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[Display omitted] The development of interfacial engineering was crucial for achieving the industrialization of high-performance carbon fiber/phenolic composites. In this study, establishing scalable interpenetrating networks (cellulose nanofiber-zeolitic imidazolate frameworks-8/aramid nanofiber-boron nitride) on the fiber/matrix interphase, was in favor of realizing precise repairation of interfacial defects, further regulating thermal conductivity, mechanical and tribological properties of the composites. Based on the physical and chemical bridging-effects arising from above spider-web networks, the flexural strength and modulus of modified sample were 74.69 MPa and 6.22 GPa, showing an increase of 135.99% and 56.68%, respectively. Meanwhile, this trans-scale spider-web structure acted as a micron skeleton-nano unit continuous thermal conductive network, significantly reduced phonon scattering and displayed a 258.33% enhancement in the thermal management capability of modified sample. This study reveals key design principles of trans-scale interfacial structure to dynamicly regulate performances and meet service requirements of next-generation carbon fiber/phenolic composites. [ABSTRACT FROM AUTHOR]

Abstract In this paper, we establish the existence of viscosity solutions of Hessian equations with singular right-hand sides and obtain the asymptotic boundary behavior of solutions. The asymptotic results generalize those for Poisson equations and Monge-Ampère equations, and are more precise than obtained from Hopf lemma. [ABSTRACT FROM AUTHOR]

In this paper, by Karamata regular variation theory and constructing super and subsolutions, we obtain the asymptotic boundary behavior of convex solutions of Monge–Ampère equations with singular righthand sides. [ABSTRACT FROM AUTHOR]

In this paper we investigate viscosity solutions of non-divergence elliptic equations in cones and obtain asymptotic behaviors at vertexes of cones and at infinity of solutions. [ABSTRACT FROM AUTHOR]

[Display omitted] • ZIS/CFO flower-like composites were prepared by a method involving ultrasonic and calcination. • Charge carriers were separated due to the formed p-n heterojunction and internal electric field. • Magnetic ZIS/CFO can be recovered under the external magnetic field. The construction of a p-n heterojunction structure is considered to be an effective method to improve the separation of electron-hole pairs in photocatalysts. A series of ZnIn 2 S 4 /CoFe 2 O 4 (ZIS/CFO) photocatalysts with p-n heterojunctions were prepared via a method involving ultrasonication and calcination. The synthesized photocatalysts were tested and analyzed via various testing techniques, and their hydrogen evolution rates were evaluated. Compared with pure ZIS, ZIS/CFO with different mass ratios of CFO to ZIS showed improved photocatalytic hydrogen production performance, and the optimal photoactivity showed a nearly 12-fold increase, which can be attributed to the formation of p-n junctions and the formed internal electric field, accelerating the separation of electron-hole pairs and effectively improving the photocatalytic hydrogen evolution rate. The excellent stability of the ZIS/CFO composite was proven by three cycle experiments. In addition, the ZIS/CFO composite also possessed excellent magnetic properties to realize facial magnetic recoverability. This work paves the way for the design and preparation of magnetically recoverable p-n heterojunction photocatalysts. [ABSTRACT FROM AUTHOR]

With the widespread use of sulfonamide antibiotics (SAs), SAs are detected as residues in aquatic environments, posing a serious threat to human life and safety. Because of their high water solubility, fast transmission rate, and strong antibacterial properties, the safe disposal of SAs has become a key constraint for water quality assurance. Therefore, an ultrasound (US)-assisted zero-valent iron (ZVI)/persulfate (PS) system was proposed to explore the rapid and effective degradation of SAs. Comparative experiments were performed to study the removal of sulfadiazine (SDZ) by US, ZVI, PS, US/ZVI, US/PS, ZVI/PS, and US-ZVI/PS systems, respectively. Experimental results indicated that the highest removal efficiency of SDZ was ahieved in US-ZVI/PS system (97.4%), which were 2–44 times higher than that in other systems. Furthermore, the degradation efficiency of five typical SAs was achieved over 95%, demonstrating the effectiveness of the US ZVI/PS system for SAs removal. Also, quantum chemical computations for potential reactive sites of SAs and intermediate product detection by HPLC‒MS/MS were performed. The radical attack on active sites of SAs, such as N atom (number 7), was the main reason for SAs removal in US-ZVI/PS system. Besides, the common degradation pathways of six typical SAs were defined as S–N bond cleavage, C–N bond cleavage, benzene ring hydroxylation, aniline oxidation, and R substituent oxidation. Interestingly, the unique pathway of "SO 2 group extraction" was observed in the degradation of six-membered ring SAs. Therefore, the US-ZVI/PS system is a promising and cost-effective method for the removal of SAs and other refractory pollutants. • Comparative experiments were executed to study SDZ removal by seven related systems. • 97.4% of SD was removed by two-stage US-ZVI/PS system within 30 min. • The removal of six typical SAs by US-ZVI/PS system were all achieved over 95%. • Specific reactive sites of SAs molecule were proved by quantum chemical computations. • The removal mechanism of six typical SAs by a US-ZVI/PS system was analyzed in detail. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is the most common neurodegenerative movement disorder, characterized by the progressive loss of nigrostriatal dopaminergic neurons (DANs), involving the dysregulation of both neurons and glial cells. Cell type- and region-specific gene expression profiles can provide an effective source for revealing the mechanisms of PD. In this study, we adopted the RiboTag approach to obtain cell type (DAN, microglia, astrocytes)- and brain region (substantia nigra, caudate-putamen)-specific translatomes at an early stage in an MPTP-induced mouse model of PD. Through DAN-specific translatome analysis, the glycosphingolipid biosynthetic process was identified as a significantly downregulated pathway in the MPTP-treated mice. ST8Sia6, a key downregulated gene related to glycosphingolipid biosynthesis, was confirmed to be downregulated in nigral DANs from postmortem brains of patients with PD. Specific expression of ST8Sia6 in DANs exerts anti-inflammatory and neuroprotective effects in MPTP-treated mice. Through cell type (microglia vs. astrocyte) and brain region (substantia nigra vs. caudate-putamen) comparisons, nigral microglia showed the most intense immune responses. Microglia and astrocytes in the substantia nigra showed similar levels of activation in interferon-related pathways and interferon gamma (IFNG) was identified as the top upstream regulator in both cell types. This work highlights that the glycosphingolipid metabolism pathway in the DAN is involved in neuroinflammation and neurodegeneration in an MPTP mouse model of PD and provides a new data source for elucidating the pathogenesis of PD. • Glycosphingolipid biosynthetic pathway is de-enriched in dopamine neurons in MPTP mice. • Gene changes of microglia and astrocytes overlap with pro-inflammatory pathways. • Nigral microglia play a major role in pro-inflammation marked by antiviral responses. • ST8Sia6 downregulation is validated in postmortem brains of Parkinson's patients. • Overexpression of ST8Sia6 in mice shows anti-inflammatory and neuroprotective effects. [ABSTRACT FROM AUTHOR]

The progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) is one of the hallmarks of Parkinson's disease (PD). Neuroinflammation has been proposed to contributes to the progressive nature of the disease. Early growth response-1 (Egr-1), a zinc finger transcription factor, has been shown to have a crucial role in both neuronal death and the inflammatory response. However, whether and how Egr-1 is involved in the pathogenesis of PD has not been investigated. Using the subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, we identified early peak induction of Egr-1 in the SNpc but not in the striatum. In situ immunofluorescent analysis showed that Egr-1 predominantly locates in the nuclei of nigral AldoC (+) astrocytes upon MPTP treatment. Genetic ablation of Egr-1 or inhibition of its transcriptional activity by Mithramycin A significantly suppresses the activation of both astrocytes and microglia, decreases proinflammatory cytokine expression, and protects dopaminergic cell bodies from degeneration in the SNpc. Taken together, these findings demonstrate that the induction of Egr-1 promotes neuroinflammation and dopaminergic cell body loss in the SNpc of MPTP-induced mouse model, suggesting an important role of astrocytic Egr-1 in neuroinflammation in PD. [ABSTRACT FROM AUTHOR]

The c-Jun N-terminal kinase (JNK)/c-Jun pathway is a known critical regulator of dopaminergic neuronal death in Parkinson's disease (PD) and is considered a potential target for neuroprotective therapy. However, whether JNK is activated within dopaminergic neurons remains controversial, and whether JNK acts through downstream effectors other than c-Jun to promote dopaminergic neuronal death remains unclear. In this study, we confirm that JNK but not p38 is activated in dopaminergic neurons after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxication. Furthermore, within the dopaminergic neurons of the substantia nigra in MPTP-treated mice, JNK2/3 phosphorylates threonine 69 (Thr69) of Activating transcription factor-2 (ATF2), a transcription factor of the ATF/CREB family, whereas the phosphorylation of Thr71 is constitutive and remains unchanged. The increased phosphorylation of ATF2 on Thr69 by JNK in the MPTP mouse model suggests a functional relationship between the transcriptional activation of ATF2 and dopaminergic neuron death. By using dopaminergic neuron-specific conditional ATF2 mutant mice, we found that either partial or complete deletion of the ATF2 DNA-binding domain in dopaminergic neurons markedly alleviates the MPTP-induced dopaminergic neurodegeneration, indicating that the activation of ATF2 plays a detrimental role in neuropathogenesis in PD. Taken together, our findings demonstrate that JNK-mediated ATF2 activation contributes to dopaminergic neuronal death in an MPTP model of PD. [ABSTRACT FROM AUTHOR]

Prechordal mesendoderm (PME) is a derivative of gastrula organizer underlying the anterior neural plate of vertebrate embryos. It has been firmly established that PME is critical for head induction and anterior–posterior patterning. Therefore, the establishment of PME in a desired shape and size at a correct position during early embryogenesis is crucial for normal head patterning. However, it remains largely unclear how the desired form and size of PME is generated at a predestined position during early embryogenesis. Here we show that in zebrafish a maternal transcription repressor Vsx1 is essential for this early developmental regulation. Knocking down maternal vsx1 resulted in impaired PME formation and progression associated with a deficient and posteriorized forebrain. Loss- and gain-of-function experiments showed that maternal Vsx1 is essential for repressing ntl ectopic expression in more animal region at early gastrula stages. Chromatin immunoprecipitation assay in combination with core consensus sequence mutation analysis further revealed that maternal Vsx1 can directly repress ntl transcription by binding to the proximal promoter at a specific site. Simultaneous inhibition of ntl function could successfully suppress the defects of both PME and forebrain formation in maternal Vsx1 knockdown embryos. Our results reveal a pivotal role for maternal Vsx1 as a direct transcriptional repressor of ntl expression at the margin of the zebrafish gastrula to ensure directional cell polarization and migration of PME cells. [ABSTRACT FROM AUTHOR]

Layered materials are generally considered to be good candidates for thermoelectric materials, and the monolayer ZrNCl and HfNCl obtained from layered material ZrNCl and HfNCl should have lower lattice thermal conductivity. Here the electronic structure and thermoelectric properties of monolayer ZrNCl and HfNCl are studied by the first principles and the semi-classical Boltzmann theory. It is found that the DOS of HfNCl is larger than that of ZrNCl near Fermi surface, which shows that Seebeck coefficient of HfNCl are also larger than that of ZrNCl. The high frequency of the acoustic branch of HfNCl is relatively low, therefore, the lattice thermal conductivity of HfNCl is lower. The electrical conductivity of HfNCl is larger than that of ZrNCl. Therefore, HfNCl have good thermoelectric transport performance and high thermoelectric optimal value. ZT as a function of temperature for monolayer ZrNCl (Left) and monolayer HfNCl (Right). The Seebeck coefficient and electrical conductivity of HfNCl is larger than that of ZrNCl, nevertheless the lattice thermal conductivity of HfNCl is smaller than that of ZrNCl. Therefore, HfNCl have good thermoelectric transport performance and high thermoelectric optimal value. Image 1 • Seebeck coefficient of HfNCl are also larger than that of ZrNCl. • High frequency of acoustic branch of HfNCl causes lower lattice thermal conductivity. • The electrical conductivity of HfNCl is larger than that of ZrNCl. • HfNCl have good thermoelectric transport performance. [ABSTRACT FROM AUTHOR]

MS-275 has been demonstrated to inhibit the growth of esophageal squamous cell carcinoma (ESCC) cells in our previous study, but its role in ESCC remains to be further explored. Cisplatin (cis-diamminedichloroplatinum II, DDP) is the first-line chemotherapeutic drug widely used in clinic for ESCC patients. However, the side effects of nephrotoxicity and drug resistance limit its clinical use. This study aimed to evaluate the anticancer effects of MS-275 combined with DDP on ESCC cell line EC9706 both in vitro and in vivo , and to investigate the possible mechanisms that mediate these effects. We found that MS-275 combined with DDP showed synergistic antitumor effects on EC9706 cells in vitro by decreasing cell proliferation, increasing apoptosis and oxidative damage, and inhibiting migration and stemness. The combination of MS-275 and DDP triggered pro-survival autophagy in EC9706. Moreover, MS-275 combined with DDP suppressed EC9706 xenografts growth and promoted apoptosis in vivo. Further study displayed that MS-275 combined with DDP suppressed Wnt/β-catenin signaling in EC9706 cells and xenografts. These results indicate that MS-275 combined with DDP exerts synergistic antitumor effects by enhancing the chemosensitivity of EC9706 cells to DDP, which may be a potential therapeutic strategy for the treatment of patients with ESCC. • MS-275 combined with DDP significantly inhibits the survival of EC9706 cells in vitro and in vivo. • The combination of MS-275 and DDP triggers pro-survival autophagy in EC9706 cells. • MS-275 combined with DDP suppresses Wnt/β-catenin signaling in EC9706 cells and xenografts. [ABSTRACT FROM AUTHOR]

Sepsis is characterized as exceed inflammation response and multiple organs dysfunction. Many articles suggested that mesenchymal stem cells can alleviate the inflammation and improve the survival rate of inflammatory animal models, however, the mechanism is still unclear. This study aimed to test the hypothesis that rat adipose-derived mesenchymal stem cells (ADMSCs) produce a amount of soluble tumour necrosis factor receptor 1 (sTNFR1), which ameliorated liver injury and inflammation and increased the survival rate of septic rat model.120 adult male Sprague-Dawley rats were randomly divided into 4 groups: sham-operated (Sham), sepsis-induced by cecal ligation and puncture (CLP), shNC (injected 1 × 106 ADMSCs with transfected with scramble shRNA 1 h after CLP), and shsTNFR1 (injected 1 × 106 ADMSCs with transfected with sTNFR1 1 h after CLP). The serum sTNFR1 levels were the lowest in Sham and highest in shNC group. ADMSCs could decrease the levels of pro-inflammatory cytokines such as TNF-α, IL-6, AP-1 c-jun and NF-κB p56 after CLP administration, whereas this result was weaken by shsTNFR1 administration. Moreover, shNC had an increased levels of the anti-inflammatory factor IL-10 compared with CLP, and this change could be weakened in shsTNFR1 administration. More importantly, ADMSCs could improve the survival rate of CLP-induced septic rats. Therapeutically administered ADMSCs secrete sTNFR1, which alleviated the liver injury and inflammatory response. Additionally, ADMSCs also ameliorated the systematic inflammation and increased the survival rate of septic rats. • ADMSCs could produce numerous sTNFR1 under inflammatory stimulation. • ADMSCs transplanted into the injury organ, liver. • ADMSCs could alleviate the liver injury and inflammation via secreting sTNFR1. [ABSTRACT FROM AUTHOR]