Unlabelled: Radiolabeled amino acids are useful for brain tumor diagnosis, but unspecific uptake near the cerebral hematoma may complicate the differentiation of a neoplastic from a nonneoplastic origin of the hematoma. The aim of this study was to investigate the pattern and time course of O-(2-(18)F-fluorethyl)-l-tyrosine ((18)F-FET) and l-(3)H-methionine ((3)H-MET) uptake in rats with cerebral hematomas.
Methods: Intracerebral hematomas were induced in the striatum of 25 Fischer 344 CDF rats by inoculation of bacterial collagenase. (18)F-FET and (3)H-MET were injected intravenously at different times up to 4 wk after bleeding. One hour after tracer injection, brains were cut in coronal sections and evaluated by dual-tracer autoradiography. Lesion-to-brain (L/B) ratios were calculated by dividing maximal uptake near the hematomas and mean uptake in normal brain tissue. An L/B ratio greater than 1.5 was considered as indicative of pathologic uptake. The autoradiograms were compared with histology and immunostainings for astrogliosis (glial fibrillary acidic protein) and macrophage infiltration (CD68).
Results: (18)F-FET exhibited significantly increased uptake near the hematomas between 3 and 14 d after bleeding. The time course of pathologic (3)H-MET uptake was similar, but after 3-4 wk there was still borderline uptake in single animals. The L/B ratios exceeded the cutoff level of 1.5 in 10 of 23 animals for (18)F-FET and in 12 of 22 animals for (3)H-MET but did not exceed a value of 3. Immunostainings indicated that increased uptake of both tracers correlated with reactive astrogliosis, whereas (3)H-MET uptake was additionally increased in areas with macrophage infiltration.
Conclusion: (18)F-FET, like (3)H-MET, may exhibit significantly increased uptake near cerebral hematomas, especially during the first 2 wk after bleeding, complicating the differentiation between a neoplastic and a nonneoplastic origin of cerebral hematomas.
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Aspartate (Asp) metabolism-mediated antioxidant functions have important implications for neonatal growth and intestinal health; however, the antioxidant mechanisms through which Asp regulates the gut microbiota and influences RIP activation remain elusive. This study reports that chronic oxidative stress disrupts gut microbiota and metabolite balance and that such imbalance is intricately tied to the perturbation of Asp metabolism. Under normal conditions, in vivo and in vitro studies reveal that exogenous Asp improves intestinal health by regulating epithelial cell proliferation, nutrient uptake, and apoptosis.
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