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• Gut microbiota contributes to the cognitive deficits induced by chronic T. gondii infection. • Gut microbiota is a vital player in the impairment of synaptic ultrastructure and cognitive function induced by T. gondii infection. • T. gondii chronic infection induces significant depletion of butyrate-producing bacterial species and decrease of serum butyrate levels. • Dietary butyrate supplementation significantly prevents cognitive decline induced by T. gondii infection. • Manipulation of gut microbiota may represent a promising prophylactic strategy against T. gondii -associated neurodegerative diseases. • Butyrate is a potential metabolite for treating T. gondii -mediated cognitive impairment. Chronic infection with Toxoplasma gondii (T. gondii) emerges as a risk factor for neurodegenerative diseases in animals and humans. However, the underlying mechanisms are largely unknown. We aimed to investigate whether gut microbiota and its metabolites play a role in T. gondii -induced cognitive deficits. We found that T. gondii infection induced cognitive deficits in mice, which was characterized by synaptic ultrastructure impairment and neuroinflammation in the hippocampus. Moreover, the infection led to gut microbiota dysbiosis, barrier integrity impairment, and inflammation in the colon. Interestingly, broad-spectrum antibiotic ablation of gut microbiota attenuated the adverse effects of the parasitic infection on the cognitive function in mice; cognitive deficits and hippocampal pathological changes were transferred from the infected mice to control mice by fecal microbiota transplantation. In addition, the abundance of butyrate-producing bacteria and the production of serum butyrate were decreased in infected mice. Interestingly, dietary supplementation of butyrate ameliorated T. gondii -induced cognitive impairment in mice. Notably, compared to the healthy controls, decreased butyrate production was observed in the serum of human subjects with high levels of anti- T. gondii IgG. Overall, this study demonstrates that gut microbiota is a key regulator of T. gondii -induced cognitive impairment. [ABSTRACT FROM AUTHOR]

In this work, a direct determination of 238Pu determination using reactive gases, CO2 and H2 in triple quadrupole ICP-MS without prior radiochemical separation resins has been established. Quantification of 0.25 pg/mL 238Pu sample mixture (1.18 pg of 238Pu) yielded satisfactory results (> 95% accuracy), uncertainties of less than 15% and in the presence of spiked natural U (0.5 ng/mL). Additional verification of this method was performed using certified ratio materials (IRMM-086, Belgium) and experimental 238Pu/239Pu and 240Pu/239Pu values are analogous to the certified values provided. [ABSTRACT FROM AUTHOR]

Background: Toxoplasma gondii (T. gondii) is a neuroinvasive parasite causing neuroinflammation, which in turn is associated with a higher risk for several psycho-behavioral disorders. There is an urgent need to identify drugs capable of improving cognitive deficits induced by T. gondii infection. β-Glucan, an active ingredient in mushrooms, could significantly enhance immunity. However, the effects of β-glucan against neuroinflammation and cognitive decline induced by T. gondii infection remain unknown. The present study aimed to investigate the neuroprotective effect of β-glucan on goal-directed behavior of mice chronically infected by T. gondii Wh6 strain. Methods: A mice model of chronic T. gondii Wh6 infection was established by infecting mice by oral gavage with 10 cysts of T. gondii Wh6. Intraperitoneal injection of β-glucan was manipulated 2 weeks before T. gondii infection. Performance of the infected mice on the Y-maze test and temporal order memory (TOM) test was used to assess the goal-directed behavior. Golgi-Cox staining, transmission electron microscopy, immunofluorescence, real-time PCR and western blot assays were used to detect prefrontal cortex-associated pathological change and neuroinflammation. Results: The administration of β-glucan significantly prevented T. gondii Wh6-induced goal-directed behavioral impairment as assessed behaviorally by the Y-maze test and TOM test. In the prefrontal cortex, β-glucan was able to counter T. gondii Wh6-induced degeneration of neurites, impairment of synaptic ultrastructure and decrease of pre- and postsynaptic protein levels. Also, β-glucan significantly prevented the hyperactivation of pro-inflammatory microglia and astrocytes, as well as the upregulation of proinflammatory cytokines caused by chronic T. gondii Wh6 infection. Conclusions: This study revealed that β-glucan prevents goal-directed behavioral impairment induced by chronic T. gondii infection in mice. These findings suggest that β-glucan may be an effective drug candidate to prevent T. gondii-associated psycho-behavioral disorders including goal-directed behavioral injury. [ABSTRACT FROM AUTHOR]

The article focuses on sensitive high resolution ion microprobe (SHRIMP) uranium-lead (U-Pb) age and its geological implications of concealed granite in the Changchong ore deposits in northeast Hunan, China. It also mentions that the major rock-forming minerals of the granodiorite porphyry in the deposit are quartz, feldspar and sericite. It further elaborates on the identification and examination of Zircon.