FD), [11C]dihydrotetrabenazine (DTBZ), and 2beta-[11 C]carbome

104 Binding potential estimates from thirty-five 11C-PBR28 PET scans from an independent sample of health

105 trol subjects (14 for 18F-AV-1451 and 15 for 11C-PK-11195).

106 s, which were negligible after adjusting for 11C-PiB.

107 components with differential affinities for 11C-PBB3 and 18F-AV-1451, and higher availability of bin

108 first (i.e. anterior temporal) component for 11C-PK11195.

109 gressive supranuclear palsy tau deposits for 11C-PBB3 than 18F-AV-1451.

110 etermine the optimal modeling parameters for 11C-MMP under its new name, 11C-CUMI-101, in Papio anubi

111 specific binding ratio across cell types for 11C-MeNTI (4.32 +/- 1.31; mean +/- SEM) was greater than

112 c deficit was observed, a third and a fourth 11C-raclopride PET were acquired to evaluate changes in

113 were observed between 18F-MK-6240 and global 11C-PiB in regions associated with Braak neurofibrillary

114 The greatest 11C-BU99008 VT increase in patients with early Parkinson

115 mpound B and 10 healthy control subjects had 11C-(R)-PK11195 positron emission tomography for compari

116 lve age-matched healthy control subjects had 11C-Pittsburgh compound B and 10 healthy control subject

117 lts showed that patients with TBI had higher 11C-PBB3 binding capacities in the neocortical grey and

118 umatic encephalopathy syndrome showed higher 11C-PBB3 binding capacity in the white matter segment th

119 ith control subjects, drug users had higher [11C]-(+)-PHNO binding in the D3-rich midbrain substantia

120 s, had asymmetrically increased hippocampal [11C]PBR28 uptake exceeding the 95% confidence interval o

121 istology: 13.9%+/-0.7%) and the hippocampus (11C-PIB BPND: 0.71+/-0.09; amyloid histology: 9.2%+/-0.9

122 However, 11C-PIB BPND and amyloid histology linearly correlated (

123 We used PET in vivo with (i) 11C-PK-11195, a marker of activated microglia and a prox

124 ft striatum as assessed by reduced change in 11C-raclopride binding compared with control subjects.

125 mes of the present study were differences in 11C-PBB3 binding capacity between groups, and the associ

126 found significant group-wise differences in 11C-PK-11195 binding between each patient group and cont

127 a widespread, approximately 20% reduction in 11C-(R)-rolipram binding (p = .002), which was not cause

128 thylphenidate induced smaller decrements in [11C]raclopride binding in left and right caudate (blunte

129 The difference in [11C]raclopride's specific binding between placebo and me

130 Increases in [11C]PiB distribution volume ratios in patients with TBI

131 In conclusion, increased 11C-PBB3 binding capacity is associated with late-onset

132 In early Parkinson's disease, increased 11C-BU99008 VT uptake was observed in frontal (P = 0.022

133 Increased [11C]5-HTP influx rate was observed in the amygdala, raph

134 LPS administration significantly increased [11C]PBR28 binding 30-60%, demonstrating microglial activ

135 nts with TBI showed significantly increased [11C]PiB distribution volume ratios in cortical gray matt

136 We injected 11C-Pittsburgh compound B (PIB) intravenously in transge

137 radiolabeled with positron emitting isotopes 11C and 18F as potential radioligands for positron emiss

138 ty, and favorable plasma and brain kinetics, 11C-CUMI-101 is an excellent candidate for imaging high-

139 Binary classification of carbon 11-labeled [11C]PMP acetylcholinesterase and caudate nucleus [11C]DT

140 e positron emission tomography (PET) ligand [11C](R)PK11195 (PK).

141 ers, using PET and the D3-preferring ligand [11C]-(+)-propyl-hexahydro-naphtho-oxazin ([11C]-(+)-PHNO

142 y metabolized to 11C-N-desmethyl-loperamide (11C-dLop), which is also a substrate for P-gp and thereb

143 There was significantly lower [11C]Ro15-4513 V(T) in the hippocampus of antipsychotic-f

144 Path analysis revealed that lower [11C]LY2795050 volume of distribution values in this circ

145 The mean 11C HED RI was 0.086 mL of blood per minute per millilit

146 ission tomography (PET) radioligand N-methyl-11C-2-(4-methylaminophenyl)-6-hydroxybenzothiazole (also

147 idinyl)ethynyl]-2-cyclohexen-1-one-O-(methyl-11C)oxime, a negative allosteric modulator of the metabo

148 ynthesis and initial evaluation of [O-methyl-11C]2-(4-(4-(2-methoxyphenyl)piperazin-1-yl)butyl)-4-met

149 st in the frontal cortex of transgenic mice (11C-PIB BPND: 0.93+/-0.08; amyloid histology: 15.1%+/-1.

150 rol subjects underwent 3 T MRI and a 120-min 11C-BU99008 PET scan with volume of distribution (VT) es

151 healthy male subjects each had two 120-min [11C]PBR28 PET scans in 1 d, before and after an LPS chal

152 In a mixed-effects model, 11C-PK11195 uptake, representing activated microglia/mac

153 This was in line with moderate 11C-PBB3 versus faint 18F-AV-1451 autoradiographic label

154 g parameters for 11C-MMP under its new name, 11C-CUMI-101, in Papio anubis.

155 Four patients had normal 11C HED studies and four had mild denervation (global ex

156 MP acetylcholinesterase and caudate nucleus [11C]DTBZ monoaminergic positron-emission tomography imag

157 Therefore, we evaluated the ability of 11C-dLop to quantify the function of P-gp at the blood-b

158 Analysis of 11C-PBR28 PET data was not inconsistent with the existen

159 n of control and AD subjects on the basis of 11C-PIB uptake.

160 This study sought to quantify the binding of 11C-(R)-rolipram, a PDE4 inhibitor, as an indirect measu

161 to improve the classification capability of 11C-PIB scans on patients with AD.

162 The concentration of 11C-dLop in the brain was low under baseline conditions

163 The brain concentrations of 11C-loperamide and the putative 11C-dLop were about 16-f

164 Should further demethylation of 11C-dLop occur, radiometabolites with low entry into the

165 in barrier, because further demethylation of 11C-dLop will generate radiometabolites that have little

166 blockade affected peripheral distribution of 11C-dLop, we measured whole-body biodistribution in 4 mo

167 The multivariate distribution of 11C-PK-11195 binding related better to clinical heteroge

168 With the exception of 11C-PK11195, all TSPO PET ligands in current clinical ap

169 The single-pass extraction of 11C-dLop is high and requires correction for blood flow

170 starting immediately after the injection of 11C-methylaminoisobutyric acid (11C-MeAIB).

171 Levels of 11C-(R)-PK11195 binding potential were measured in a sel

172 major limitations are the short half-life of 11C and the rapid catabolism of thymidine after injectio

173 n patients with Parkinson's disease, loss of 11C-BU99008 VT in cortical regions, striatum, thalamus a

174 derate/advanced Parkinson's disease, loss of 11C-BU99008 VT in the frontal (r = 0.79; P = 0.001), tem

175 derate/advanced Parkinson's disease, loss of 11C-BU99008 VT was observed across frontal (P = 0.002),

176 ysis was used to generate parametric maps of 11C-(R)-PK11195 binding potential.

177 s; 166.5 MBq +/- 43.0 (4.50 +/- 1.16 mCi) of 11C-CUMI-101 were injected as an intravenous bolus, and

178 The major metabolites of 11C-choline were phosphocholine in HCC and betaine and c

179 Dynamic PET scans of 11C-choline were acquired using the woodchuck models of

180 1.31; mean +/- SEM) was greater than that of 11C-CFN (2.42 +/- 1.17) but lower than that of 18F-FDG (

181 ction for cerebral blood flow, the uptake of 11C-dLop was fairly uniform among brain regions, suggest

182 Asymmetry of [11C]DPA-713 was greater than that of [11C]PBR28 (F = 29.

183 tion did not affect the specific binding of [11C]cocaine in the striatum.

184 Binding of [11C]PBR28 was increased significantly in thalamus.

185 The specific binding of [11C]raclopride in the striatum and thalamus were signifi

186 The binding potential (BPF) of [11C]WAY-100635 (calculated as the number of receptors av

187 Amphetamine-induced displacement of [11C]FLB 457 binding potential (DeltaBPND) was significan

188 After injection of [11C](-)-12a, there was high uptake and retention of radi

189 P < .001; r = -0.70; P < .001), but not of [11C]PiB binding.

190 cant difference in the binding potential of [11C]DASB between the recovered depressed patients and he

191 The binding properties of [11C]MeDAS for myelin were systematically evaluated by in

192 Polar radiometabolites of [11C](-)-12a appeared moderately slowly in plasma.

193 The influx rate of [11C]5-HTP as a measure of serotonin synthesis rate capac

194 olated rat hearts, neuronal uptake rates of [11C]1a-m ranged from 0.24 to 1.96 mL min-1 (g wet wt)-1,

195 odistribution and acute toxicity studies of [11C]MeDAS were also conducted.

196 ry of [11C]DPA-713 was greater than that of [11C]PBR28 (F = 29.4; P = .001).

197 PET studies showed that the tumor uptake of [11C]14 in the NCI-H1975 xenografts was significantly hig

198 levated amyloid-beta and tau status based on 11C-Pittsburgh compound B (PiB) and 18F-MK-6240 PET imag

199 d brain beta-amyloidosis (A+ or A-) based on 11C-Pittsburgh compound B positron emission tomography.

200 l of innate immune activation as measured on 11C-PK11195 PET.

201 nzothiazole (also known as 11C-6-OH-BTA-1 or 11C-PIB) binds to amyloid-beta (Abeta), which accumulate

202 in prostate cancer, namely 18F-FDG, 18F- or 11C-acetate, and 18F- or 11C-choline.

203 ly 18F-FDG, 18F- or 11C-acetate, and 18F- or 11C-choline.

204 ns between measures of brain AD pathology or 11C-PiB beta-amyloid load and glucose intolerance or ins

205 patially extended-when grey matter volume or 11C-PiB uptake maps were added as covariates.

206 [11C]-(+)-propyl-hexahydro-naphtho-oxazin ([11C]-(+)-PHNO).

207 nt baseline assessment with 18F-AV-1451 PET, 11C-PK11195 PET, and structural MRI.

208 en 54 and 77 years underwent 11C-(R)PK11195, 11C-PIB positron emission tomography and magnetic resona

209 ntrations of 11C-loperamide and the putative 11C-dLop were about 16-fold greater in P-gp knockout mic

210 Quantitative [11C]14-PET studies showed that the tumor uptake of [11C]

211 itron emission tomography with radiolabeled [11C]ABP688, which binds to an allosteric site with high

212 ng with the translocator protein radioligand 11C-PBR28 was performed at baseline.

213 Radioligand [11C](-)-12a is promising for the study of brain CB1 rece

214 itron emission tomography (PET) radioligand [11C]raclopride directly to subsecond dopamine release ev

215 ecific dopamine transporter PET radioligand, 11C-PE2I, to assess the association between neuromelanin

216 -loperamide and its putative radiometabolite 11C-dLop are avid P-gp substrates.

217 itron emission tomography (PET) radiotracer [11C]PBR28, which binds to translocator protein, a molecu

218 micro-opioid receptor-selective radiotracer [11C]carfentanil after each 1-week inactive and active or

219 ed positron emission tomography radiotracer [11C]GSK931145 was used to quantify the relationship betw

220 y identifying and describing a radiotracer, [11C]GV1-57, that appears to specifically label olfactory

221 Here, we have evaluated a PET radiotracer, [11C]GV1-57, that specifically binds mature OSNs and quan

222 release during speech production and reduced 11C-raclopride binding to D2/D3 receptors at rest was se

223 with control subjects, patients had reduced 11C-raclopride binding to D2/D3 receptors at rest in the

224 tapping overlapped with a region of reduced 11C-raclopride binding to D2/D3 receptors at rest.

225 ween groups, and the association of regional 11C-PBB3 binding capacity with neuropsychiatric symptoms

226 hted magnetic resonance imaging and relative 11C-PBR28 uptake in the normal-appearing white matter wa

227 Relative [11C]PBR28 and [11C]DPA-713 uptakes were higher ipsilater

228 In a case-control study, relative [11C]Martinostat uptake was compared between 14 patients

229 was administered 180 min before the second [11C]PBR28 scan.

230 orophenyl)methylamide, termed [11C]SU11274 ([11C]14) for in vivo imaging of mesenchymal-epithelial tr

231 18F]AV-1451) (formerly known as [18F]T807), [11C]PiB PET, magnetic resonance imaging (MRI), neurologi

232 ic acid (3-chlorophenyl)methylamide, termed [11C]SU11274 ([11C]14) for in vivo imaging of mesenchymal

233 ron emission tomography (PET) probe, termed [11C]MeDAS, that is capable of longitudinally imaging cen

234 .2%+/-0.9%), and was lowest in the thalamus (11C-PIB BPND: 0.40+/-0.07; amyloid histology: 6.6%+/-0.6

235 se, with TSPO-binding PET ligands other than 11C-PBR28, for TSPO present in peripheral blood, and wit

236 All metabolites are more polar than 11C-CUMI-101, and no significant change in metabolites w

237 ased uptake after P-gp blockade suggest that 11C-dLop will be useful to measure a wide range of P-gp

238 in LPC and EAE rat models demonstrate that [11C]MeDAS uptake changes correlate with associated myeli

239 These studies demonstrated that [11C]14-PET is an appropriate imaging marker for quantifi

240 This study demonstrates that [11C]CUMI-101 is a selective 5-HT1AR ligand for in vivo a

241 The 11C-PIB PET data were quantified to nondisplaceable bind

242 le image, was calculated on the basis of the 11C-MeAIB images.

243 The [11C]-(+)-PHNO binding ratio in D3-rich SN versus D2-rich

244 The [11C]methylreboxetine-binding potential of NET availabili

245 The [11C]PBR28 distribution volume (VT) corrected for free fr

246 The [11C]PBR28 VT to fp ratio was higher in patients with TLE

247 monitored via temporal fluctuations in the [11C]raclopride PET signal.

248 evoke detectable temporal variations in the [11C]raclopride signal.

249 We quantified the [11C]PiB distribution volume ratio and standardized uptak

250 teral to seizure foci in patients with TLE ([11C]PBR28: 2%-6%; [11C]DPA-713: 4%-9%).

251 ein (P-gp), but it is rapidly metabolized to 11C-N-desmethyl-loperamide (11C-dLop), which is also a s

252 11C-dLop may be superior to 11C-loperamide in measuring P-gp function at the blood-b

253 resection.Increased uptake of the PET tracer 11C-alpha-methyl tryptophan shows promise for localizing

254 The PET tracer 11C-PK11195 targets the translocator protein expressed b

255 rols) aged between 54 and 77 years underwent 11C-(R)PK11195, 11C-PIB positron emission tomography and

256 mean [SD] age, 34.7 [9.2] years) underwent [11C]5-HTP PET imaging.

257 We used 11C-donepezil PET/CT to assess cholinergic (parasympathe

258 The agreement using 11C-MeAIB, parametric imaging, and fixed thresholding of

259 Our dual-modality imaging approach using 11C-PIB PET/7 T MR imaging and 16.4 T microscopic MR ima

260 esonance imaging and were dichotomized using 11C-labelled Pittsburgh compound B positron emission tom

261 o in patients with Parkinson's disease using 11C-BU99008 PET, a novel radioligand with high specifici

262 MEE and MVO(2) were evaluated using 11C-acetate positron emission tomography.

263 sms in LIDs development in PD patients using 11C-DASB PET to evaluate serotonin terminal function and

264 tic minimally conscious state patients using 11C-raclopride PET to estimate dopamine 2-like receptors

265 y amyloid positron emission tomography using 11C-Pittsburgh B compound (PiB-PET).

266 Using [11C]DPA-713 positron emission tomographic data from 12 a

267 with SCZ and matched healthy controls using [11C]Martinostat positron emission tomography (PET).

268 Furthermore, using [11C]MeDAS-PET, the efficacy of myelin repair therapy wit

269 eled with carbon-11 (t1/2 ) 20.4 min) using [11C]cyanide ion as labeling agent and evaluated as PET r

270 r-olds (n = 79) we also performed PET using [11C]dihydrotetrabenazine (DTBZ), a measure of presynapti

271 cortical Abeta deposition, quantified using [11C] Pittsburgh-compound-B (PIB)-PET.

272 raphy-based regional measures of TSPO using [11C]DPA-713, diffusion tensor imaging measures of region

273 cose metabolism in three PPA variants using [11C]-Pittsburgh compound B ([11C]PIB) and [18F]-labeled

274 rther control for local grey matter volumes, 11C-PiB uptake, or both.

275 erived U87MG tumor volumes was achieved with 11C-MeAIB, MAP3D reconstruction, and fixed thresholding

276 Imaging with 11C-thymidine has been tested for detecting tumors and t

277 Monkeys were injected with 11C-loperamide, and PET brain images were acquired for 1

278 were 122.1 mm3 using 18F-FDG, 118.3 mm3 with 11C-MeAIB, and 125.4 mm3 by histology.

279 was 35.0 mm3 using 18F-FDG and 34.1 mm3 with 11C-MeAIB, compared with 33.7 mm3 by histology.

280 Cardiac PET was performed with 11C HED in 27 patients with IPD (20 men and seven women

281 Using PET with 11C-acetate, 18FDG, and 18F-fluoro-thiaheptadecanoic aci

282 PET with 11C-choline showed an HCC detection rate of 9 of 10.

283 nd choline tracer uptake in HCC for PET with 11C-choline.

284 PET with 11C-dLop can quantify P-gp function at the blood-brain b

285 ts in long-term survivors of TBI by PET with 11C-PBB3, and evaluated those associations with late-lif

286 I with a gradient echo sequence and PET with 11C-PK11195.

287 gone 3 T MRI scan, 985 amyloid PET scan with 11C-Pittsburgh compound B (PIB) and MRI, and 577 PIB-PET

288 labelling of Alzheimer's disease slices with 11C-PBB3 and 18F-AV-1451 were noted.

289 sured with positron emission tomography with 11C altropane.

290 h human brain PET data acquired in vivo with 11C-PBR28.

291 to measure brain microglial activation with [11C]PBR28 PET provides an approach to test new medicatio

292 he association of [18F]AV-1451 binding with [11C]PiB binding, and the association of [18F]AV-1451 bin

293 PET imaging with [11C] dihydrotetrabenazine, insulin staining, and microva

294 individuals underwent amyloid imaging with [11C]PiB PET.

295 ing positron emission tomography (PET) with [11C]-WAY-100635 before and after treatment of MDD with a

296 point, the subjects were also scanned with [11C]-raclopride PET and structural MRI to measure concur

297 8 patients and 7 controls were scanned with [11C]DPA-713.

298 d 11 age-matched controls were scanned with [11C]PBR28, and 8 patients and 7 controls were scanned wi

299 by PET imaging of the transplant site with [11C] dihydrotetrabenazine.

300 yl))-N-(2-pyridyl)-cyclohexanecarbo xamide ([11C]WAY-100635), a serotonin1A antagonist; a subset of 5