The intestinal tract serves as a critical regulator for nutrient absorption and overall health. However, its involvement in anti-parasitic infection and immunity has been largely neglected, ...especially when a parasite is not transmitted orally. The present study investigated the colonic histopathology and functional reprogramming in mice with intraperitoneal infection of the larval
(
).
Compared with the control group, the
-infected mice exhibited deteriorated secreted mucus, shortened length, decreased expression of tight junction proteins zonula occludens-1 (ZO-1), and occludin in the colon. Moreover, RNA sequencing was employed to characterize colonic gene expression after infection. In total, 3,019 differentially expressed genes (1,346 upregulated and 1,673 downregulated genes) were identified in the colon of infected mice. KEGG pathway and GO enrichment analysis revealed that differentially expressed genes involved in intestinal immune responses, infectious disease-associated pathways, metabolism, or focal adhesion were significantly enriched. Among these, 18 tight junction-relative genes, 44 immune response-associated genes, and 23 metabolic genes were annotated. Furthermore, mebendazole treatment could reverse the colonic histopathology induced by
infection.
Intraperitoneal infection with
induced the pathological changes and functional reprogramming in the colon of mice, and mebendazole administration alleviated above alternations, highlighting the significance of the colon as a protective barrier against parasitic infection. The findings provide a novel perspective on host-parasite interplay and propose intestine as a possible target for treating parasitic diseases that are not transmitted orally.
Toxoplasma gondii (T. gondii) is increasingly considered a risk factor for neurodegenerative diseases. However, there is only limited information on the development of drugs for T. gondii infection. ...Lentinan from Lentinula edodes is a bioactive ingredient with the potential to enhance anti-infective immunity. The present study aimed to investigate the neuroprotective effect of lentinan on T. gondii-associated cognitive deficits in mice.
A chronic T. gondii infection mouse model was established by administering 10 cysts of T. gondii by gavage. Lentinan was intraperitoneally administered 2 weeks before infection. Behavioral tests, RNA sequencing, immunofluorescence, transmission electron microscopy and Golgi-Cox staining were performed to assess the effect of lentinan on cognitive deficits and neuropathology in vivo. In vitro, the direct and indirect effects of lentinan on the proliferation of T. gondii tachyzoites were evaluated in the absence and presence of BV-2 cells, respectively.
Lentinan prevented T. gondii-induced cognitive deficits and altered the transcriptome profile of genes related to neuroinflammation, microglial activation, synaptic function, neural development and cognitive behavior in the hippocampus of infected mice. Moreover, lentinan reduced the infection-induced accumulation of microglia and downregulated the mRNA expression of proinflammatory cytokines. In addition, the neurite and synaptic ultrastructural damage in the hippocampal CA1 region due to infection was ameliorated by lentinan administration. Lentinan decreased the cyst burden in the brains of infected mice, which was correlated with behavioral performance. In line with this finding, lentinan could significantly inhibit the proliferation of T. gondii tachyzoites in the microglial cell line BV2, although lentinan had no direct inhibitory effect on parasite growth.
Lentinan prevents cognitive deficits via the improvement of neurite impairment and synaptic loss induced by T. gondii infection, which may be associated with decreased cyst burden in the brain. Overall, our findings indicate that lentinan can ameliorate T. gondii-related neurodegenerative diseases.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
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.
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.
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.
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.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Abstract An increasing number of distributed energy resources, acting as Supplier nodes, are participating in electricity market transactions. In order to meet the demand for large-scale renewable ...energy participation in the market, this article proposes a multi-layered electricity trading framework based on blockchain technology. This framework, with consortium chain technology at its core, is divided into network layer, regulatory layer, and physical layer. The feasibility of the proposed electricity trading model has been verified through simulation. Furthermore, this study divides the electricity trading process into stages, adopting noncooperative game theory for the bidding and clearing stages of trading nodes. After listing the remaining untraded nodes following the cycle auction, the node electricity price eventually converges to around 0.7 yuan/kW·h in the simulation game. By solving the game, rational node matching is achieved, while also matching untraded nodes with trading partners. The established electricity trading model in this article aims to provide trading services to nodes under different trading scenarios as much as possible, thereby enhancing the utilization of distributed energy resources. Future work will focus on refining the blockchain technology used in our framework, particularly exploring optimizations for scalability and efficiency in handling a larger volume of transactions involving distributed energy resources.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Both the assembly of naturally occurring resources into functional catalytic materials and upgrading of biomass-derived alcohols are of significant importance in the green chemistry community, which ...have achieved significant attention. Herein, we constructed several earth-abundant metal phosphates (MPOs) by the pyrolysis of the assembly structure of plant-originated sodium phytate (Na-PhyA) and the corresponding metal ions. It was discovered that the obtained aluminum phosphate (AlPO) was highly efficient for the transesterification of diethyl carbonate (DEC) with various biomass-derived alcohols (except for methoxy-substituted aromatic alcohols) to produce unsymmetrical organic carbonates with high selectivities (>96%). Detailed investigations revealed that the excellent catalytic activity of the phytic acid (PhyA)-derived AlPO originated mainly from the high content of Lewis acidic sites to activate the carbonyl groups in DEC and the hydroxyl group in alcohols simultaneously. Besides, its relative high surface area could also boost the reaction. Notably, the fact of combining bioderived catalysts and upgrading of important biomass derivatives enabled this work to be highly promising and practical from the viewpoint of green chemistry.
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IJS, KILJ, NUK, PNG, UL, UM
Abstract With the rapid evolution of the electricity market and the significant surge in power transactions, anomalies in data could wield substantial influence and pose risks to market participants, ...regulatory bodies, and the overall market operation. This study addresses the voluminous nature of power trading data and the imperative for real-time processing by introducing an anomaly detection method based on the local outlier factor (LOF) algorithm to identify anomalous data points in the electricity market. Simultaneously, this research enhances the LOF algorithm by incorporating the closest distance to center (CDC) algorithm and leveraging the introduction of local reachability density based on k-nearest neighbors, termed as the CDCLOF-k model. The F1 score of the two-stage identification method generally surpasses that of the single-stage method, achieving optimal effectiveness even with smaller values of k, with minimal fluctuation as k varies. Simulation experiments demonstrate that the improved algorithm not only ensures the accuracy of outlier detection but also enhances its efficiency. Future endeavors may delve into more intricate trading anomaly scenarios to further enhance the performance and applicability of this algorithm.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Obesity is a risk factor for cognitive dysfunction and neurodegenerative disease, including Alzheimer's disease (AD). The gut microbiota-brain axis is altered in obesity and linked to cognitive ...impairment and neurodegenerative disorders. Here, we targeted obesity-induced cognitive impairment by testing the impact of the probiotic Clostridium butyricum, which has previously shown beneficial effects on gut homeostasis and brain function. Firstly, we characterized and analyzed the gut microbial profiles of participants with obesity and the correlation between gut microbiota and cognitive scores. Then, using an obese mouse model induced by a Western-style diet (high-fat and fiber-deficient diet), the effects of Clostridium butyricum on the microbiota-gut-brain axis and hippocampal cognitive function were evaluated. Finally, fecal microbiota transplantation was performed to assess the functional link between Clostridium butyricum remodeling gut microbiota and hippocampal synaptic protein and cognitive behaviors. Our results showed that participants with obesity had gut microbiota dysbiosis characterized by an increase in phylum Proteobacteria and a decrease in Clostridium butyricum, which were closely associated with cognitive decline. In diet-induced obese mice, oral Clostridium butyricum supplementation significantly alleviated cognitive impairment, attenuated the deficit of hippocampal neurite outgrowth and synaptic ultrastructure, improved hippocampal transcriptome related to synapses and dendrites; a comparison of the effects of Clostridium butyricum in mice against human AD datasets revealed that many of the genes changes in AD were reversed by Clostridium butyricum; concurrently, Clostridium butyricum also prevented gut microbiota dysbiosis, colonic barrier impairment and inflammation, and attenuated endotoxemia. Importantly, fecal microbiota transplantation from donor-obese mice with Clostridium butyricum supplementation facilitated cognitive variables and colonic integrity compared with from donor obese mice, highlighting that Clostridium butyricum's impact on cognitive function is largely due to its ability to remodel gut microbiota. Our findings provide the first insights into the neuroprotective effects of Clostridium butyricum on obesity-associated cognitive impairments and neurodegeneration via the gut microbiota-gut-brain axis.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Scope
Hepatic steatosis is a major health issue that can be attenuated by a healthy diet. This study investigates the effects and molecular mechanisms of butyrate, a dietary fiber metabolite of gut ...microbiota, on lipid metabolism in hepatocytes.
Methods and results
This study examines the effects of butyrate (0–8 mM) on lipid metabolism in primary hepatocytes. The results show that butyrate (2 mM) consistently inhibits lipogenic genes and activates lipid oxidation‐related gene expression in hepatocytes. Furthermore, butyrate modulates lipid metabolism genes, reduces fat droplet accumulation, and activates the calcium/calmodulin‐dependent protein kinase II (CaMKII)/histone deacetylase 1 (HDAC1)‐cyclic adenosine monophosphate response element binding protein (CREB) signaling pathway in the primary hepatocytes and liver of wild‐type (WT) mice, but not in G‐protein‐coupled receptor 41 (GPR41) knockout and 43 (GPR43) knockout mice. This suggests that butyrate regulated hepatic lipid metabolism requires GPR41 and GPR43. Finally, the study finds that dietary butyrate supplementation (5%) ameliorates hepatic steatosis and abnormal lipid metabolism in the liver of mice fed a high‐fat and fiber‐deficient diet for 15 weeks.
Conclusion
This work reveals that butyrate improves hepatic lipid metabolism through the GPR41/43‐CaMKII/HDAC1‐CREB pathway, providing support for consideration of butyrate as a dietary supplement to prevent the progression of NAFLD induced by the Western‐style diet.
Butyrate decreases body weight, improves insulin sensitivity and prevents hepatic steatosis induced by a high‐fat and fiber‐deficient diet. The underlying molecular mechanism of butyrate in preventing hepatic steatosis is attributed to activating the calcium/calmodulin‐dependent protein kinase II/histone deacetylase 1‐cyclic adenosine monophosphate response element binding protein (CaMKII/HDAC1‐CREB) signaling pathway via hepatic G‐protein‐coupled receptors 41 and 43.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
