Contribution of intramacrophage stages to Pseudomonas aeruginosa infection outcome in zebrafish embryos: insights from mgtC and oprF mutants.

Pseudomonas aeruginosa often colonizes immunocompromised patients, causing acute and chronic infections. This bacterium can reside transiently inside cultured macrophages, but the contribution of the intramacrophic stage during infection remains unclear. MgtC and OprF have been identified as important bacterial factors when P. aeruginosa resides inside cultured macrophages. In this study, we showed that P. aeruginosa mgtC and oprF mutants, particular the latter one, had attenuated virulence in both mouse and zebrafish animal models of acute infection. To further investigate P. aeruginosa pathogenesis in zebrafish at a stage different from acute infection, we monitored bacterial load and visualized fluorescent bacteria in live larvae up to 4 days after infection. Whereas the attenuated phenotype of the oprF mutant was associated with a rapid elimination of bacteria, the mgtC mutant was able to persist at low level, a feature also observed with the wild-type strain in surviving larvae. Interestingly, these persistent bacteria can be visualized in macrophages of zebrafish. In a short-time infection model using a macrophage cell line, electron microscopy revealed that internalized P. aeruginosa wild-type bacteria were either released after macrophage lysis or remained intracellularly, where they were localized in vacuoles or in the cytoplasm. The mgtC mutant could also be detected inside macrophages, but without causing cell damage, whereas the oprF mutant was almost completely eliminated after phagocytosis, or localized in phagolysosomes. Taken together, our results show that the main role of OprF for intramacrophage survival impacts both acute and persistent infection by this bacterium. On the other hand, MgtC plays a clear role in acute infection but is not essential for bacterial persistence, in relation with the finding that the mgtC mutant is not completely eliminated by macrophages.

Case report: Cheek acupuncture exhibits an immediate effect in relieving severe pain associated with nerve compression or damage of central nervous system and its potential mechanism of action.

Peripheral nerve compression or permanent damage of central nervous system (CNS) can trigger severe neuralgia to patients. Analgesic medicine or even surgery to remove nerve compression is commonly used for pain relief. But these treatments either are ineffective, have side-effect or can cause subsequent complications. Acupuncture, a technique that has been widely used in China and other Asian countries for thousands of years, is an alternative to relieve pain, although the mechanism of action is not fully understood. In this study, two patients who had symptoms of severe neuralgia associated with peripheral nerve compression or permanent damage/dysfunction of CNS and analgesic medicines are ineffective, underwent cheek acupuncture, a new technique established recent years by the author with the features of painless, standardization, simplicity, and precision. An immediate analgesic effect of the cheek acupuncture was observed without any side effects, and clinical remission was achieved after several sessions of treatments. It suggests that this new approach is an efficient alternative for pain relief induced by nerve impairment. The authors proposed a biological holographic model of triplet homunculi existing at the level of the local cheek, spinal cord, and cerebral cortex, to explain the immediate and accurate analgesic effect of the cheek acupuncture. These homunculi have the same structure, and synchronized sensations and actions that are mediated by afferent and efferent neurons, as the integrated human body. Therefore, the nociception and needling signals are sensed, transmitted, analyzed, and manipulated cooperatively and simultaneously among these homunculi with the subsequent pain relief in the body.

Modulation of Airway Expression of the Host Bactericidal Enzyme, sPLA2-IIA, by Bacterial Toxins.

Host molecules with antimicrobial properties belong to a large family of mediators including type-IIA secreted phospholipase A2 (sPLA2-IIA). The latter is a potent bactericidal agent with high selectivity against Gram-positive bacteria, but it may also play a role in modulating the host inflammatory response. However, several pathogen-associated molecular patterns (PAMPs) or toxins produced by pathogenic bacteria can modulate the levels of sPLA2-IIA by either inducing or inhibiting its expression in host cells. Thus, the final sPLA2-IIA concentration during the infection process is determined by the orchestration between the levels of toxins that stimulate and those that downregulate the expression of this enzyme. The stimulation of sPLA2-IIA expression is a process that participates in the clearance of invading bacteria, while inhibition of this expression highlights a mechanism by which certain bacteria can subvert the immune response and invade the host. Here, we will review the major functions of sPLA2-IIA in the airways and the role of bacterial toxins in modulating the expression of this enzyme. We will also summarize the major mechanisms involved in this modulation and the potential consequences for the pulmonary host response to bacterial infection.

A burns and COVID-19 shared stress responding gene network deciphers CD1C-CD141- DCs as the key cellular components in septic prognosis.

Differential body responses to various stresses, infectious or noninfectious, govern clinical outcomes ranging from asymptoma to death. However, the common molecular and cellular nature of the stress responsome across different stimuli is not described. In this study, we compared the expression behaviors between burns and COVID-19 infection by choosing the transcriptome of peripheral blood from related patients as the analytic target since the blood cells reflect the systemic landscape of immune status. To this end, we identified an immune co-stimulator (CD86)-centered network, named stress-response core (SRC), which was robustly co-expressed in burns and COVID-19. The enhancement of SRC genes (SRCs) expression indicated favorable prognosis and less severity in both conditions. An independent whole blood single-cell RNA sequencing of COVID-19 patients demonstrated that the monocyte-dendritic cell (Mono-DC) wing was the major cellular source of SRC, among which the higher expression of the SRCs in the monocyte was associated with the asymptomatic COVID-19 patients, while the quantity-restricted and function-defected CD1C-CD141-DCs were recognized as the key signature which linked to bad consequences. Specifically, the proportion of the CD1C-CD141-DCs and their SRCs expression were step-wise reduced along with worse clinic conditions while the subcluster of CD1C-CD141-DCs from the critical COVID-19 patients was characterized of IFN signaling quiescence, high mitochondrial metabolism and immune-communication inactivation. Thus, our study identified an expression-synchronized and function-focused gene network in Mono-DC population whose expression status was prognosis-related and might serve as a new target of diagnosis and therapy.

Modulating the electronic structure of CoS2 by Sn doping boosting urea oxidation for efficient alkaline hydrogen production.

Urea electrocatalytic oxidation afforded by renewable energies is highly promising to replace the sluggish oxygen evolution reaction in water splitting for hydrogen production while realizing the treatment of urea-rich waste water. Therefore, the development of efficient and cost-effective catalysts for water splitting assisted by urea is highly desirable. Herein, Sn-doped CoS2 electrocatalysts were reported with the engineered electronic structure and the formation of Co-Sn dual active sites for urea oxidation reaction (UOR) and hydrogen evolution reaction (HER), respectively. Consequently, the number of active sites and the intrinsic activity were enhanced simultaneously and the resultant electrodes exhibited outstanding electrocatalytic activity with a very low potential of 1.301 V at 10 mA·cm-2 for UOR and an overpotential of 132 mV at 10 mA·cm-2 for HER. Therefore, a two-electrode device was assembled by employing Sn(2)-CoS2/CC and Sn(5)-CoS2/CC and the constructed cell required only 1.45 V to approach a current density of 10 mA·cm-2 along with good durability for at least 95 h assisted by urea. More importantly, the assembled electrolyzer can be powered by commercial dry battery to generate numerous gas bubbles on the surface of the electrodes, demonstrating the high potential of the as-fabricated electrodes for applications in hydrogen production and pollutant treatment at a low-voltage electrical energy input.

Interference with Lipoprotein Maturation Sensitizes Methicillin-Resistant Staphylococcus aureus to Human Group IIA-Secreted Phospholipase A2 and Daptomycin.

Methicillin-resistant Staphylococcus aureus (MRSA) has been classified as a high priority pathogen by the World Health Organization underlining the high demand for new therapeutics to treat infections. Human group IIA-secreted phospholipase A2 (hGIIA) is among the most potent bactericidal proteins against Gram-positive bacteria, including S. aureus. To determine hGIIA-resistance mechanisms of MRSA, we screened the Nebraska Transposon Mutant Library using a sublethal concentration of recombinant hGIIA. We identified and confirmed the role of lspA, encoding the lipoprotein signal peptidase LspA, as a new hGIIA resistance gene in both in vitro assays and an infection model in hGIIA-transgenic mice. Increased susceptibility of the lspA mutant was associated with enhanced activity of hGIIA on the cell membrane. Moreover, lspA deletion increased susceptibility to daptomycin, a last-resort antibiotic to treat MRSA infections. MRSA wild type could be sensitized to hGIIA and daptomycin killing through exposure to LspA-specific inhibitors globomycin and myxovirescin A1. Analysis of >26,000 S. aureus genomes showed that LspA is highly sequence-conserved, suggesting universal application of LspA inhibition. The role of LspA in hGIIA resistance was not restricted to MRSA since Streptococcus mutans and Enterococcus faecalis were also more hGIIA-susceptible after lspA deletion or LspA inhibition, respectively. Overall, our data suggest that pharmacological interference with LspA may disarm Gram-positive pathogens, including MRSA, to enhance clearance by innate host defense molecules and clinically applied antibiotics.

Pseudomonas aeruginosa Production of Hydrogen Cyanide Leads to Airborne Control of Staphylococcus aureus Growth in Biofilm and In Vivo Lung Environments.

Diverse bacterial volatile compounds alter bacterial stress responses and physiology, but their contribution to population dynamics in polymicrobial communities is not well known. In this study, we showed that airborne volatile hydrogen cyanide (HCN) produced by a wide range of Pseudomonas aeruginosa clinical strains leads to at-a-distance in vitro inhibition of the growth of a wide array of Staphylococcus aureus strains. We determined that low-oxygen environments not only enhance P. aeruginosa HCN production but also increase S. aureus sensitivity to HCN, which impacts P. aeruginosa-S. aureus competition in microaerobic in vitro mixed biofilms as well as in an in vitro cystic fibrosis lung sputum medium. Consistently, we demonstrated that production of HCN by P. aeruginosa controls S. aureus growth in a mouse model of airways coinfected by P. aeruginosa and S. aureus. Our study therefore demonstrates that P. aeruginosa HCN contributes to local and distant airborne competition against S. aureus and potentially other HCN-sensitive bacteria in contexts relevant to cystic fibrosis and other polymicrobial infectious diseases. IMPORTANCE Airborne volatile compounds produced by bacteria are often only considered attractive or repulsive scents, but they also directly contribute to bacterial physiology. Here, we showed that volatile hydrogen cyanide (HCN) released by a wide range of Pseudomonas aeruginosa strains controls Staphylococcus aureus growth in low-oxygen in vitro biofilms or aggregates and in vivo lung environments. These results are of pathophysiological relevance, since lungs of cystic fibrosis patients are known to present microaerobic areas and to be commonly associated with the presence of S. aureus and P. aeruginosa in polymicrobial communities. Our study therefore provides insights into how a bacterial volatile compound can contribute to the exclusion of S. aureus and other HCN-sensitive competitors from P. aeruginosa ecological niches. It opens new perspectives for the management or monitoring of P. aeruginosa infections in lower-lung airway infections and other polymicrobial disease contexts.

Engineering the electronic structure of Ni3FeS with polyaniline for enhanced electrocatalytic performance of overall water splitting.

Developing highly efficient and stable electrocatalysts for oxygen evolution reaction is of significant importance for applications in energy conversion and storage. Modulation of electronic structure of catalysts is critical for improving the performance of the resulting electrodes. Here, we report a facile way to engineer the electronic structure of Ni3FeS by coating a thin polyaniline (PANI) layer for improving electrocatalytic activity for overall water splitting. Experimental investigations unveil that the strong electronic interactions between the lone electron pairs of nitrogen in PANI and d orbitals of iron, nickel in Ni3FeS result in an electron-rich structure of Ni and Fe, and consequently optimize the adsorption and desorption processes to promote the OER activity. Remarkably, the resulting PANI/Ni3FeS electrode exhibited much enhanced OER performance with a low overpotential of 143 mV at a current density of 10 mA·cm-2and good stability. Promisingly, coupled with the reported MoNi4/MoO2electrode, the two-electrode electrolyzer achieved a current density of 10 mA·cm-2with a relatively low potential of 1.55 V, and can generate oxygen and hydrogen bubbles steadily driven by a commercial dry battery, endowed the composite electrocatalyst with high potential for practical applications.

Identification of pathological-related and diagnostic potential circular RNAs in Stanford type A aortic dissection.

Introduction: Stanford type A aortic dissection (TAAD) is one of the lethal macrovascular diseases caused by the invasion of blood into the media layer of ascending aortic wall. Inflammation, smooth muscle dysfunction, and extracellular matrix (ECM) degradation were regarded as the major pathology in affected tissue. However, the expression pattern and its regulation especially through circular RNAs (circRNAs) as an overall characteristic of TAAD molecular pathology remain unclear. Methods: We employed CIRCexplorer2 to identify circRNAs based on the RNA sequencing (RNA-seq) data of human ascending aortic tissues to systematically assess the role of circRNA in the massive alterations of gene expression in TAAD aortas. The key circRNAs were determined by LASSO model and functionally annotated by competing endogenous RNAs (ceRNA) network and co-analysis with mRNA profile. The expression level and diagnostic capability of the 4 key circRNAs in peripheral serum were confirmed by real-time polymerase chain reaction (RT-PCR). Results: The 4 key circRNAs, namely circPTGR1 (chr9:114341075-114348445[-]), circNOX4 (chr11:89069012-89106660[-]), circAMN1 (chr12:31854796-31862359[-]) and circUSP3 (chr15:63845913-63855207[+]), demonstrated a high power to discriminate between TAAD and control tissues, suggesting that these molecules stand for a major difference between the tissues at gene regulation level. Functionally, the ceRNA network of circRNA-miRNA-mRNA predicted by the online databases, combining gene set enrichment analysis (GSEA) and cell component prediction, revealed that the identified circRNAs covered all the aspects of primary TAAD pathology, centralized with increasing inflammatory factors and cells, and ECM destruction and loss of vascular inherent cells along with the circRNAs. Importantly, we validated the high concentration and diagnostic capability of the 4 key circRNAs in the peripheral serum in TAAD patients. Discussion: This study reinforces the vital status of circRNAs in TAAD and the possibility of serving as promising diagnostic biomarkers.

Primary ectocervical epithelial cells display lower permissivity to Chlamydia trachomatis than HeLa cells and a globally higher pro-inflammatory profile.

The tumoral origin and extensive passaging of HeLa cells, a most commonly used cervical epithelial cell line, raise concerns on their suitability to study the cell responses to infection. The present study was designed to isolate primary epithelial cells from human ectocervix explants and characterize their susceptibility to C. trachomatis infection. We achieved a high purity of isolation, assessed by the expression of E-cadherin and cytokeratin 14. The infectious progeny in these primary epithelial cells was lower than in HeLa cells. We showed that the difference in culture medium, and the addition of serum in HeLa cultures, accounted for a large part of these differences. However, all things considered the primary ectocervical epithelial cells remained less permissive than HeLa cells to C. trachomatis serovar L2 or D development. Finally, the basal level of transcription of genes coding for pro-inflammatory cytokines was globally higher in primary epithelial cells than in HeLa cells. Transcription of several pro-inflammatory genes was further induced by infection with C. trachomatis serovar L2 or serovar D. In conclusion, primary epithelial cells have a strong capacity to mount an inflammatory response to Chlamydia infection. Our simplified purification protocol from human explants should facilitate future studies to understand the contribution of this response to limiting the spread of the pathogen to the upper female genital tract.

Strong In-Plane Magnetic Field-Induced Reemergent Superconductivity in the van der Waals Heterointerface of NbSe2 and CrCl3.

A magnetic field is generally considered to be incompatible with superconductivity as it tends to spin-polarize electrons and breaks apart the opposite-spin singlet superconducting Cooper pairs. Here, an experimental phenomenon is observed that an intriguing reemergent superconductivity evolves from a conventional superconductivity undergoing a hump-like intermediate phase with a finite electric resistance in the van der Waals heterointerface of layered NbSe2 and CrCl3 flakes. This phenomenon merely occurred when the applied magnetic field is parallel to the sample plane and perpendicular to the electric current direction as compared to the reference sample of a NbSe2 thin flake. The strong anisotropy of the reemergent superconducting phase is pointed to the nature of the Fulde-Ferrell-Larkin-Ovchinnikov (FFLO) state driven by the strong interfacial spin-orbit coupling between NbSe2 and CrCl3 layers. The theoretical picture of FFLO state nodes induced by Josephson vortices collectively pinning is presented for well understanding the experimental observation of the reemergent superconductivity. This finding sheds light on an opportunity to search for the exotic FFLO state in the van der Waals heterostructures with strong interfacial spin-orbit coupling.

Effective p-wave Fermi-Fermi Interaction Induced by Bosonic Superfluids.

We study the two-dimensional Bose-Fermi mixture on square lattice at finite temperature by using the determinant quantum Monte Carlo method within the weakly interacting regime. Here we consider the attractive Bose-Hubbard model and free spinless fermions. In the absence of boson-fermion interactions, we obtain the boundary of the collapsed state of the attractive bosons. In the presence of boson-fermion interactions, an effective p-wave interaction between fermions will be induced as far as the bosons are in a superfluid state. Moreover, we find the emergence of the composite fermion pairs at low temperatures.

FLCN-regulated miRNAs suppressed reparative response in cells and pulmonary lesions of Birt-Hogg-Dubé syndrome.

BACKGROUND: Birt-Hogg-Dubé Syndrome (BHDS) characterised by skin fibrofolliculomas, kidney tumour and pulmonary cysts/pneumothorax is caused by folliculin (FLCN) germline mutations. The pathology of both neoplasia and focused tissue loss of BHDS strongly features tissue-specific behaviour of the gene. Isolated cysts/pneumothorax is the most frequent atypical presentation of BHDS and often misdiagnosed as primary spontaneous pneumothorax (PSP). Deferential diagnosis of BHDS with isolated pulmonary presentation (PSP-BHD) from PSP is essential in lifelong surveillance for developing renal cell carcinoma. METHODS: The expression profiles of microRNAs (miRNAs) in cystic lesions of PSP-BHD and PSP were determined via microarray. The selected upregulated miRNAs were further confirmed in the plasma of an expanded cohort of PSP-BHD patients by reverse transcription quantitative PCR (RT-qPCR). Their diagnostic accuracy was evaluated. Moreover, the cellular functions and targeted signalling pathways of FLCN-regulated miRNAs were assessed in various cell lines and in the lesion tissue contexts. RESULTS: Cystic lesions of PSP-BHD and PSP showed different miRNAs profiles with a significant upregulation of miR-424-5p and let-7d-5p in PSP-BHD. The combination of the two effectively predicted BHDS patients. In vitro studies revealed a suppressive effect of FLCN on miR-424-5p and let-7d-5p expressions specifically in lung epithelial cells. The ectopic miRNAs triggered epithelial apoptosis and epithelial transition of mesenchymal cells and suppressed the reparative responses in cells and tissues with FLCN deficiency. CONCLUSION: The upregulation of miR-424-5p and let-7d-5p by FLCN deficiency occurred in epithelial cells and marked the PSP-BHD condition, which contributed to a focused degenerative pathology in the lung of PSP-BHD patients.

Type IIA Secreted Phospholipase A2 in Host Defense against Bacterial Infections.

The enzyme type IIA secreted phospholipase A2 (sPLA2-IIA) is crucial for mammalian innate host defense against bacterial pathogens. Most studies have investigated the role of sPLA2-IIA in systemic bacterial infections, identifying molecular pathways of bacterial resistance against sPLA2-IIA-mediated killing, and providing insight into sPLA2-IIA mechanisms of action. Sensitization of (antibiotic-resistant) bacteria to sPLA2-IIA action by blocking bacterial resistance or by applying sPLA2-IIA to treat bacterial infections might represent a therapeutic option in the future. Because sPLA2-IIA is highly expressed at mucosal barriers, we also discuss how sPLA2-IIA is likely to be an important driver of microbiome composition; we anticipate that future research in this area may bring new insights into the role of sPLA2-IIA in health and disease.

Infection-driven activation of transglutaminase 2 boosts glucose uptake and hexosamine biosynthesis in epithelial cells.

Transglutaminase 2 (TG2) is a ubiquitously expressed enzyme with transamidating activity. We report here that both expression and activity of TG2 are enhanced in mammalian epithelial cells infected with the obligate intracellular bacteria Chlamydia trachomatis. Genetic or pharmacological inhibition of TG2 impairs bacterial development. We show that TG2 increases glucose import by up-regulating the transcription of the glucose transporter genes GLUT-1 and GLUT-3. Furthermore, TG2 activation drives one specific glucose-dependent pathway in the host, i.e., hexosamine biosynthesis. Mechanistically, we identify the glucosamine:fructose-6-phosphate amidotransferase (GFPT) among the substrates of TG2. GFPT modification by TG2 increases its enzymatic activity, resulting in higher levels of UDP-N-acetylglucosamine biosynthesis and protein O-GlcNAcylation. The correlation between TG2 transamidating activity and O-GlcNAcylation is disrupted in infected cells because host hexosamine biosynthesis is being exploited by the bacteria, in particular to assist their division. In conclusion, our work establishes TG2 as a key player in controlling glucose-derived metabolic pathways in mammalian cells, themselves hijacked by C. trachomatis to sustain their own metabolic needs.

Borneol alleviates brain injury in sepsis mice by blocking neuronal effect of endotoxin.

AIM: Brain injury after sepsis leads to high mortality and long-term brain dysfunction in patients. Previous studies revealed that borneol has a protective effect on the brain, but its function on sepsis associated encephalopathy (SAE) remains unknown. Herein, we investigated the protective effect of borneol against sepsis-related brain injury. MAIN METHODS: Lipopolysaccharide (LPS)-induced sepsis mice and cells were treated with borneol at the dose of 100 mg/kg by gavage or 10 µg/ml in culture, respectively. The protective effect of borneol on neurons and the microglia were assessed in vivo and in vitro. KEY FINDINGS: We observed that borneol attenuated brain neuronal and microglial inflammation in LPS-induced sepsis mice with a suppression of p-p65 and p38 signaling that were initially activated by LPS in the brain. In vitro examination confirmed that the protective effect of borneol on both neurons and microglia, and its suppressive effect on p-p65 and p38 pathways were, at least in part, direct. SIGNIFICANCE: An early protection of neurons and microglia from bacterial endotoxin during sepsis is beneficial, and borneol has the potential to protect these cells.

Puerarin prevents high-fat diet-induced obesity by enriching Akkermansia muciniphila in the gut microbiota of mice.

Growing evidence indicates that the gut microbiota plays a significant role in the pathophysiological processes of obesity and its related metabolic symptoms in the host. Puerarin, an active ingredient in the root of Pueraria lobate has been suggested to have a potent anti-obesity effect. Herein, we tested whether this effect of puerarin is associated with changes in the gut microbiota. In addition to reducing body weight, inflammation, and insulin resistance, puerarin administration significantly altered the composition of the gut microbiota. Notably, puerarin treatment greatly increased the abundance of Akkermansia muciniphila, a mucin-degrading bacterium known to be beneficial for host metabolism and significantly downregulated in high-fat diet-fed mice. Further experiments revealed that puerarin increased intestinal expression levels of Muc2 and Reg3g and protected intestinal barrier function (normal permeability) by increasing the expression of ZO-1 and occludin in vivo and in vitro. These data suggest that puerarin's enriching effect on A. muciniphila is mediated, at least in part, by a host cellular response to protect the host from diet-induced metabolic disorders and other diseases.

Rapid histology of laryngeal squamous cell carcinoma with deep-learning based stimulated Raman scattering microscopy.

Maximal resection of tumor while preserving the adjacent healthy tissue is particularly important for larynx surgery, hence precise and rapid intraoperative histology of laryngeal tissue is crucial for providing optimal surgical outcomes. We hypothesized that deep-learning based stimulated Raman scattering (SRS) microscopy could provide automated and accurate diagnosis of laryngeal squamous cell carcinoma on fresh, unprocessed surgical specimens without fixation, sectioning or staining. Methods: We first compared 80 pairs of adjacent frozen sections imaged with SRS and standard hematoxylin and eosin histology to evaluate their concordance. We then applied SRS imaging on fresh surgical tissues from 45 patients to reveal key diagnostic features, based on which we have constructed a deep learning based model to generate automated histologic results. 18,750 SRS fields of views were used to train and cross-validate our 34-layered residual convolutional neural network, which was used to classify 33 untrained fresh larynx surgical samples into normal and neoplasia. Furthermore, we simulated intraoperative evaluation of resection margins on totally removed larynxes. Results: We demonstrated near-perfect diagnostic concordance (Cohen's kappa, κ > 0.90) between SRS and standard histology as evaluated by three pathologists. And deep-learning based SRS correctly classified 33 independent surgical specimens with 100% accuracy. We also demonstrated that our method could identify tissue neoplasia at the simulated resection margins that appear grossly normal with naked eyes. Conclusion: Our results indicated that SRS histology integrated with deep learning algorithm provides potential for delivering rapid intraoperative diagnosis that could aid the surgical management of laryngeal cancer.

Possible cluster pairing correlation in the checkerboard Hubbard model: a quantum Monte Carlo study.

Constrained-path quantum Monte Carlo method is applied to study the pairing correlation in the checkerboard Hubbard model with inhomogeneous nearest-neighbor hopping at a low doping of holes. The inhomogeneous hopping can enhance the pairing correlation among different plaquette clusters. An obvious maximum for the pairing correlation is observed at a certain inhomogeneous hopping. The cluster pairing correlation shows the strongest long-range behavior at the optimal inhomogeneity. The enhancement of cluster pairing correlation might be associated with the transition of the Fermi surface structure. This work indicates that the inhomogeneous hopping could tailor the pairing correlation effectively.

Integrating the Z-scheme heterojunction into a novel Ag2O@rGO@reduced TiO2 photocatalyst: Broadened light absorption and accelerated charge separation co-mediated highly efficient UV/visible/NIR light photocatalysis.

A photocatalyst with good electron-transfer property and wide spectrum response is of great interest. Herein, visible/NIR-light-driven Ag2O nanoparticles (NPs) and UV/visible-responsive reduced TiO2 nanosheets (TiO2-x NSs) anchored onto reduced graphene oxide (rGO) forming Ag2O@rGO@TiO2-x composites are synthesized in this study. The as-synthesized Ag2O@rGO@TiO2-x composites exhibit a superior full solar spectrum (UV, visible and NIR) response, showing their potential for effective use of solar energy. Compared to single component (TiO2 NSs and Ag2O NPs) or binary composites (Ag2O@TiO2), Ag2O@rGO@TiO2-x ternary composite has exhibited improved photocatalytic activity under UV, visible, NIR and nature sunlight irradiation and excellent photostability. The outstanding photocatalytic performance of Ag2O@rGO@TiO2-x composites depends on three sides: firstly, synergistic effect among the reduced TiO2, Ag2O, and rGO improves the wide spectrum response ability; Secondly, Ag2O@rGO@TiO2-x builds a Z-scheme structure, which promotes the separation of electron/hole pairs and retains prominent redox ability; Thirdly, the electrons of Ag2O are transferred to rGO to suppress the photo-corrosion of Ag2O during the photocatalytic process and the stability of Ag2O@rGO@TiO2-x composite has been enhanced greatly.