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Correlation between virological response and portal vein thrombosis in patients with chronic hepatitis B
An adaptive deep learning approach based on InBNFus and CNNDen-GRU networks for breast cancer and maternal fetal classification using ultrasound images
Optogenetic restoration of high-sensitivity vision using ChRmine- and ChroME-based channelrhodopsins
Abstract Optogenetic gene therapy is a promising mutation-independent treatment that aims to restore visual perception in patients blinded by retinal diseases that cause photoreceptor degeneration. Still, low sensitivity or slow kinetics of currently utilized optogenetic proteins limit the efficacy of such approaches. Here, we evaluated the therapeutic potential of three channelrhodopsin variants: ChRmine, from the algae Rhodomonas lens, ChRmine-T119A, a faster-closing ChRmine variant, and ChroME2s, a second-generation Chronos-based opsin.We expressed these opsins in retinal ganglion cells of rd1 mice, a model of severe retinal degeneration. Single cell electrophysiology demonstrates opsin’s large sensitivity to a range of light intensities as well as opsin-expressing retinal ganglion cells generated action potentials in response to light stimulation. Behavioral tests showed ChRmine-T119A’s efficacy at 360 lux compared to unmodified ChRmine and ChroME2s. ChRmine and ChroME2s did restore light perception at higher light intensities. Additionally, our dose–response study with ChRmine-T119A revealed that lower viral titers were more effective at restoring light sensitivity. Our study demonstrates that these ChRmine- and ChroME-based opsins can enhance vision in late-stage blinding diseases.
Suppression of interfacial polarization via enhancement of entropy, grain resistance and optical band-gap strategies in perovskite ceramics
Pressure-driven electronegativity inversion in alkali liquids
Liquid–liquid phase transitions (LLPTs) are typically characterized as two-state systems, where transitions occur between two distinct liquid phases driven by local structural rearrangements. In this study, we observed a continuous LLPT with an inversion of electronegativity in a K–Rb binary alloy. This uniquely exhibits a three-state system behavior. The transition, induced by pressure-driven reordering of electronic orbital energies, progresses through a sequence from s -metal to electride to d -metal, accompanied by a valence reversal: Potassium transitions from a negative to a positive valence, while rubidium undergoes the opposite shift. This process is marked by two successive anomalies in the alloy’s optical, thermodynamic, and dynamic properties over a broad pressure range. The observation of similar LLPT phenomena in other alkali and alkaline earth metal liquids suggests that this three-state system mechanism may provide broader insights into the nature of continuous phase transitions.
EZH2 loss promotes gastric squamous cell carcinoma
Non-C2 symmetric chiral ligand dictating allyl-allyl coupling
Cryo-EM structures of the E. coli Ton and Tol motor complexes
Abstract The Ton and Tol motor proteins use the proton gradient at the inner membrane of Gram-negative bacteria as an energy source. The generated force is transmitted through the periplasmic space to protein components associated with the outer membrane, either to maintain the outer membrane integrity for the Tol system, or to allow essential nutrients to enter the cell for Ton. We have solved the high-resolution structures of the E. coli TonB-ExbB-ExbD and TolA-TolQ-TolR complexes, revealing the inner membrane embedded engine parts of the Ton and Tol systems, and showing how TonB and TolA interact with the ExbBD and TolQR subcomplexes. Structural similarities between the two motor complexes suggest a common mechanism for the opening of the proton channel and the propagation of the proton motive force into movement of the TonB and TolA subunits. Because TonB and TolA bind at preferential ExbB or TolQ subunits, we propose a new mechanism of assembly of TonB and TolA with their respective ExbBD and TolQR subcomplexes and discuss its impact on the mechanism of action for the Ton and Tol systems.
Halogen Bonding Enable Improved Performance and Stability of Dion–Jacobson Perovskite Solar Cells
Abstract The undesired phase distribution and intrinsic residual lattice strain remain the bottleneck for high‐performance and stable 2D or Q‐2D perovskite solar cells (PSCs), especially for the Dion–Jacobson (DJ) type Q‐2D PSCs. Here, we showcase employing halogen bonds to stabilize the halide anions and fine‐tuning the residual lattice strain by introducing perfluorodecyl iodide (PFI). It reduces the density of iodide species defects and releases the residual tensile strain, leading to more homogenous phase distribution, suppressed carrier recombination, promoted charge transport, enhanced efficiency, and stability. Therefore, DJ PSCs maintain over 81% of initial efficiency after thermal‐light aging (i.e., under 85 °C and 1 sun illumination) for 952 h, and remain over 91% of initial efficiency after under reverse bias (−2.5 V, under ISOS‐V aging tests) for over 21 h, representing one of the most bias‐stable Q‐2D PSCs reported so far.
Mitogenome characterization and phylogeny of Neohydatothrips gracilipes (Thripidae: Sericothripinae)
A subcellular study on reactive oxygen species generation by PFAS in HepG2 cells
Abstract Per- and polyfluoroalkyl substances (PFAS) hepatotoxicity is well documented, especially for legacy compounds such as PFHxS, PFOA, PFOS, and PFNA. However, the mechanism(s) involved are yet to be fully understood. The present study aims to investigate the origin of PFAS-induced formation of reactive oxygen species (ROS) and their relevance for the decrease of cell viability of HepG2 cells after exposure to PFASs. Moreover, a structure–activity relationship was assessed using PFASs with different headgroups (carboxylic, sulfonic, and alcoholic) and variable carbon-chain lengths (4–10 C). The link between ROS generation and cell viability was assessed using two antioxidants: quercetin, a generic antioxidant, and mito-tempo, a mitochondria-targeted antioxidant. Both antioxidants were demonstrated to be effective in reducing PFAS-induced ROS generation. The mechanism behind PFAS-induced ROS might be headgroup-dependent, as quercetin increased cell viability after both perfluoroalkyl carboxylic acids (PFCA) and perfluorosulfonic acids (PFSA) exposure, while mito-tempo only improved cell viability after PFCAs exposure. The two major sources of ROS generation in HepG2 cells are the peroxisomes and mitochondria. However, exposure to PFASs did not impact peroxisomal or mitochondrial activity after 24 h. Uncommon sources of ROS generation, such as lysosomal leakage or lipid peroxidation, have been demonstrated to result from previously generated ROS and not from PFASs exposure. Indeed, lysosomal leakage caused by PFASs exposure is negated by either quercetin or mito-tempo treatment, while lipid peroxidation only occurs after 24 h of exposure, long after the initial ROS generation by PFASs. This indicates that both events are a result of previously generated ROS. However, exposure to both PFOA and PFOS was demonstrated to reduce catalase activity in HepG2. In conclusion, the present study demonstrates that ROS generation after PFASs exposure might be due to inhibition of HepG2 endogenous antioxidants. Moreover, a headgroup-dependent mechanism of action has been observed, indicating that PFCAs and PFSAs exposure might lead to hepatotoxicity through different pathways.
China’s energy economic efficiency evaluation based on novel dynamic network DEA
Fermented grapeseed oil repairs chemically damaged hair via enhanced permeability mechanisms
Abstract Human hair is a biopolymer composed of keratin filaments, lipids, pigments, and water. Chemical treatments of hair, such as dyeing, perming, and bleaching, can impair the integrity of the hair protein structure and accelerate the loss of water and lipids, resulting in increased fragility, breakage, and rapid colour fading. This study investigates compositional changes in fermented grapeseed oil (F-GO) compared to grapeseed oil (GO) and identifies its enhanced hair permeability, highlighting its substantial potential to mitigate hair damage from bleaching and dyeing. The fluorescent labelling results verified that the ability to permeate hair was significantly improved by F-GO compared to GO and silicone oil. Fourier transform infrared spectroscopy (FT-IR) and thermal weight analyser (TGA) results illustrate that F-GO-treated hair can form additional intermolecular hydrogen bonds and might cause a conformational change in the protein structure. The in vitro assessments demonstrate that F-GO delays hair colour loss and enhances mechanical properties. The colour fixation mechanism of F-GO is attributed to its ability to act as an anti-oxygen barrier on the outer layer and a lipid barrier in the inner layer. Together, they protect against pigment loss and degradation. F-GO enhances damaged hair strength by forming hydrogen bonds with keratin residues and preserving lipids and moisture contents. Therefore, F-GO has broad application prospects for bleaching and dyeing damaged hair improvement.
Genetic variation associated with increased lambda-cyhalothrin resistance in Spodoptera frugiperda (Lepidoptera: Noctuidae) in West Africa
Lipid accumulation product and cardiometabolic index as indicators for sarcopenia: A cross-sectional study from NHANES 2011–2018
A lightweight anomaly detection model for network traffic using multi scale spatio temporal residual learning
Pumice soil stabilisation using alkali-activated waste glass for sustainable road subgrade applications
<i>PIK3CA</i> gain-of-function mutation in Schwann cells leads to severe neuropathy and aerobic glycolysis through a non-cell autonomous effect
PIK3CA -related disorders are rare genetic disorders due to somatic gain-of-function mutations in PIK3CA during embryonic development, a pathway involved in cell growth, proliferation, and metabolism. Accumulating evidence from patients with PIK3CA -related disorders indicates that peripheral nerves are frequently affected, leading to severe neurological symptoms. However, the exact underlying mechanism of these disorders remains unclear. To address this, we developed a mouse model with a PIK3CA gain-of-function mutation specifically in Schwann cells, which successfully mirrored the clinical features observed in patients. In this model, we observed that PIK3CA -mutated cells communicate with neighboring healthy cells, such as adipocytes and hair follicles, through a unique crosstalk mechanism that triggers their growth, proliferation, and anagen phase expansion. Additionally, we demonstrated that PIK3CA mutation in peripheral nerves leads to a metabolic shift through glycolytic activation. We investigated the effects of alpelisib, an approved pharmacological inhibitor of PIK3CA, in the model. Early administration of alpelisib significantly improved the signs and symptoms in the mice. However, when treatment was delayed, its efficacy was diminished due to the drug’s inability to penetrate the myelin sheath effectively. In summary, our study offers a valuable mouse model for studying PIK3CA -related neuropathy, uncovers a unique communication between healthy and affected tissues, and highlights the potential benefits of early pharmacological intervention using alpelisib.