Glial cell activation occurs in response to brain injury and is present in a wide variety of inflammatory processes including dementia associated with human immunodeficiency virus (HIV). HIV-infected glial cells release cytokines and chemokines that, along with viral neurotoxins, contribute to neuronal damage and apoptosis. The purpose of this study was to determine if glial cell activation in HIV-positive (HIV+) patients could be detected noninvasively, in vivo, using [11C]-R-PK11195 with positron emission tomography (PET). [11C]-R-PK11195 is a selective radioligand for the peripheral benzodiazepine receptor (PBR), and is known to reflect the extent of glial cell activation. A subaim was to determine if nondemented HIV+ patients could be distinguished from those with HIV-associated dementia (HAD) on the basis of [11C]-R-PK11195 binding. Five healthy volunteers and 10 HIV+ patients underwent PET with [11C]-R-PK11195. Time-radioactivity curves (TACs) were generated from dynamic PET images in nine regions of interest (ROIs) drawn on coregistered magnetic resonance imaging (MRI) scans. The average radioactivity was calculated in each ROI and was normalized to the average radioactivity in white matter. Patients with HAD showed significantly higher [11C]-R-PK11195 binding than controls in five out of eight brain regions (P < .05, Mann-Whitney U test). Nondemented HIV+ patients did not show significantly increased binding compared to controls. HIV+ patients overall (demented and nondemented) showed significantly higher radioligand binding than controls in five brain regions (P < 0.05). Patients with HAD did not show significant differences in binding when compared to HIV+ nondemented patients. The findings of this pilot study support a role for glial cell activation in HAD, and that PET with [11C]-R-PK11195 can detect the concomitants of neuronal damage in individuals infected with HIV.

The medical literature states that solid gastric-emptying studies are more sensitive for the detection of gastroparesis than are liquid studies; thus, liquid studies are rarely required. However, we have seen patients with normal solid but delayed liquid emptying. The purpose of this investigation was to determine whether a study of clear liquid gastric empting has added value for the diagnosis of gastroparesis over a study of solid emptying alone. Methods: A total of 101 patients underwent both solid and liquid gastric-emptying studies, acquired sequentially on the same day. A 30-min (1-min frames) liquid study (300 mL of water with 7.4 MBq [0.2 mCi] of 111 In-diethylenetriaminepentaacetic acid) was followed by a standardized 4-h solid-meal study (a 99m Tcsulfur colloid-labeled egg-substitute sandwich meal). Emptying was quantified as a best-fit exponential emptying rate (T1/2) for liquids and percentage emptying at 4 h for solid empting. Thirty healthy volunteers underwent a study of clear liquid emptying to establish normal values. The results of the liquid and solid studies were compared. 111 In liquid downscatter into the subsequent 99m Tc solid meal results was analyzed. Results: The upper range of normal for clear liquid emptying (T1/2) for healthy volunteers was 22 min (mean 6 3 SDs) and 19 min (mean 6 2 SDs). Of 101 patients, delayed emptying was found in 36% of liquid and 16% of solid studies. Of all patients with normal solid emptying, 32% had delayed liquid emptying. 111 In downscatter into the 99m Tc window was not generally significant. Conclusion: For the detection of gastroparesis, a 30-min study of clear liquid gastric-emptying has considerable added diagnostic value over a study of solid emptying alone. The radionuclide gastric-emptying study has long been the standard clinical diagnostic test for the detection of gastroparesis. Both solid and liquid studies have been used over the years, either as individual or as dual-phase studies, for investigative and clinical purposes. Standard teaching has been that only a solid study is needed for clinical purposes because the liquid study is less sensitive for the detection of gastroparesis, and liquid studies should be reserved for patients who cannot tolerate solids (1-6).However, we have observed patients who have had delayed liquid but normal solid emptying (7). The primary purpose of this investigation was to determine, in a large patient population, whether liquid gastric emptying provided added diagnostic value over solid emptying alone for the diagnosis of gastroparesis.We chose to perform the studies on the same day to avoid potential problems (e.g., different fasting conditions, different medications, and possible intercurrent clinical conditions that might affect emptying) that might arise from separate-day studies. Thus, the clear liquid and solid gastricemptying studies were performed sequentially; that is, a 30-min water study was performed, followed by the 4-h simplified and standardized solid protocol recommended by recently published...

Liquid gastric emptying is commonly abnormal in patients who have normal solid studies. Liquid studies should be routinely performed in addition to solid studies to fully evaluate gastric motility in patients with symptoms suggestive of gastroparesis.

Because of the ultrashort tracer half-life and high positron energy of 82 Rb, PET images acquired with this tracer are noisier and of lower resolution than those obtained with other PET tracers. The validity of electrocardiographic gating using 82 Rb for assessment of left ventricular (LV) function is not well established. To support feasibility, we compared functional parameters from gated 82 Rb PET with simultaneous high-resolution contrastenhanced CT ventriculography, obtained as a byproduct a CT coronary angiography during hybrid cardiac PET/CT. Methods: A total of 24 patients underwent PET/CT, consisting of rest and dipyridamole 82 Rb perfusion studies and contrast-enhanced CT angiography, using a 64-slice scanner, for the workup of coronary artery disease. From gated PET images, LV ejection fraction (EF), end-diastolic volume (EDV), and end-systolic volume (ESV) were calculated using 2 commercial products. For functional CT analysis, commercial software using endocardial contour detection was applied. Results: Inter-and intraobserver agreement was good for all methods. On CT, EF was 66% 6 13%, ESV was 41 6 29 mL, and EDV was 115 6 36 mL. On PET, EF during dipyridamole was 56% 6 15% and 52% 6 15% using the 2 commercial products (P , 0.05 vs. CT), ESV was 36 6 28 and 47 6 35 mL (P 5 not significant vs. CT), and EDV was 75 6 30 and 91 6 33 mL (P , 0.05 vs. CT). Correlations with CT were 0.85 and 0.87 for EF using commercial software, 0.76 and 0.88 for ESV, and 0.60 and 0.68 for EDV (P , 0.01 for all). Bland-Altman analysis confirmed systematic underestimation of EF and EDV by PET versus CT but did not show a significant deviation from linearity. Conclusion: Global LV function can be measured reproducibly from gated 82 Rb PET, using different available software products. However, underestimation of EF by 82 Rb PET, compared with CT ventriculography, is present, which is a result of underestimation of EDV from countpoor ED frames. This underestimation needs to be considered for clinical interpretation of 82 Rb PET.

Understanding the relationship between activity recorded in sympathetic nerves and the action potentials of the axons that contribute to that activity is important for understanding the processing of sympathetic activity by the central nervous system. Because this relationship cannot be determined experimentally and is difficult to predict analytically, we simulated the summed action potentials of 300 axons. This simulation closely resembled actual sympathetic activity and permitted us to know how many action potentials contributed to each burst of simulated sympathetic activity and the durations and amplitudes of each burst. We used these simulated data to examine a statistical method (cluster analysis) that has been used to identify and quantify bursts of sympathetic activity. Simulation indicated that the integrals of bursts, whether determined directly from the simulation or by integrating bursts detected by cluster analysis, were linearly correlated to the number of action potentials contributing to bursts. The variances of samples of the simulated signal were also linearly correlated to the number of action potentials. The amplitudes of bursts of sympathetic activity were less well correlated to the number of underlying action potentials. A linear relationship existed between the average number of action potentials contributing to simulated bursts and the integral of the amplitude spectra obtained by Fourier transform of the simulated activity. Finally, simulated experiments indicated that relatively brief recordings might be sufficient to detect statistically significant changes in sympathetic activity.