PSMA-Positive Low Malignant Gastrointestinal Stromal Tumor in the Stomach on F-18-PSMA-1007 PET/CT.

A 76-year-old man with newly diagnosed high-risk prostate cancer was referred for primary staging with F-18-PSMA-1007 PET/CT. The PET/CT scan showed no lymph node or bone metastases, only localized disease within the prostate gland. Additionally, the F-18-PSMA PET/CT scan showed a PSMA-positive lesion correlating to a polyp located in the body of the stomach on the greater curvature. A prior F-18-FDG PET/CT showed low FDG uptake in the polyp, but this was not reported initially in the written report. The patient had no upper gastrointestinal symptoms. A gastroscopy with biopsies was performed, and the histopathology results showed chronic unspecific inflammation with no granulomas, dysplastic or malignant changes in three out of three biopsies. A repeated gastroscopy with biopsy showed an epithelioid variant of a gastrointestinal stromal tumor (Ki-67 index 2%). A laparoscopic tumor extirpation was planned after radiation treatment in combination with endocrine therapy of the localized prostate cancer. To our knowledge, this is one of very few reported cases of a PSMA-positive gastrointestinal stromal tumor (GIST), and can be added to the list of malignant pitfalls of PSMA PET/CT in prostate cancer patients.

Reverse Mismatch Pattern in Cardiac 18F-FDG Viability PET/CT Is Not Associated With Poor Outcome of Revascularization: A Retrospective Outcome Study of 91 Patients With Heart Failure.

PURPOSE: Revascularization strategies in patients with ischemic heart failure (HF) should be based on evidence of reversible perfusion defects and myocardial viability. Myocardial viability assessment is preferably based on dual isotope PET using perfusion and metabolism tracers. However, in a nonnegligible subset of HF patients, reverse mismatch (RM) pattern (reduced glucose uptake relative to perfusion) of unknown origin is observed. We aimed to investigate determinants of RM and the impact of RM on the subsequent improvement in left ventricular function by revascularization. PATIENTS AND METHODS: Ninety-one patients (12 women, 25 with diabetes) with HF undergoing Rb perfusion PET and hyperinsulinemic-euglycemic clamp F-FDG viability PET were retrospectively reviewed. RESULTS: Follow-up time was 12 to 33 months. In 30 of 91 patients, hypometabolic myocardium exceeded the percentage of hypoperfused myocardium; however, only in 12 of 91 patients was the RM considered significant (percentage RM in the left ventricle, 42.5 ± 12.9 [reverse patients] vs 14.1 ± 8.6 [scar and hibernation patients]; P < 0.001). Diabetes status per se did not predict RM, but a significant inverse correlation between insulin sensitivity and RM was observed. The frequency of hospitalization, cardiac death, and myocardial infarctions were not significantly higher in RM patients. Reverse mismatch patients benefited from revascularization to the same extent as patient with normal metabolic patterns. CONCLUSIONS: Reverse mismatch is common among HF patients (~15%) and is inversely correlated to insulin sensitivity. It is not, however, associated with increased cardiac morbidity and mortality and does not predict a worse outcome after revascularization.

Intrinsic Ca2+-dependent theta oscillations in apical dendrites of hippocampal CA1 pyramidal cells in vitro.

Behavior-associated theta-frequency oscillation in the hippocampal network involves a patterned activation of place cells in the CA1, which can be accounted for by a somatic-dendritic interference model predicting the existence of an intrinsic dendritic oscillator. Here we describe an intrinsic oscillatory mechanism in apical dendrites of in vitro CA1 pyramidal cells, which is induced by suprathreshold depolarization and consists of rhythmic firing of slow spikes in the theta-frequency band. The incidence of slow spiking (29%) increased to 78% and 100% in the presence of the ß-adrenergic agonist isoproterenol (2 µM) or 4-aminopyridine (2 mM), respectively. Prior depolarization facilitated the induction of slow spiking. Applied electrical field polarization revealed a distal dendritic origin of slow spikes. The oscillations were largely insensitive to tetrodotoxin, but blocked by nimodipine (10 µM), indicating that they depend on activation of L-type Ca2+ channels. Antagonists of T-, R-, N-, and P/Q-type Ca2+ channels had no detectable effect. The slow spike dimension and frequency was sensitive to 4-aminopyridine (0.1-2 mM) and TEA (10 mM), suggesting the contribution from voltage-dependent K+ channels to the oscillation mechanism. α-Dendrotoxin (10 µM), stromatoxin (2 µM), iberiotoxin (0.2 µM), apamin (0.5 µM), linorpidine (30 µM), and ZD7288 (20 µM) were without effect. Oscillations induced by sine-wave current injection or theta-burst synaptic stimulation were voltage-dependently attenuated by nimodipine, indicating an amplifying function of L-type Ca2+ channels on imposed signals. These results show that the apical dendrites have intrinsic oscillatory properties capable of generating rhythmic voltage fluctuations in the theta-frequency band.