Evaluation of Data-Driven Respiration Gating in Continuous Bed Motion in Lung Lesions.

Respiration gating is used in PET to prevent image quality degradation due to respiratory effects. In this study, we evaluated a type of data-driven respiration gating for continuous bed motion, OncoFreeze AI, which was implemented to improve image quality and the accuracy of semiquantitative uptake values affected by respiratory motion. Methods: 18F-FDG PET/CT was performed on 32 patients with lung lesions. Two types of respiration-gated images (OncoFreeze AI with data-driven respiration gating, device-based amplitude-based OncoFreeze with elastic motion compensation) and ungated images (static) were reconstructed. For each image, we calculated SUV and metabolic tumor volume (MTV). The improvement rate (IR) from respiration gating and the contrast-to-noise ratio (CNR), which indicates the improvement in image noise, were also calculated for these indices. IR was also calculated for the upper and lower lobes of the lung. As OncoFreeze AI assumes the presence of respiratory motion, we examined quantitative accuracy in regions where respiratory motion was not present using a 68Ge cylinder phantom with known quantitative accuracy. Results: OncoFreeze and OncoFreeze AI showed similar values, with a significant increase in SUV and decrease in MTV compared with static reconstruction. OncoFreeze and OncoFreeze AI also showed similar values for IR and CNR. OncoFreeze AI increased SUVmax by an average of 18% and decreased MTV by an average of 25% compared with static reconstruction. From the IR results, both OncoFreeze and OncoFreeze AI showed a greater IR from static reconstruction in the lower lobe than in the upper lobe. OncoFreeze and OncoFreeze AI increased CNR by 17.9% and 18.0%, respectively, compared with static reconstruction. The quantitative accuracy of the 68Ge phantom, assuming a region of no respiratory motion, was almost equal for the static reconstruction and OncoFreeze AI. Conclusion: OncoFreeze AI improved the influence of respiratory motion in the assessment of lung lesion uptake to a level comparable to that of the previously launched OncoFreeze. OncoFreeze AI provides more accurate imaging with significantly larger SUVs and smaller MTVs than static reconstruction.

Achievements of true whole-body imaging using a faster acquisition of the lower extremities in variable-speed continuous bed motion.

Variable-speed continuous bed motion 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT), a reliable imaging technique, allows setting the bed motion speed for arbitrary sections of the body. The purpose of this study was to evaluate the relationship between the PET image quality and the bed speed following shortening of the scanning time for the lower extremities to achieve whole-body acquisition optimization of the examination time. Four sets of images were created by editing four-phase dynamic whole-body PET/CT images acquired at a bed speed of 6 and 14 mm/s in the trunk and lower extremities, respectively. The signal-to-noise ratio (SNR) was calculated using regions of interest in the liver, gluteus muscles, thigh, and lower legs, and the relationship between the bed speed and the SNR was assessed. The number of patients with findings in the lower extremities among 967 cases was evaluated. Based on this relationship between the SNR and bed motion speed, it is reasonable to increase the speed of the lower extremities by up to three times that of the trunk. The findings from whole-body FDG-PET imaging revealed that the number of patients with detected lesions in the lower extremities was 6.6% (64/967), bone metastases were found in 2.6%, soft lesions in 1.8%, and inflammation in 2.3%. Images of the lower extremities, which have a better SNR than the trunk, can be acquired at a faster bed speed using the variable-speed continuous bed motion PET.

Comparison between dynamic whole-body FDG-PET and early-delayed imaging for the assessment of motion in focal uptake in colorectal area.

OBJECTIVES: Serial changes of focal uptake in whole-body dynamic positron emission tomography (PET) imaging were assessed and compared with those in early-delayed imaging to differentiate pathological uptake from physiological uptake in the colorectal area, based on the change in uptake shape. METHODS: In 60 patients with at least 1 pathologically diagnosed colorectal cancer or adenoma, a serial 3 min dynamic whole-body PET/computed tomography imaging was performed four times around 60 min after the administration of 18F-fluorodeoxyglucose (FDG) to create a conventional (early) image by summation. Delayed imaging was performed separately at 110 min after FDG administration. High focal uptake lesions in the colorectal area were visually assessed as "changed" or "unchanged" on serial dynamic imaging and early-delayed imaging, based on the alteration in uptake shape over time. These criteria on the images were used to differentiate pathological uptake from physiological uptake. RESULTS: In this study, 334 lesions with high focal FDG uptake were observed. Among 73 histologically proven pathological FDG uptakes, no change was observed in 69 on serial dynamic imaging and 72 on early-delayed imaging (sensitivity of 95 vs. 99%, respectively; ns). In contrast, out of 261 physiological FDG uptakes, a change in uptake shape was seen in 159 on dynamic PET imaging and 66 on early-delayed imaging (specificity of 61 vs. 25%, respectively; p < 0.01). High and similar negative predictive values for identifying pathological uptake were obtained by both methods (98 vs 99%, respectively). Thus, the overall accuracy for differentiating pathological from physiological FDG uptake based on change in uptake shape tended to be higher on serial dynamic imaging (68%) than on early-delayed imaging (41%; p < 0.01). CONCLUSIONS: Dynamic whole-body FDG imaging enables differentiation of pathological uptake from physiological uptake based on the serial changes in uptake shape in the colorectal area. It may provide greater diagnostic value than early-delayed PET imaging. Thus, this technique holds a promise for minimizing the need for delayed imaging.

Hydrogen sulfide induces Ca2+ release from intracellular Ca2+ stores and stimulates lactate production in spinal cord astrocytes.

Hydrogen sulfide (H2S) is a well-known inhibitor of the mitochondrial electron transport chain (ETC). H2S also increases intracellular Ca2+ levels in astrocytes, which are glial cells and that supply lactate as an energy substrate to neurons. Here, we examined the relationship between H2S-induced metabolic changes and Ca2+ responses in spinal cord astrocytes. Na2S (150 µM), an H2S donor, increased the intracellular Ca2+ concentration, which was inhibited by an ETC inhibitor and an uncoupler of mitochondrial oxidative phosphorylation. Na2S also increased the accumulation of extracellular lactate. Na2S alone did not change intracellular ATP content, but decreased it when glycolysis was inhibited. The Na2S-induced Ca2+ increase and accumulation of extracellular lactate were inhibited by emetine, an inhibitor of translocon complex, which mediates Ca2+ leak from the endoplasmic reticulum (ER). Furthermore, an inhibitor of the Ca2+-sensitive NADH shuttle decreased Na2S-mediated accumulation of lactate. We conclude that inhibition of the mitochondrial ETC by H2S induces Ca2+ release from mitochondria and the ER in spinal cord astrocytes, which increases lactate production. H2S may promote glycolysis by activating the Ca2+-sensitive NADH shuttle and facilitating the supply of lactate from astrocytes to neurons.

Hydrogen sulfide induces Ca2+ release from the endoplasmic reticulum and suppresses ATP-induced Ca2+ signaling in rat spinal cord astrocytes.

Hydrogen sulfide (H2S) has a variety of physiological functions. H2S reportedly increases intracellular Ca2+ concentration ([Ca2+]i) in astrocytes. However, the precise mechanism and functional role of this increase are not known. Here, we examined the effects of H2S on [Ca2+]i in astrocytes from the rat spinal cord and whether H2S affects ATP-induced Ca2+ signaling, which is known to be involved in synaptic function. Na2S (150 µM), an H2S donor, produced a nontoxic increase in [Ca2+]i. The [Ca2+]i increase by Na2S was inhibited by Ca2+ depletion in the endoplasmic reticulum (ER) but not by removal of extracellular Ca2+, indicating that H2S releases Ca2+ from the ER. On the other hand, Na2S inhibited ATP-induced [Ca2+]i increase when Na2S clearly increased [Ca2+]i in the astrocytes, which was not suppressed by a reducing agent. In addition, Na2S had no effect on intracellular cyclic AMP (cAMP) level. These results indicate that oxidative post-translational modification of proteins and cAMP are not involved in the inhibitory effect of H2S on ATP-induced Ca2+ signaling. We conclude that H2S indirectly inhibits ATP-induced Ca2+ signaling by decreasing Ca2+ content in the ER in astrocytes. In this way, H2S may influence intercellular communication between astrocytes and neurons, thereby contributing to neuronal signaling in the nervous system.