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MeSH Review:

Positron-Emission Tomography

Bailer, U.F. et al., Frazier, O.H. et al., Koepp, M.J. et al., Shively, C.A. et al., Chugani, H.T. et al., et al.

Beanlands, Hendry, Masters, deKemp, Woodend, Ruddy, Okubo, Suhara, Suzuki, Kobayashi, Inoue, Terasaki, Someya, Sassa, Sudo, Matsushima, Iyo, Tateno, Toru, May, Bahra, Büchel, Frackowiak, Goadsby, Düzel, Cabeza, Picton, Yonelinas, Scheich, Heinze, Tulving, Kapur, Zipursky, Remington, Shively, Friedman, Gage, Bounds, Brown-Proctor, Blair, Henderson, Smith, Buchheimer, Otonkoski, Näntö-Salonen, Seppänen, Veijola, Huopio, Hussain, Tapanainen, Eskola, Parkkola, Ekström, Guiot, Rahier, Laakso, Rintala, Nuutila, Minn, Clark, Eder, Ryan, Lathia, Lenz, Kuhl, Koeppe, Snyder, Minoshima, Frey, Kilbourn,

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Disease relevance of Positron-Emission Tomography

Cerebral uptake of benzodiazepine measured by positron emission tomography in hepatic encephalopathy [1].
METHODS: We used positron-emission tomography to measure presynaptic accumulation of fluorodopa F 18 tracer in the dopaminergic regions of the brains of 12 patients with Lesch-Nyhan disease (age, 10 to 20 years) and 15 healthy controls (age, 12 to 23) [2].
Synaptic dopamine release from embryonic nigral transplants has been monitored in the striatum of a patient with Parkinson's disease using [11C]-raclopride positron emission tomography to measure dopamine D2 receptor occupancy by the endogenous transmitter [3].
We studied whether whole-body positron emission tomography (PET) with 18F-fluorodeoxyglucose (18FDG) would improve the preoperative detection of metastases [4].
Whole-body 18F-fluorodeoxyglucose positron emission tomography in preoperative evaluation of lung cancer [4].

Psychiatry related information on Positron-Emission Tomography

To this end, we used positron emission tomography (fludeoxyglucose F 18 method) to study 24 patients with clinical diagnoses of probable Alzheimer's disease [5].
The cerebral metabolic rate for glucose was studied in 18 adults with childhood-onset obsessive-compulsive disorder (OCD) and in age- and sex-matched controls using positron emission tomography and fludeoxyglucose F 18 [6].
METHODS: We used positron emission tomography and fludeoxyglucose F 18 to measure brain metabolism in Vietnam combat veterans with PTSD (n = 10) and healthy age-matched control subjects (n = 10), following administration of yohimbine (0.4 mg/kg) or placebo in a randomized, double-blind fashion [7].
OBJECTIVE: To further characterize the 5-HT system in AN, we investigated 5-HT1A receptor activity using positron emission tomography imaging because this receptor is implicated in anxiety and feeding behavior [8].
Benzodiazepine receptor binding in Huntington's disease: [11C]flumazenil uptake measured using positron emission tomography [9].

High impact information on Positron-Emission Tomography

When used in conjunction with a radioactive glucose analog, positron-emission tomography has proven useful for detecting malignant tissue and quantitating changes in tumor glycolysis during and after treatment [10].
We used positron-emission tomography with [(11)C]hydroxyephedrine, an analogue of norepinephrine, to delineate sympathetic innervation [11].
VHL-deficient tumors show increased uptake of the positron emission tomography (PET) tracer fluorodeoxyglucose (FDG) in an mTOR-dependent manner [12].
Here we use 11C-labelled raclopride and positron emission tomography scans to provide evidence that endogenous dopamine is released in the human striatum during a goal-directed motor task, namely a video game [13].
D2R is expressed most highly in the striatum, but most of the recent positron emission tomography (PET) studies have failed to show any change in D2R densities in the striatum of schizophrenics, raising the possibility that other receptors may also be involved [14].

Chemical compound and disease context of Positron-Emission Tomography

METHODS: Positron emission tomography (PET) and a radiolabelled acetylcholine analogue with high hydrolytic specificity to acetylcholinesterase [11C]N-methyl-4-piperidyl acetate (MP4A), was used in eight elderly healthy controls and five patients with Alzheimer's disease who had mild dementia [15].
METHODS: We used positron emission tomography (PET) to assess the changes in rCBF, as an index of synaptic activity, during nitroglycerin-induced cluster headache attacks in nine patients who had chronic cluster headache [16].
Myocardial blood flow response to pacing tachycardia and to dipyridamole infusion in patients with dilated cardiomyopathy without overt heart failure. A quantitative assessment by positron emission tomography [17].
Delay in revascularization is associated with increased mortality rate in patients with severe left ventricular dysfunction and viable myocardium on fluorine 18-fluorodeoxyglucose positron emission tomography imaging [18].
Diagnosis of deep septic thrombophlebitis in cancer patients by fluorine-18 fluorodeoxyglucose positron emission tomography scanning: a preliminary report [19].

Biological context of Positron-Emission Tomography

We studied the mechanism of action of eniluracil by measuring with positron emission tomography (PET) the effect of eniluracil on tumour and normal-tissue pharmacokinetics of fluorine-18-labelled fluorouracil [20].
Quantitative in-vivo measurements of glial activation were obtained with positron emission tomography (PET) and carbon-11-labelled (R)-PK11195, a specific ligand for the peripheral benzodiazepine binding site [21].
Brain glucose metabolism during non-rapid eye movement sleep in major depression. A positron emission tomography study [22].
Herein we report a combined positron emission tomography and event-related potential (ERP) experiment that was designed to distinguish between neural correlates of task-related and item-related processes of memory retrieval [23].
BACKGROUND--Imaging of myocardial glucose metabolism using [18F]fluorodeoxyglucose (FDG) with positron emission tomography (PET) has been proposed for identification of tissue viability in patients with advanced coronary artery disease [24].

Anatomical context of Positron-Emission Tomography

Whole body glucose uptake was determined with a 2-h euglycemic hyperinsulinemic clamp, and regional glucose uptake in femoral and arm muscles, and myocardium using 18F-fluoro-2-deoxy-D-glucose and positron emission tomography [25].
We investigated insulin-induced glucose metabolism of skeletal muscle by positron-emission tomography to identify possible defects of muscle glucose metabolism in these patients [26].
Dynamic positron emission tomography with 15O-labelled water was used in 12 patients with angina and angiographically proven coronary artery disease to measure regional cerebral blood flow changes during angina induced by intravenous dobutamine [27].
We measured the relationship between decreased relative prefrontal cortex glucose metabolism (hypofrontality) using positron emission tomography and evaluated the severity of negative symptoms in 20 chronic schizophrenics who underwent scanning while not receiving neuroleptic drugs [28].
MAIN OUTCOME MEASURES: Serotonin 1A receptor BP was examined by positron emission tomography using the radioligand 4,2"-(methoxyphenyl)-1-[2"-(N-2"-pyridinyl)-p-fluorobenzamido]ethylpiperazine in the raphe, amygdala, hippocampus, and anterior cingulate cortex in monkeys characterized by behavioral observation as depressed or not depressed [29].

Associations of Positron-Emission Tomography with chemical compounds

Here we use positron emission tomography (PET) to examine the regulatory role of dopamine on cortical function in normal subjects and unmedicated schizophrenic patients [30].
We have used positron emission tomography to determine what level of DAT occupancy is required to produce a subjective 'high' in human volunteers who regularly abuse cocaine [31].
In this study we examined mu opioid receptor binding in ten cocaine-dependent men and seven nonaddicted controls using positron emission tomography and [11C] carfentanil [32].
Positron emission tomography. Progress in brain imaging [33].
Maturational changes in cerebral function in infants determined by 18FDG positron emission tomography [34].

Gene context of Positron-Emission Tomography

Positron emission tomography scans in AD patients (n = 15) and control subjects (n = 12) measured both BuChE (using [(11)C]BMP) and AChE activity (using N-[(11)C] methylpiperidin-4-yl propionate, an established method) [35].
We have assessed the feasibility of positron emission tomography (PET) and ex vivo gamma-counting to measure the pattern of expression of telomerase promoter fragments in vivo [36].
We evaluated the utility of fluorine-18 l-3,4-dihydroxyphenylalanine ([(18)F]-DOPA) positron emission tomography (PET) to identify focal pancreatic lesions in 14 CHI patients, 11 of which carried mutations in the ABCC8 gene (age 1-42 months) [37].
METHOD: Forty-four patients with schizophrenia (16 taking risperidone, 2-12 mg/day; 17 taking olanzapine, 5-60 mg/day; and 11 taking clozapine, 75-900 mg/day) had their D2 and 5-HT2 occupancies determined with the use of [11C]raclopride and [18F]setoperone, respectively, and positron emission tomography imaging [38].
Stable disease was achieved in five patients: one patient showed reduced tumor activity (positron emission tomography scan) and reduced mitogen-activated protein kinase signaling (lower phospho-ERK); one patient remained on treatment until study end point [39].

Analytical, diagnostic and therapeutic context of Positron-Emission Tomography

METHODS AND RESULTS: Thirty-one patients were evaluated with positron emission tomography (PET), dobutamine echocardiography, 201Tl single-photon emission computed tomography (201Tl-SPECT), and multigated acquisition radionuclide ventriculography (MUGA) [40].
BACKGROUND: Dual positron emission tomography (PET) imaging with a perfusion tracer and 18F-fluorodeoxyglucose (FDG) can detect myocardial viability [41].
PURPOSE: To address the role of positron emission tomography (PET) using [(18)F]fluorodeoxyglucose (FDG) to monitor primary (neoadjuvant) chemotherapy in patients with locally advanced breast cancer [42].
While the [18F]FDG PET scan cannot currently localize an epileptogenic zone independently, the absence of focal hypometabolism or its presence contralateral to a presumed EEG focus suggests the need for additional electrophysiological data [43].
Fifty-four chorea-free persons were evaluated by neurological examination, positron emission tomography measurement of glucose metabolism, radiographic computerized tomographic measurement of caudate size, and genetic testing at the polymorphic DNA loci D4S10, D4S43, and D4S125 [44].

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