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Positron emission tomography was used to measure local cerebral glucose utilization by the 2-[18F]fluoro-2-deoxy-D-glucose technique in 23 patients with cerebral gliomas. All 10 high-grade (III and IV) astrocytomas demonstrated a region of high activity with a glucose consumption of 7.4 ± 3.5 (SD) mg/100 gm per minute. The 13 low-grade (I and II) gliomas had a glucose metabolic rate of 4.0 ± 1.8 mg/100 gm per minute, with no distinctly visible hot spot. Thus, we found a correlation between rate of glycolysis and malignancy in primary cerebral tumors. Cerebral cortical glucose utilization was often depressed in areas adjacent to or neurally connected to the tumor site, and there was focal irregular delta wave EEG activity in these areas.

Using the Greene melanoma In the hamster (Syrian Golden), the radlopharmaceutical, 123I-4(3-dimethylaminopropylamino)-7-iodoquinoline, was tested for Its ability to localize melanoma. This quinoline analog has been described for use in the detection of melanoma, but this Is the first report, to our knowledge, of its being used with an 123I label.Hamsters with either skin or eye melanomas were studied. Both melanomas could be seen with a gamma camera at three hours after injection. In vitro analysis confirmed the tumor specificity. Thus, it appears that this preclinical trial of a new radiopharmaceutical justifies clinical testing to determine its value in the localization of melanomas of the eyes and skin of humans.

A new model for the perfusion of human term-placentas has been developed for studies on the placental biogenesis of C-18 and C-19 steroids. For viability criteria, the glucose- and oxygen-consumption, regional perfusion control by dye-infusions or scanning after injection of 99Tc-labelled macroparticles, and the histological qualification were chosen. The recycled perfusate was investigated for the steroids oestrone (Oe1), oestradiol-17β (Oe2), oestriol (Oe3), 4-androstene-3,17-dione (A), testosterone (T), and human placental lactogen (HPL) by radioimmunoassay in controls and perfusions with the foetal steroid precursor dehydroepiandrosterone sulphate (DHA-S). In control perfusions, steroid hormones were found in constant ratios (Oe1:Oe2:Oe3:T:A = 30:1.5:100:0.35:1). Following the administration of 10 mg DHA-S for testing the metabolic capacity of the organ, high concentrations of Oe1(90–720 ng/ml = 250–3970 % as compared to 100% pre-injection values) were found, shortly preceded by a rapid increase of A (66–1000 ng/ml = 100–16 000 %). A typical surge of T (5.3–147 ng/ml = 265–4640 %) preceded the normally slower increment of Oe2(22–220 ng/ml = 1570–4330 %). The concentrations of Oe3and HPL remained nearly unchanged. From different steroid patterns after DHA-S-load, two distinct responses of term-placentas could be differentiated: Group I (n=12) showed high concentrations of Oe1(3200 ± 940 %), a small increase of T (1020 ± 500%), as well as low and delayed values of Oe2(1660 ± 450%). In Group II (n = 5), values were high for T (3160 ± 1020%) and Oe2(3300 ± 1110%), whereas Oe1was found in a lower range (508 ± 302%).In contrast to in vivofindings in maternal venous blood after DHS-S injection to the mother, oestrone was found in perfusions as the main oestrogen fraction from DHA-S. Thus, the analysis of such metabolic differences might be of help in the interpretation of complex results from the DHA-S-loading test.

• Frontal lobe dysfunction is widely suspected to underlie negative symptoms of schizophrenia. This hypothesis is based largely on long-standing observations of the similarities between the effects of frontal lobe lesions and negative symptoms. However, there is little direct evidence specifically for such an association in schizophrenic patients. 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. We found a close relationship between negative symptoms and prefrontal hypometabolism, particularly in the right dorsolateral convexity. This association was regionally specific. Furthermore, there was no evidence that this relationship was an artifact of age, cerebral atrophy, or severity of positive symptoms.

• Thirteen diagnosed schizophrenics and 11 normal controls were studied with a method using the PETT III positron emission tomograph (PET) and fluorodeoxyglucose labeled with fluorine 18. Each subject also had a computed tomographic (CT) scan. For each subject, two brain levels, one through the basal ganglia and one through the semioval center, were analyzed for the mean regional metabolic glucose rate. Specifically, relationships between frontal and posterior regions were evaluated. The CT scans of matching levels were superimposed on the functional PET images to provide anatomic criteria for region of interest selection. While no wholeslice metabolic differences were apparent between groups, schizophrenics had significantly lower activity in the frontal lobes, relative to posterior regions. The medicated and drugfree groups did not differ from one another in these regards. Trait v state dependency of the phenomenon was analyzed, and several technological limitations were considered.

Positron emission tomography (PET) can probe biochemical pathways in vivo and can provide quantitative data; for that purpose, tracers labeled with positron-emitting radioisotopes are essential. This report describes the tracers that are being used or that may have future use, their production by cyclotrons, and other needed resources for PET imaging. Current routine and automated methods for convenient production of labeled compounds, coupled with simple computer-controlled accelerators, can support the creation of clinical PET centers in any large medical institution, obviating the need for in-depth research teams. An alternate approach involves the development of regional centers that provide in-house service and that supply fluorine 18— and carbon 11—labeled compounds to nearby hospitals with PET machines.(JAMA 1988;259:1854-1860)

This report describes the current and potential uses of positron emission tomography in clinical medicine and research related to oncology. Assessment will be possible of metabolism and physiology of tumors and their effects on adjacent tissues. Specific probes are likely to be developed for target sites on tumors, including monoclonal antibodies and specific growth factors that recognize tumors. To date, most oncological applications of positron emission tomography tracers have been qualitative; in the future, quantitative metabolic measurements should aid in the evaluation of tumor biology and response to treatment.(JAMA 1988;259:2126-2131)

This report discusses experimental and clinical applications of positron emission tomography to the heart, including measurements of blood flow to the myocardium and studies of metabolism and experimental injury. Most initial clinical studies have concentrated on ischemic heart disease, but the technique also has potential for investigation of cardiomyopathies, studying the neural control of the heart, and evaluating the effects of drugs on cardiac tissues.(JAMA 1988;259:2438-2445)

The synthesis of 4-[18F]fluoroantipyrine (1) and its biodistribution in mice are described. Compound 1 was synthesized either by direct fluorination of antipyrine with [18F]F2 or CH3CO218F, or by an isotopic exchange method. While direct fluorination of antipyrine with [18F]F2 gave compound 1 in about a 20% yield, the isotopic exchange method gave compound 1 in only a 1%–2% yield. The biodistributions of compound 1 and 4-[131I]iodoantipyrine (3) in mice indicated that both compounds reached apparent equilibrium concentration in the bloodstream at approximately 0.5 min postinjection and compound 1 was found in higher concentrations than the iodinated analog in the well-perfused tissues. The 18F activity in the mouse brain persisted for about 2 min. The ratio of activity in the brain to bone was approximately 2:1. After 10 min, the 18F activity in the brain decreased markedly while the 18F activity in bones rose sharply resulting in a brain to bone ratio of approximately 1:2. This would suggest that compound 1 defluorinated in vivo to give fluoride as one of the metabolites.