Naphthenic acid removal from bitumen-derived HVGO by thermal cracking and catalytic decarboxylation was investigated. With MgO and ZnO, naphthenic acid removal proceeds mainly via catalytic ...decarboxylation. With CaO, multiple pathways were responsible for naphthenic acid conversion. With BaO, naphthenic acid conversion is mainly through neutralization. All BaO is converted to Ba(OH)
2 during the reaction.
Naphthenic acid removal from bitumen-derived HVGO by thermal cracking and catalytic decarboxylation was investigated over alkaline earth-metal oxides and ZnO catalysts in a batch reactor and a continuous fixed-bed reactor. The fresh and spent catalysts were characterized by XRD, TG-DTA, CO
2-TPD, and SEM. With MgO and ZnO, naphthenic acid removal proceeds mainly via catalytic decarboxylation, and no crystalline phase changes are observed after reaction. With CaO, multiple pathways (catalytic decarboxylation, neutralization, and thermal cracking) were responsible for naphthenic acid conversion. Ca(OH)
2 and CaCO
3 were identified in the spent catalysts. With BaO, naphthenic acid conversion is mainly through neutralization. All BaO is converted to Ba(OH)
2 during the reaction.
To evaluate the effect of disease sites and prior therapy on response and toxicity after iodine-131-metaiodobenzylguanidine (131I-MIBG) treatment of patients with resistant neuroblastoma.
One hundred ...sixty-four patients with progressive, refractory or relapsed high-risk neuroblastoma, age 2 to 30 years, were treated in a limited institution phase II study. Patients with cryopreserved hematopoietic stem cells (n = 148) were treated with 18 mCi/kg of 131I-MIBG. Those without hematopoietic stem cells (n = 16) received 12 mCi/kg. Patients were stratified according to prior myeloablative therapy and whether they had measurable soft tissue involvement or only bone and/or bone marrow disease.
Hematologic toxicity was common, with 33% of patients receiving autologous hematopoietic stem cell support. Nonhematologic grade 3 or 4 toxicity was rare, with 5% of patients experiencing hepatic, 3.6% pulmonary, 10.9% infectious toxicity, and 9.7% with febrile neutropenia. The overall complete plus partial response rate was 36%. The response rate was significantly higher for patients with disease limited either to bone and bone marrow, or to soft tissue (compared with patients with both) for patients with fewer than three prior treatment regimens and for patients older than 12 years. The event-free survival (EFS) and overall survival (OS) times were significantly longer for patients achieving response, for those older than 12 years and with fewer than three prior treatment regimens. The OS was 49% at 1 year and 29% at 2 years; EFS was 18% at 1 year.
The high response rate and low nonhematologic toxicity with 131I-MIBG suggest incorporation of this agent into initial multimodal therapy of neuroblastoma.
This review provides a general overview of microwave applications in oil sands bitumen or shale oil production in petroleum upgrading. The vast oil reserves in the oil sands of Alberta will become a ...major source of petroleum products in the near future and a number of alternative technologies have been explored for the production and upgrading of oil sands and heavy oil. This study is based primarily on the unique selective heating capacity associated with exposure of materials to microwaves. Of particular interest are applications of microwaves for bitumen extraction, upgrading heavy oils, removing heteroatoms, and the underground heating of oil sands to reduce bitumen viscosity and allow it to be pumped to the surface. The fundamentally different method of transferring energy from the source to the sample is the main advantage of utilizing microwave energy. By directly delivering energy to microwave-absorbing materials, conventional issues such as long heating periods and energy loses can be minimized. Microwave energy was shown to be effective in some applications; however, it is not used commercially at the present time.
To evaluate the safety and efficacy of high-dose (131)Imetaiodobenzylguanidine ((131)IMIBG) in the treatment of malignant pheochromocytoma (PHEO) and paraganglioma (PGL).
Fifty patients with ...metastatic PHEO or PGL, age 10 to 64 years, were treated with (131)IMIBG doses ranging from 492 to 1,160 mCi (median, 12 mCi/kg). Cumulative (131)IMIBG administered ranged from 492 to 3,191 mCi. Autologous hematopoietic stem cells were collected and cryopreserved before treatment with (131)IMIBG greater than 12 mCi/kg or with a total dose greater than 500 mCi. Sixty-nine (131)IMIBG infusions were given, which included infusions to 35 patients treated once and infusions to 15 patients who received two or three treatments. Response was evaluated by (123)IMIBG scans, computed tomography/magnetic resonance imaging, urinary catecholamines/metanephrines, and chromogranin A.
The overall complete response (CR) plus partial response (PR) rate in 49 evaluable patients was 22%. Additionally, 35% of patients achieved a CR or PR in at least one measure of response without progressive disease, and 8% of patients maintained stable disease for greater than 12 months. Thirty-five percent of patients experienced progressive disease within 1 year after therapy. The estimated 5-year overall survival rate was 64%. Toxicities included grades 3 to 4 neutropenia (87%) and thrombocytopenia (83%). Grades 3 to 4 nonhematologic toxicity included acute respiratory distress syndrome (n = 2), bronchiolitis obliterans organizing pneumonia (n = 2), pulmonary embolism (n = 1), fever with neutropenia (n = 7), acute hypertension (n = 10), infection (n = 2), myelodysplastic syndrome (n = 2), and hypogonadism (n = 4).
Although serious toxicity may occur, the survival and response rates achieved with high-dose (131)IMIBG suggest its utility in the management of selected patients with metastatic PHEO and PGL.
Iodine-131-metaiodobenzylguanidine ((131)I-MIBG) provides targeted radiotherapy with more than 30% response rate in refractory neuroblastoma, but activity infused is limited by radiation safety and ...hematologic toxicity. The goal was to determine the maximum-tolerated dose of (131)I-MIBG in two consecutive infusions at a 2-week interval, supported by autologous stem-cell rescue (ASCR) 2 weeks after the second dose.
The (131)I-MIBG dose was escalated using a 3 + 3 phase I trial design, with levels calculated by cumulative red marrow radiation index (RMI) from both infusions. Using dosimetry, the second infusion was adjusted to achieve the target RMI, except at level 4, where the second infusion was capped at 21 mCi/kg.
Twenty-one patients were enrolled onto the study at levels 1 to 4, with 18 patients assessable for toxicity and 20 patients assessable for response. Cumulative (131)I-MIBG given to achieve the target RMI ranged from 22 to 50 mCi/kg, with cumulative RMI of 3.2 to 8.92 Gy. No patient had a dose-limiting toxicity. Reversible grade 3 nonhematologic toxicity occurred in six patients at level 4, establishing the recommended cumulative dose as 36 mCi/kg. The median time to absolute neutrophil count more than 500/microL after ASCR was 13 days (4 to 27 days) and to platelet independence was 17 days (6 to 47 days). Responses included two partial responses, eight mixed responses, three stable disease, and seven progressive disease. Responses by semiquantitative MIBG score occurred in eight patients, soft tissue responses occurred in five of 11 patients, but bone marrow responses occurred in only two of 13 patients.
The lack of toxicity with this approach allowed dramatic dose intensification of (131)I-MIBG, with minimal toxicity and promising activity.
The metaiodobenzylguanidine (MIBG) scan is one of the most sensitive noninvasive lesion detection modalities for neuroblastoma. Unlike
I-MIBG,
I-MIBG allows high-resolution PET. We evaluated
I-MIBG ...PET/CT for its diagnostic performance as directly compared with paired
I-MIBG scans.
Before
I-MIBG therapy, standard
I-MIBG imaging (5.2 MBq/kg) was performed on 7 patients, including whole-body (anterior-posterior) planar imaging, focused-field-of-view SPECT/CT, and whole-body
I-MIBG PET/CT (1.05 MBq/kg). After therapy, 2 of 7 patients also completed
I-MIBG PET/CT as well as paired
I-MIBG planar imaging and SPECT/CT. One patient underwent
I-MIBG PET/CT only after therapy. We evaluated all 8 patients who showed at least 1
I-MIBG-positive lesion with a total of 10 scans. In 8 pairs,
I-MIBG and
I-MIBG were performed within 1 mo of each other. The locations of identified lesions, the number of total lesions, and the curie scores were recorded for the
I-MIBG and
I-MIBG scans. Finally, for 5 patients who completed at least 3 PET/CT scans after administration of
I-MIBG, we estimated the effective dose of
I-MIBG.
I-MIBG whole-body planar scans, focused-field-of-view SPECT/CT scans, and whole-body
I-MIBG PET scans found 25, 32, and 87 total lesions, respectively. There was a statistically significant difference in lesion detection for
I-MIBG PET/CT versus
I-MIBG planar imaging (
< 0.0001) and
I-MIBG SPECT/CT (
< 0.0001). The curie scores were also higher for
I-MIBG PET/CT than for
I-MIBG planar imaging and SPECT/CT in 6 of 10 patients.
I-MIBG PET/CT demonstrated better detection of lesions throughout the body, including the chest, spine, head and neck, and extremities. The effective dose estimated for patient-specific
I-MIBG was approximately 10 times that of
I-MIBG; however, given that we administered a very low activity of
I-MIBG (1.05 MBq/kg), the effective dose was only approximately twice that of
I-MIBG despite the large difference in half-lives (100 vs. 13.2 h).
The first-in-humans use of low-dose
I-MIBG PET for monitoring disease burden demonstrated tumor detection capability superior to that of
I-MIBG planar imaging and SPECT/CT.
Objective
The objective of this report is to compare computed tomography (CT) and magnetic resonance (MR) myelography with radioisotope cisternography (RC) for detection of spinal cerebrospinal (CSF) ...leaks.
Methods
We retrospectively reviewed 12 spontaneous intracranial hypotension (SIH) patients; CT and RC were performed simultaneously. Three patients had MR myelography.
Results
CT and/or MR myelography identified CSF leaks in four of 12 patients. RC detected spinal leaks in all three patients confirmed by CT myelography; RC identified the CSF leak location in two of three cases, and these were due to osteophytic spicules and/or discs. RC showed only enlarged perineural activity. Only intrathecal gadolinium MR myelography clearly identified a slow leak from a perineural cyst. In eight remaining cases, the leak site was unknown; however, two of these showed indirect signs of CSF leak on RC. CSF slow leaks from perineural cysts were the most common presumed etiology; and the cysts were best visualized on myelography.
Conclusion
RC is comparable to CT myelography but has spatial limitations and should be limited to atypical cases.
Purpose
Newer high-performance time-of-flight (TOF) positron emission tomography (PET) systems have the capability to preserve diagnostic image quality with low count density, while maintaining a ...high raw photon detection sensitivity that would allow for a reduction in injected dose or rapid data acquisition. To assess this, we performed quantitative and visual assessments of the PET images acquired using a highly sensitive (23.3 cps/kBq) large field of view (25-cm axial) silicon photomultiplier (SiPM)-based TOF PET (400-ps timing resolution) integrated with 3 T-MRI in comparison to PET images acquired on non-TOF PET/x-ray computed tomography (CT) systems.
Procedures
Whole-body 2-deoxy-2-
18
Ffluoro-D-glucose (
18
FFDG) PET/CT was acquired for 15 patients followed by whole body PET/magnetic resonance imaging (MRI) with an average injected dose of 325 ± 84 MBq. The PET list mode data from PET/MRI were reconstructed using full datasets (4 min/bed) and reduced datasets (2, 1, 0.5, and 0.25 min/bed). Qualitative assessment between PET/CT and PET/MR images were made. A Likert-type scale between 1 and 5, 1 for non-diagnostic, 3 equivalent to PET/CT, and 5 superior quality, was used. Maximum and mean standardized uptake values (SUV
max
and SUV
mean
) of normal tissues and lesions detected were measured and compared.
Results
Mean visual assessment scores were 3.54 ± 0.32, 3.62 ± 0.38, and 3.69 ± 0.35 for the brain and 3.05 ± 0.49, 3.71 ± 0.45, and 4.14 ± 0.44 for the whole-body maximum intensity projections (MIPs) for 1, 2, and 4 min/bed PET/MR images, respectively. The SUV
mean
values for normal tissues were lower and statistically significant for images acquired at 4, 2, 1, 0.5, and 0.25 min/bed on the PET/MR, with values of – 18 ± 28 % (
p
< 0.001), − 16 ± 29 % (
p
= 0.001), − 16 ± 31 % (
p
= 0.002), − 14 ± 35 % (
p
< 0.001), and − 13 ± 34 % (
p
= 0.002), respectively. SUV
max
and SUV
peak
values of all lesions were higher and statistically significant (
p
< 0.05) for 4, 2, 1, 0.50, and 0.25 min/bed PET/MR datasets.
Conclusion
High-sensitivity TOF PET showed comparable but still better visual image quality even at a much reduced activity in comparison to lower-sensitivity non-TOF PET. Our data translates to a seven times reduction in either injection dose for the same time or total scan time for the same injected dose. This “ultra-sensitivity” PET system provides a path to clinically acceptable extremely low-dose FDG PET studies (e.g., sub 1 mCi injection or sub-mSv effective dose) or PET studies as short as 1 min/bed (e.g
.
, 6 min of total scan time) to cover whole body without compromising diagnostic performance.
Background:
Evolving immune-mediated therapeutic strategies for rheumatoid arthritis (RA) may benefit from an improved understanding of the complex role that T-cell activation plays in RA. This study ...assessed the potential of fluorine-18-labeled 9-β-d-arabinofuranosylguanine (18FF-AraG) positron emission tomography (PET) imaging to report immune activation in vivo in an adjuvant-induced arthritis (AIA) small animal model.
Methods:
Using positron emission tomography–computed tomography imaging, uptake of 18FF-AraG in the paws of mice affected by arthritis at 6 (acute) and 20 (chronic) days following AIA induction in a single paw was assessed and compared to uptake in contralateral control paws. Fractions of T cells and B cells demonstrating markers of activation at the 2 time points were determined by flow cytometry.
Results:
Differential uptake of 18FF-AraG was demonstrated on imaging of the affected joint when compared to control at both acute and chronic time points with corresponding changes in markers of T-cell activation observed on flow cytometry.
Conclusion:
18FF-AraG may serve as an imaging biomarker of T-cell activation in inflammatory arthritis. Further development of this technique is warranted and could offer a tool to explore the temporal link between activated T cells and RA as well as to monitor immune-mediated therapies for RA in clinical trials.
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