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Metal-organic frameworks (MOFs) with diverse chemistry, structures, and properties have emerged as appealing materials for miniaturized solid-state devices. The incorporation of MOF films in these devices, such as the integrated microelectronics and nanophotonics, requires robust patterning methods. However, existing MOF patterning methods suffer from some combinations of limited material adaptability, compromised patterning resolution and scalability, and degraded properties. Here we report a universal, crosslinking-induced patterning approach for various MOFs, termed as CLIP-MOF. Via resist-free, direct photo- and electron-beam (e-beam) lithography, the ligand crosslinking chemistry leads to drastically reduced solubility of colloidal MOFs, permitting selective removal of unexposed MOF films with developer solvents. This enables scalable, micro-/nanoscale (≈70 nm resolution), and multimaterial patterning of MOFs on large-area, rigid or flexible substrates. Patterned MOF films preserve their crystallinity, porosity, and other properties tailored for targeted applications, such as diffractive gas sensors and electrochromic pixels. The combined features of CLIP-MOF create more possibilities in the system-level integration of MOFs in various electronic, photonic, and biomedical devices. Precise and scalable patterning is essential for the use of metal-organic frameworks (MOFs) in solid-state electronics and photonics. Here, the authors report on resistance-free, direct photo- and electron-beam lithography of MOF films using crosslinking chemistry.

During autophagy the enzyme Atg3 catalyzes the covalent conjugation of LC3 to the amino group of phosphatidylethanolamine (PE) lipids, which is one of the key steps in autophagosome formation. Here, we have demonstrated that an N-terminal conserved region of human Atg3 (hAtg3) communicates information from the N-terminal membrane curvature-sensitive amphipathic helix (AH), which presumably targets the enzyme to the tip of phagophore, to the C-terminally located catalytic core for LC3–PE conjugation. Mutations in the putative communication region greatly reduce or abolish the ability of hAtg3 to catalyze this conjugation in vitro and in vivo, and alter the membrane-bound conformation of the wild-type protein, as reported by NMR. Collectively, our results demonstrate that the N-terminal conserved region of hAtg3 works in concert with its geometry-selective AH to promote LC3–PE conjugation only on the target membrane, and substantiate the concept that highly curved membranes drive spatial regulation of the autophagosome biogenesis during autophagy. The E2-like enzyme human Atg3 catalyses the transfer of ubiquitin-like mammalian LC3 to the lipid phosphatidylethanolamine during autophagosome formation. Here, the authors combine NMR measurements with in vitro biochemical and in vivo cellular assays and show that the N-terminal conserved region of human Atg3 communicates information from the curvature-sensing domain to its active site.

The mechanism of phagophore closure remains unclear due to technical limitations in distinguishing unclosed and closed autophagosomal membranes. Here, we report the HaloTag-LC3 autophagosome completion assay that specifically detects phagophores, nascent autophagosomes, and mature autophagic structures. Using this assay, we identify the endosomal sorting complexes required for transport (ESCRT)-III component CHMP2A as a critical regulator of phagophore closure. During autophagy, CHMP2A translocates to the phagophore and regulates the separation of the inner and outer autophagosomal membranes to form double-membrane autophagosomes. Consistently, inhibition of the AAA-ATPase VPS4 activity impairs autophagosome completion. The ESCRT-mediated membrane abscission appears to be a critical step in forming functional autolysosomes by preventing mislocalization of lysosome-associated membrane glycoprotein 1 to the inner autophagosomal membrane. Collectively, our work reveals a function for the ESCRT machinery in the final step of autophagosome formation and provides a useful tool for quantitative analysis of autophagosome biogenesis and maturation. During autophagy, phagophores elongate to form double-membrane vesicles but the mechanism behind their closure is unknown. Here, the authors develop an autophagy assay and find a role for the endosomal sorting complexes required for transport component CHMP2A as a phagophore closure regulator.

Autophagosomal membranes can serve as activation platforms for intracellular death-inducing signaling complexes (iDISCs) to initiate Caspase-8-dependent apoptosis. In this study, we explore the impact of ESCRT-III-dependent phagophore closure on iDISC assemblies and cell death in osteosarcoma and neuroblastoma cells. Inhibition of phagophore closure by conditional depletion of CHMP2A, an ESCRT-III component, stabilizes iDISCs on immature autophagosomal membranes and induces Caspase-8-dependent cell death. Importantly, suppression of the iDISC formation via deletion of ATG7, an E1 enzyme for ubiquitin-like autophagy-related proteins, blocks Caspase-8 activation and cell death following CHMP2A depletion. Although DR5 expression and TRAIL-induced apoptosis are enhanced in CHMP2A-depleted cells, the canonical extrinsic pathway of apoptosis is not responsible for the initiation of cell death by CHMP2A depletion. Furthermore, the loss of CHMP2A impairs neuroblastoma tumor growth associated with decreased autophagy and increased apoptosis in vivo. Together, these findings indicate that inhibition of the ESCRT-III-dependent autophagosome sealing process triggers noncanonical Caspase-8 activation and apoptosis, which may open new avenues for therapeutic targeting of autophagy in cancer.

Autophagosomal membranes are emerging as platforms for various cell survival and death signaling networks beyond autophagy. While autophagy-dependent cell death has been reported in response to a variety of stimuli, the underlying molecular mechanisms remain far from clear. Here, we demonstrate that inhibition of autophagosome completion by Atg2A/B deletion accumulates immature autophagosomal membranes that promote non-canonical caspase-8 activation in response to nutrient starvation via an intracellular death-inducing signaling complex (iDISC). Importantly, iDISC-induced caspase-8 dimerization and activation occurs on accumulated autophagosomal membranes and requires the LC3 conjugation machinery but is independent from the extrinsic pathway of apoptosis. Moreover, we have identified NF-κB signaling and c-FLIP as negative regulators of iDISC-mediated caspase-8 activation and apoptosis. Collectively, these findings reveal autophagosomal membrane completion as a novel target to switch cytoprotective autophagy to apoptosis.

Objectives The study investigates the role of Cell Division Cycle Associated (CDCA) genes in colorectal cancer (COAD) by analyzing their differential expression, epigenetic alterations, prognostic significance, and functional associations. Methodology This study employed a detailed in silico and in vitro experiments-based methodology. Results RT-qPCR assays reveal significantly elevated mRNA levels of CDCA2, CDCA3, CDCA4, CDCA5, CDCA7, and CDCA8 genes in COAD cell lines compared to controls. Bisulfite sequencing indicates reduced promoter methylation of CDCA gene promoters in COAD cell lines, suggesting an epigenetic regulatory mechanism. Analysis of large TCGA datasets confirms increased CDCA gene expression in COAD tissues. Survival analysis using cSurvival database demonstrates negative correlations between CDCA gene expression and patient overall survival. Additionally, Lasso regression-based models of CDCA genes predict survival outcomes in COAD patients. Investigating immune modulation, CDCA gene expression inversely correlates with immune cell infiltration and immune modulators. miRNA-mRNA network analysis identifies regulatory miRNAs targeting CDCA genes, validated by RT-qPCR showing up-regulation of has-mir-10a-5p and has-mir-20a-5p in COAD cell lines and tissues. Drug sensitivity analysis suggests resistance to specific drugs in COAD patients with elevated CDCA gene expression. Furthermore, CDCA gene expression correlates with crucial functional states in COAD, including “angiogenesis, apoptosis, differentiation, hypoxia, inflammation, and metastasis.” Additional in vitro experiments revealed that CDCA2 and CDCA3 knockdown in SW480 and SW629 cells significantly reduced cell proliferation and colony formation while enhancing cell migration. Conclusion Overall, the study elucidates the multifaceted role of CDCA genes in COAD progression, providing insights into potential diagnostic, prognostic, and therapeutic implications.

In hypersonic flight the shock wave and turbulent boundary layer interaction (STBLI) sharply increases wall heat transfer that intensifies the aerodynamic heating problems. In this work the STBLI is modelled by compression ramp flow with a Mach number of 5, a Reynolds number based on momentum thickness of 4652 and a wall to recovery temperature ratio of 0.5. The aerodynamic heat generation and transport mechanisms are investigated in the interaction based on theoretical analysis and direct numerical simulation (DNS) that agrees with previous studies. A prediction correlation of wall heat flux in STBLI is deduced theoretically and validated by some representative data including the present DNS, which improves the prediction accuracy and can be applied to a wider $Ma$ range compared with the canonical Q-P theory. The correlation indicates that the sharp increase of wall heat transfer in the STBLI can be explained by the boundary layer compression and the convection transport enhancement. Based on the DNS results, the aerodynamic heat generation and transport mechanisms are revealed in the separation, recirculation and reattachment zones in the STBLI. From this perspective, the peak heat flux can be further explained by the enhancement of near-wall turbulent energy dissipation, compression aerodynamic heat generation and the near-wall turbulent transport. The generation and transport of compression aerodynamic heat reveal the underlying mechanism of the strong correlation between the peak heat flux ratios and the pressure ratios in STBLIs.

Purpose – The jet impingement usually accompanying large interface movement is studied by the in-house solver MLParticle-SJTU based on the modified moving particle semi-implicit (MPS) method, which can provide more accurate pressure fields and deformed interface shape. The comparisons of the pressure distribution and the shape of free surface between the presented numerical results and the analytical solution are investigated. The paper aims to discuss these issues. Design/methodology/approach – To avoid the instability in traditional MPS, a modified MPS method is employed, which include mixed source term for Poisson pressure equation (PPE), kernel function without singularity, momentum conservative gradient model and highly precise free surface detection approach. Detailed analysis on improved schemes in the modified MPS is carried out. In particular, three kinds of source term in PPE are considered, including: particle number density (PND) method, mixed source term method and divergence-free method. Two typical kernel functions containing original kernel function with singularity and modified kernel function without singularity are analyzed. Three kinds of pressure gradient are considered: original pressure gradient (OPG), conservative pressure gradient (CPG) and modified pressure gradient (MPG). In addition, particle convergence is performed by running the simulation with various spatial resolutions. Finally, the comparison of the pressure fields by the modified MPS and by SPH is presented. Findings – The modified MPS method can provide a reliable pressure distribution and the shape of the free surface compared to the analytical solution in a steady state after the water jet impinging on the wall. Specifically, mixed source term in PPE can give a reasonable profile of the shape of free surface and pressure distribution, while PND method adopted in the traditional MPS is not stable in simulation, and divergence-free method cannot produce rational pressure field near the wall. Two kernel functions show similar pressure field, however, the kernel function without singularity is preferred in this case to predict the profile of free surface and pressure on the wall. The shape of free surface by CPG and MPG is agreement with the analytical solution, while a great discrepancy can be observed by OPG. The pressure peak by MPG is closer to the analytical solution than that by CPG, while the pressure distribution on the right hand side of the pressure peak by latter is better match with the analytical solution than that by former. Besides, fine spatial resolution is necessary to achieve a good agreement with analytical results. In addition, the pressure field by the modified MPS is also quite similar to that by SPH, and this can further validate the reliable of current modified MPS. Originality/value – The present modified MPS appears to be a stable and reliable tool to deal with the impinging jet flow problems involving large interface movement. Mixed source term in PPE is superior to PND adopted in the traditional MPS and divergence-free method. The kernel function without singularity is preferred to improve the computational accuracy in this case. CPG is a good choice to obtain the shape of free surface and the pressure distribution by jet impingement.

In the present study, a novel layered cathodic compound, Li 1-x Ni 0.58 Co 0.12 Mn 0.19 Fe 0.07 Cr 0.04 Mg x O 2 , was synthesized using an economically feasible oxalic acid co-precipitation method. The microstructure, morphology, and electrochemical properties of the synthesized compounds were studied by X-ray diffraction (XRD), scanning electron microscope (SEM), charge–discharge tests, cyclic voltammetry (CV), and electrochemical impedance spectroscopy (EIS). Electrochemical test results showed that the sample containing Cr = 0.04 and Mg = 0.02 exhibited the best electrochemical performance with an initial specific capacity of 181.76 mAh·g −1 at 0.1 C, the capacity retention ratios of 88.81% at 200 cycles at 0.5 C. In addition, the 4Cr-2 Mg electrode exhibits superior rate capability with discharge capacities of 182.56, 171.13, 158.51, 133.41, and 121.01 mAh·g −1 at 0.1, 0.2, 0.5, 1, and 2 C, respectively. Replacing Cr can play an essential role in improving maintenance capacity and cycling behavior. Additionally, the diffusibility of lithium-ion batteries (LIBs) was significantly improved as a result of Mg doping, which could be related to the reduction in Li + /Ni 2+ cation mixing and its ionic radius. Graphical Abstract

Though silicon suboxide (SiO x , 0 < x < 2) has been considered a new generation of anode material for lithium-ion batteries, the large volume expansion and intrinsic conductivity hinder its commercial applications. In this work, silicon dioxide (SiO 2 ) was prepared via tetraethyl orthosilicate (TEOS) hydrolyzed, and lithium fluoride (LiF) was introduced in situ, and then SiO 2 /LiF was covered with pyrolyzed sucrose to obtain SiO x /LiF@C. Large elastic modulus, low solubility in a carbonate solution, and high chemical stability LiF was designed to induce the formation of a stable solid-electrolyte interface (SEI) layer on the electrode surface. The more stable interface minimizes the continuous growth of the SEI layer, thereby reducing the resistance and the irreversible decay of capacity. Compared with SiO x @C-3, the SiO x /LiF@C-3 anode displays better electrochemical performance, especially cycle performance at high current density. Benefiting from the cooperation of amorphous carbon coating and stable SEI layer, SiO x /LiF@C-3 activated by low current maintains a specific capacity of 504.2 mAh g −1 and a capacity retention rate of 96% after 300 cycles at a current density of 0.3 A g −1 . The great potential of LiF‑introduced for silicon suboxide anode is demonstrated.