In this work, a binder-free layered Ni(OH)2 nanosheet-like structure was synthesized using a facile vapour-assisted hydrothermal growth technique. The effect of the hydrothermal reaction duration on the structural development and electrch emical efficiency of the electrodes is thoroughly investigated. The uniquelayered structureof Ni(OH)2helps to enhance its electrochemical activity. The electrochemical measurements of the optimizedNiH-8electrode(Ni(OH)2 over Ni foam formed by 8 hours of hydrothermal treatment) showan ultra-high areal capacitance of 16.66 F/cm2 and a specific capacity of 7.49 C/cm2 at acurrent density of 2 mA/cm2. A rate capability of 56.4% could be maintained even at a current density of 30 mA/cm2. The enhanced electrochemical activity was attributed to the highly accessible, interconnected layered architecture of Ni(OH)2, which improved rate kinetics. Additionally,an asymmetric supercapacitor device was fabricated with NiH-8 as the positive electrode and activated carbon-coated Ni foam as the negative electrode, and it exhibitedan outstanding energy density of 0.49 mWh/cm2and a power density of 29.9 mW/cm2. Cyclic stability studies over5000 cycles were also conducted for the assembled asymmetric supercapacitor, yieldinga capacitance retention of 98% and aCoulombic efficiency of 93%.This work also demonstrates the device prototype's practical applicabilityby powering red and white LEDs. Therefore, the developed NiH-8 electrode is a promising candidate for high-performance supercapacitors.
Deoxysphingolipids (dSLs) are atypical sphingolipids that accumulate in several pathological settings, yet their impact on hematologic malignancies is poorly understood. Here, we investigate the pathways and mechanisms of deoxysphinganine (dSA) cytotoxicity in lymphoma cells and its potential as a therapeutic agent. dSA exhibited markedly greater cytotoxicity than canonical sphingoid bases in lymphoma cell lines, yet induced only cytostatic effects in normal human T cells, indicating a therapeutically exploitable window. Inhibition of ceramide synthase blocked the generation of deoxy(dihydro)ceramides, prevented mitochondrial depolarization, caspase activation, ER stress, and DNA damage, establishing CerS-dependent deoxysphingolipids as essential mediators of dSA-induced death. Mechanistically, dSA engaged a mitochondrial apoptotic pathway, with DNA damage occurring downstream of mitochondrial permeabilization and caspase activation, while PERK-driven ER stress occurred in parallel and was dispensable for cytotoxicity. Subtype-specific engagement of ER stress and DNA damage further suggests that dSL signaling is shaped by lineage context. The differential sensitivity between malignant lymphoid cells and normal T cells, together with the central role of CerS-derived deoxy(dihydro)ceramides, highlights deoxysphingolipid metabolism as a druggable vulnerability in lymphoma. These findings support further exploration of dSA-based strategies and targeted modulation of dSL synthesis as a novel therapeutic avenue for non-solid hematologic malignancies.
Developing a convenient catalyst preparation strategy capable of efficiently activating peroxymonosulfate (PMS) holds crucial significance for facilitating the large-scale application of advanced oxidation technologies. Herein, the leaf-like zeolitic imidazolate framework (ZIF-L) was in situ grown on stainless steel mesh (SS) through impregnation at room temperature, and the derivatives of ZIF-L/SS were obtained via rapid combustion to form CoOx@C/SS. The CoOx@C/SS catalyst was employed for activating PMS to degrade the sulfamethoxazole (SMX). In cyclic experiments, ZIF-L/SS could be rapidly recovered and reused in subsequent reactions. Structural evolution studies reveal that after the unstable carbon nanotubes on the catalyst surface detach during the initial reaction cycle, the catalytic performance stabilizes, and metal leaching is significantly suppressed. Reactive species capture experiments and electron paramagnetic resonance (EPR) tests demonstrated that superoxide radicals (O2•-) and high-valent cobalt oxygen species (Co(IV)=O) played crucial roles in SMX degradation. Considering its simple preparation process, low cost, as well as its effectiveness and stability, CoOx@C/SS undoubtedly represents a promising catalyst for environmental applications.
Methanol contamination in ethanol-based systems remains a major concern in both beverage safety and fuel-quality monitoring. In this work, a dual-defect one-dimensional topological photonic crystal is proposed for sensitive methanol detection. The structure consists of alternating Si and SiO2 layers with two cavities for analyte. This configuration supports four coupled defect modes inside the photonic band gap with strong field localization within the cavity regions. Optical characteristics are investigated using the transfer matrix method along with wavelength-dependent refractive index modelling and Bruggeman effective medium theory. The proposed sensor exhibits simultaneous concentration-dependent shifting of four defect modes, enabling easier spectral tracking with a maximum sensitivity of 916.15 nm/RIU and a figure of merit of 1624/RIU. The influence of spacer-layer engineering on mode coupling and sensing performance is also systematically investigated. At very low methanol concentrations, the resonance shifts become extremely small due to the minimal refractive index variation of the analyte. To address this limitation, three machine learning models are employed using multiple spectral descriptors extracted from all defect modes. The combined photonic crystal-machine learning framework enables reliable prediction of ultra-low methanol concentration variations in ethanol-based beverage and fuel systems.
Nanofibers with nominal compositions LaFe1−xCuxO3, x = 0, 0.05 and 0.10, were synthesized by electrospinning and evaluated for photo-Fenton degradation of methyl orange (MO) under UVB/UVA–visible–near-infrared irradiation in acidic H2O2 solution. XRD Rietveld refinements confirmed single orthorhombic Pbnm perovskite phases, while EDX and XPS verified Cu incorporation close to the nominal compositions. Cu incorporation reduced fiber thickness from 228 ± 82 nm for LaFeO3 to 151 ± 72 and 138 ± 53 nm for LaFe0.95Cu0.05O3 and LaFe0.9Cu0.1O3, but produced more compact fibers with lower accessible surface area. Despite this unfavorable textural change, MO decolorization after 24 h increased from 6.4% for LaFeO3 to 34.2% and 26.1% for LaFe0.95Cu0.05O3 and LaFe0.9Cu0.1O3, respectively. LaFe0.95Cu0.05O3 retained most of its activity after three cycles, while XRD confirmed preservation of crystalline structure. XPS detected predominantly Fe3+ in all samples, mixed Cu+ and Cu2+ in the doped fibers and higher non-lattice oxygen contributions after Cu incorporation. UV-Vis-NIR diffuse reflectance spectroscopy suggested extended visible and infrared absorption after Cu incorporation, while DFT + U assigned low energy transitions to Cu–O hybridized in-gap states. Electronic levels calculated by DFT + U were referenced using the valence band maximum obtained from UPS. This band alignment showed that photogenerated electrons from conduction band regions can reduce Cu2+ to Cu+. Hence, the higher activity is mainly associated with surface Cu + sites reacting with H2O2 to generate •OH radicals, together with Cu+ generation and regeneration during irradiation. The superior activity of the 5% Cu fibers was attributed to higher specific surface area and lower radiative recombination response.
Whether the fecal metabolome differs according to intensive low-density lipoprotein cholesterol (LDL-C) target achievement among statin-treated patients is unclear. In this cross-sectional study, 124 statin-treated adults with chronic disease were stratified by fasting LDL-C into a target-achieved group (< 70 mg/dL, n = 52) and a target-not-achieved group (≥ 70 mg/dL, n = 72). Stool samples were profiled by untargeted ultra-high-performance liquid chromatography-tandem mass spectrometry, and multivariable models adjusted for age, sex, chronic kidney disease, and angiotensin-converting enzyme inhibitor/angiotensin receptor blocker use were used to identify metabolites independently associated with target achievement. Statin dose, treatment duration and glucose-lowering therapy were also compared between the groups. Paired 16S rRNA gene sequencing data available for a subset (n = 86) were used for integrative correlation and network analyses. Partial least-squares discriminant analysis showed separation between the two groups. Eight annotated metabolites-glutamine, glutamate, phenylalanine, N-acetyl-L-phenylalanine, L-methionine, N-acetyl-L-methionine, lysine, and N-methyl-D-aspartic acid, predominantly amino acids and their derivatives-were present at lower fecal levels in participants who achieved the LDL-C target. Metabolite set enrichment analysis implicated amino acid and nitrogen metabolism, and multiomics network analysis identified an Anaerotruncus-centered amino acid module with high degree centrality. In conclusion, LDL-C target achievement under statin therapy was associated with a coherent "low fecal amino acid" signature and an Anaerotruncus-linked microbe-metabolite hub. These findings suggest that intestinal nutrient handling and gut microbial amino acid metabolism may contribute to variability in LDL-C response, and they warrant prospective mechanistic evaluation.
Metabolic dysfunction-associated liver disease (MASLD) arises from the accumulation of triglycerides within the liver. MASLD can advance to metabolic dysfunction-associated steatohepatitis (MASH), cirrhosis, and hepatocellular carcinoma. Monoacylglycerol acyltransferase 2 (MOGAT2) is essential for triglyceride synthesis and plays a significant role in regulating lipid metabolism. Here, we demonstrate the ability of a new human MOGAT 2 inhibitor, VB-85387, to inhibit the development of MASLD/MASH and further define its effects on the key metabolic pathways that progress MASH development. MASLD/MASH was induced using a methionine, choline-deficient diet (LMCD) or by streptozotocin treatment combined with high fat diet feeding (STAM-HFD). VB-85387 significantly mitigated the severity of MASLD and reduced signs of MASH in mice subjected to these two distinct diets. VB-85387-treated mice exhibited decreased fibrosis, evidenced by reduced hepatic triglyceride concentrations, hydroxyproline levels, and collagen deposition. NAS scores were consistently lower in VB-85387-treated mice across both models. VB-85387-treated mice showed induced PPARα signaling and reduced SREBP transcription, demonstrating a likely role for VB-85387 in regulating lipogenesis and fatty acid β-oxidation. STAM-HFD treated mice showed lower NF-κBp65 activation, which was associated with lower TNFα expression. IL-1β and IFNβ levels were also both reduced, suggesting VB-85387 can reduce pro-inflammatory pattern recognition receptor signaling. In addition, treatment suppressed IL-4/IL-6-dependent JAK activation. Overall, VB-85387 inhibited MASLD development by reducing liver triglyceride levels, fibrosis, and meta-inflammatory signaling. VB-85387 was as effective or superior to the MOGAT2 inhibitor phase I clinical trial drug BMS-963272 in reducing MASLD and fibrosis. VB-85387 has considerable potential for developing therapeutics targeting MASLD/MASH.
