A generative adversarial network model fused with a self‐attention mechanism for the super‐resolution reconstruction of ancient murals

Abstract The problem that the texture details of low‐resolution (LR) digital images of ancient murals are ambiguous persists. To solve this problem, this study proposes a super‐resolution (SR) reconstruction method for fuzzy murals based on a generative adversarial network with self‐attention (SA). The network uses a blur kernel and realistic noise data to add blur and noise, respectively, to a high‐resolution (HR) image to obtain an original LR image. Then, a feature image with the same size as that of the input image is obtained through a SA module. Finally, the feature information extracted from the image is input into the high‐resolution image space by using a subpixel convolution layer to realize the image enlargement process from an LR to an HR. Experiments evaluate the proposed approach both objectively and subjectively. The objective evaluation results show that compared with other SR reconstruction algorithms, the proposed algorithm's peak signal‐to‐noise ratio (PSNR) is increased by 0.04 to 3.78 dB on average, and its structural similarity is increased by 0.002 to 0.191. A subjective perception evaluation shows that the developed algorithm can better reconstruct the texture details of murals, thus better meeting the visual perception needs of the public. The method proposed in this study can satisfactorily reconstruct the texture details of murals, which may provide technical guidance for the development of mural protection plans. Furthermore, it may be of certain practical significance for the SR reconstruction of ancient murals

MCC950 ameliorates cognitive function by reducing white matter microstructure damage in rats after SAH

Neuroinflammation and white matter microstructure damage are important causes of cognitive impairment after subarachnoid hemorrhage (SAH). Nod-like receptor protein 3 (NLRP3) plays an important role in neuroinflammation after SAH and may be a potential therapeutic target for treatment of white matter microstructure injury. In this study, we observed whether MCC950, a specific inhibitor of the NLRP3 inflammasome, exerted a therapeutic effect after SAH. The SAH model was induced by endovascular perforation in SpragueDawley rats. MCC950 was injected intraperitoneally 1 h after SAH at a dose of 10 mg/kg. The results showed that MCC950 significantly attenuated white matter microstructure damage in some brain regions, and behavioral experiments confirmed that MCC950 ameliorated cognitive function in rats after SAH, which may provide a new method for the treatment of cognitive dysfunction in SAH patients

Photostable epoxy polymerized carbon quantum dots luminescent thin films and the performance study

High photostable epoxy polymerized carbon quantum dots (C-dots) luminescent thin films were prepared and their performances were compared with the CdTe quantum dots (QDs). First, water soluble C-dots (λem = 543.60 nm) were synthesized. Poly (ethylene glycol) diglycidyl ether (PEG) and diaminooctane were used as the polymer matrix to make the epoxy resin films. FT-IR spectra showed that there were vibration at 3448 cm−1 and 1644 cm−1 which contributed to -OH and -NH respectively. SEM observations showed that the polymerizations of the films were uniform and there were no structure defects. Mechanical tests showed the tensile modulus of C-dots composite films were 4.6, 4.9, 6.4 and 7.8 MPa respectively with corresponding 0%, 1%, 2% and 5% mass fraction of C-dots, while the tensile modulus of CdTe QDs films were 4.6 MPa under the same mass fraction of CdTe QDs. Compared with semiconductor QDs, the decay of quantum yield were 5% and 10% for the C-dots and CdTe QDs, respectively. The pictures in the continuous irradiation of 48 h showed that the C-dots film was more photostable. This study provides much helpful and profound towards the fluorescent enhancement films in the field of flexible displays. Keywords: Carbon-dots, Waterborne epoxy resin, Luminescent materials, Quantum dots display

p21-Activated Kinase 4 Signaling Promotes Japanese Encephalitis Virus-Mediated Inflammation in Astrocytes

Japanese encephalitis virus (JEV) targets central nervous system, resulting in neuroinflammation with typical features of neuronal death along with hyper activation of glial cells. Exploring the mechanisms responsible for the JEV-caused inflammatory response remains a pivotal area of research. In the present study, we have explored the function of p21-activated kinase 4 (PAK4) in JEV-mediated inflammatory response in human astrocytes. The results showed that JEV infection enhances the phosphorylation of PAK4 in U251 cells and mouse brain. Knockdown of PAK4 resulted in decreased expression of inflammatory cytokines that include tumor necrosis factor alpha, interleukin-6, interleukin-1β, and chemokine (C-C motif) ligand 5 and interferon β upon JEV infection, suggesting that PAK4 signaling promotes JEV-mediated inflammation. In addition, we found that knockdown of PAK4 led to the inhibition of MAPK signaling including ERK, p38 MAPK and JNK, and also resulted in the reduced nuclear translocation of NF-κB and phosphorylation of AP-1. These results demonstrate that PAK4 signaling actively promotes JEV-mediated inflammation in human astrocytes via MAPK-NF-κB/AP-1 pathway, which will provide a new insight into the molecular mechanism of the JEV-induced inflammatory response

IP-10 Promotes Blood–Brain Barrier Damage by Inducing Tumor Necrosis Factor Alpha Production in Japanese Encephalitis

Japanese encephalitis is a neuropathological disorder caused by Japanese encephalitis virus (JEV), which is characterized by severe pathological neuroinflammation and damage to the blood–brain barrier (BBB). Inflammatory cytokines/chemokines can regulate the expression of tight junction (TJ) proteins and are believed to be a leading cause of BBB disruption, but the specific mechanisms remain unclear. IP-10 is the most abundant chemokine produced in the early stage of JEV infection, but its role in BBB disruption is unknown. The administration of IP-10-neutralizing antibody ameliorated the decrease in TJ proteins and restored BBB integrity in JEV-infected mice. In vitro study showed IP-10 and JEV treatment did not directly alter the permeability of the monolayers of endothelial cells. However, IP-10 treatment promoted tumor necrosis factor alpha (TNF-α) production and IP-10-neutralizing antibody significantly reduced the production of TNF-α. Thus, TNF-α could be a downstream cytokine of IP-10, which decreased TJ proteins and damaged BBB integrity. Further study indicated that JEV infection can stimulate upregulation of the IP-10 receptor CXCR3 on astrocytes, resulting in TNF-α production through the JNK-c-Jun signaling pathway. Consequently, TNF-α affected the expression and cellular distribution of TJs in brain microvascular endothelial cells and led to BBB damage during JEV infection. Regarding regulation of the BBB, the IP-10/TNF-α cytokine axis could be considered a potential target for the development of novel therapeutics in BBB-related neurological diseases

Selective sphingosine-1-phosphate receptor 1 modulator attenuates blood–brain barrier disruption following traumatic brain injury by inhibiting vesicular transcytosis

Abstract Background Traumatic brain injury (TBI) provokes secondary pathological damage, such as damage to the blood–brain barrier (BBB), ischaemia and inflammation. Major facilitator superfamily domain-containing 2a (Mfsd2a) has been demonstrated to be critical in limiting the increase in BBB vesicle transcytosis following brain injury. Recent studies suggest that a novel and selective modulator of the sphingosine-1-phosphate receptor 1 (S1P1), CYM-5442, maintains the integrity of the BBB by restricting vesicle transcytosis during acute ischaemic stroke. In the current study, we investigated whether CYM-5442, evaluated in a short-term study, could protect the brains of mice with acute-stage TBI by reversing the increase in vesicle transport due to reduced Mfsd2a expression after TBI. Methods We used the well-characterized model of TBI caused by controlled cortical impact. CYM-5442 (0.3, 1, 3 mg/kg) was intraperitoneally injected 30 min after surgery for 7 consecutive days. To investigate the effect of CYM-5442 on vesicle transcytosis, we downregulated and upregulated Mfsd2a expression using a specific AAV prior to evaluation of the TBI model. MRI scanning, cerebral blood flow, circulating blood counts, ELISA, TEM, WB, and immunostaining evaluations were performed after brain injury. Results CYM-5442 significantly attenuated neurological deficits and reduced brain oedema in TBI mice. CYM-5442 transiently suppressed lymphocyte trafficking but did not induce persistent lymphocytopenia. After TBI, the levels of Mfsd2a were decreased significantly, while the levels of CAV-1 and albumin were increased. In addition, Mfsd2a deficiency caused inadequate sphingosine-1-phosphate (S1P) transport in the brain parenchyma, and the regulation of BBB permeability by Mfsd2a after TBI was shown to be related to changes in vesicle transcytosis. Downregulation of Mfsd2a in mice markedly increased the BBB permeability, neurological deficit scores, and brain water contents after TBI. Intervention with CYM-5442 after TBI protected the BBB by significantly reducing the vesicle transcytosis of cerebrovascular endothelial cells. Conclusion In addition to transiently suppressing lymphocytes, CYM-5442 alleviated the neurological deficits, cerebral edema and protective BBB permeability in TBI mice by reducing the vesicle transcytosis of cerebrovascular endothelial cells

Microarray Analysis Identifies the Potential Role of Long Non-Coding RNA in Regulating Neuroinflammation during Japanese Encephalitis Virus Infection

Japanese encephalitis virus (JEV) is the leading cause of epidemic encephalitis worldwide. JEV-induced neuroinflammation is characterized by profound neuronal cells damage accompanied by activation of glial cells. Albeit long non-coding RNAs (lncRNAs) have been emerged as important regulatory RNAs with profound effects on various biological processes, it is unknown how lncRNAs regulate JEV-induced inflammation. Here, using microarray approach, we identified 618 lncRNAs and 1,007 mRNAs differentially expressed in JEV-infected mice brain. The functional annotation analysis revealed that differentially regulated transcripts were predominantly involved in various signaling pathways related to host immune and inflammatory responses. The lncRNAs with their potential to regulate JEV-induced inflammatory response were identified by constructing the lncRNA-mRNA coexpression network. Furthermore, silencing of the two selected lncRNAs (E52329 and N54010) resulted in reducing the phosphorylation of JNK and MKK4, which are known to be involved during inflammatory response. Collectively, we first demonstrated the transcriptomic landscape of lncRNAs in mice brain infected with JEV and analyzed the coexpression network of differentially regulated lncRNAs and mRNAs during JEV infection. Our results provide a better understanding of the host response to JEV infection and suggest that the identified lncRNAs may be used as potential therapeutic targets for the management of Japanese encephalitis

H3K27me3 of Rnf19a promotes neuroinflammatory response during Japanese encephalitis virus infection

Abstract Histone methylation is an important epigenetic modification that affects various biological processes, including the inflammatory response. In this study, we found that infection with Japanese encephalitis virus (JEV) leads to an increase in H3K27me3 in BV2 microglial cell line, primary mouse microglia and mouse brain. Inhibition of H3K27me3 modification through EZH2 knockdown and treatment with EZH2 inhibitor significantly reduces the production of pro-inflammatory cytokines during JEV infection, which suggests that H3K27me3 modification plays a crucial role in the neuroinflammatory response caused by JEV infection. The chromatin immunoprecipitation-sequencing (ChIP-sequencing) assay revealed an increase in H3K27me3 modification of E3 ubiquitin ligases Rnf19a following JEV infection, which leads to downregulation of Rnf19a expression. Furthermore, the results showed that Rnf19a negatively regulates the neuroinflammatory response induced by JEV. This is achieved through the degradation of RIG-I by mediating its ubiquitination. In conclusion, our findings reveal a novel mechanism by which JEV triggers extensive neuroinflammation from an epigenetic perspective