{ "labelLang" : "hun", "responseDate" : "2024-03-29 02:07", "content" : { "otype" : "JournalArticle", "mtid" : 3371867, "status" : "VALIDATED", "published" : true, "comment" : "CROmed Translational Research Centers, Budapest, H-1047, Hungary \n Department of Biophysics and Radiation Biology, Semmelweis Univ, Budapest, H-1094, Hungary \n Laboratory of Neuroimmunology, Institute of Experimental Medicine, Budapest, Hungary \n Helmholz-Zentrum Dresden-Rossendorf, Radiopharmazie Radiopharmaceutische Biologie, Dresden, Germany \n Nuclear Physics Institute of the CAS, Rez, CZ 250 68, Czech Republic \n Biological Nanochemistry Research Group, Institute of Materials and Environmental Chemistry, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary \n Progressio Fine Chemical Engineering Ltd, Székesfehérvár, Hungary \n Cited By :9 \n Export Date: 2 March 2022 \n CODEN: CPIMF \n Correspondence Address: Szigeti, K.; Department of Biophysics and Radiation Biology, Hungary; email: szigeti.krisztian@med.semmelweis-univ.hu \n Chemicals/CAS: fluorodeoxyglucose f 18, 63503-12-8; glutathione, 70-18-8; protein tyrosine phosphatase; receptor type tyrosine protein phosphatase C; glucose, 50-99-7, 84778-64-3; Fluorodeoxyglucose F18; Glucose; Iodine Radioisotopes; Iodine-125; Lipopolysaccharides; Radioactive Tracers; Technetium Tc 99m Exametazime \n Funding details: HEALTH.2011.2.2.1-2 \n Funding details: Seventh Framework Programme, FP7, 278850 \n Funding details: Seventh Framework Programme, FP7, VKSZ-14-1-2005-0151 \n Funding text 1: This work was funded in part by INMiND (HEALTH.2011.2.2.1-2 No.278850) of FP7 and by VKSZ-14-1-2005-0151. We thank Mediso Ltd. for technical background of NanoSPECT/CT Plus and nanoScan PET/MRI. K Szigeti was supported by the Janos Bolyai Research Fellowship program of the Hungarian Academy of Science. The authors declare that they have no conflict of interest. \n Funding text 2: Acknowledgements. This work was funded in part by INMiND (HEALTH.2011.2.2.1-2 No.278850) of FP7 and by VKSZ-14-1-2005-0151. We thank Mediso Ltd. for technical background of NanoSPECT/CT Plus and nanoScan PET/MRI. 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model of sepsis-associated encephalopathy (SAE). The lipopolysaccharide (LPS)-induced murine systemic inflammation model was selected as a model of SAE. PROCEDURES: C57BL/6 mice were used. A multimodal imaging protocol was carried out on each animal 4 h following the intravenous administration of LPS using the following tracers: [(99m)Tc][2,2-dimethyl-3-[(3E)-3-oxidoiminobutan-2-yl]azanidylpropyl]-[(3E)-3-hyd roxyiminobutan-2-yl]azanide ([(99m)Tc]HMPAO) and ethyl-7-[(125)I]iodo-5-methyl-6-oxo-4H-imidazo[1,5-a][1,4]benzodiazepine-3-carbox ylate ([(125)I]iomazenil) to measure brain perfusion and neuronal damage, respectively; 2-deoxy-2-[(18)F]fluoro-D-glucose ([(18)F]FDG) to measure cerebral glucose uptake. We assessed microglia activity on another group of mice using 2-[6-chloro-2-(4-[(125)I]iodophenyl)-imidazo[1,2-a]pyridin-3-yl]-N-ethyl-N-methyl -acetamide ([(125)I]CLINME). Radiotracer uptakes were measured in different brain regions and correlated. Microglia activity was also assessed using immunohistochemistry. Brain glutathione levels were measured to investigate oxidative stress. RESULTS: Significantly reduced perfusion values and significantly enhanced [(18)F]FDG and [(125)I]CLINME uptake was measured in the LPS-treated group. Following perfusion compensation, enhanced [(125)I]iomazenil uptake was measured in the LPS-treated group's hippocampus and cerebellum. In this group, both [(18)F]FDG and [(125)I]iomazenil uptake showed highly negative correlation to perfusion measured with ([(99m)Tc]HMPAO uptake in all brain regions. No significant differences were detected in brain glutathione levels between the groups. The CD45 and P2Y12 double-labeling immunohistochemistry showed widespread microglia activation in the LPS-treated group. CONCLUSIONS: Our results suggest that [(125)I]CLINME and [(99m)Tc]HMPAO SPECT can be used to detect microglia activation and brain hypoperfusion, respectively, in the early phase (4 h post injection) of systemic inflammation. We suspect that the enhancement of [(18)F]FDG and [(125)I]iomazenil uptake in the LPS-treated group does not necessarily reflect neural hypermetabolism and the lack of neuronal damage. 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