2-((1E,3E)-4-(6-( 11 C-methylamino)pyridin-3-yl)buta-1,3-dienyl) benzo [d]thiazol-6-ol ( 11 C-PBB3) is a clinically useful PET probe that we developed for in vivo imaging of tau pathology in the human brain. To ensure the availability of this probe among multiple PET facilities, in the present study we established protocols for the radiosynthesis and quality control of 11 C-PBB3 and for the characterization of its photoisomerization, biodistribution, and metabolism. Methods: 11 C-PBB3 was synthesized by reaction of the tert-butyldimethylsilyl desmethyl precursor (1) with 11 C-methyl iodide using potassium hydroxide as a base, followed by deprotection. Photoisomerization of 11 C-PBB3 under fluorescent light was determined. The biodistribution and metabolite analysis of 11 C-PBB3 was determined in mice using the dissection method. Results: 11 C-PBB3 was synthesized with 15.4% ± 2.8% radiochemical yield (decay-corrected, n 5 50) based on the cyclotron-produced 11 C-CO 2 and showed an averaged synthesis time of 35 min from the end of bombardment. The radiochemical purity and specific activity of 11 C-PBB3 were 98.0% ± 2.3% and 180.2 ± 44.3 GBq/μmol, respectively, at the end of synthesis (n 5 50). 11 C-PBB3 showed rapid photoisomerization, and its radiochemical purity decreased to approximately 50% at 10 min after exposure to fluorescent light. After the fluorescent light was switched off, 11 C-PBB3 retained more than 95% radiochemical purity over 60 min. A suitable brain uptake (1.92% injected dose/g tissue) of radioactivity was observed at 1 min after the probe injection, which was followed by rapid washout from the brain tissue. More than 70% of total radioactivity in the mouse brain homogenate at 5 min after injection represented the unchanged 11 C-PBB3, despite its rapid metabolism in the plasma. Conclusion: 11 C-PBB3 was produced with sufficient radioactivity and high quality, demonstrating its clinical utility. The present results of radiosynthesis, photoisomerization, biodistribution, and metabolite analysis could be helpful for the reliable production and application of 11 C-PBB3 in diverse PET facilities.

Background: Helicobacter pylori ( H. pylori ) is the major cause of chronic active gastritis and peptic ulcer disease. Recent studies have shown that H. pylori produces various cytokines that are related to neutrophil or mononuclear cell accumulation. Interleukin-17 (IL-17) is the founding member of an emerging family of inflammatory cytokines whose biological activities remain incompletely defined. In this study, the contributions of IL-17 to the induction of gastric inflammation and to the protection from H. pylori infection were investigated using IL-17 gene-knockout

H. pylori infection induces IL-18 in the gastric mucosa. H. pylori-infected patients with IL18 -607C/C and -137G/G have higher IL-18 levels, which causes severe gastric inflammation. IL18 genotype might be a marker for predicting the effects of eradication therapy.

Parkinson's disease (PD) is a prevalent degenerative disorder affecting the CNS that is primarily characterized by resting tremor and movement deficits. Group I metabotropic glutamate receptor subtypes 1 and 5 (mGluR1 and mGluR5, respectively) are important targets for investigation in several CNS disorders. In the present study, we investigated the in vivo roles of mGluR1 and mGluR5 in chronic PD pathology by performing longitudinal positron emission tomography (PET) imaging in A53T transgenic (A53T-Tg) rats expressing an abnormal human ␣-synuclein (

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