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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 721 records · Page 40

Hepatotoxic Dose Thresholds by Positron-Emission Tomography After Yttrium-90 Radioembolization of Liver Tumors: A Prospective Single-Arm Observational Study

PurposeTo define a threshold radiation dose to non-tumoral liver from {sup 90}Y radioembolization that results in hepatic toxicity using pair-production PET.Materials and MethodsThis prospective single-arm study enrolled 35 patients undergoing radioembolization. A total of 34 patients (27 with HCC and 7 with liver metastases) were included in the final analysis. Of 27 patients with underlying cirrhosis, 22 and 5 patients were Child–Pugh A and B, respectively. Glass and resin microspheres were used in 32 (94%) and 2 (6%) patients, respectively. Lobar and segmental treatment was done in 26 (76%) and 8 (24%) patients, respectively. Volumetric analysis was performed on post-radioembolization time-of-flight PET imaging to determine non-tumoral parenchymal dose. Hepatic toxicity was evaluated up to 120 days post-treatment, with CTCAE grade ≤ 1 compared to grade ≥ 2.ResultsThe median dose delivered to the non-tumoral liver in the treated lobe was 49 Gy (range 0–133). A total of 15 patients had grade ≤ 1 hepatic toxicity, and 19 patients had grade ≥ 2 toxicity. Patients with a grade ≥ 2 change in composite toxicity (70.7 vs. 43.8 Gy), bilirubin (74.1 vs. 43.3 Gy), albumin (84.2 vs. 43.8 Gy), and AST (94.5 vs. 47.1 Gy) have significantly higher non-tumoral parenchymal doses than those with grade ≤ 1. Liver parenchymal dose and Child–Pugh status predicted grade ≥ 2 toxicity, observed above a dose threshold of 54 Gy.ConclusionIncreasing delivered {sup 90}Y dose to non-tumoral liver measured by internal pair-production PET correlates with post-treatment hepatic toxicity. The likelihood of toxicity exceeds 50% at a dose threshold of 54 Gy.ClinicalTrials.gov identifier: NCT02848638.

62 RADIOLOGY AND NUCLEAR MEDICINE↗

Early risk stratification using Rubidium-82 positron emission tomography in STEMI patients

Background: Assessment of infarct size after myocardial infarction is predictive of subsequent morphological changes and clinical outcome. This study aimed to assess subacute post-intervention Rubidium-82 ({sup 82}Rb)-PET imaging in predicting left ventricle ejection fraction, regional wall motion, and final infarct size by CMR at 3-months after STEMI. Methods: STEMI patients undergoing percutaneous coronary intervention were included prospectively. Rest-only {sup 82}Rb-PET perfusion imaging was performed at median 36 hours [IQR: 22 to 50] after the treatment. The extent of hypoperfusion and absolute blood flow (mL·min·g) were estimated on a global and a 17-segment model with dedicated software. At 3-months follow-up patients completed the CMR functional and late gadolinium enhancement imaging. Results: 42 patients were included, but only 35 had follow-up CMR and constituted the study population. Absolute blood flow was significantly lower in the infarct-related territory compared to remote myocardium, P < .005. Extent of hypoperfusion correlated with final infarct size, r = 0.58, P < .001, while blood flow correlated with ejection fraction, r = 0.41, P < .05. In linear mixed models, higher subacute absolute blood flow (β = 4.6, confidence interval [3.5; 5.2], P < .001, R{sup 2} = 0.67) was associated with greater wall motion. Segmental extent of subacute hypoperfusion (β = 0.43 [0.38; 0.49], P < .001, R{sup 2} = 0.58) was associated with the degree of late gadolinium enhancement at 3-months. Conclusions: Subacute rest-only {sup 82}Rb-PET is feasible following STEMI and seems predictive of myocardial function and infarct size at 3-months.

62 RADIOLOGY AND NUCLEAR MEDICINE↗

Positron Emission Tomography Imaging of Functional Transforming Growth Factor β (TGFβ) Activity and Benefit of TGFβ Inhibition in Irradiated Intracranial Tumors

Transforming growth factor β (TGFβ) promotes cell survival by endorsing DNA damage repair and mediates an immunosuppressive tumor microenvironment. Thus, TGFβ activation in response to radiation therapy is potentially targetable because it opposes therapeutic control. Strategies to assess this potential in the clinic are needed.

62 RADIOLOGY AND NUCLEAR MEDICINE↗