Stimuli-Responsive Hydrogels for Antibacterial Applications.

Hydrogels have emerged as promising candidates for biomedical applications, especially in the field of antibacterial therapeutics, due to their unique structural properties, highly tunable physicochemical properties, and excellent biocompatibility. The integration of stimuli-responsive functions into antibacterial hydrogels holds the potential to enhance their antibacterial properties and therapeutic efficacy, dynamically responding to different external or internal stimuli, such as pH, temperature, enzymes, and light. Therefore, this review describes the applications of hydrogel dressings responsive to different stimuli in antibacterial therapy. The collaborative interaction between stimuli-responsive hydrogels and antibacterial materials was discussed. This synergistic approach, in contrast to conventional antibacterial materials, not only amplifies the antibacterial effect but also alleviates adverse side effects and diminishes the incidence of multiple infections and drug resistance. The review provides a comprehensive overview of the current challenges and outlines future research directions for stimuli-responsive antibacterial hydrogels. It underscores the imperative for ongoing interdisciplinary research aimed at unraveling the mechanisms of wound healing. This understanding is crucial for optimizing the design and implementation of stimuli-responsive antibacterial hydrogels. Ultimately, this review aims to offer scientific guidance for the development and practical clinical application of stimuli-responsive antibacterial hydrogel dressings. This article is protected by copyright. All rights reserved.

CD14 facilitates perinatal human cytomegalovirus infection in biliary epithelial cells via CD55.

Background & Aims: A high human cytomegalovirus (HCMV) infection rate accompanied by an increased level of bile duct damage is observed in the perinatal period. The possible mechanism was investigated. Methods: A total of 1,120 HCMV-positive and 9,297 HCMV-negative children were recruited, and depending on age, their liver biochemistry profile was compared. Fetal and infant biliary epithelial cells (F-BECs and I-BECs, respectively) were infected with HCMV, and the differences in cells were revealed by proteomic analysis. Protein-protein interactions were examined by coimmunoprecipitation and mass spectrometry analyses. A murine cytomegalovirus (MCMV) infection model was established to assess treatment effects. Results: Perinatal HCMV infection significantly increased the level of bile duct damage. Neonatal BALB/c mice inoculated with MCMV showed obvious inflammation in the portal area with an abnormal bile duct structure. Proteomics analysis showed higher CD14 expression in F-BECs than in I-BECs. CD14 siRNA administration hindered HCMV infection, and CD14-knockout mice showed lower MCMV-induced bile duct damage. HCMV infection upregulated CD55 and poly ADP-ribose polymerase-1 (PARP-1) expression in F-BECs. Coimmunoprecipitation and mass spectrometry analyses revealed formation of the CD14-CD55 complex. siRNA-mediated inhibition of CD55 expression reduced sCD14-promoted HCMV replication in F-BECs. In MCMV-infected mice, anti-mouse CD14 antibody and PARP-1 inhibitor treatment diminished cell death, ameliorated bile duct damage, and reduced mortality. Conclusions: CD14 facilitates perinatal HCMV infection in BECs via CD55, and PARP-1-mediated cell death was detected in perinatal cytomegalovirus-infected BECs. These results provide new insight into the treatment of perinatal HCMV infection with bile duct damage. Impact and implications: Perinatal human cytomegalovirus (HCMV) infection is associated with bile duct damage, but the underlying mechanism is still unknown. We discovered that CD14 expression is increased in biliary epithelial cells during perinatal HCMV infection and facilitates viral entry through CD55. We also detected PARP-1-mediated cell death in perinatal HCMV-infected biliary epithelial cells. We showed that blocking CD14 or inhibiting PARP-1 reduced bile duct damage and mortality in a mouse model of murine cytomegalovirus infection. Our findings provide a new insight into therapeutic strategies for perinatal HCMV infection.

Y-tube assisted coprecipitation synthesis of iron-based Prussian blue analogues cathode materials for sodium-ion batteries.

Prussian blue analogues possess numerous advantages as cathode materials for sodium-ion batteries, including high energy density, low cost, sustainability, and straightforward synthesis processes, making them highly promising for practical applications. However, during the synthesis, crystal defects such as vacancies and the incorporation of crystal water can lead to issues such as diminished capacity and suboptimal cycling stability. In the current study, a Y-tube assisted coprecipitation method was used to synthesize iron-based Prussian blue analogues, and the optimized feed flow rate during synthesis contributed to the successful preparation of the material with a formula of Na1.56Fe[Fe(CN)6]0.90□0.10·2.42H2O, representing a low-defect cathode material. This approach cleverly utilizes the Y-tube component to enhance the micro-mixing of materials in the co-precipitation reaction, featuring simplicity, low cost, user-friendly, and the ability to be used in continuous production. Electrochemical performance tests show that the sample retains 69.8% of its capacity after 200 cycles at a current density of 0.5C (1C = 140 mA g-1) and delivers a capacity of 71.9 mA h g-1 at a high rate of 10C. The findings of this research provide important insights for the development of high-performance Prussian blue analogues cathode materials for sodium-ion batteries.

Proteomics Defines Plasma Biomarkers for the Early Diagnosis of Biliary Atresia.

Early diagnosis of biliary atresia (BA) is crucial for improving the chances of survival and preserving the liver function of pediatric patients with BA. Herein, we performed proteomics analysis using data-independent acquisition (DIA) and parallel reaction monitoring (PRM) to explore potential biomarkers for the early diagnosis of BA compared to other non-BA jaundice cases. Consequently, we detected and validated differential protein expression in the plasma of patients with BA compared to the plasma of patients with intrahepatic cholestasis. Bioinformatics analysis revealed the enriched biological processes characteristic of BA by identifying the differential expression of specific proteins. Signaling pathway analysis revealed changes in the expression levels of proteins associated with an alteration in immunoglobulin levels, which is indicative of immune dysfunction in BA. The combination of polymeric immunoglobulin receptor expression and immunoglobulin lambda variable chain (IGL c2225_light_IGLV1-47_IGLJ2), as revealed via machine learning, provided a useful early diagnostic model for BA, with a sensitivity of 0.8, specificity of 1, accuracy of 0.89, and area under the curve value of 0.944. Thus, our study identified a possible effective plasma biomarker for the early diagnosis of BA and could help elucidate the underlying mechanisms of BA.

Spectroscopy and absolute quantum efficiency of near-infrared electrochemiluminescence for a macrocyclic palladium complex.

Electrochemiluminescence (ECL) is widely applied as a reliable tool in clinical diagnosis, including immunoassays, cancer biomarker detection, etc. Metal complexes with emission in the near-infrared (NIR) range possess distinct features such as high transmission and minimal tissue auto-absorption, making them versatile for applications in biosensing and other fields. Through ECL spectral studies of an O-linked nonaromatic benzitripyrrin (C^N^N^N) macrocyclic palladium complex (Pd1) with multiple pyrrole structures, we observed emission peaks from the Qx(0,0) and its vibronic Qx(0,1) bands during both photoluminescence (PL) and ECL. Notably, the emission from the Qx(0,1) band was significantly enhanced in the ECL spectrum, demonstrating higher selectivity for near-infrared light at 743 nm. In the ECL annihilation pathway, the appearance of ECL signals showed a strong correlation with the redox processes of the tri-pyrrin structure, revealing a cyclic tri-pyrrin ligand-centered nature with contributions from the metal center. Upon the introduction of tripropylamine (TPrA) and benzoyl peroxide (BPO) coreactants, the ECL signals exhibited enhancements ranging from several hundred to tens of times. Various reaction routes within different coreactant systems are extensively discussed. Additionally, the absolute quantum efficiencies of the Pd1/TPrA coreactant system were determined, showing efficiencies of 0.0032% ± 0.0005% and 0.000074% ± 0.000016% during pulsing and CV scan processes, respectively. This work addresses gaps in the study of palladacycle complexes in ECL and provides insights into the design of NIR luminescent structures that contribute to the fast screening and deep tissue penetration bioimaging techniques.

High-fidelity intracellular imaging of multiple miRNAs via stimulus-responsive nanocarriers and catalytic hairpin assembly.

An advanced nanoplatform was developed by integrating catalytic hairpin assembly (CHA) with glutathione-responsive nanocarriers, enabling superior imaging of dual cancer-related miRNAs. Two distinct CHA circuits for the sensing of miRNA-21 and miRNA-155 were functionalized on biodegraded MnO2. In the presence of GSH and the corresponding miRNAs, the degraded MnO2 released the DNA cargos, activating the CHA circuits and recovering the fluorescence. This approach offers a reliable sensing performance with highly selective cell-identification capacity, positioning it as a pivotal tool for imaging multiple biomarkers in living cells.

Superhydrophilic Triazine-Based Covalent Organic Frameworks via Post-Modification of FeOOH Clusters for Boosted Photocatalytic Performance.

The triazine-based covalent organic frameworks (tCOF), an intriguing subtype of COFs, are expected as highly promising photocatalysts for various photocatalytic applications owing to their fully conjugated structures and nitrogen-rich skeletons. However, the inherent hydrophobicity and fast recombination of photoexcited electron-hole pairs are two main factors hindering the application of tCOF in practical photocatalytic reactions. Here, a post-synthetic modification strategy to fabricate superhydrophilic tCOF-based photocatalysts is demonstrated by in situ growing FeOOH clusters on TaTz COF (TaTz-FeOOH) for efficient photocatalytic oxidation of various organic pollutants. The strong polar FeOOH endows TaTz-FeOOH with good hydrophilic properties. The well-defined heterogeneous interface between FeOOH and TaTz allows the photoelectrons generated by TaTz to be consumed by Fe (III) to transform into Fe (II), synergistically promoting the separation of holes and the generation of free radicals. Compared with the unmodified TaTz, the optimized TaTz-FeOOH (1%) shows excellent photocatalytic performance, where the photocatalytic degrade rate (k) of rhodamine B is increased by about 12 times, and the degradation rate is maintained at 99% after 5 cycles, thus achieving efficient removal of quinolone antibiotics from water. This study provides a new avenue for the development of COF-based hydrophilic functional materials for a wide range of practical applications.

Single cell RNA-sequencing analysis reveals that N-acetylcysteine partially reverses hepatic immune dysfunction in biliary atresia.

Background & Aims: Our previous study indicated that CD177+ neutrophil activation has a vital role in the pathogenesis of biliary atresia (BA), which is partially ameliorated by N-acetylcysteine (NAC) treatment. Here, we evaluated the clinical efficacy of NAC treatment and profiled liver-resident immune cells via single cell RNA-sequencing (scRNA-seq) analysis to provide a comprehensive immune landscape of NAC-derived immune regulation. Methods: A pilot clinical study was conducted to evaluate the potential effects of intravenous NAC treatment on infants with BA, and a 3-month follow-up was carried out to assess treatment efficacy. scRNA-seq analysis of liver CD45+ immune cells in the control (n = 4), BA (n = 6), and BA + NAC (n = 6) groups was performed and the effects on innate cells, including neutrophil and monocyte-macrophage subsets, and lymphoid cells were evaluated. Results: Intravenous NAC treatment demonstrated beneficial efficacy for infants with BA by improving bilirubin metabolism and bile acid flow. Two hepatic neutrophil subsets of innate cells were identified by scRNA-seq analysis. NAC treatment suppressed oxidative phosphorylation and reactive oxygen species production in immature neutrophils, which were transcriptionally and functionally similar to CD177+ neutrophils. We also observed the suppression of hepatic monocyte-mediated inflammation, decreased levels of oxidative phosphorylation, and M1 polarisation in Kupffer-like macrophages by NAC. In lymphoid cells, enhancement of humoral immune responses and attenuation of cellular immune responses were observed after NAC treatment. Moreover, cell-cell interaction analysis showed that innate/adaptive proinflammatory responses were downregulated by NAC. Conclusions: Our clinical and scRNA-seq data demonstrated that intravenous NAC treatment partially reversed liver immune dysfunction, alleviated the proinflammatory responses in BA by targeting innate cells, and exhibited beneficial clinical efficacy. Impact and implications: BA is a serious liver disease that affects newborns and has no effective drug treatment. In this study, scRNA-seq showed that NAC treatment can partially reverse the immune dysfunction of neutrophil extracellular trap-releasing CD177+ neutrophils and Kupffer cells, and lower the inflammatory responses of other innate immune cells in BA. In consequence, intravenous NAC treatment improved the clinical outcomes of patients with BA in term of bilirubin metabolism.

DNA-modulated single-atom nanozymes with enhanced enzyme-like activity for ultrasensitive detection of dopamine.

Despite the current progress in optimizing and tailoring the performance of nanozymes through structural and synthetic adaptation, there is still a lack of dynamic modulation approaches to alter their catalytic activity. Here, we demonstrate that DNA can act as an auxiliary regulator via a straightforward incubation method with Fe-N-C single-atom nanozymes (SAzymes), causing a leap in the enzyme-like activity of Fe-N-C from moderate to a higher level. The DNA-assisted enhancement is attributed to the increased substrate affinity of Fe-N-C nanozymes through electrostatic attraction between the substrate and DNA. Based on the prepared DNA/Fe-N-C system, colorimetric sensors for dopamine (DA) detection were constructed. Surprisingly, the incorporation of DNA not only enabled the detection of DA in a low concentration range, but also greatly improved the sensitivity with a 436-fold decrease in detection limit. The quantitative determination of DA was achieved in two-segment linear ranges of 0.01-4 µM and 5-100 µM with an ultralow detection limit of 9.56 nM. The DNA/Fe-N-C system shows superior performance compared to the original Fe-N-C system, making it an ideal choice for nanozyme-based biosensors. This simple design approach has paved the way for enhancing nanozyme activity and is expected to serve as a general strategy for optimizing biosensor performance.

Regulating highly photoelectrochemical activity of Zr-based mixed-linker metal-organic frameworks toward sensitive electrogenerated chemiluminescence sensing of α-glucosidase.

The conductivity and emission efficiency of metal-organic frameworks (MOFs) remain challenging factors that limit their electrogenerated chemiluminescence (ECL) sensing applications. Herein, we report a facile approach to address these challenges by integrating an electroactive linker (H2-TCPP) with an ECL active electrogenerated chemiluminescence linker (H4-TBAPy) to construct a highly photoelectrochemical active mixed-linker MOFs (ML-MOFs). ECL results revealed a remarkable 15.4-fold enhancement for the top-performing ML-MOFs (M6-MOFs), surpassing the single linker MOFs. In addition, M6-MOFs also exhibit a remarkable 73-fold enhancement in ECL efficiency compared to commercial Ru (bpy)32+. This improvement should be attributed to the synergistic effects resulting from the combination of two linkers. Furthermore, M6-MOFs are found to be served as a model ECLphore for sensitive and selective detection of α-glucosidase for the first time with good potential practicability in human serum samples. This work represents a promising direction to guide for designing good conductivity and high ECL efficiency MOFs in terms of linker functionalization and thus bandgap modulation for advancing their ECL sensing applications.

The association of immune-related genes and the potential role of IL10 with biliary atresia.

BACKGROUND: Biliary atresia (BA) is a severe immune-related disease that is characterized by biliary obstruction and cholestasis. The etiology of BA is unclear, our aim was to explore the relationship between biliary tract inflammation and immune-related genes. METHODS: We selected 14 SNPs in 13 immune-related genes and investigated their associations with BA by using a large case‒control cohort with a total of 503 cases and 1473 controls from southern China. RESULTS: SNP rs1518111 in interleukin10 (IL10) was identified as associated with BA (P = 5.79E-03; OR: 0.80; 95% CI: 0.68-0.94). The epistatic effects of the following pairwise interactions among these SNPs were associated with BA: signal transducer and activator of transcription 4 (STAT4) and chemokine (C-X-C motif) ligand 3 (CXCL3); STAT4 and damage-regulated autophagy modulator1 (DRAM1); CXCL3 and RAD51 paralog B (RAD51B); and interferon gamma (IFNG) and interleukin26 (IL26). Furthermore, we explored the potential role of IL-10 in the pathogenesis of the neonatal mouse model of BA. IL-10 effectively prevented biliary epithelial cell injury and biliary obstruction in murine BA as well as inhibit the activation of BA-related immune cells. CONCLUSIONS: In conclusion, this study provided strong evidence implicating IL10 as a susceptibility gene for BA in the southern Chinese population. IMPACT: This study provided strong evidence implicating IL10 as a susceptibility gene for BA in the southern Chinese population. This study could infer that IL-10 may play a protective role in BA mouse model. We found that four SNPs (rs7574865, rs352038, rs4622329, and rs4902562) have genetic interactions.

Dual-Site Activation Coupling with a Schottky Junction Boosts the Electrochemiluminescence of Carbon Nitride.

Robust electrochemiluminescence (ECL) of carbon nitride (CN) requires efficient electron-hole recombination and the suppression of electrode passivation. In this work, Au nanoparticles and single atoms (AuSA+NP ) loaded on CN serve as dual active sites that significantly accelerate charge transfer and activate peroxydisulfate. Meanwhile, the well-established Schottky junctions between Au NPs and CN act as electron sinks, effectively trapping over-injected electrons to prevent electrode passivation. As a result, the porous CN modified with AuSA+NP exhibits an enhanced and stable ECL emission, with a minimal relative standard deviation of 0.24 %. Furthermore, the designed ECL biosensor based on AuSA+NP -CN shows a remarkable performance in detecting organophosphorus pesticides. This innovative strategy has the potential to offer new insights into strong and stable ECL emission for practical applications.

Endogenous glutathione-activated DNA nanoprobes for spatially controllable imaging of microRNA in living cells.

A DNA nanoprobe, activated by glutathione (GSH), was designed to enable spatially selective sensing and imaging of miRNA in living cells. The nanoprobe was constructed using nano-sized metal-organic frameworks (MOFs) and DNA hairpin probes tethered to the surface of the MOFs, with the loop portion of the hairpin structure containing a disulfide bond. Cleavage of the disulfide bond by GSH triggers a strand-displacement reaction with target miRNAs, facilitating in situ readout of the fluorescence signal. The synergy of endogenous GSH activation and MOF improves the spatial resolution of miRNA detection and imaging.

A case report of Gitelman syndrome in children.

RATIONALE: Giltelman syndrome (GS) is an autosomal recessive infectious disease, which is caused by the mutation of SLC12A3 gene encoding thiazide diuretic sensitive sodium chloride cotransporter located in the distal convoluted tubule of the kidney. PATIENT CONCERNS: A 7-year-old and 3-month-old male patient has poor appetite, slow growth in height and body weight since the age of 3, body weight: 16 kg (-3 standard deviation), height: 110 cm (-3 standard deviation), normal exercise ability and intelligence. One year ago, he was diagnosed with hypokalemia. After potassium supplement treatment, the blood potassium returned to normal. The patient developed abdominal pain, vomiting, limb weakness, and tetany 1 day before admission. DIAGNOSES: After admission examination, the patient was found to have hypokalemia (2.27-2.88 mmol/L), hypomagnesemia (0.47 mmol/L), hypophosphatemia (1.17 mmol/L), hypocalcemia (1.06 mmol/24 hours), and metabolic alkalosis (PH 7.60). The blood pressure is normal, and the concentration of aldosterone is 791.63 pg/mL. The adrenocorticotropic hormone and cortisol detected at 8 am are 4.95 pmol/L and 275.09 nmol/L, respectively. Twenty-four hours of urine potassium is 32.52 mmol. Gene sequencing results showed 2 pathogenic variants in the GS-related SLC12A3 gene, which are related to the phenotype of the subject. INTERVENTIONS: After admission, the patients were given potassium and magnesium supplements, as well as oral spironolactone. The symptoms of limb weakness and tetany were significantly relieved. After discharge, the patients continued to maintain treatment to keep the blood potassium at more than 3.0 mmol/L, and the blood magnesium at more than 0.6 mmol/L. OUTCOMES: Follow-up at 1 month after discharge, in the patient's self-description, he had no symptoms such as limb weakness and tetany, and his height was increased by 1 cm and the body weight increased by 1.5 kg. LESSONS: For patients with hypokalemia, hypomagnesemia, and metabolic alkalosis, the possibility of GS should be given priority. After the diagnosed by gene sequencing of SLC12A3 gene, potassium and magnesium supplementation could significantly improve symptoms.

Association between GPC2 polymorphisms and neuroblastoma risk in Chinese children.

BACKGROUND: The cell surface glycoprotein glypican 2 (GPC2) has been shown to increase susceptibility to neuroblastoma, which is the most common malignancy in children. However, associations between single nucleotide polymorphism(s) of GPC2 and neuroblastoma risk remain unclarified. METHODS: We conducted a case-control study to investigate two GPC2 polymorphisms (rs1918353 G>A and rs7799441 C>T) in 473 healthy controls and 402 pediatric patients with neuroblastoma. Single nucleotide polymorphism (SNP) genotyping was conducted on the samples by the TaqMan technique, and the data were subsequently analyzed by the t test, chi-squared test, and logistic regression model. In addition, we further performed stratification analysis by age, sex, tumor site of origin, or clinical stage to control confounding factors. RESULTS: According to the data of dominant models (GA/AA vs. GG: adjusted OR = 0.99, 95% CI = 0.76-1.29, p = 0.943; CT/TT vs. CC: adjusted OR = 0.91, 95% CI = 0.70-1.19, p = 0.498) or other comparisons, as well as the conjoint analysis (adjusted OR = 1.22, 95% CI = 0.93-1.59, p = 0.152), we unfortunately proved that the analysis of single or multiple loci did not support any significant association of GPC2 polymorphisms with susceptibility to neuroblastoma. CONCLUSION: GPC2 polymorphisms (rs1918353 G>A and rs7799441 C>T) are unable to statistically affect neuroblastoma risk in Chinese children. Therefore, more samples, especially from patients of various ethnic backgrounds, are required to increase the sample size and verify the effect of GPC2 polymorphisms on neuroblastoma risk in the presence of ethnic factor.

Self-enhanced peroxidase-like activity in a wide pH range enabled by heterostructured Au/MOF nanozymes for multiple ascorbic acid-related bioenzyme analyses.

Nanozymes, a class of catalytic nanomaterials, have shown great potential to substitute natural enzymes in various applications. Nevertheless, the pursuit of high-efficiency peroxidase-like activity in a wide pH range is one of the major challenges existing in designing nanozymes. A feasible strategy is to construct an artificial active center by using porous materials as stable supporting structures, which can actively modulate biocatalytic activities via their porous atomic structures and more active sites. Herein, a gold nanoparticles/metal-organic framework (MOF) heterostructure was prepared using UiO-66 as a stable support structure (Au NPs/UiO-66), which demonstrates enhanced peroxidase-like activity, ∼8.95 times higher than that of pure Au NPs. Strikingly, Au NPs/UiO-66 exhibits excellent stability (maintains above 80% activity at 40-70 °C and retains 93% activity after 3 months of storage) and sustained high relative activity (above 90%) over a pH range of 5.0-9.0 due to the homogeneous dispersibility of free-ligand Au NPs and the strong chemical interaction between the Au NPs and the UiO-66 host. Moreover, a colorimetric assay of ascorbic acid (AA) and three AA-related biological enzymes was developed based on Au NPs/UiO-66 nanozyme, which has a good linear detection range and excellent anti-interference ability. This work provides important guidance for the expansion of metal NPs/MOF heterostructure nanozymes and their application prospects in the development of biosensors.

Nitrogen- and sulfur-doped graphene quantum dots for chemiluminescence.

Graphene quantum dots (GQDs), as one of the most promising luminescent nanomaterials, have been receiving increasing attention in various applications. However, it is still a challenge to improve their chemiluminescence (CL) quantum efficiency. Herein, the CL emissions of nitrogen- and sulfur-doped GQDs (NS-GQDs), nitrogen-doped GQDs (N-GQDs) and undoped GQDs synthesized through one-pot high-temperature pyrolysis are investigated in their chemical reactions with bis(2-carbopentyloxy-3,5,6-trichlorophenyl) oxalate (CPPO) and hydrogen peroxide (H2O2). A bright blue emission, and yellowish green and yellowish white light from NS-GQDs, N-GQDs and GQDs can be observed, respectively, in the mixture solutions with CPPO and H2O2. For the first time, spooling CL spectroscopy was used to investigate the CL reaction mechanisms, illuminant decays and the absolute CL efficiencies of these three GQD systems. Compared with the same system of undoped GQDs, it has been found that the NS-GQDs not only present slower illuminant decay, but also display an absolute CL quantum efficiency of 0.01%, 5-fold enhancement, due to the increase in N and S doping for a well-defined band gap energy. Moreover, three peak wavelengths attributed to intrinsic emission at 425 nm, aggregation-induced emission (AIE) at 575 nm and S-doped emissive surface states at 820 nm are observed for the first time in the NS-GQD system. The CL spectrum of N-GQDs displays two emission peaks at 395 and 575 nm attributed to intrinsic emission and AIE, whereas the CL spectrum of undoped GQDs demonstrates 500 nm and 600 nm peak wavelengths attributed to core emission and AIE. Absolute CL quantum efficiencies from these emissions at these various peaks can be determined quantitatively. This study provides guidance on tuning the surface states of GQD for more conducive injection of electrons and holes, facilitating the production of CL emission, which is beneficial for promoting the development of optical, bioassay and energy conversion applications.

A Mouse Model of Chronic Liver Fibrosis for the Study of Biliary Atresia.

Biliary atresia (BA) is a fatal disease involving obstructive jaundice, and it is the most common indication for liver transplantation in children. Due to the complex etiology and unknown pathogenesis, there are still no effective drug treatments. At present, the classic BA mouse model induced by rhesus rotavirus (RRV) is the most commonly used model for studying the pathogenesis of BA. This model is characterized by growth retardation, jaundice of the skin and mucosa, clay stools, and dark yellow urine. The histopathology shows severe liver inflammation and obstruction of the intrahepatic and extrahepatic bile ducts, which are similar to the symptoms of human BA. However, the livers of end-stage mice in this model lack fibrosis and cannot fully simulate the characteristics of liver fibrosis in clinical BA. The presented study developed a novel BA mouse model of chronic liver fibrosis by injecting 5-10 µg of anti-Ly6G antibody four times, with gaps of 2 days after each injection. The results showed that some of the mice successfully formed chronic BA with typical fibrosis after the time lapse, meaning these mice represent a suitable animal model for the virus-induced liver fibrosis mechanistic study of BA and a platform for developing future BA treatments.

Mechanistic explorations on the decarboxylative allylation of amino esters via dual photoredox and palladium catalysis.

Mechanistic studies reveal that the decarboxylative allylation of amino esters via dual photoredox and palladium catalysis occurs via oxidation giving π-allyl-Pd(II) species and carboxylate, which is oxidized by *Ir(III)-catalyst offering benzyl radicals. The alkylated product is formed via an SN2 pathway. Single-electron transfer between Pd(I)-species and Ir(II)-catalysis restores both catalysts.