查找使用阿拉丁产品的科研文献

d-Cysteine functionalised silver nanoparticles surface with a “disperse-then-kill” antibacterial synergy

Luyao Huang,Yuntian Lou,Dawei Zhang,Lingwei Ma,Hongchang Qian,Yuting Hu,Pengfei Ju,Dake Xu,Xiaogang Li

In this study, antibacterial surfaces with a “disperse-then-kill” synergy were prepared by embedding d -cysteine ( d -cys) functionalised silver nanoparticles (AgNPs) onto polydopamine-coated stainless steel. The as-prepared surface exhibited excellent antibacterial performance against the gram-negative Escherichia coli and Pseudomonas aeruginosa PAO1 and gram-positive Staphylococcus aureus . This component of d -cys could inhibit the formation of mature biofilms and maintain bacteria in dispersed and planktonic states, which further facilitates the bacterial-killing action enabled by the AgNPs. The cooperation of these two components presents a new strategy for developing antibacterial surfaces with a stronger and more durable performance. Furthermore, the as-prepared surface did not exhibit an apparent cytotoxicity based on the results of real-time cell analyzer (RTCA) and a cell viability kit-8 assay (CCK-8 assay). Given these results, the proposed antibacterial strategy demonstrated a potential to inhibit bacterial adhesion and biofilm formation on surgical devices and medical implants.

Trunk Health Condition Inspection Using Integrated 3-D Photogrammetry and Holographic Radar Tomography

Lilong Zou,Xuan Feng,Hai Liu,Amir M. Alani,Cai Liu

Forests are vital components of the ecosystem of the Earth, regulating climate, conserving soil and water, and fostering biodiversity. Sustainable forest management offers crucial long-term benefits, but challenges such as disease threaten tree health. Disease-infected trees in both forests and urban areas pose risks to safety, property, and culture, leading to economic losses. Traditional inspection methods, such as resistance drilling, are invasive and laborious, while nondestructive techniques such as ground penetrating radar (GPR), offer promising alternatives. Although GPR shows potential, complexities such as tree structure and electromagnetic properties hinder accurate disease detection. In order to address these challenges, a new approach integrates structure-from-motion (SfM) photogrammetry with GPR measurement, and a novel holographic radar tomography processing approach has been proposed in this article. These methodologies accurately reconstruct tree trunks in 3-D, enabling precise GPR positioning and the obtaining of trunk permittivity. An arc-shaped Kirchhoff migration algorithm, moreover, helps mitigate irregular trunk shapes, enhancing data accuracy. The proposed framework demonstrates efficacy in real-tree measurement, offering high-precision disease monitoring. This innovation not only aids in preserving biodiversity but also enhances ecosystem services by promoting sustainable forest management. Effective disease monitoring ensures timely intervention, safeguarding valuable old trees and ecosystems while minimizing economic and cultural losses.

D-peptide-nanodrug conjugates synergize VISTA blockade and innate activation for cancer immunotherapy

Beibei Li,Qingchao Wang,Xiaoxi Wang,Peixin Chen,Xinyu Zi,Yanping Ma,Qiaoya Xuan,Ying Cheng,Shihan Zhang,Hanke Feng,Wenjie Zhai,Yahong Wu,Yumiao Zhao,Xiaowen Zhou,Xiaoshuang Niu,Wenshan Zhao

Effective cancer immunotherapy is often hindered by V-domain Ig suppressor of T cell activation (VISTA) signaling and myeloid-derived suppressor cells (MDSCs) within tumor microenvironment (TME). Here, we report D-peptide-nanodrug conjugates that synergize VISTA blockade and innate activation to overcome these constraints. We developed Reorpn7, a proteolytically stable D-peptide VISTA inhibitor with high binding affinity and in vitro serum stability. This inhibitor was co-loaded with a toll-like receptor 7/8 (TLR7/8) agonist (R848) into an matrix metalloproteinase-2 (MMP-2) responsive poly lactic-co-glycolic acid (PLGA) nanoplatform (r7PL-PLGA@R848). Upon enrichment in the TME, MMP-2 responsive cleavage enables the precise release of the VISTA-targeting peptide Reorpn7 and the TLR7/8 agonist R848, thereby achieving synergistic therapeutic effect of VISTA blockade and innate immune activation. In MC38 tumor models, this nanosystem significantly increased intratumoral CD8 + T cell infiltration and achieved robust antitumor efficacy without obvious systemic toxicity. Mechanistically, the platform reshaped the TME from an inhibitory milieu into an immunosupportive one by coordinating checkpoint blockade, myeloid reprogramming, and T cell recruitment. This stimuli-responsive paradigm offers a translatable strategy to overcome immune checkpoint blockade resistance in challenging malignancies.

Shielding the interaction between Pt-d and S-p orbitals through carbon encapsulation

Qingpo Yang,Shangkang Xie,Zixiang Xing,Jie Liu,Yufeng Shen,Ling Huang,Rubo Fang,Feng Feng,Chunshan Lu,Qingtao Wang,Chong Yao,Qunfeng Zhang,Xiaonian Li

The shielding effect effectively suppresses the chemical adsorption between platinum and sulfur species and hinders the formation of Pt-S bonds. • Electrons transfer from Pt to the carbon encapsulation layer to construct metal-carbon interfacial structures, which endows the catalyst with superior hydrogenation activity in sulfur-containing environments. • Carbon-encapsulated structure enhances the structural stability and sulfur resistance of the catalyst. • Experimental characterizations combined with DFT calculations elucidate the underlying reaction mechanism. The presence of sulfur-containing impurities in industrial feedstocks leads to the rapid deactivation of metal-based catalysts, which originates from the specific recognition between the d orbitals of metallic active sites and the p orbitals of sulfur. In this work, a carbon-encapsulation catalyst strategy was employed to shield this specific d–p orbital recognition effect. The Pt-base catalyst showed a sharp 92.28% loss in activity after sulfur poisoning, whereas the carbon-encapsulated catalyst maintained high efficiency and stability, sustaining a reaction rate of 83.41 min –1 even at high mercaptan concentrations (7945 ppm). Moreover, it exhibited excellent reusability with negligible deactivation after five cycles. Characterization and density functional theory (DFT) calculations revealed that the carbon shell serves as “armor” for Pt active sites, physically isolating them from sulfur impurities and suppressing the hybridization between Pt nanoparticles (Pt NPs) and the S 2p orbitals. Meanwhile, Pt nanoparticles induce electron transfer to the carbon layer, converting it into a conductive “metallic carbon” that enhances hydrogenation activity. This work provides new insights into the anti-sulfur poisoning mechanism of catalytic hydrogenation. Download: Download high-res image (255KB) Download: Download full-size image

Rehmannioside D directly targets PTP1B to ameliorate metabolic dysfunction-associated fatty liver disease

Daiyu Xu,Ruidi Liu,Zhenqiang Zhang,Xiaowei Zhang,Gai Gao,Zhishen Xie

Ethnopharmacological relevance Rehmanniae Radix Praeparata, the processed root of Rehmannia glutinosa Steud. (Orobanchaceae), a traditional Chinese medicine, has traditionally been used for metabolic disorders related deficiency patterns in traditional Chinese medicine. As a pharmacopoeial quality control marker of Rehmanniae Radix Praeparata, rehmannioside D (RD) possesses hepatoprotective and metabolic regulatory potential; however, its therapeutic role in MAFLD remains unclear. Aim of the study This study aimed to evaluate the therapeutic effects of RD against MAFLD and to elucidate its underlying molecular mechanisms. Materials and methods db/db mice and free fatty acid (FFA)-induced HepG2 cells were used to assess the effects of RD in vivo and in vitro . Lipid accumulation, liver injury, insulin signaling, and endoplasmic reticulum (ER) stress were evaluated. Limited proteolysis-mass spectrometry (LiP-MS) was used to identify potential targets of RD. Molecular docking, cellular thermal shift assay (CETSA), and molecular dynamics (MD) simulations were performed to validate the interaction between RD and the target protein. Results Marked amelioration of lipid metabolic disorders was observed in both db/db mice and FFA-induced HepG2 cells following RD treatment. This intervention effectively attenuated ALT and AST elevations while mitigating histopathological hepatic injury. LiP-MS identified PTP1B as a potential target of RD; molecular docking, CETSA, and MD simulation further corroborated stable binding between RD and PTP1B, identifying Asp181 as an important residue contributing to the RD–PTP1B interaction. Mechanistically, RD inhibited PTP1B activity, suppressed SREBP-1c transcription and expression, and downregulated lipogenesis-related genes. RD also inhibited the PERK/eIF2α pathway, alleviated ER stress, and restored the PI3K/AKT insulin signaling. Conclusion RD ameliorates MAFLD by inhibiting PTP1B, orchestrating a concerted improvement in lipid metabolism, ER stress resolution, and insulin signaling, supporting its potential as a therapeutic agent for MAFLD management.

Biochemical characterization of 1,5-anhydro-D-glucitol kinase from Clostridium symbiosum ATCC 14940

Dan Guo,Bangyu Li,Hua Huang,Xinshuai Zhang

1,5-Anhydro-D-glucitol (1,5-AG), a 1-deoxy form of glucopyranose, is a major dietary-derived polyol in the human body and serves as a sensitive clinical marker for short-term glycemic control in diabetic patients. Its phosphorylated derivative, 1,5-anhydro-D-glucitol-6-phosphate (1,5-AG6P), is a non-canonical metabolite formed when glucose phosphorylating enzymes erroneously act on 1,5-AG. Accumulation of 1,5-AG6P is associated with neutrophil dysfunction. Recently, the Zhang group reported a gut bacterial pathway for 1,5-AG catabolism, in which the key enzyme is a glycyl radical enzyme (GRE) responsible for the ring-opening C−O cleavage of 1,5-AG6P. In this report, through a synergistic analysis of sequence similarity network (SSN) and genome neighborhood network (GNN) of this GRE homologs, we uncovered novel ATP-dependent 1,5-AG kinases belonging to the ROK family (PF00480). These enzymes exhibit higher catalytic efficiencies for 1,5-AG than for D-glucose, driven by both a smaller K M and a larger k cat . The substrate preference contrasts with that of other hexokinases and ADP-dependent glucokinases, which typically show a marked preference for D-glucose. This study expands the biocatalytic toolbox for the enzymatic synthesis of 1,5-AG6P, offering a more efficient and convenient approach, and reinforces the value of the “genomic enzymology” strategy applicable for enzyme function discovery.

Inhibition of d-ribose-induced glycation of metalloprotein human myoglobin by bioactive quinones

Jing-Jing Liu,Si-Dian Miao,Zhan-Yi Wang,Ya-Han Zhu,Bin-Bin Jiang,Shuang-Shuang Long,Shu-Qin Gao,Ying-Wu Lin

The anti-glycation effects and mechanisms of eight quinone-related compounds, primarily sourced from medicinal and edible plants, were evaluated in this study. In vitro glycation experiments were conducted to study the structural perturbation induced by d -ribose on human myoglobin (HMb) in the presence of the tested compounds. Spectroscopic and electrophoretic analyses indicated that among the four benzoquinone-related substances, thymoquinone and its structurally closest analogue 2,5-dimethyl-1,4-benzoquinone, exhibited significant inhibitory effects on the d -ribose-induced glycation, thereby maintaining protein structural stability, reducing advanced glycation end products (AGEs) formation, and attenuating the covalent protein modification by d -ribose. In contrast, 1,4-benzoquinone and hydroquinone (a reduction product of 1,4-benzoquinone) promoted HMb denaturation through the Michael addition mechanism. Of the two naphthoquinones, juglone and plumbagin, showed anti-glycation effects, whereas the anthraquinones emodin and chrysophanol showed no significant effects. Nano-HPLC-MS/MS analysis further showed that thymoquinone was more effective in preventing glycation than juglone and plumbagin. This study investigates the mechanisms underlying glycation inhibition by quinones, revealing that the presence of dual β -substituted carbons on the benzoquinone ring is critical for stabilizing protein conformations and suppressing glycation. It provides a preliminary mechanistic basis and identifies candidate molecules for potential applications of quinones in retarding glycation, such as in managing diabetic complications or inhibiting glycation reactions during food processing.

A methyl-β-D-galactopyranoside breath probe for early detection of hepatocellular carcinoma

Fuping Wang,Xinyi Peng,Zhengpeng Zhong,Mingchen He,Qinyan Lu,Yifan Li,Huaiyang Liu,Wang Li,Guobao Chen,Bo Zhou,Zhongmin Chen

A non-isotopic methanol-releasing probe detects HCC early via breath. • Selectively cleaved by β-galactosidase in HCC for tumor-specific signal. • A low-cost dual-sensor array enables real-time exhaled methanol detection. • Distinguishes early-stage tumor-bearing mice from controls (< 2 mm). • Offers a portable, affordable screening tool for primary healthcare. Early detection is crucial for improving therapeutic outcomes in hepatocellular carcinoma (HCC), yet the widespread implementation of low-cost, accessible screening for high-risk populations remains a significant challenge. To address this issue, we investigated the β-galactosidase–methanol signaling axis using a hydrophilic, cell-membrane-impermeable probe, methyl-β-D-galactopyranoside (MGP). This probe is selectively hydrolyzed by β-galactosidase, which is overexpressed in the HCC microenvironment, releasing methanol—an easily volatile, non-isotopic, and metabolically inert volatile organic compounds (VOCs). Methanol levels in exhaled breath were quantified using a custom-designed sensor array. Through in vitro enzymatic assays, cellular studies, and animal experiments, we demonstrated that methanol concentrations in tumor-bearing mice (with tumor diameters <2 mm) were significantly elevated compared to healthy controls, and these levels positively correlated with tumor volume. Our findings highlight the potential of Me-β-Gal in addressing critical barriers to early HCC detection. With further validation, this approach could potentially improve clinical management for high-risk populations, including patients with liver cirrhosis.

Thermostable D-Allulose 3-Epimerase for Long-Term Food-Compatible Continuous Production Systems

Jiawei Cui,Yan Li,Ming Yan

D-allulose is a rare sugar with promising applications in food and health industries, owing to its low caloric value and multiple health benefits. In this study, we systematically investigated a thermostable D-allulose 3-epimerase (TcDAEase) fromThermogemmatispora carboxidivoransfor food-compatible continuous production. The enzyme exhibited remarkable thermostability, with over 70% activity retained at 80 °C, and showed broad pH tolerance across the range of 8.0 to 13.0. Notably, TcDAEase exhibited high catalytic activity toward D-allulose and D-fructose even without the addition of metal ions. Moreover, food-grade Mg2+was identified as enhancing enzyme activity by 14.3%, thus ensuring compliance with Generally Recognized as Safe (GRAS) standards for food applications. To improve industrial applicability, the enzyme was immobilized using a chitosan-diatomaceous earth (DE) matrix via three-step adsorption–crosslinking–embedding strategy. The immobilized TcDAEase achieved 48.7% ± 2.4% activity recovery and retained 90.3% ± 1.5% activity over seven reaction cycles. Furthermore, continuous production of D-allulose was realized in a packed-bed reactor, operating stably at 60 °C, pH 8.0 and 5 mM Mg2+for 150 days, producing 756 kg of D-allulose with a conversion yield exceeding 89.7% of the theoretical maximum. Overall, this study provides a feasible strategy for the continuous and efficient production of high-value-added D-allulose in the food industry.

A Hybrid Wireless Electrodeless QCM-D for the Discrimination of Volatile Organic Compounds

Ruifen Hu,Xuefei Su,Ye Wang,You Wang,Adrian Carl Stevenson,Guang Li

Gasdermin D permeabilization of mitochondrial inner and outer membranes accelerates and enhances pyroptosis

Rui Miao,Cong Jiang,Winston Y. Chang,Haiwei Zhang,Jinsu An,Felicia Ho,Pengcheng Chen,Han Zhang,Caroline Junqueira,Dulguun Amgalan,Felix G. Liang,Junbing Zhang,Charles L. Evavold,Iva Hafner-Bratkovič,Zhibin Zhang,Pietro Fontana,Shiyu Xia,Markus Waldeck-Weiermair,Youdong Pan,Thomas Michel,Liron Bar-Peled,Hao Wu,Jonathan C. Kagan,Richard N. Kitsis,Peng Zhang,Xing Liu,Judy Lieberman

Gasdermin D (GSDMD)-activated inflammatory cell death (pyroptosis) causes mitochondrial damage, but its underlying mechanism and functional consequences are largely unknown. Here, we show that the N-terminal pore-forming GSDMD fragment (GSDMD-NT) rapidly damaged both inner and outer mitochondrial membranes (OMMs) leading to reduced mitochondrial numbers, mitophagy, ROS, loss of transmembrane potential, attenuated oxidative phosphorylation (OXPHOS), and release of mitochondrial proteins and DNA from the matrix and intermembrane space. Mitochondrial damage occurred as soon as GSDMD was cleaved prior to plasma membrane damage. Mitochondrial damage was independent of the B-cell lymphoma 2 family and depended on GSDMD-NT binding to cardiolipin. Canonical and noncanonical inflammasome activation of mitochondrial damage, pyroptosis, and inflammatory cytokine release were suppressed by genetic ablation of cardiolipin synthase (Crls1) or the scramblase (Plscr3) that transfers cardiolipin to the OMM. Phospholipid scramblase-3 (PLSCR3) deficiency in a tumor compromised pyroptosis-triggered anti-tumor immunity. Thus, mitochondrial damage plays a critical role in pyroptosis.

Dietary D-xylose promotes intestinal health by inducing phage production in Escherichia coli

Hu Jie,Wu Yifan,Kang Luyuan,Liu Yisi,Ye Hao,Wang Ran,Zhao Jinbiao,Zhang Guolong,Li Xilong,Wang Junjun,Han Dandan

Elimination of specific enteropathogenic microorganisms is critical to gut health. However, the complexity of the gut community makes it challenging to target specific bacterial organisms. Accumulating evidence suggests that various foods can change the abundance of intestinal bacteria by modulating prophage induction. By using pathogenic Escherichia coli ( E. coli ) ATCC 25922 as a model in this research, we explored the potential of dietary modulation of prophage induction and subsequent bacterial survival. Among a panel of sugars tested in vitro, D -xylose was shown to efficiently induce prophages in E. coli ATCC 25922, which depends, in part, upon the production of D -lactic acid. In an enteric mouse model, prophage induction was found to be further enhanced in response to propionic acid. Dietary D -xylose increased the proportion of Clostridia which converted D -lactic acid to propionic acid. Intestinal propionic acid levels were diminished, following either oral gavage with the dehydrogenase gene ( ldhA )-deficient E. coli ATCC 25922 or depletion of intestinal Clostridia by administration of streptomycin. D -Xylose metabolism and exposure to propionic acid triggered E. coli ATCC 25922 SOS response that promoted prophage induction. E. coli ATCC 25922 mutant of RecA, a key component of SOS system, exhibited decreased phage production. These findings suggest the potential of using dietary components that can induce prophages as antimicrobial alternatives for disease control and prevention by targeted elimination of harmful gut bacteria.