Orthodontic maxillary molar movement-induced zygomatic pillar remodeling and its consequences on occlusal characteristics and stress distribution.

OBJECTIVE: We aimed to evaluate changes in the zygomatic pillar during orthodontic treatment involving premolar extraction, analyze the effects of maxillary first molar movement on zygomatic pillar remodeling, and examine occlusal characteristics and stress distribution after remodeling. METHODS: Twenty-five patients who underwent premolar extraction were included in the study. The zygomatic pillar measurement range was defined, and cross-sectional areas, surface landmark coordinates, alveolar and cortical bone thicknesses, and density changes were assessed using Mimics software based on the cone-beam computed tomography scans taken before (T0) and after the treatment (T1). Multiple linear regression analysis was performed to determine the correlation between changes in the zygomatic pillar and maxillary first molar three-dimensional (3D) movement and rotation. Additionally, the correlation between pillar remodeling and occlusal characteristics was analyzed by Teetester. Pre- and post-reconstruction 3D finite element models were constructed and loaded with an average occlusal force of two periods. RESULTS: The morphological and structural remodeling of the zygomatic pillar after orthodontic treatment involving premolar extraction showed a decreased cross-sectional area of the lower segment of the zygomatic pillar. The zygomatic process point moved inward and backward, whereas the zygomatico-maxillary suture point moved backward. The thicknesses of the zygomatic pillar alveolar and cortical bones were thinner, and reduced alveolar bone density was observed. Simultaneously, the movement and angle change of the maxillary first molar could predict zygomatic pillar reconstruction to a certain extent. With decreasing the total occlusal force and the occlusal force of the first molar, occlusal force distribution was more uniform. With zygomatic pillar remodeling, occlusal stress distribution in the zygomatic alveolar ridge decreased, and occlusal stress was concentrated at the junction of the vertical and horizontal parts of the zygomatic bone and the posterior part of the zygomatic arch. CONCLUSIONS: Orthodontic treatment involving premolar extraction led to zygomatic pillar remodeling, making it more fragile than before and reducing the occlusal force of the maxillary first molar and the entire dentition with stress concentrated in weak areas. CLINICAL RELEVANCE: No other study has focused on the effects of orthodontics on pillar structures. The present study indicates that the mesial movement of the maxillary first molar weakened the zygomatic pillar and reduced occlusal function, thereby providing insights for inserting anchorage screws and facial esthetics.

Biofilm-associated metabolism via ERG251 in Candida albicans.

Biofilm formation by the fungal pathogen Candida albicans is the basis for its ability to infect medical devices. The metabolic gene ERG251 has been identified as a target of biofilm transcriptional regulator Efg1, and here we report that ERG251 is required for biofilm formation but not conventional free-living planktonic growth. An erg251Δ/Δ mutation impairs biofilm formation in vitro and in an in vivo catheter infection model. In both in vitro and in vivo biofilm contexts, cell number is reduced and hyphal length is limited. To determine whether the mutant defect is in growth or some other aspect of biofilm development, we examined planktonic cell features in a biofilm-like environment, which was approximated with sealed unshaken cultures. Under those conditions, the erg251Δ/Δ mutation causes defects in growth and hyphal extension. Overexpression in the erg251Δ/Δ mutant of the paralog ERG25, which is normally expressed more weakly than ERG251, partially improves biofilm formation and biofilm hyphal content, as well as growth and hyphal extension in a biofilm-like environment. GC-MS analysis shows that the erg251Δ/Δ mutation causes a defect in ergosterol accumulation when cells are cultivated under biofilm-like conditions, but not under conventional planktonic conditions. Overexpression of ERG25 in the erg251Δ/Δ mutant causes some increase in ergosterol levels. Finally, the hypersensitivity of efg1Δ/Δ mutants to the ergosterol inhibitor fluconazole is reversed by ERG251 overexpression, arguing that reduced ERG251 expression contributes to this efg1Δ/Δ phenotype. Our results indicate that ERG251 is required for biofilm formation because its high expression levels are necessary for ergosterol synthesis in a biofilm-like environment.

Enhanced Corrosion Inhibition of Q235 Steel by N,S Co-Doped Carbon Dots: A Sustainable Approach for Industrial Pickling Corrosion Inhibitors.

A high yield of environmentally friendly N,S-codoped (N,S-CDs) and N-doping carbon points (N-CDs) carbon dots was achieved through a biochemical oxidation reaction at room temperature in this study. Acetaldehyde, sodium hydroxide, benzotriazole (BTA), and 2-mercaptobenzimidazole (MB) with a similar structure were used as raw materials. The microstructure and properties of the corrosion inhibitor for Q235 steel were evaluated by various experiments. The results demonstrated enhanced corrosion inhibition rates of the N,S-CDs compared to the N-CDs using electrochemical tests (93.83% vs 77.65%) and weight loss experiments (96.35% vs 91.65%) at 50 mg/L, respectively, compared to the blank material, indicating that N,S codoping can significantly improve the corrosion inhibition effect of carbon dots. The significant improvements were attributed to the formation of dense adsorption films and the hydrophobic properties of N and S-CDs nanoparticles on the steel surface, leading to an effective barrier against corrosion. The findings from this study provide important experimental data for potential industrial applications and hold important practical value in the field of pickling corrosion inhibitors.

Regulatory features of Candida albicans hemin-induced filamentation.

Candida albicans is a prominent fungal pathogen that can infect the bloodstream and deep tissues. One key pathogenicity trait is the ability to transition between yeast and hyphal growth. Hyphae are critical for the formation of biofilms, which in turn enable device-associated infection. Among signals that drive hypha formation is the presence of hemin, an oxidized Fe(III)-containing heme derivative found in blood. In this study, we asked 4 questions. First, how uniform is the filamentation response to hemin among C. albicans strains? We tested 26 diverse isolates and found that the strength of a strain's filamentation response to hemin reflected its filamentation level in the absence of hemin. Second, does hemin induce biofilm formation? Hemin biofilm induction was evident in 5 out of 10 isolates tested, including most of the weaker biofilm formers tested. Third, what is the gene expression response to hemin? We compared RNA-seq data for type strain SC5314 grown in pH 5.5 minimal media with or without hemin. We also compared that response to SC5314 grown in pH 7.0 minimal media, where it undergoes well-studied pH-dependent filamentation. We found a common set of 72 genes with upregulated RNA levels in response to both signals, including many known hypha-associated genes. Surprisingly, overlap among those 72 genes with 2 recent consensus definitions of hypha-associated genes was limited to only 16 genes. Fourth, which regulators govern hemin-induced filamentation? A mutant survey indicated that the response depends upon filamentation regulators Efg1, Brg1, and Rim101, but not upon heme acquisition regulator Hap1 or its target genes HMX1, RBT5, PGA10, PGA7, and CSA2. These findings argue that hemin induces hypha formation independently of its utilization.

WDR12/RAC1 axis promoted proliferation and anti-apoptosis in colorectal cancer cells.

BACKGROUND: WD repeat domain 12 (WDR12) plays a crucial role in the ribosome biogenesis pathway. However, its biological function in colorectal cancer (CRC) remains poorly understood. Therefore, this study aims to investigate the roles of WDR12 in the occurrence and progression of CRC, as well as its underlying mechanisms. METHODS: The expression of WDR12 was assessed through The Cancer Genome Atlas (TCGA) and the Human Protein Atlas (HPA) database. Functional experiments including Celigo assay, MTT assay, and Caspase-3/7 assay were conducted to validate the role of WDR12 in the malignant progression of CRC. Additionally, mRNA chip-sequencing and ingenuity pathway analysis (IPA) were performed to identify the molecular mechanism. RESULTS: WDR12 expression was significantly upregulated in CRC tissues compared to normal colorectal tissues. Knockdown of WDR12 reduced proliferation and promoted apoptosis of CRC cell lines in vitro and in vivo experiments. Furthermore, WDR12 expression had a significantly inverse association with diseases and functions, including cancer, cell cycle, DNA replication, recombination, cellular growth, proliferation and repair, as revealed by IPA analysis of mRNA chip-sequencing data. Moreover, the activation of cell cycle checkpoint kinases proteins in the cell cycle checkpoint control signaling pathway was enriched in the WDR12 knockdown CRC cell lines. Additionally, downregulation of rac family small GTPase 1 (RAC1) occurred upon WDR12 knockdown, thereby facilitating the proliferation and anti-apoptosis of CRC cells. CONCLUSION: Our study demonstrates that the WDR12/RAC1 axis promotes tumor progression in CRC. Therefore, WDR12 may serve as a novel oncogene and a potential target for individualized therapy in CRC. These findings provide an experimental foundation for the clinical development of drugs targeting the WDR12/RAC1 axis.

Intraperitoneal vancomycin plus levofloxacin for the treatment of peritoneal dialysis-related peritonitis in patients with no response to cefazolin plus ceftazidime.

INTRODUCTION: Peritoneal dialysis-related peritonitis (PDRP) should be treated as soon as possible by an empirical regimen without waiting for effluent bacterial culture results. We retrospectively investigated patients treated with vancomycin plus levofloxacin as a treatment regimen if there was no response to cefazolin plus ceftazidime. MATERIALS AND METHODS: We collected records of adult patients with PDRP from January 1, 2013, to November 30, 2020. The characteristics of episodes of PDRP with no response to cefazolin plus ceftazidime treated by intraperitoneal (IP) injection of vancomycin plus levofloxacin were analyzed. RESULTS: 118 episodes of PDRP were recorded, among which 115 episodes were treated with IP antibiotics. 93 episodes were treated with cefazolin plus ceftazidime. In 38 episodes, treatment was switched to IP injection of vancomycin plus levofloxacin if there was no response to cefazolin plus ceftazidime. 26/38 (68.4%) episodes were cured by vancomycin plus levofloxacin. Fever, diabetes, fasting glucose, a decrease in effluent leukocytes on day 3 and day 5, and Charlson Comorbidity Index (CCI) scores were significantly different between uncured and cured episodes. No variable was associated with treatment failure after multiple logistic regression. Fever, diabetes, a decrease in effluent leukocytes on day 3, and CCI score were associated with treatment failure after univariable logistic regression. CONCLUSION: Vancomycin plus levofloxacin may be effective if patients are not responsive to cefazolin plus ceftazidime.

Thiol-Ene Click Reaction in Constructing Liquid Separation Membranes for Water Treatment.

In the evolving landscape of water treatment, membrane technology has ascended to an instrumental role, underscored by its unmatched efficacy and ubiquity. Diverse synthesis and modification techniques are employed to fabricate state-of-the-art liquid separation membranes. Click reactions, distinguished by their rapid kinetics, minimal byproduct generation, and simple reaction condition, emerge as a potent paradigm for devising eco-functional materials. While the metal-free thiol-ene click reaction is acknowledged as a viable approach for membrane material innovation, a systematic elucidation of its applicability in liquid separation membrane development remains conspicuously absent. This review elucidates the pre-functionalization strategies of substrate materials tailored for thiol-ene reactions, notably highlighting thiolation and introducing unsaturated moieties. The consequential implications of thiol-ene reactions on membrane properties-including trade-off effect, surface wettability, and antifouling property-are discussed. The application of thiol-ene reaction in fabricating various liquid separation membranes for different water treatment processes, including wastewater treatment, oil/water separation, and ion separation, are reviewed. Finally, the prospects of thiol-ene reaction in designing novel liquid separation membrane, including pre-functionalization, products prediction, and solute-solute separation membrane, are proposed. This review endeavors to furnish invaluable insights, paving the way for expanding the horizons of thiol-ene reaction application in liquid separation membrane fabrication.

Bibliometric analysis of global research trends between gut microbiota and pancreatic cancer: from 2004 to 2023.

Background: Pancreatic cancer (PC) is one of the most lethal malignancies of the digestive system and is expected to be the second leading cause of cancer-related death in the United States by 2030. A growing body of evidence suggests that the gut microbiota (GM) is intimately involved in the clinical diagnosis, oncogenic mechanism and treatment of PC. However, no bibliometric analysis of PC and GM has been reported. Methods: The literature on PC and GM was retrieved from the Web of Science Core Collection (WoSCC) database for the period from January 1, 2004 to April 25, 2023. Microsoft Excel 2021, CiteSpace, VOSviewer, Scimago Graphica, Graphpad Prism, Origin, the R package "bibliometrics" and the bibliometric online analysis program were used to visualize the publishing trends and hot spots in this field. Results: A total of 1,449 articles were included, including 918 articles and 531 reviews. Publishing had grown rapidly since 2017, with the 2023 expected to publish 268 articles. Unsurprisingly, the United States ranked highest in terms of number of literatures, H index and average citations. The University of California System was the most active institution, but Harvard University tended to be cited the most on average. The three most influential researchers were Robert M. Hoffman, Zhao Minglei, and Zhang Yong. Cancers had published the most papers, while Nature was the most cited journal. Keyword analysis and theme analysis indicated that "tumor microenvironment," "gemcitabine-resistance," "ductal adenocarcinoma," "gut microbiota" and "diagnosis" will be the hotspots and frontiers of research in the future. Conclusion: In summary, the field is receiving increasing attention. We found that future hotspots of PC/GM research may focus on the mechanism of oncogenesis, flora combination therapy and the exploitation of new predictive biomarkers, which provides effective suggestions and new insights for scholars.

Higher D-dimer and activated partial thromboplastin time are poor prognostic factors in patients with peritoneal dialysis-related peritonitis.

INTRODUCTION: Coagulation system dysfunction is associated with adverse outcomes of peritoneal dialysis (PD) and bacterial infection. We investigated the association between coagulation system and treatment failure of peritoneal dialysis-related peritonitis (PDRP). METHODS: We collected records of patients aged ≥18 years with PDRP. PDRP episodes were divided into: shortened activated partial thromboplastin time (APTT) group and prolonged APTT group, low D-dimer (DD) group and high DD group. The baseline characteristics of the groups were collected and compared. The association between APTT, DD and treatment failure of PDRP was analyzed using logistic regression analysis. RESULTS: Thirty episodes of treatment failure were observed in 110 episodes of PDRP in our study. After adjusting for variables, prolonged APTT (OR = 1.166 [1.049-1.296], p = 0.004) or high level of DD (OR = 1.374 [1.057-1.787], p = 0.017) was associated with treatment failure of PDRP. CONCLUSION: Prolonged baseline APTT or high level of DD increased the risk of treatment failure of PDRP.

MiR-92a regulates PTEN/Akt signaling axis to promote paclitaxel resistance in ovarian cancer cells.

To investigate the function and possible mechanism of miR-92a in malignant behaviors such as paclitaxel resistance in ovarian cancer (OC) cells. The miR-92a and PTEN expression were detected by real-time PCR (RT-PCR). The cell viability and apoptosis were detected by MTT, colony formation and flow cytometry assay, respectively. Dual-luciferase reporter assay was adopted to verify the targeting relationship between miR-92a and PTEN. Besides, we measured the relative protein levels of PTEN and p-AKT/AKT by Western blot. MiR-92a was significantly highly expressed in OC cells, and its high expression could notably enhance paclitaxel resistance, cell proliferation and colony formation, as well as inhibit apoptosis in SKOV3-Tax cells. Further luciferase reporter assay and expression detection showed that miR-92a could target and regulate PTEN and that there was a targeted relationship between them. In addition, further exploration of the mechanism revealed that miR-92a regulated PTEN/Akt signaling pathway. MiR-92a not only promotes the proliferation, colony formation and paclitaxel resistance of SKOV3-Tax cells in OC, but also inhibits apoptosis, and it may be related to the regulation of the PTEN/Akt signaling pathway. MiR-92a serves as a potential biomarker for the malignant biological behavior of OC cells.

Cerium oxide nanoparticles protect against chondrocytes and cartilage explants from oxidative stress via Nrf2/HO-1 pathway in temporomandibular joint osteoarthritis.

Oxidative stress is closely linked to the etiology of temporomandibular joint osteoarthritis. (TMJ-OA) and is an important therapeutic target. Cerium oxide nanoparticles (CNPs) have been broadly studied owing to their powerful antioxidant properties and potential preventive and therapeutic effects against chronic diseases. The current study was designed to explore the protective effects of CNPs on the progression of TMJ-OA and their potential mechanisms. We detected the ability of CNPs to eliminate reactive oxygen species (ROS) in chondrocytes. Moreover, their protective effects on chondrocytes were detected in the level of gene and protein. Furthermore, TUNEL assay, histology and safranin O-fast green staining were used to detect the beneficial effects of CNPs on cartilage explants. The mechanism of CNPs, protecting condylar cartilage by reducing inflammation, was further explored by knocking down the Nuclear factor-erythroid 2-related factor (Nrf2) gene. CNPs could reduce the ROS levels in chondrocytes and cartilage explants and reverse the IL-1ß-induced imbalance of cartilage matrix metabolism and apoptosis. The protective effects of CNPs on cartilage were lost after key antioxidant factors including Nrf2 and heme-oxygenase 1(HO-1) were significantly reduced. In conclusion, this study demonstrated for the first time that activating the Nrf2/HO-1 signaling pathway by CNPs might have therapeutic potential for TMJ-OA.

High glucose levels contribute to vascular fibrosis via the activation of the endothelial-to-mesenchymal transition in periodontitis.

OBJECTIVE: To determine the changes of Porphyromonas gingivalis (P. gingivalis) growth and metabolism and identify whether the vascular epithelium change could be induced in diabetic periodontitis. BACKGROUND: Maintaining favourable vascular function is a precondition for periodontal regeneration. In diabetic periodontitis, high glucose levels could enhance the metabolism of pathogens, and a complex condition involving inflammation and high glucose levels would disrupt homeostasis of the epithelium and promote fibrosis by endothelial-to-mesenchymal transition (EndMT). METHODS: Porphyromonas gingivalis was cultured with glucose to judge its metabolic activity. Human umbilical vein endothelial cells (HUVECs) were treated with P. gingivalis-lipopolysaccharide (LPS) (10 µg/ml) and/or high glucose concentrations (25 mM), and transforming growth factor (TGF)-ß inhibitor was used to block EndMT. Inflammation level was assessed by flow cytometry. Multiple biological functions including EndMT, angiopoiesis, and cell migration were analysed. Additionally, gene expressions and protein levels were determined with qPCR and western blot, respectively. Finally, blood vessels were cultured ex vivo, and EndMT and fibrosis markers were detected by immunohistochemistry. RESULTS: Glucose could promote P. gingivalis growth and biofilm formation as well as the expression of virulence factor genes including FimA, RgpA, RgpB, and Kgp. P. gingivalis-LPS and glucose could increase intracellular reactive oxygen species (ROS) and promote fibrosis via EndMT in HUVECs, along with attenuating angiopoiesis and cell migration, which could be resumed by blocking EndMT with TGF-ß inhibitor. Vascular fibrosis was observed after the addition of glucose via EndMT regulation. CONCLUSION: Glucose augmented the growth and metabolism of P. gingivalis and promoted fibrosis by the activation of EndMT, as well as the inhibition of angiopoiesis and cell migration.

Estimation of gingival crevicular fluid oxidative stress markers in school-aged children and teenagers with insufficient sleep.

BACKGROUND: Sleep is crucial for survival. Sleep deprivation causes ROS accumulation and, consequently, oxidative stress. The goal of the study was to evaluate gingival crevicular fluid (GCF) levels of the oxidative stress status hydrogen peroxide (H2O2), superoxide glutathione (GSH), and cellular oxidative damage marker malondialdehyde (MDA) in school-aged children and teenagers with insufficient sleep. METHODS: This study investigated sleep duration in 80 participants from two different developmental stages: school-aged children (6-13 years) and teenagers (14-17 years). GCF samples were obtained from all individuals, and samples were investigated to detect H2O2, GSH, and MDA levels using the micro method. RESULTS: Results reveal that GCF MDA and H2O2 in school-age children and teenagers with insufficient sleep were significantly higher than in children with sufficient sleep. GCF GSH with insufficient sleep was insignificantly lower than in children with sufficient sleep. There was no significant difference between school-age and teenage populations. CONCLUSION: Sleep deprivation causes increased levels of oxidative stress in gingival crevicular fluid, and adequate sleep is essential for maintaining redox balance.

The effectiveness and safety of corticosteroid therapy for IgA nephropathy with crescents: a prospective, randomized, controlled study.

BACKGROUND: Pozzi protocol (methylprednisolone intravenous infusion in 1st-3rd-5th months and oral steroid for 6 months) has been thought to be the classic therapy for IgA nephropathy (IgAN) patients with proteinuria> 1.0 g/24 h. There is no consensus on the treatments for IgAN with active pathological changes, especially for IgAN patients with crescents proportion < 50%. This study aimed to evaluate the effectiveness and safety of the treatment protocol of methylprednisolone intravenous infusion at the 1st-2nd-3rd months for IgAN patients with crescents. METHODS: In this prospective, randomized, controlled, non-blind study, 68 IgAN patients with crescents proportion < 50% were divided into the 1-2-3 group receiving 0.25 g/d methylprednisolone intravenously for 3 consecutive days in the 1st-2nd-3rd months, and oral prednisone 0.5 mg/kg/d on consecutive days for 6 months and the 1-3-5 group with the same intravenous methylprednisolone treatment in the 1st-3rd-5th months, and the same oral prednisone. The primary outcome measure was remission of proteinuria (complete or partial); while the secondary outcome measures were deterioration of renal function (evidenced by a 50% rise from baseline serum creatinine levels, or a 25% decline from baseline eGFR levels). RESULTS: There was no significant difference in incidence of crescents (median 14.66% vs. 11.45%, p = 0.143) between the 1-2-3 and 1-3-5 groups. From month 1 to month 6, there was a decreasing trend in the levels of urine protein and serum creatinine and an increasing trend in eGFR in both groups. The mean period of remission in the 1-2-3 group seemed shorter. Overall, there were 55 (80.89%) patients meeting remission. The rates of remission in the 1-2-3 group and 1-3-5 group were 85.3 and 76.47%, respectively (P = 0.644). The 1-2-3 group had lower creatinine and higher eGFR than the 1-3-5 group, but the difference was not significant. The complication rate was 11.11 and 15.79% in the two groups, respectively. There was no significant difference in the complications between groups. CONCLUSIONS: Both the 1st-3rd-5th and 1st-2nd-3rd protocols can effectively alleviate proteinuria and protect renal function in IgAN patients with crescents but the 1st-2nd-3rd protocol seemed to have better effectiveness. TRIAL REGISTRATION: ClinicalTrials.gov, Identifier: NCT02160132 , Registered June 10, 2014.

Hypertriglyceridemia is a risk factor for treatment failure in patients with peritoneal dialysis-related peritonitis.

OBJECTIVE: Disorders of triglycerides (TG) are common in patients with peritoneal dialysis (PD). Hypertriglyceridemia has been demonstrated in various infections. The association between triglycerides and the outcomes of peritoneal dialysis-related peritonitis (PDRP) was investigated in this study. METHODS: We retrospectively investigated patients with PDRP from January 1, 2013 to October 31, 2020. Hypertriglyceridemia was defined as triglycerides ≥ 1.7 mmol/L. PDRP episodes were divided into two groups: hypertriglyceridemia and normal levels of triglycerides. The clinical and laboratory baseline data of the two groups were collected and compared. The association between triglycerides and treatment failure was analyzed by logistic regression analysis. RESULTS: Ninety episodes in 66 patients were recorded in our center. Hypertriglyceridemia occurred in 38% (34/90) of episodes. Twenty-five episodes were not cured in 90 episodes (27.8%, 25/90). The levels of thrombocytes, high-sensitivity C-reactive protein (hs-CRP), low-density lipoprotein cholesterol (LDL-C) and glycated hemoglobin, were higher in hypertriglyceridemia episodes of PDRP at baseline. The bacterial classification was different between elevated triglyceride group and normal triglyceride group. Adjusted for age, duration of dialysis, residual renal function, diabetes, thrombocytes, hs-CRP, serum albumin, cholesterol, HDL-C, LDL-C, intact parathyroid hormone (iPTH), glycated hemoglobin and spectrum of bacteria, hypertriglyceridemia were associated significantly with treatment failure of PDRP in our study (OR 3.416, 95% CI 1.223-9.540 p < 0.05). CONCLUSION: Hypertriglyceridemia at baseline was an independent risk factor for treatment failure of PDRP.

Synthesis and Structure of Water-Soluble Sb Quantum Dots and Enhanced Corrosion Inhibition Performance and Mechanisms.

Generally, single organic or inorganic inhibitors could effectively inhibit corrosion for metallic materials; however, there are rarely reports about the hybrid corrosion inhibitors consisting of organic and inorganic inhibitors. Thus, in this work, we synthesize a hybrid environment-friendly water-soluble corrosion inhibitor (Sb quantum dots) containing Sb, Sb2O3, Sb2O4, and carbon using the electrochemical exfoliation method. The inhibition effectiveness in short- and long-term immersion tests is measured using electrochemical methods, weight loss, and surface analysis. The results exhibit that the corrosion inhibition efficiency sensitively relates to the concentration of Sb quantum dots (SQDs), which achieves the largest value as the concentration of SQDs increases to 200 mg/L. Atomic force microscopy, scanning electron microscopy, and contact angle analysis reveal that the SQDs well-disperse on and cover the Q235 steel surface at 200 mg/L. According to the Langmuir adsorption data, the physicochemical adsorption and effective antioxidation of SQDs on the passivated Q235 steel surface are in charge of the effective corrosion inhibition efficiency in 0.5 M H2SO4 solution.

PD-L1 induces macrophage polarization toward the M2 phenotype via Erk/Akt/mTOR.

PD-L1 (programmed death-ligand 1) is the ligand of PD-1 (programmed cell death protein 1) and regulates inhibitory immune responses. It is well known that PD-L1 suppresses T cell function via binding to PD-1. However, little is known about the role of the PD-1/PD-L1 axis in macrophage polarization. According to previous studies, the function of the PD-1/PD-L1 axis in macrophage polarization is controversial, and the underlying mechanism has not been fully elucidated. Thus, we treated THP-1-derived macrophages with human PD-L1 Fc to determine the role of the PD-1/PD-L1 axis in macrophage polarization. To further explore the mechanism, we performed RNA sequencing and used specific inhibitors to identify the implicated signalling pathways. In this study, we found that PD-L1 induces the upregulation of CD206 expression, which is inhibited by nivolumab, LY294002, U0126, and rapamycin. Evaluation of differentially expressed genes (DEGs) and bioinformatics analysis indicated that PD-L1 also induces the upregulation of the expression of genes that maintain mitochondrial function and mediate metabolic switching. In addition, we did not detect PD-L1-induced CD86 alterations, indicating that PD-L1 treatment has no significant influence on M1 polarization. Taken together, these results suggest that PD-L1 binds to PD-1 and promotes M2 polarization accompanied by mitochondrial function enhancement and metabolic reprogramming via Erk/Akt/mTOR. This study elucidates the role of PD-L1 in macrophage polarization and verifies the underlying mechanisms for the first time. Considering that aberrantly upregulated PD-L1 expression contributes to a wide variety of diseases, targeting PD-L1-mediated macrophage polarization is a prospective therapeutic strategy for both neoplastic and nonneoplastic diseases.

Analysis of methylparaben in cosmetics based on a chemiluminescence H2 O2 -NaIO4 -CNQDs system.

In this article, a simple, effective chemiluminescence (CL) method for the detection of methylparaben (MP) in cosmetic samples was developed based on an IO4 - -H2 O2 -carbon nitrogen quantum dots (CNQDs) system without a separation process. The results indicated that the redox reaction between periodate and hydrogen peroxide released hydroxide radicals and superoxide radical anions in the presence of bicarbonate. These two radicals were responsible for the formation of excited luminophor CNQD* with a maximum wavelength at 480 nm. Due to the competitive reaction with hydroxide radicals, CL intensity was markedly diminished in the presence of MP. The relative standard deviation in the intraday assay was below 5.5% (n = 9), and the detection limit was as low as 0.50 µmol/L. The proposed method allowed for the successful, selective determination of MP in cosmetics.

In Situ Friction-Induced Graphene Originating from Methanol at the Sliding Interface between the WC Self-Mated Tribo-Pair and Its Tribological Performance.

Alcohols are reported to have superlubricity at low loads during sliding; however, their lubricity under high loads has rarely been reported. Meanwhile, the lubrication mechanism of alcohols under high loads is still not well understood. Here, we first report the lubricity of methanol under 98 N and 1450 rpm and demonstrate the formation of graphene and fullerene-like nanostructures induced by tribochemical reactions. Results show that the lubrication mechanism was mainly attributed to the friction-induced graphene under boundary lubrication condition. Besides that, the wear rate of a YG8 hard alloy ball mainly occurred at the run-in processes, and the friction-induced graphene effectively inhibited further wear after the run-in processes. The formation mechanism of graphene was well investigated, and the flash temperature rise and catalyst (WC, WO2, and WO3) were the major causes for the formation of graphene.

Drp1-mediated mitochondrial fission promotes renal fibroblast activation and fibrogenesis.

Excessive mitochondrial fission acts as a pro-proliferative marker in some cancers and organ fibrosis; its potential role in renal fibroblast activation and fibrogenesis has never been investigated. Here, we showed more pronounced fragmented mitochondria in fibrotic than in non-fibrotic renal fibroblast in humans and mice. In a mouse model of obstructive nephropathy, phosphorylation of Drp1 at serine 616 (p-Drp1S616) and acetylation of H3K27(H3K27ac) was increased in fibrotic kidneys; pharmacological inhibition of mitochondrial fission by mdivi-1 substantially reduced H3K27ac levels, fibroblasts accumulation, and interstitial fibrosis. Moreover, mdivi-1 treatment was able to attenuate the established renal fibrosis. In cultured renal interstitial fibroblasts, targeting Drp1 using pharmacological inhibitor or siRNA suppressed TGF-ß1-elicited cell activation and proliferation, as evidenced by inhibiting expression of α-smooth muscle actin (α-SMA) and collagen I, as well as by reducing DNA synthesis. In contrast, Drp1 deletion enhanced cell apoptosis, along with decreased mitochondrial fragmentation, mtROS elevation, and glycolytic shift upon TGF-ß1 stimulation. In Drp1 deletion fibroblasts, re-expression of wild-type Drp1 rather than Drp1S616A mutant restores the reduction of TGF-ß-induced-Drp1 phosphorylation, H3K27ac, and cell activation. Moreover, TGF-ß1 treatment increased the enrichment of H3K27ac at the promoters of α-SMA and PCNA, which was reversed in Drp1-knockdown fibroblasts co-transfected with empty vector or Drp1S616A, but not wild-type Drp1. Collectively, our results imply that inhibiting p-Drp1S616-mediated mitochondrial fission attenuates fibroblast activation and proliferation in renal fibrosis through epigenetic regulation of fibrosis-related genes transcription and may serve as a therapeutic target for retarding progression of chronic kidney disease.