T1 - Implications of ambient glucose variation on the target-to-background ratio of hepatic tumors by 18FDG-PET imaging Therefore, correction by the glucose sensitivity factor will result in more accurate SUV measurements and make semi-quantitative analysis of 18FDG PET scans more reliable.', Conclusion: The tumor FDG uptake is much more sensitive to ambient glucose level variation than the background liver. Simulation studies showed that the SUV in malignant lesions will decrease rapidly when Glc level is >120 mg/dl, while background liver remains relatively constant up to 250 mg/dl. Results: By logarithmic transformation and linear regression, g for metastasis was significantly higher than that for normal liver (-0.636 ± 0.144 vs.-0.0536 ± 0.0583 P = 0.00092). Simulations using glucose level from 70 to 250 mg/dl were performed to evaluate the effects of Glc on the maximum SUV of malignant hepatic lesions and normal liver. The inverse relationship of SUV to glucose can be defined as d (SUV)/d (Glc) = gFNx01SUV/(Glc), where g is the glucose sensitivity. The serum glucose level (Glc) was recorded prior to imaging, and the maximum standardized uptake value (SUV) in the hepatic tumors and the average SUV in normal liver were determined. Patients and Methods: Eighty-six patients with hepatic lesions identified on 18FDG PET/computed tomography (CT) were analyzed. Therefore, correction by the glucose sensitivity factor will result in more accurate SUV measurements and make semi-quantitative analysis of 18FDG PET scans more reliable.Ībstract = 'Objectives: To investigate the effects of ambient glucose on quantitative analysis of hepatic tumors on 2-deoxy-2-(18F)-fluoro-D-glucose (18FDG) positron emission tomography (PET) and to establish a method for glucose correction. All rights reserved.Objectives: To investigate the effects of ambient glucose on quantitative analysis of hepatic tumors on 2-deoxy-2-( 18F)-fluoro-D-glucose ( 18FDG) positron emission tomography (PET) and to establish a method for glucose correction. These compounds may be candidates for treatment of spinal-cord injury and neurodegeneration.Ĭopyright © 2011 Elsevier Inc. Co-incubation of PC12 cells in H(2)O(2), and ACM collected from AP1 treated astrocytes did not prevent cell death.ĪP1 and AP2 effectively ameliorated astrocytic pro-inflammatory reactions and prevented PC12 cell death with different efficacies. AP1 protected H(2)O(2)-treated PC12 cells cultured in ACM. Astrocyte-conditioned medium (ACM) and TNF-α-stimulated astrocyte-conditioned medium (SACM) were used to assess the effects of AP2 on PC12 cells treated with H(2)O(2).ĪP1 and AP2 reduced pro-inflammatory cytokines, reactive oxygen species (ROS), and CSPG in TNF-α stimulated astrocytes. Reduction of H(2)O(2)-induced death was tested in PC12 cells. The reduction of chondroitin sulfate proteoglycan (CSPG) in stimulated astrocytes was tested using the dot blot method. In addition, the abilities of AP1 and AP2 to reduce oxidative stress in astrocytes were tested using an oxidative-sensitive fluorescent dye. The abilities of AP1 and AP2 to reduce the secretion of pro-inflammatory cytokines Interleukin (IL)-1, IL-6, and Tumor necrosis factor (TNF)-α from stimulated astrocytes were tested. To test the effects of andrographolide (AP1) and 14-deoxy-11,12-didehydroandrographolide (AP2) on pheochromocytoma cell line 12 (PC12) cells in an astrocyte-rich environment.

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