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In this letter, a lightweight and effective deep steganalysis network (DSN) with less than 400,000 parameters, called LWENet, is proposed, which focuses on increasing the performance as well as significantly reducing the number of parameters (NP) from three perspectives. Firstly, in the preprocessing part, several lightweight bottleneck residual blocks are combined into the spatial rich model filters to improve the signal-to-noise ratio of stego signals while slightly increasing NP, thereby improving the subsequent performance. Secondly, a depthwise separable convolution layer is exploited at the end of the feature extraction part to largely reduce NP and increase the performance by capturing salient correlations while ignoring trivial ones among feature maps. Finally, to keep LWENet lightweight, we have to select only one fully connected (FC) layer. Simultaneously, multi-view global pooling is employed prior to the FC layer to yield multi-view features and further improve the detection performance. Extensive experiments demonstrate that our network achieves better performance than several state-of-the-art DSNs. [ABSTRACT FROM AUTHOR]

B and Ga co-doped ZnO films were fabricated by RF magnetron sputtering method. The effects of sputtering pressure on the electrical, optical, structural and morphological properties of the films (BGZO) were investigated. As sputtering pressure increased up to 6mTorr, the film crystallinity was improved. At the sputtering pressure of 6mTorr, the films showed smooth and dense of film surface, lower resistivity and higher Hall mobility. It was also observed that all films showed high transparency in the visible range. The film showed blue shift of optical band gap with increaseing of sputtering pressure.

Neurodegenerative diseases are considered to be among the diseases most threatening to human beings. Increasing evidence shows that antioxidant hydrolysates/peptides with neuroprotective effects may relieve neurodegenerative diseases. However, related research in mushrooms, one of the richest sources of antioxidant hydrolysates/peptides, is in its infancy. Therefore, the in vitro neuroprotective effects of protein hydrolysates from Pleurotus geesteranus were researched in this study. Proteins were extracted from P. geesteranus and then hydrolyzed by simulated gastrointestinal digestion. The neuroprotective effects of the protein hydrolysates were evaluated by H2O2‐injured PC12 cells. The hydrolysates showed a superior antioxidative ability and had a higher abundance of hydrophobic amino acids (e.g., leucine, alanine, and phenylalanine). Neither cytotoxicity nor the increase of ROS in PC12 cells was observed under treatment with the hydrolysates. However, pre‐treatment with the hydrolysates in PC12 cells, which were then injured by H2O2, markedly attenuated ROS generation and enhanced the activities and mRNA expression of the endogenous antioxidant enzymes (catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD)), leading to a 26.68% increase in cell viability. The hydrolysates exhibited strong neuroprotective activity in H2O2‐injured PC12 cells, possibly by reducing ROS generation and enhancing the activity of the antioxidant enzymatic system. Practical applications: Antioxidant hydrolysates with neuroprotection were obtained from Pleurotus geesteranus proteins by simulating gastrointestinal digestion, which exhibited an excellent pre‐protective effect in oxidatively damaged PC12 cells. Further study showed that hydrolysates pre‐protection may exert antioxidant activities not only as an exogenous antioxidant to scavenge ROS but also as a gene regulator to modulate the endogenous antioxidant enzymes gene expression. These results indicated that the potential of antioxidant peptides, derived from P. geesteranus through gastrointestinal digestion, could serve as a source of bioactive molecules in the prevention, relief or even treatment of neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

In this study, the ameliorative effect of purified polyphenols from Arctium lappa L (ALPP) on doxorubicin (DOX)‐induce heart failure was investigated. Results indicated that ALPP pretreatment significantly reduced the activities of casein kinase and lactate dehydrogenase, lowered the levels of inflammatory indexes (TNF‐α and NO), and alleviated antioxidant stress in DOX‐induce mice, thus leading to a reduced heart failure syndrome. In addition, according to 16s high‐throughput sequencing, the increased abundance of Lactobacillaceae,Muribaculaceae, and Ruminococcaceae and the decreased abundance of Proteobacteria,Enterobacteriaee, and Escherichia_Shigella were observed in ALPP treatment group. ALPP could significantly enhance the abundance of bacteria producing short chain fatty acids (SCFAs) and then promote the increase of SCFAs. Consequently, ALPP might be a therapeutic alternative in the treatment of DOX‐induced heart failure. Practical applications: The effect of Arctium lappa L (ALPP) on doxorubicin (DOX)‐induced heart failure was investigated. It provided experimental basis for further studies on the biological activity of polyphenols from ALPP. The results demonstrated that ALPP could significantly ameliorate DOX‐induced heart failure and improve the gut microbiota composition. The obtained results could provide the potential application of ALPP as an alternative therapy for heart failure in the functional food industry. [ABSTRACT FROM AUTHOR]

Arbuscular mycorrhizal fungi (AMF) significantly contribute to plant resource acquisition and play important roles in mediating plant interactions and soil carbon (C) dynamics. However, it remains unclear how AMF communities respond to climate change. We assessed impacts of warming and precipitation alterations (30% increase or decrease) on soil AMF communities, and examined major ecological processes shaping the AMF community assemblage in a Tibetan alpine meadow. Our results showed that warming significantly increased root biomass, and available nitrogen (N) and phosphorus (P) in soil. While precipitation alterations increased AMF abundances, they did not significantly affect the composition or diversity of AMF communities. In contrast, warming altered the composition of AMF communities and reduced their Shannon–Wiener index and Pielou's evenness. In particular, warming shifted the AMF community composition in favor of Diversisporaceae over Glomeraceae, likely through its impact on soil N and P availability. In addition, AMF communities were phylogenetically random in the unwarmed control but clustered in warming plots, implying more deterministic community assembly under climate warming. Warming enhancement of root growth, N and P availability likely reduced plant C‐allocation to AMF, imposing stronger environmental filtering on AMF communities. We further proposed a conceptual framework that integrates biological and geochemical processes into a mechanistic understanding of warming and precipitation changes' effects on AMF. Taken together, these results suggest that soil AMF communities may be more sensitive to warming than expected, highlighting the need to monitor their community structure and associated functional consequences on plant communities and soil C dynamics under the future warmer climate. [ABSTRACT FROM AUTHOR]

Background: Olfactory inflammation in chronic rhinosinusitis (CRS) is associated with cytokines that may result in the death of olfactory sensory neurons. The principal signaling molecules involved in the apoptotic pathway are c‐Jun N‐terminal kinases (JNK). Although the JNK pathway has emerged as a key player in programmed cell death in neuroinflammation, its specific role in CRS‐associated olfactory loss has not been thoroughly investigated. Methods: JNK activation was studied in human tissue samples from 9 control and 11 CRS patients by immunohistochemical staining for phosphorylated c‐Jun. A mouse model of inducible olfactory cytokine expression was used to experimentally control inflammation and assess JNK activation over time. Results: In patients with CRS, activation of c‐Jun is significantly increased relative to non‐CRS control subjects, and there is an associated loss of sensory neurons. In the olfactory inflammation mouse model, prolonged induction of inflammation results in elevation of c‐Jun expression and neuronal apoptosis. Conclusion: Activation of neuronal JNK is a feature of chronic olfactory inflammation that is associated with neuronal apoptosis. Given that inhibition of JNK activity is neuroprotective in other settings, antagonism of this pathway may have therapeutic potential in the management of inflammatory olfactory loss or other disorders linked to olfactory neuronal apoptosis. [ABSTRACT FROM AUTHOR]

Induced pluripotent stem cells (iPSCs) possess the capacity to differentiate into multiple cell types including retinal neurons. Despite substantial progress in the transcriptional regulation of iPSC differentiation process, the efficiency of generation of retinal neurons from iPSCs is still low. In this study, we investigated the role of transcription factor NeuroD1 in the differentiation of iPSCs into retinal neurons. We observed that retrovirus-mediated NeuroD1 overexpression in iPSCs increased the efficiency of neuronal differentiation. Immunostaining analysis showed that NeuroD1 overexpression increased the expression of retina ganglion cell markers including Islet-1, Math5, Brn3b, and Thy1.2. Retinoid acid (RA) and taurine further improved the differentiation efficiency of iPSCs overexpressing NeuroD1. However, RA and taurine did not promote differentiation in the absence of NeuroD1 overexpression. Together, our study provides new evidence in transcription factor-regulated stem cell differentiation in vitro. [ABSTRACT FROM AUTHOR]

Background To understand mechanisms of human olfactory dysfunction in chronic rhinosinusitis, an inducible olfactory inflammation (IOI) model has been utilized to chronically express inflammatory cytokines locally, resulting in neuronal loss, diminished odorant responses, and repressed olfactory regeneration. Knockout of the minor tumor necrosis factor α receptor 2 (TNFR2) was previously shown to partially rescue these olfactory changes. The purpose of current study was to investigate the role of the major TNF receptor, TNFR1, in chronic olfactory inflammation. Methods Two experimental groups of mice were studied: TNFR1 knockout in IOI background and TNFR1 knockout with allergen-induced inflammation. Olfactory function was assayed by electro-olfactogram (EOG), and olfactory tissue was processed for histology and immunohistochemical staining. Results TNF-α was dramatically induced in IOI-TNFR1 knockout mice, but the olfactory epithelium did not show inflammation. EOG responses were normal after either 2 or 8 weeks of TNF-α expression. Ovalbumin-sensitized TNFR1 knockout mice developed markedly diminished eosinophilic inflammatory infiltration. Conclusion Genetic deletion of TNFR1 completely blocks TNF-α-induced inflammation and reduces allergen-induced inflammation. Preserved EOG responses suggest a TNFR1-dependent mechanism of TNF-α-induced olfactory neuron dysfunction. [ABSTRACT FROM AUTHOR]