Systematical identification of key genes and regulatory genetic variants associated with prognosis of esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) stands as a highly lethal malignancy characterized by pronounced recurrence and metastasis, resulting in a bleak 5-year survival rate. Despite extensive investigations, encompassing genome-wide association studies, the identification of robust prognostic markers has remained elusive. In this study, leveraging four independent data sets comprising 404 ESCC patients, we conducted a systematic analysis to unveil pivotal genes influencing overall survival. our meta-analysis identified 278 genes significantly associated with ESCC prognosis. Further exploration of the prognostic landscape involved an examination of expression quantitative trait loci for these genes, leading to the identification of six tag single nucleotide polymorphisms predictive of overall survival in a cohort of 904 ESCC patients. Notably, functional annotation spotlighted rs11227223, residing in the enhancer region of nuclear paraspeckle assembly transcript 1 (NEAT1), as a crucial variant likely exerting a substantive biological role. Through a series of biochemistry experiments, we conclusively demonstrated that the rs11227223-T allele, indicative of a poorer prognosis, augmented NEAT1 expression. Our results underscore the substantive role of NEAT1 and its regulatory variant in prognostic predictions for ESCC. This comprehensive analysis not only advances our comprehension of ESCC prognosis but also unveils a potential avenue for targeted interventions, offering promise for enhanced clinical outcomes.

Increased ten-eleven translocation methylcytosine dioxygenase one in dorsal root ganglion contributes to inflammatory pain in CFA rats.

DNA hydroxylation catalyzed by Tet dioxygenases occurs abundantly in neurons in mammals. However, effects of ten-eleven translocation methylcytosine dioxygenase 1 (TET1) expression and hydroxymethylation status on neuron injury remain unclear. This study was designed to explore the effects of TET1 and TET2 expression in the inflammatory pain of rats induced by complete Freund's adjuvant (CFA). Mechanical paw withdrawal threshold (PWT) and thermal withdrawal latency (TWL) were detected to assess pain behavior. The expression of TET1 and TET2 were measured in the dorsal root ganglion (DRG) with western blotting analysis. Immunofluorescence staining is employed to detect the expression and co-location of TRPV1 with TET1. Intrathecal administration of Bobcat339 was used to inhibit TET1 function in dorsal root ganglion. The paw withdrawal threshold and thermal withdrawal latency of rats were significantly reduced after CFA Injection. Western blot results showed that the expression of TET1 was significantly increased at 3 days after CFA injection, but TET2 had no statistical difference. Immunofluorescence results showed that TET1 was co-localized with TRPV1. Intrathecal administration of Bobcat339 improved mechanical and thermal pain threshold in CFA rats. Our findings highlight the role of TET1 in chronic inflammatory pain model. The expression of TET1 was increased in CFA rats, and suppression of TET1 will ameliorate inflammatory pain.

Food with calorie restriction reduces the development of atherosclerosis in apoE-deficient mice.

Calorie restriction (CR) ameliorates various diseases including cardiovascular disease. However, its protection and underlying mechanisms against atherosclerosis remain un-fully elucidated. In this study, we fed apoE deficient (apoE-/-) mice in Control group a high-fat diet (HFD, 21% fat plus 0.5% cholesterol) or in CR group a CR diet (CRD, 2% fat plus 0.5% cholesterol, ∼40% calorie restriction and same levels of cholesterol, vitamins, minerals and amino acids as in HFD). After 16 weeks feeding, compared with HFD, CRD substantially reduced atherosclerosis in mice. CRD increased SMC and collagen content but reduced macrophage content, necrotic core and vascular calcification in lesion areas. Mechanistically, CRD attenuated bodyweight gain, improved lipid profiles but had little effect on macrophage lipid metabolism. CRD also inhibited expression of inflammatory molecules in lesions. Taken together, our study demonstrates CRD effectively reduces atherosclerosis in apoE-/- mice, suggesting it as a potent and reproducible therapy for atherosclerosis management.

PTPN23[Thr] variant reduces susceptibility and tumorigenesis in esophageal squamous cell carcinoma through dephosphorylation of EGFR.

Post-translational modifications (PTMs) have emerged as pivotal regulators of the development of cancers, including esophageal squamous cell carcinoma (ESCC). Here, we conducted a comprehensive analysis of PTM-related genetic variants associated with ESCC risk using large-scale genome-wide and exome-wide association datasets. We observed significant enrichment of PTM-related variants in the ESCC risk loci and identified five variants that were significantly associated with ESCC risk. Among them, rs6780013 in PTPN23 exhibited the highest level of significance in ESCC susceptibility in 9,728 ESCC cases and 10,977 controls (odds ratio [OR] = 0.85, 95 % confidence interval [CI] = 0.81- 0.89, P = 9.77 × 10-14). Further functional investigations revealed that PTPN23[Thr] variant binds to EGFR and modulates its phosphorylation at Thr699. PTPN23[Thr] variant substantially inhibited ESCC cell proliferation both in vitro and in vivo. Our findings underscore the critical role of PTPN23[Thr]-EGFR interaction in ESCC development, providing more insights into the pathogenesis of this cancer.

Single-cell analysis identified POSTN+ cells associated with the aggressive phenotype and risk of esophageal squamous cell carcinoma.

Tumors are intricate and heterogeneous systems characterized by mosaic cancer cell populations with diverse expression profiles. Leveraging single-cell technologies, we employed the Scissor algorithm to delineate an epithelial subpopulation associated with the aggressive phenotype in esophageal squamous cell carcinoma (ESCC). This identified subpopulation exhibited elevated expression of genes involved in critical pathways, such as epithelial-mesenchymal transition and PI3K-Akt. Key signature genes within this subpopulation, namely CAV1, COL3A1, COL6A1, POSTN, and TAGLN, demonstrated significant upregulation concomitant with both tumorigenesis and tumor progression across independent single-cell datasets. Furthermore, we selected 1,450 expression quantitative trait loci of the top 62 signature genes of this cell subpopulation to investigate their potential in predicting ESCC risk. The results showed that the POSTN loci were predominantly associated with ESCC susceptibility. Through functional annotation and replication analyses, we identified that the rs1028728 in the POSTN promoter was significantly associated with increased ESCC risk in 7,049 ESCC cases and 8,063 controls (odds ratio = 1.29, 95% confidence interval: 1.18-1.42, p = 4.03 × 10-8). Subsequent biochemical experiments showed that the rs1028728[T] allele enhanced POSTN expression by affecting the binding of PRRX1 in the POSTN promoter. In summary, our meticulous single-cell analysis delineates an invasive epithelial subpopulation in ESCC, with POSTN emerging as an important marker for the aggressive phenotype. These findings offer more insights into potential strategies for the prevention and intervention of ESCC, enriching our understanding of this complex cancer landscape.

Moscatilin inhibits vascular calcification by activating IL13RA2-dependent inhibition of STAT3 and attenuating the WNT3/ß-catenin signalling pathway.

INTRODUCTION: Vascular calcification, a devastating vascular complication accompanying atherosclerotic cardiovascular disease and chronic kidney disease, increases the incidence of adverse cardiovascular events and compromises the efficacy of vascular interventions. However, effective therapeutic drugs and treatments to delay or prevent vascular calcification are lacking. OBJECTIVES: This study was designed to test the therapeutic effects and mechanism of Moscatilin (also known as dendrophenol) from Dendrobium huoshanense (an eminent traditional Chinese medicine) in suppressing vascular calcification in vitro, ex vivo and in vivo. METHODS: Male C57BL/6J mice (25-week-old) were subjected to nicotine and vitamin D3 (VD3) treatment to induce vascular calcification. In vitro, we established the cellular model of osteogenesis of human aortic smooth muscle cells (HASMCs) under phosphate conditions. RESULTS: By utilizing an in-house drug screening strategy, we identified Moscatilin as a new naturally-occurring chemical entity to reduce HASMC calcium accumulation. The protective effects of Moscatilin against vascular calcification were verified in cultured HASMCs. Unbiased transcriptional profiling analysis and cellular thermal shift assay suggested that Moscatilin suppresses vascular calcification via binding to interleukin 13 receptor subunit A2 (IL13RA2) and augmenting its expression. Furthermore, IL13RA2 was reduced during HASMC osteogenesis, thus promoting the secretion of inflammatory factors via STAT3. We further validated the participation of Moscatilin-inhibited vascular calcification by the classical WNT/ß-catenin pathway, among which WNT3 played a key role in this process. Moscatilin mitigated the crosstalk between WNT3/ß-catenin and IL13RA2/STAT3 to reduce osteogenic differentiation of HASMCs. CONCLUSION: This study supports the potential of Moscatilin as a new naturally-occurring candidate drug for treating vascular calcification via regulating the IL13RA2/STAT3 and WNT3/ß-catenin signalling pathways.

Selection of DNA aptamer recognizing CD44 for high-efficiency capture of circulating tumor cells.

Cancer stem cells play critical roles in cancer progression, cancer invasion and metastasis, and cancer recurrence. CD44 is known as a specific surface marker of cancer stem cells, which has been well-studied in cancer invasion and metastasis. Herein, we successfully selected the DNA aptamers for recognizing CD44+ cells using Cell-SELEX strategy, in which the engineered CD44 overexpression cells were used as target cells for selection. The optimized aptamer candidate C24S showed high binding affinity with the Kd value of 14.54 nM and good specificity. Then, the aptamer C24S was employed to prepare the functional aptamer-magnetic nanoparticles (C24S-MNPs) for CTC capture. To investigate the capture efficiency and sensitivity of C24S-MNPs, series of cell capture tests were performed using artificial samples with 10-200 of HeLa cells spiked into 1 mL PBS or PBMCs isolated from 1 mL peripheral blood, obtaining an efficiency of 95% and 90%, respectively. More importantly, we finally explored the facility of C24S-MNPs for CTC detection in blood samples from clinical cancer patients, indicating a potential and feasible strategy for cancer diagnostic technology in clinical applications.

Purification of Circulating Tumor Cells Based on Multiantibody-Modified Magnetic Nanoparticles and Molecular Analysis toward Epithelial Ovarian Cancer Detection.

Circulating tumor cells (CTCs) are valuable circulating biomarkers of cancer, which carry primary tumor information and may provide real-time assessment of tumor status as well as treatment response in cancer patients. Herein, we developed a novel assay for accurate diagnosis and dynamic monitoring of epithelial ovarian cancer (EOC) using CTC RNA analysis. Multiantibody-modified magnetic nanoparticles were prepared for purification of EOC CTCs from whole blood samples of clinical patients. Subsequently, nine EOC-specific mRNAs of purified CTCs were quantified using droplet digital PCR. The EOC CTC Score was generated using a multivariate logistic regression model for each sample based on the transcripts of the nine genes. This assay exhibited a distinguishing diagnostic performance for the detection of EOC (n = 17) from benign ovarian tumors (n = 30), with an area under the receiver operating characteristic curve (AUC) of 0.96 (95% CI = 0.91-1.00). Moreover, dynamic changes of the EOC CTC Score were observed in patients undergoing treatment, demonstrating the potential of the assay for monitoring EOC. In conclusion, we present an accurate assay for the diagnosis and monitoring of EOC via CTC RNA analysis, and the results suggest that it may provide a promising solution for the detection and treatment response assessment of EOC.

MEK1/2 inhibitor inhibits neointima formation by activating miR-126-3p/ C-X-C motif chemokine ligand 12 (CXCL12)/C-X-C motif chemokine receptor 4 (CXCR4) axis.

Endothelial dysfunction is an initial and essential step in vascular-remodeling diseases, including atherosclerosis and neointima formation. During vascular remodeling, activated endothelial cells can release pro-inflammatory factors that promote phenotypic switching of vascular smooth muscle cells (VSMCs) to the proliferative phenotype. We previously reported that MEK1/2 inhibitor, U0126, has a protective effect on the development of atherosclerosis and vascular calcification. However, the effect of MEK1/2 inhibitors on neointimal formation and the underlying mechanism is not fully understood. We determined that MEK1/2 inhibitor reduced carotid artery ligation-induced neointimal formation, while increased collagen and elastin levels and vascular integrality. Mechanistically, MEK1/2 inhibitor or ERK1/2 siRNA increased miR-126-3p level in endothelial cells, thereby inhibiting expression of regular of G-protein signaling 16 (RGS16), a miR-126-3p target gene, to activate the C-X-C motif chemokine ligand 12 (CXCL12)/C-X-C motif chemokine receptor 4 (CXCR4) signaling pathway. Accordingly, miR-126-3p was also increased by U0126 in serum and carotid artery. RGS16 was inhibited while CXCR4 and CXCL12 was increased by U0126 in neointimal areas, especially in the endothelium. Moreover, similar results were observed in atherosclerotic plaques of high-fat diet-fed apolipoprotein E deficiency (apoE-/-) mice. In addition, vascular cell adhesion molecule 1 (VCAM-1), another miR-126-3p target gene, was reduced by U0126 in the neointimal areas, resulting reduced monocytes/macrophages accumulation. Taken together, our results indicate that MEK1/2 inhibitor can reduce neointima formation by activating endothelial miR-126-3p production to facilitate endothelium repair while reduce monocyte adhesion/infiltration.

Folic Acid-Modified Fluorescent-Magnetic Nanoparticles for Efficient Isolation and Identification of Circulating Tumor Cells in Ovarian Cancer.

Ovarian cancer (OC) is a lethal disease occurring in women worldwide. Due to the lack of obvious clinical symptoms and sensitivity biomarkers, OC patients are often diagnosed in advanced stages and suffer a poor prognosis. Circulating tumor cells (CTCs), released from tumor sites into the peripheral blood, have been recognized as promising biomarkers in cancer prognosis, treatment monitoring, and metastasis diagnosis. However, the number of CTCs in peripheral blood is low, and it is a technical challenge to isolate, enrich, and identify CTCs from the blood samples of patients. This work develops a simple, effective, and inexpensive strategy to capture and identify CTCs from OC blood samples using the folic acid (FA) and antifouling-hydrogel-modified fluorescent-magnetic nanoparticles. The hydrogel showed a good antifouling property against peripheral blood mononuclear cells (PBMCs). The FA was coupled to the hydrogel surface as the targeting molecule for the CTC isolation, held a good capture efficiency for SK-OV-3 cells (95.58%), and successfully isolated 2-12 CTCs from 10 OC patients' blood samples. The FA-modified fluorescent-magnetic nanoparticles were successfully used for the capture and direct identification of CTCs from the blood samples of OC patients.

Effects of Transcranial Direct Current Stimulation on Episodic Memory in Older Adults: A Meta-analysis.

OBJECTIVES: In the last two decades, the number of intervention studies using transcranial direct current stimulation (tDCS) has grown enormously. Though some studies have shown positive influences on episodic memory among older adults, disagreement exists in the literature. Therefore, the current meta-analysis aimed to provide a quantitative assessment of the efficacy of tDCS in modulating episodic memory functions in older adults. METHOD: Eligible studies were sham-controlled trials examining the effects of anodal tDCS on episodic memory in older adults. Twenty-four articles comprising 566 participants aged over 60 qualified for inclusion. RESULTS: Compared to the sham tDCS group, the active tDCS group showed significant memory improvements at both immediate poststimulation (Hedges' g = 0.625, p = .001) and long-term follow-up (Hedges' g = 0.404, p = .002). There were no differences in effect sizes between cognitively healthy and impaired older adults. Moderator analyses suggested that tDCS having a duration of 20 min or less, bilateral stimulation, or a larger stimulation area would produce greater benefits for episodic memory performance in older adults. DISCUSSION: These findings suggest that tDCS holds great promise to ameliorate memory decline in older individuals. In the future, well-designed randomized controlled trials are expected to verify the optimal stimulation protocols and determine the factors impacting the long-term effects of tDCS in enhancing episodic memory.

Upregulation of Sec22b plays a neuroprotective role in a rat model of traumatic brain injury via inducing protective autophagy.

Cortical neuronal cell death following traumatic brain injury (TBI) evoked by the cortical impact is a significant factor that contributes to neurological deficits. In the current study, we harvested the injured area and perilesional area of the injured brain induced by TBI. We explored the functions of Sec22b, an apoptosis-promoting kinase, and a pivotal bridge builder of apoptotic signaling in the etiopathogenesis of an experimental rat model of TBI. We found that Sec22b was expressed in neurons in the injured cortical area, and the expression level significantly decreased after TBI, especially at 24 h. Administration of Sec22b overexpressed plasmid significantly ameliorated TBI-induced apoptosis, neurological deficits, and blood-brain barrier permeability, accompanied by the activation of autophagy. However, the administration of Sec22b knockdown resulted in the opposite eff ;ects. Altogether, these findings indicated that Sec22b plays a neuroprotective role after TBI, suggesting that Sec22b may be a potential therapeutic target for TBI. We speculated that this neuroprotective effect might be achieved by upregulating autophagy levels and required further studies to explore.

Intermittent Fasting Inhibits High-Fat Diet-Induced Atherosclerosis by Ameliorating Hypercholesterolemia and Reducing Monocyte Chemoattraction.

Atherosclerosis is a major pathology for cardiovascular diseases (CVDs). Clinically, the intermittent fasting (IF) has been observed to reduce the risk of CVDs. However, the effect of IF on the development of atherosclerosis has not been fully elucidated. Herein, we determined the protection of IF against high-fat diet-induced atherosclerosis in pro-atherogenic low-density lipoprotein receptor deficient (LDLR-/-) mice and the potentially involved mechanisms. The LDLR-/- mice were scheduled intermittent fasting cycles of 3-day HFD feeding ad libitum and 1 day fasting, while the mice in the control group were continuously fed HFD. The treatment was lasted for 7 weeks (∼12 cycles) or 14 weeks (∼24 cycles). Associated with the reduced total HFD intake, IF substantially reduced lesions in the en face aorta and aortic root sinus. It also increased plaque stability by increasing the smooth muscle cell (SMC)/collagen content and fibrotic cap thickness while reducing macrophage accumulation and necrotic core areas. Mechanistically, IF reduced serum total and LDL cholesterol levels by inhibiting cholesterol synthesis in the liver. Meanwhile, HFD-induced hepatic lipid accumulation was attenuated by IF. Interestingly, circulating Ly6Chigh monocytes but not T cells and serum c-c motif chemokine ligand 2 levels were significantly reduced by IF. Functionally, adhesion of monocytes to the aortic endothelium was decreased by IF via inhibiting VCAM-1 and ICAM-1 expression. Taken together, our study indicates that IF reduces atherosclerosis in LDLR-/- mice by reducing monocyte chemoattraction/adhesion and ameliorating hypercholesterolemia and suggests its potential application for atherosclerosis treatment.

Peroxisome Proliferator-Activated Receptor-Gamma Reduces ER Stress and Inflammation via Targeting NGBR Expression.

Increased Nogo-B receptor (NGBR) expression in the liver improves insulin sensitivity by reducing endoplasmic reticulum stress (ER stress) and activating the AMPK pathway, although it remains elusive the mechanisms by which NGBR is induced. In this study, we found that PPARγ ligands (rosiglitazone or pioglitazone) increased NGBR expression in hepatic cells and HUVECs. Furthermore, promoter analysis defined two PPREs (PPARγ-responsive elements) in the promoter region of NGBR, which was further confirmed by the ChIP assay. In vivo, using liver-specific PPARγ deficient (PPARγLKO) mice, we identified the key role of PPARγ expression in pioglitazone-induced NGBR expression. Meanwhile, the basal level of ER stress and inflammation was slightly increased by NGBR knockdown. However, the inhibitory effect of rosiglitazone on inflammation was abolished while rosiglitazone-inhibited ER stress was weakened by NGBR knockdown. Taken together, these findings show that NGBR is a previously unrecognized target of PPARγ activation and plays an essential role in PPARγ-reduced ER stress and inflammation.

Thermally robust and valence-variation-induced white-light emission of a novel stannate phosphor Sr3Al10SnO20:Dy3+: crystal structure, luminescence property, and mechanism investigation.

The development of novel white-light-emission phosphors is of great importance for applications in lighting and display fields. Trivalent Dy3+ is widely used as a potential luminescence center for white-light emission. However, Dy3+-doped phosphors often suffer a poor yellow to blue ratio due to the deficiency of its 4F9/2 → 6H15/2 transition, low luminescence efficiency, and unsatisfactory thermal stability. The importance of the present research work is that we have achieved a tunable white light in a single phased stannate phosphor Sr3Al10SnO20:Dy3+ with robust thermal stability. The crystal structure, phase purity, and chemical composition were investigated via X-ray diffraction Rietveld structure refinement, scanning electron microscopy, and energy dispersive spectrometry. The luminescence spectra indicated that Sr3Al10SnO20:Dy3+ not only exhibited characteristic 4F9/2 → 6HJ/2 (J=11, 13, and 15) inherent transition emissions of Dy3+, but also showed an abnormal blue band emission, which was identified through X-ray photoelectric spectroscopy as the T1 → S0 transitions of Sn2+, resulting from the valence variation of Sn4+. The efficient energy transfer from Sn2+ to Dy3+ was also confirmed and the transfer efficiency was calculated. Owing to the valence-variation-induced emission of Sn2+, a tunable white light could be realized from a cool to warm white light region, with Commission Internationale de l'Eclairage coordinates and a correlative color temperature varying from (0.277, 0.333) and 8634 K to (0.353, 0.404) and 4913 K, respectively. The luminescent and defects formation mechanism as well as the luminescence kinetics were further investigated. Moreover, Sr3Al10SnO20:Dy3+ had a high quantum efficiency (∼34.6%) and a super-stable thermal stability behavior (82.5% at 240 °C of the initial integral emission intensity at 30 °C) with a large activation energy (ΔE ∼ 0.1654 eV). Finally, a charge-compensation test was performed to further verify the effect of defects on the luminescence property and the related mechanism was discussed. The current work provides a novel method to achieve tunable white-light emission in Dy3+ single-doped phosphors and the related mechanism is effectual for other rare earths for potential applications in lighting and display fields.

3D-QSAR studies of D3R antagonists and 5-HT1AR agonists.

Combination of dopamine D3 antagonism and serotonin 5-HT1A agonism leads to an effective way to atypical antipsychotics. In this work, two predictive 3D-QSAR models were bulit for D3R antagonists and 5-HT1AR agonists, respectively. Based on the steric and electrostatic information of contour maps, four compounds with improved predicted activities were newly designed. In addition, molecular docking and ADMET properties suggested that designed molecules had strong interactions with receptors and low hepatotoxicity. This work sheds light on the design of bifunctional novel antipsychotic drugs for D3R antagonists and 5HT1AR agonists.

Potential Roles of NIX/BNIP3L Pathway in Rat Traumatic Brain Injury.

NIX/BNIP3L is known as a proapoptotic protein that is also related to mitophagy. Previous reports have shown that NIX could be involved in neuronal apoptosis after intracerebral hemorrhage, but it also plays a protective role in mitophagy in ischemic brain injury. How NIX works in traumatic brain injury (TBI) is unclear. Thus, this study was designed to observe the expression of NIX and perform a preliminary exploration of the possible effects of NIX in a rat TBI model. The results showed that NIX expression decreased after damage, and colocalized with neuronal cells in cortical areas. Moreover, when we induced upregulation of NIX, autophagy was increased, while neuronal apoptosis and brain water content decreased along with neurological deficits. These findings remind us that NIX probably plays a neuroprotective role in TBI through autophagy and apoptosis pathways.

A bottom-up synthesis of rare-earth-hydrotalcite monolayer nanosheets toward multimode imaging and synergetic therapy.

Recently, ultrathin two-dimensional (2D) nanomaterials have attracted considerable research interest in biomedical applications, owing to their intriguing quantum size and surface effects. In this work, a one-step "bottom-up" method is developed to prepare rare-earth (Gd3+ and Yb3+) co-doped layered double hydroxide (LDH) monolayer nanosheets, with a precisely controlled composition and uniform morphology. Due to the successful introduction of Gd3+ and Yb3+ into the LDH host layer, the Gd&Yb-LDH monolayer nanosheets exhibit excellent magnetic resonance (MR)/X-ray computed tomography (CT) dual-mode imaging functionality. Moreover, the Gd&Yb-LDH monolayer nanosheets achieve an ultrahigh loading of a chemotherapeutic drug (SN38) with a loading content (LC) of 925%, which is a one order of magnitude enhancement compared with previously reported delivery systems of hydrophobic drugs. Interestingly, by further combination with indocyanine green (ICG), in vivo tri-mode imaging, including CT, MR and near infrared fluorescence (NIRF) imaging, is achieved, which enables a noninvasive visualization of cancer cell distribution with deep spatial resolution and high sensitivity. In addition, in vitro and in vivo therapeutic evaluations demonstrate an extremely high tri-mode synergetic anticancer activity and superior biocompatibility of SN38&ICG/Gd&Yb-LDH. Therefore, this work demonstrates a paradigm for the synthesis of novel multifunctional 2D monolayer materials via a facile "bottom-up" route, which shows promising applications in cancer synergetic theranostics.

Mechanism and dynamic study of reactive red X-3B dye degradation by ultrasonic-assisted ozone oxidation process.

The effectiveness of ozone combined with ultrasound techniques in degrading reactive red X-3B is evaluated. A comparison among ozone (O3), ultrasonic (US), ozone/ultrasonic (O3/US) for degradation of reactive red X-3B has been performed. Results show that O3/US system was the most effective and the optimally synergetic factor reaches to 1.42 in O3/US system. The cavitation of ultrasound plays an important role during the degradation process. It is found that 99.2% of dye is degraded within 6min of reaction at the initial concentration of 100mg·L-1, pH of 6.52, ozone flux of 40L·h-1 and ultrasonic intensity of 200W·L-1. Ozonation reactions in conjunction with sonolysis indicate that the decomposition followed pseudo-first-order reaction kinetics but the degradation efficiencies are affected by operating conditions, particularly initial pH and ultrasonic intensity. A kinetic model is established based on the reaction corresponding to operational parameters. In addition, the main reaction intermediates, such as p-benzoquinone, catechol, hydroquinone, phthalic anhydride and phthalic acid, are separated and identified using GC/MS and a possible degradation pathway is proposed during the O3/US process.