Patients undergoing 2-[fluorine 18]fluoro-2-deoxy-d-glucose (FDG) whole-body oncologic positron emission tomography (PET)/computed tomography (CT) are studied while fasting. Cardiac FDG uptake in fasted patients has been widely reported as variable. It is important to understand the normal patterns of cardiac FDG activity that can be seen in oncologic FDG PET/CT studies. These include focal and regional patterns of increased FDG myocardial activity. Focal activity can be observed in papillary muscles, the atria, the base, and the distal anteroapical region of the left ventricle. Regional increased cardiac FDG activity may be diffuse or localized in the posterolateral wall or the base of the left ventricle. Abnormal patterns of cardiac FDG activity not related to malignancy include those associated with lipomatous hypertrophy of the interatrial septum, epicardial and pericardial fat, increased atrial activity associated with atrial fibrillation or a prominent crista terminalis, cardiac sarcoidosis, endocarditis, myocarditis, and pericarditis. Knowledge of these patterns of cardiac FDG activity is important to be able to recognize malignant disease involving the paracardiac spaces, myocardium, and pericardium. With a better understanding of the range of normal and abnormal patterns of cardiac FDG activity, important benign and malignant diseases involving the heart and pericardium can be recognized and diagnosed.

Remyelination is a critical step for recovery of function after demyelination and defines the ability to generate new myelin. This repair process is dependent on the presence of resident oligodendrocyte progenitors (OLPs) that have been shown to remyelinate axons after demyelination. We have previously shown that the levels of the cell cycle inhibitor p27Kip-1 modulate the number of neonatal cortical OLPs. We now asked whether this cell cycle molecule plays also a role in regulating the number of adult OLP in the spinal cord after demyelination induced by lysolecithin injection. The proliferative response of OLP in the spinal cord of injected wild-type (wt) and p27Kip-1 null mice was evaluated 3 days after lesion. In vivo labeling with bromodeoxyuridine (BrdU) was used to identify cells in S phase. Double immunofluorescence for the OLP marker NG2, and for BrdU was used to count the number of proliferating progenitors. Consistent with a role of p27Kip-1 in regulating the number of adult OLP in the injured spinal cord, a larger number of proliferating OLPs was observed in p27Kip-1null mice compared with wild-type controls. These cells were able to differentiate as assessed by the presence of MBP+ cells in the spinal cord 14 days after injury. We conclude that the cellular levels of the cell cycle inhibitor p27Kip-1 modulate the repair response of OLPs to injury in the adult spinal cord.

No abstract

This study confirms variable fasting FDG cardiac activity with a predominant basal pattern not associated with radiation injury. Knowledge of these patterns is important for recognition of possible underlying cardiac ischemia, tumor, or other inflammatory conditions encountered during interpretation of oncologic positron emission tomography computed tomography studies.

No abstract