Development of a method to measure kinetics of radiolabelled monoclonal antibody in human tumour with applications to microdosimetry: positron emission tomography studies of iodine-124 labelled 3F8 monoclonal antibody in glioma

1993 ◽  
Vol 20 (5) ◽  
Author(s):  
Farhad Daghighian ◽  
KeithS. Pentlow ◽  
StevenM. Larson ◽  
MartinC. Graham ◽  
GeneR. DiResta ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Monoclonal Antibody ◽  
Emission Tomography ◽  
Human Tumour ◽  
Positron Emission ◽  
Kinetics Of

scholarly journals Noninvasive and Quantitative Monitoring of the Distributions and Kinetics of MicroRNA-Targeting Molecules in Vivo by Positron Emission Tomography

2019 ◽  
Vol 16 (4) ◽  
pp. 1507-1515 ◽  
Author(s):  
Jussi Mäkilä ◽  
Anu Kiviniemi ◽  
Tiina Saanijoki ◽  
Heidi Liljenbäck ◽  
Meeri Käkelä ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Emission Tomography ◽  
Positron Emission ◽  
Quantitative Monitoring ◽  
Kinetics Of

scholarly journals Evaluation of 89Zr-Labeled Human Anti-CD147 Monoclonal Antibody as a Positron Emission Tomography Probe in a Mouse Model of Pancreatic Cancer

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e61230 ◽  
Author(s):  
Aya Sugyo ◽  
Atsushi B. Tsuji ◽  
Hitomi Sudo ◽  
Kotaro Nagatsu ◽  
Mitsuru Koizumi ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Positron Emission Tomography ◽  
Monoclonal Antibody ◽  
Mouse Model ◽  
Emission Tomography ◽  
Positron Emission

A Double-Injection Technique for in vivo Measurement of Dopamine D2-Receptor Density in Monkeys with 3-(2'-[18F] Fluoroethyl)Spiperone and Dynamic Positron Emission Tomography

1989 ◽  
Vol 9 (6) ◽  
pp. 850-858 ◽  
Author(s):  
Sung-Cheng Huang ◽  
Mark M. Bahn ◽  
Jorge R. Barrio ◽  
John M. Hoffman ◽  
Nagichettiar Satyamurthy ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Receptor Binding ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Emission Tomography ◽  
Injection Technique ◽  
Receptor Density ◽  
Dopamine D2 ◽  
Positron Emission ◽  
Kinetics Of

Dopamine D2-receptor density in striatum of monkey was measured with 3-(2'-[18F]fluoroethyl)spiperone (FESP) and dynamic positron emission tomography (PET), using a double-injection technique. A first bolus of high specific activity (SA) FESP (5 mCi; ≃ 1 Ci/μmol) was injected i.v.; 90 min later, a second bolus of lower SA FESP (5 mCi; ≃ 0.04 Ci/μmol) was injected. A dynamic PET study was performed to measure the kinetics of FESP in striatum over 180 min, and the metabolite-corrected concentration of FESP in plasma as a function of time was obtained from arterial blood samples. A nonlinear compartmental model that took into account the saturability of the receptor binding was used to describe the kinetics of FESP in striatum. Model parameters were estimated by regression with a constraint based on information about the equilibrium dissociation constant of the ligand–receptor binding. Dopamine D2-receptor density in striatum was estimated to be 25.9 ± 12.7 pmol/g in seven Macaca nemestrina monkeys. The method does not require the use of cerebellum as a reference tissue region and an estimate of dopamine D2-receptor density can be obtained from a single study.

Kinetics of 11C-Labeled Opiates Studied with Positron Emission Tomography in the Brain of the Rhesus Monkey

1985 ◽  
pp. 97-100
Author(s):  
P. O. Lundberg ◽  
P. Hartvig ◽  
K. Bergström ◽  
B. Lindberg ◽  
H. Lundqvist ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Rhesus Monkey ◽  
Emission Tomography ◽  
Positron Emission ◽  
Kinetics Of ◽  
The Brain

scholarly journals Positron Emission Tomography Study of Brain Benzodiazepine Receptors in Friedreich's Ataxia

1990 ◽  
Vol 17 (4) ◽  
pp. 404-409 ◽  
Author(s):  
C. Chavoix ◽  
Y. Samson ◽  
S. Pappata ◽  
C. Prenant ◽  
M. Mazière ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Benzodiazepine Receptors ◽  
Friedreich’S Ataxia ◽  
Friedreich's Ataxia ◽  
Emission Tomography ◽  
Tracer Injection ◽  
Central Type ◽  
Positron Emission ◽  
Specific Antagonist ◽  
Kinetics Of

ABSTRACT:Central type benzodiazepine receptors were studied in 9 patients with Friedreich's ataxia and 12 healthy subjects using positron emission tomography (PET) and [11C]Ro 15-1788, a specific antagonist of the central type benzodiazepine receptors, as radioligand. A standard PET procedure was used in 5 patients and 8 controls to obtain brain kinetics of the total binding of the radioligand. The remaining subjects were intravenously injected with a saturating dose of unlabeled Ro 15-1788, 30 minutes after the tracer injection, to determine the nondisplaceable binding of [11C]Ro 15-1788. A semi-quantitative method was used to quantify the [11C]Ro 15-1788 data. None of the quantification indices in the cerebellar hemispheres, or in the other brain areas investigated, was significantly modified in patients with Friedreich's ataxia. These findings suggest that brain benzodiazepine receptors are unaffected in Friedreich's ataxia.

scholarly journals Cerebral rituximab uptake in multiple sclerosis: A 89Zr-immunoPET pilot study

2017 ◽  
Vol 24 (4) ◽  
pp. 543-545 ◽  
Author(s):  
Marloes HJ Hagens ◽  
Joep Killestein ◽  
Maqsood M Yaqub ◽  
Guus AMS van Dongen ◽  
Adriaan A Lammertsma ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Positron Emission Tomography ◽  
Central Nervous System ◽  
Monoclonal Antibody ◽  
Emission Tomography ◽  
Positron Emission ◽  
Central Nervous System Penetration ◽  
Relapsing Remitting ◽  
Rapid Effect ◽  
Relapsing Remitting Multiple Sclerosis

Previous studies have demonstrated that the chimeric monoclonal antibody rituximab significantly reduces clinical and radiological disease activity in relapsing-remitting multiple sclerosis as early as 4 weeks after the first administration. The exact mechanisms leading to this rapid effect have not yet been clarified. The aim of this positron emission tomography study was to assess central nervous system penetration as a possible explanation, using zirconium-89-labelled rituximab. No evidence was found for cerebral penetration of [89Zr]rituximab.

scholarly journals Comparison of [11C]Diprenorphine and [11C]Carfentanil Binding to Opiate Receptors in Humans by Positron Emission Tomography

1990 ◽  
Vol 10 (4) ◽  
pp. 484-492 ◽  
Author(s):  
J. James Frost ◽  
Helen S. Mayberg ◽  
Bernard Sadzot ◽  
Robert F. Dannals ◽  
John R. Lever ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Specific Binding ◽  
Regional Distribution ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Total Radioactivity ◽  
Emission Tomography ◽  
Receptor Subtypes ◽  
Positron Emission ◽  
Kinetics Of

The kinetics and regional distribution of [11C]carfentanil, a μ-selective opiate receptor agonist, and [11C]diprenorphine, a nonselective opiate receptor antagonist, were compared using paired positron emission tomography studies in two normal volunteers. Kinetics of total radioactivity (counts/mCi/pixel) was greater for [11C]diprenorphine than [11C]carfentanil in all regions. [11C]Carfentanil binding (expressed as the total/nonspecific ratio) reached near equilibrium at ∼40 min, whereas [11C]diprenorphine showed a linear increase until ∼60 min. Kinetics of specific binding demonstrated significant dissociation of [11C]carfentanil from opiate receptors, whereas little dissociation of [11C]diprenorphine was observed during the 90-min scan session. Regional distributions of [11C]carfentanil and [11C]diprenorphine were qualitatively and quantitatively different: Relative to the thalamus (a region with known predominance of μ-receptors), [11C]diprenorphine displayed greater binding in the striatum and cingulate and frontal cortex compared to [11C]carfentanil, consistent with labeling of additional, non-μ sites by [11C]diprenorphine. We conclude from these studies that [11C]diprenorphine labels other opiate receptor subtypes in addition to the μ sites selectively labeled by [11C]carfentanil. The nonselective nature of diprenorphine potentially limits its usefulness in defining abnormalities of specific opiate receptor subtypes in various diseases. Development of selective tracers for the δ- and κ-opiate receptor sites, or alternatively use of unlabeled inhibitors to differentially displace μ, δ, and κ subtypes, will help offset these limitations.

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