Platinum single atoms anchored on ultra-thin carbon nitride nanosheets for photoreforming of glucose

Photoreforming of biomass is a fascinating process that harnesses renewable sunlight and biomass to produce hydrogen under ambient conditions, holding a significant promise for future energy sustainability. However, the main challenge lies in developing highly active and stable photocatalysts with high light harvesting efficiency. In this study, we adopted a simple yet effective approach that combines thermal exfoliation and photodeposition to anchor Pt single atoms onto ultra-thin g-C3N4 nanosheets (MCNN). The incorporation of Pt single atoms induced a distinct red-shift in the visible light region, augmenting the solar energy absorption capacity, while the enlarged surface area of g-C3N4 nanosheets improved the mass transfer. Moreover, the enhanced photoelectric properties further contributed to the superior performance of Pt-MCNN-3.0 % in the photoreforming of glucose for hydrogen evolution. Remarkably, Pt-MCNN-3.0 % demonstrated an impressive hydrogen generation rate, approximately 59 times higher than that of MCNN, after a 3 h visible-light irradiation, maintaining a satisfied photo-stability. This work addresses the critical need for design of efficient photocatalysts, bringing us one step closer to realizing the potential of biomass photoreforming as a sustainable and clean energy conversion technology

Peroxisome Proliferator-Activated Receptor γ

Lipid phosphate phosphohydrolase 1 (LPP1), a membrane ectophosphohydrolase regulating the availability of bioactive lipid phosphates, plays important roles in cellular signaling and physiological processes such as angiogenesis and endothelial migration. However, the regulated expression of LPP1 remains largely unknown. Here, we aimed to examine a role of peroxisome proliferator-activated receptor γ (PPARγ) in the transcriptional control of LPP1 gene expression. In human umbilical vein endothelial cells (HUVECs), quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) demonstrated that activation of PPARγ increased the mRNA level of LPP1. Chromatin immunoprecipitation assay showed that PPARγ binds to the putative PPAR-responsive elements (PPREs) within the 5′-flanking region of the human LPP1 gene. Genomic fragment containing 1.7-kilobase of the promoter region was cloned by using PCR. The luciferase reporter assays demonstrated that overexpression of PPARγ and rosiglitazone, a specific ligand for PPARγ, could significantly upregulate the reporter activity. However, site-directed mutagenesis of the PPRE motif abolished the induction. In conclusion, our results demonstrated that PPARγ transcriptionally activated the expression of LPP1 gene in ECs, suggesting a potential role of PPARγ in the metabolism of phospholipids

Tandem internal electric fields in intralayer/interlayer carbon nitride homojunction with a directed flow of photo-excited electrons for photocatalysis

Photocatalytic hydrogen production is a green technology while significantly impeded by the sluggish and uncontrolled charge dynamics for less electron accumulation on catalyst surface. Herein, we proposed an effective strategy of epitaxial growth of a van der Waals (VDW) homojunction on an intralayer homojunction of carbon nitride for a controlled charge flow. Experimental and simulation collectively disclosed a tandem internal electric field (IEF) in the integrated hybrid, stringing a lateral IEF along the intralayer homojunction with a vertical IEF within the VDW homojunction. The planar IEF dominates laterally dispersive movement of charge carriers for their efficient separations and mobilities, meanwhile the vertical IEF induces an oriented accumulation of the dispersive hot electrons to the catalyst surface for intensified hydrogen reduction. The tandem IEF renders the hydrogen evolution rate at 3.5-fold higher than in-planar homojunction, and 6.3 times higher than g-C3N4 benchmark. This work realizes charge-directing dynamics for robust photocatalysis

Multipoint-Interconnected Quantum Communication Networks

As quantum computers with sufficient computational power are becoming mature, the security of classical communication and cryptography may compromise, which is based on the mathematical complexity. Quantum communication technology is a promising solution to secure communication based on quantum mechanics. To meet the secure communication requirements of multiple users, multipoint-interconnected quantum communication networks are specified, including quantum key distribution networks and quantum teleportation networks. The enabling technologies for quantum communication are the important bases for multipoint-interconnected quantum communication networks. To achieve the better connection, resource utilization, and resilience of multipoint-interconnected quantum communication networks, the efficient network architecture and optimization methods are summarized, and open issues in quantum communication networks are discussed

Effects of the pyrE deletion mutant from Bacillus thuringiensis on gut microbiota and immune response of Spodoptera exigua

The gut microbiota is essential for the growth and development of insects, and the intestinal immune system plays a critical role in regulating the homeostasis of intestinal microorganisms and their interactions with pathogenic bacteria. Infection with Bacillus thuringiensis (Bt) can disrupt the gut microbiota of insects, but the regulatory factors governing the interaction between Bt and gut bacteria are not well understood. Uracil secreted by exogenous pathogenic bacteria can activate DUOX-mediated reactive oxygen species (ROS) production, which helps maintain intestinal microbial homeostasis and immune balance. To elucidate the regulatory genes involved in the interaction between Bt and gut microbiota, we investigate the effects of uracil derived from Bt on gut microbiota, and host immunity using a uracil deficient Bt strain (Bt GS57△pyrE) obtained by homologous recombination. We analyze the biological characteristics of the uracil deficient strain and found that the deletion of uracil in Bt GS57 strain changed the diversity of gut bacteria in Spodoptera exigua, as investigated using Illumina HiSeq sequencing. Furthermore, qRT-PCR analysis showed that compared with Bt GS57 (control), the expression of the SeDuox gene and the level of ROS were significantly decreased after feeding with Bt GS57△pyrE. Adding uracil to Bt GS57△pyrE restored the expression level of DUOX and ROS to a higher level. Additionally, we observed that PGRP-SA, attacin, defensin and ceropin genes were significant different in the midgut of S. exigua infected by Bt GS57 and Bt GS57△pyrE, with a trend of increasing first and then decreasing. These results suggest that uracil regulates and activates the DUOX-ROS system, affects the expression of antimicrobial peptide genes, and disturb intestinal microbial homeostasis. We preliminarily speculate that uracil is a key factor in the interaction between Bt and gut microbiota, and these findings provide a theoretical basis for clarifying the interaction between Bt, host, and intestinal microorganisms, as well as for gaining new insights into the insecticidal mechanism of B. thuringiensis in insects

An Integrative Pharmacology Model for Decoding the Underlying Therapeutic Mechanisms of Ermiao Powder for Rheumatoid Arthritis

As a systemic inflammatory arthritis disease, rheumatoid arthritis (RA) is complex and hereditary. Traditional Chinese medicine (TCM) has evident advantages in treating complex diseases, and a variety of TCM formulas have been reported that have effective treatment on RA. Clinical and pharmacological studies showed that Ermiao Powder, which consists of Phellodendron amurense Rupr. (PAR) and Atractylodes lancea (Thunb.) DC. (ALD), can be used in the treatment of RA. Currently, most studies focus on the anti-inflammatory mechanism of PAR and ALD and are less focused on their coordinated molecular mechanism. In this research, we established an integrative pharmacological strategy to explore the coordinated molecular mechanism of the two herbs of Ermiao Powder in treating RA. To explore the potential coordinated mechanism of PAR and ALD, we firstly developed a novel mathematical model to calculate the contribution score of 126 active components and 85 active components, which contributed 90% of the total contribution scores that were retained to construct the coordinated functional space. Then, the knapsack algorithm was applied to identify the core coordinated functional components from the 85 active components. Finally, we obtained the potential coordinated functional components group (CFCG) with 37 components, including wogonin, paeonol, ethyl caffeate, and magnoflorine. Also, functional enrichment analysis was performed on the targets of CFCG to explore the potential coordinated molecular mechanisms of PAR and ALD. The results indicated that the CFCG could treat RA by coordinated targeting to the genes involved in immunity and inflammation-related signal pathways, such as phosphatidylinositol 3‑kinase/protein kinase B signaling pathway, mitogen-activated protein kinase signaling pathway, tumor necrosis factor signaling pathway, and nuclear factor-kappa B signaling pathway. The docking and in vitro experiments were used to predict the affinity and validate the effect of CFCG and further confirm the reliability of our method. Our integrative pharmacological strategy, including CFCG identification and verification, can provide the methodological references for exploring the coordinated mechanism of TCM in treating complex diseases and contribute to improving our understanding of the coordinated mechanism

Neuronal MicroRNA Deregulation in Response to Alzheimer's Disease Amyloid-β

Normal brain development and function depends on microRNA (miRNA) networks to fine tune the balance between the transcriptome and proteome of the cell. These small non-coding RNA regulators are highly enriched in brain where they play key roles in neuronal development, plasticity and disease. In neurodegenerative disorders such as Alzheimer's disease (AD), brain miRNA profiles are altered; thus miRNA dysfunction could be both a cause and a consequence of disease. Our study dissects the complexity of human AD pathology, and addresses the hypothesis that amyloid-β (Aβ) itself, a known causative factor of AD, causes neuronal miRNA deregulation, which could contribute to the pathomechanisms of AD. We used sensitive TaqMan low density miRNA arrays (TLDA) on murine primary hippocampal cultures to show that about half of all miRNAs tested were down-regulated in response to Aβ peptides. Time-course assays of neuronal Aβ treatments show that Aβ is in fact a powerful regulator of miRNA levels as the response of certain mature miRNAs is extremely rapid. Bioinformatic analysis predicts that the deregulated miRNAs are likely to affect target genes present in prominent neuronal pathways known to be disrupted in AD. Remarkably, we also found that the miRNA deregulation in hippocampal cultures was paralleled in vivo by a deregulation in the hippocampus of Aβ42-depositing APP23 mice, at the onset of Aβ plaque formation. In addition, the miRNA deregulation in hippocampal cultures and APP23 hippocampus overlaps with those obtained in human AD studies. Taken together, our findings suggest that neuronal miRNA deregulation in response to an insult by Aβ may be an important factor contributing to the cascade of events leading to AD

Cytoplasmic Accumulation and Aggregation of TDP-43 upon Proteasome Inhibition in Cultured Neurons

Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are characterized by intraneuronal deposition of the nuclear TAR DNA-binding protein 43 (TDP-43) caused by unknown mechanisms. Here, we studied TDP-43 in primary neurons under different stress conditions and found that only proteasome inhibition by MG-132 or lactacystin could induce significant cytoplasmic accumulation of TDP-43, a histopathological hallmark in disease. This cytoplasmic accumulation was accompanied by phosphorylation, ubiquitination and aggregation of TDP-43, recapitulating major features of disease. Proteasome inhibition produced similar effects in both hippocampal and cortical neurons, as well as in immortalized motor neurons. To determine the contribution of TDP-43 to cell death, we reduced TDP-43 expression using small interfering RNA (siRNA), and found that reduced levels of TDP-43 dose-dependently rendered neurons more vulnerable to MG-132. Taken together, our data suggests a role for the proteasome in subcellular localization of TDP-43, and possibly in disease