Intricate Ionic Behaviors in High-Performance Self-Powered Hydrothermal Chemical Generator Using Water and Iron (III) Gate.

Utilizing the ionic flux to generate voltage output has been confirmed as an effective way to meet the requirements of clean energy sources. Different from ionic thermoelectric (i-TE) and hydrovoltaic devices, a new hydrothermal chemical generator is designed by amorphous FeCl3 particles dispersing in MWCNT and unique ferric chloride or water gate. In the presence of gate, the special ion behaviors enable the cell to present a constant voltage of 0.60 V lasting for over 96 h without temperature difference. Combining the differences of cation concentration, humidity and temperature between the right and left side of sample, the maximum short-circuit current and power output can be obtained to 168.46 µA and 28.11 µW, respectively. The generator also can utilize the low-grade heat to produce electricity wherein Seebeck coefficient is 6.79 mV K-1 . The emerged hydrothermal chemical generator offers a novel approach to utilize the low-grade heat, water and salt solution resources, which provides a simple, sustainable and low-cost strategy to realize energy supply.

Progranulin from different gliocytes in the nucleus accumbens exerts distinct roles in FTD- and neuroinflammation-induced depression-like behaviors.

BACKGROUND: Neuroinflammation in the nucleus accumbens (NAc) is well known to influence the progression of depression. However, the molecular mechanisms triggering NAc neuroinflammation in depression have not been fully elucidated. Progranulin (PGRN) is a multifunctional growth factor that is linked to the innate immune response and inflammation, and PGRN plays a key role in neurodegenerative diseases such as frontotemporal dementia (FTD). Here, the purpose of this study was to validate whether PGRN was involved in the NAc neuroinflammation-promoted depressive-like phenotype. METHODS: A NAc neuroinflammation-relevant depression-like model was established using wild-type (WT) and PGRN-knockout (KO) mice after NAc injection with lipopolysaccharide (LPS), and various behavioral tests related to cognition, social recognition, depression and anxiety were performed with WT and PGRNKO mice with or without NAc immune challenge. RT‒PCR, ELISA, western blotting and immunofluorescence staining were used to determine the expression and function of PGRN in the neuroinflammatory reaction in the NAc after LPS challenge. The morphology of neurons in the NAc from WT and PGRNKO mice under conditions of NAc neuroinflammation was analyzed using Golgi-Cox staining, followed by Sholl analyses. The potential signaling pathways involved in NAc neuroinflammation in PGRNKO mice were investigated by western blotting. RESULTS: Under normal conditions, PGRN deficiency induced FTD-like behaviors in mice and astrocyte activation in the NAc, promoted the release of the inflammatory cytokines interleukin (IL)-6 and IL-10 and increased dendritic complexity and synaptic protein BDNF levels in the NAc. However, NAc neuroinflammation enhanced PGRN expression, which was located in astrocytes and microglia within the NAc, and PGRN deficiency in mice alleviated NAc neuroinflammation-elicited depression-like behaviors, seemingly inhibiting astrocyte- and microglia-related inflammatory reactions and neuroplasticity complexity in the NAc via the p38 and nuclear factor of kappa (NF-κB) signaling pathways present in the NAc after neuroinflammation. CONCLUSIONS: Our results suggest that PGRN exerts distinct function on different behaviors, showing protective roles in the FTD-like behavior and detrimental effects on the neuroinflammation-related depression-like behavior, resulting from mediating astrocyte and microglial functions from the NAc in different status.