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Interleukin-1β (IL-1β) plays a crucial role in mediating inflammation and innate immunity response in the central nervous system. Death-associated protein kinase 1 (DAPK1) was shown to be involved in several cellular processes. Here, we investigated the effects of DAPK1 on IL-1β production in microglial cells. We used a combination of in vitro (Bv2 microglial cell cultures) and in vivo (mice injected with amyloid-β (Aβ)) techniques to address the role of caspase-1 activation in release of IL-1β. DAPK1 involvement was postulated through genetic approaches and pharmacological blockade of this enzyme. We found that Aβ25–35 stimulation induced IL-1β production and caspase-1 activation in LPS-primed Bv2 cells and mice. DAPK1 knockdown and catalytic activity inhibition reduced IL-1β maturation and caspase-1 activation, nevertheless, DAPK1 overexpression attenuated these effects. Aβ25–35-induced lysosomal cathepsin B leakage was required for DAPK1 activation. Furthermore, repeated DAPK1 inhibitor treatment ameliorated the memory impairment in Aβ25–35-injected mice. Taken together, our findings suggest that DAPK1 facilitates Aβ25–35-induced IL-1β production through regulating caspase-1 activation in microglial cells.

Fluoxetine, one of the selective serotonin reuptake inhibitor (SSRI) antidepressants, has been thought to be effective for treating post-stroke depression (PSD). Recent work has shown that fluoxetine may exert an antidepressive effect through increasing the level of brain-derived neurotrophic factor (BDNF), but the underlying mechanism still remains unclear. In the present study, we successfully established the PSD model using male C57BL/6 J mice by photothrombosis of the left anterior cortex combined with isolatied-housing conditions. In the process, we confirmed that fluoxetine could improve the depression-like behaviors of PSD mice and upregulate the expression of BDNF in the hippocampus. However, depletion of BDNF by transfecting lentivirus-derived shBDNF in hippocampus suppressed the effect of fluoxetine. Furthermore, we demonstrated the epigenetic mechanisms involved in regulation of BDNF expression induced by fluoxetine. We found a statistically significant increase in DNA methylation at specific CpG sites (loci 2) of Bdnf promoter IV in the hippocampus of PSD mice. We also found that fluoxetine treatment could disassociate the MeCP2-CREB-Bdnf promoter IV complex via phosphorylation of MeCP2 at Ser421 by Protein Kinase A (PKA). Our research highlighted the importance of fluoxetine in regulating BDNF expression which could represent a potential strategy for preventing PSD.

Biochar derived from waste biomass has proven as a promising sorbent for removal of heavy metals from wastewater. However, proper disposal of such a heavy metal-containing biochar is challengeable. The major objective of this study is to create a reuse way by converting the heavy metal-loaded biochar into supercapacitor. Two biochars were produced from dairy manure and sewage sludge, respectively, and subjected to sorption of Ni from solution, and then the Ni-loaded biochar underwent microwave treatments for fabrication of supercapacitor. The specific capacitance of biochar supercapacitor increased with Ni loading, especially the Ni-loaded biochar further treated with microwave in which the capacitance increased by over 2 times, compared to the original biochar supercapacitors. The increase of capacitance in the Ni-loaded biochar supercapacitor following microwave treatment was mainly attributed to the conversion of Ni into NiO and NiOOH, which was evidenced by X-ray diffraction and X-ray photoelectron spectroscopy. The biochar supercapacitors, especially microwave-treated Ni-loaded biochar supercapacitors exhibited the high stability of specific capacitance, with less than 2% loss after 1000 charge-discharge cycles. This study demonstrated that Ni-loaded biochar can be further utilized for generation of supercapacitor, providing a potential way for the reuse of exhausted carbonaceous sorbents.

MicroRNAs (miRNAs) have been considered to be potent biomarkers for early disease diagnosis and for cancer therapy. The rapid and selective detection of miRNAs without reverse transcription and labelling is highly desired. Herein, we report a simple and label-free miRNA detection method that is based on the Duplex-Specific Nuclease (DSN)-Assisted simple target miRNA recycling procedure. The interaction of the G-quadruplex DNA structure with N-methyl mesoporphyrin IX (NMM) led to a label-free signal output. Under the optimised conditions, this method allowed for simple, rapid, and sequence-specific detection of miR-141 over a dynamic range from 1 fM to 100 nM with a linear range from 1 pM to 100 nM. Moreover, our method offered an excellent capacity to discriminate between miRNA family members with just one mismatched nucleotide. This simple and label-free strategy holds great potential in applications in biomedical research and in early clinical diagnostics.