Ubiquitous nanocolloids suppress the conjugative transfer of plasmid-mediated antibiotic resistance in aqueous environment.

Nanocolloids (Nc) are widespread in natural water environment, whereas the potential effects of Nc on dissemination of antibiotic resistance remain largely unknown. In this study, Nc collected from the Yellow River in Henan province was tested for its ability to influence the conjugative transfer of resistant plasmid in aqueous environment. The results revealed that the conjugative transfer of RP4 plasmid between Escherichia coli was down-regulated by 52%-91% upon exposure to 1-10 mg/L Nc and the reduction became constant when the dose became higher (20-200 mg/L). Despite the exposure of Nc activated the anti-oxidation and SOS response in bacteria through up-regulating genes involved in glutathione biosynthesis and DNA recombination, the inhibition on the synthesis and secretion of extracellular polysaccharide induced the prevention of cell-cell contact, leading to the reduction of plasmid transfer. This was evidenced by the decreased bacterial adhesion and lowered levels of genes and metabolites relevant to transmembrane transport and D-glucose phosphorylation, as clarified in phenotypic, transcriptomics and metabolomics analysis of E. coli. The significant down-regulation of glycolysis/gluconeogenesis and TCA cycle was associated with the shortage of ATP induced by Nc. The up-regulation of global regulatory genes (korA and trbA) and the reduction of plasmid genes (trfAp, trbBp, and traG) expression also contributed to the suppressed conjugation of RP4 plasmid. The obtained findings remind that the role of ubiquitous colloidal particles is nonnegligible when practically and comprehensively assessing the risk of antibiotic resistance in the environment.

Componential and molecular-weight-dependent effects of natural organic matter on the colloidal behavior, transformation, and toxicity of MoS2 nanoflakes.

The potential widespread applications in water processing have rendered the necessity for investigations of the fate and hazard of molybdenum disulfide (MoS2) nanosheets. Herein, it was found that humic acid (HA) had better performances toward stabilizing pure 2H phase MoS2 and chemical-exfoliated MoS2 (ce-MoS2) in electrolyte solutions than fulvic acid (FA), and molecular weight (MW)-dependent manners were disclosed due to steric repulsions. Compared with darkness, the extent to which the aggregation and sedimentation of ce-MoS2 facilitated by visible light irradiation was greater in the presence of HA and FA fractions, likely due to the introduction of stronger plasmonic dipole-dipole interaction and Van der Waals attraction forces. HA-triggered structural disintegration of nanosheets was performed after irradiation and it was observed to be more significant with the increase in MWs, whereas the MW-dependent dissolution of MoS2 caused by FA was much quicker than that by HA owing to the higher generation of singlet oxygen. Moreover, FA lowered the bioavailability of MoS2 and relieved its toxicity to zebrafish more effectively than HA. Our findings boost the insights into the effects of organic molecules on the fates and hazards of MoS2, providing guidance for the MoS2-based nanotechnological development on environment.

Effect of Sintering Temperatures on Grain Coarsening Behaviors and Mechanical Properties of W-NiTi Heavy Tungsten Alloys.

W-NiTi tungsten heavy alloys were prepared by an infiltration process using submicron W powders, and the effect of sintering temperatures on grain-coarsening behaviors and the mechanical properties of W-NiTi tungsten heavy alloys were investigated. The microstructures and mechanical properties were investigated using scanning electron microscopy, X-ray diffraction and compression tests. The results showed that tungsten particles were uniformly distributed in the NiTi binder. The W-NiTi tungsten heavy alloys consisted of B19'-NiTi and body-centered cubic W phases. The average tungsten particle sizes of W-NiTi tungsten heavy alloys sintered at 1400 °C, 1480 °C and 1560 °C were 2.62 µm, 4.04 µm and 5.20 µm, respectively. The average tungsten particle size increased with sintering temperatures, while the densities decreased at higher temperatures. The cavities retained in the W-NiTi tungsten heavy alloy sintered at 1560 °C, which degraded the mechanical properties. The calculated grain growth activation energy of W particles in the NiTi binder was 330 kJ/mol, which was higher than those in conventional W-NiFe and W-NiCo tungsten heavy alloys. The higher activation energy means more difficult diffusion process of W atoms in NiTi binders during sintering. Therefore, finer-grained heavy tungsten alloys were more easily obtained by using NiTi binders. Yield strength of W-NiTi tungsten heavy alloys decreased with increasing sintering temperatures due to coarsened tungsten particles.

Bioinformatics analysis of potential glioblastoma circular RNA sponge network.

Background: Circular RNA is emerging functional molecule for glioblastoma. However, the function and regulatory of circular RNA (circRNA) remains unclear. In this study, the circRNA sequencing and array data of glioblastoma were analyzed by multiple bioinformatics methods to establish a potential molecular sponge mechanism regulation network. Methods: Gene Expression Omnibus datasets were used to extract circRNAs. CircInteractome was used to predict microRNAs binding to circRNAs. Chinese Glioma Gene Atlas database was used to screen the microRNAs with expression and survival trends. MiRabel database was used to predict potential gene targets of microRNAs. The Cancer Genome Atlas database was used to screen the gene targets of sponge network. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis were to explain the gene targets functions. R software, Cytoscape software and Bioinformatics website were used to establish the network and visualize the results. Results: Hsa_circ_0000219, hsa_circ_0001073 and hsa_circ_0070700 were selected from more than 2000 differentially expressed circRNAs of Gene Expression Omnibus Series (GSE) GSE146463, GSE92322 and GSE86202 datasets. Hsa-miR-1248 and hsa-miR-1290 were up regulated and related to glioblastoma poor prognosis. Targets of these microRNAs including ARHGEF7, CELA2b, RNF11, YPEL1 and ZNF37a were also screened via expression and survival data. Gene targets function were mainly enriched in signal transduction, cell plasma membrane, ATP binding and calcium signaling pathway. Conclusions: A circRNA molecular sponge regulatory network including hsa-miR-1248 and hsa-miR-1290 has been established. In this network, hsa_circ_0001073, hsa_circ_0070700, hsa_circ_0000219, hsa-miR-1248, hsa-miR-1290, and RNF11 may have the potential being emerging glioblastoma therapeutic targets. However, their function and significance for glioblastoma need further experiments to verify.

RAB1A regulates glioma cellular proliferation and invasion via the mTOR signaling pathway and epithelial-mesenchymal transition.

Aim: We aimed at investigating the mechanism of RAB1A proliferation and invasion in gliomas. Materials & methods: Genome-wide expression profile data and immunohistochemistry were analyzed to assess RAB1A expression in gliomas. The Transwell assay, wound healing assay, brain slice coculture model, cellular fluorescence and intracranial xenograft model of nude mice were used to determine the proliferation and invasion of glioma cells. Results & conclusion: RAB1A was highly expressed in gliomas compared with normal brain tissue. The overall survival time of glioma patients with high RAB1A expression was significantly shortened. RAB1A regulated the activity of RAC1 by inhibiting the mTOR signaling pathway, affecting actin polymerization, cell morphology and cell polarity. RAB1A downregulation inhibited the epithelial-mesenchymal transition, proliferation and invasion of glioma cells.

ACT001 reduces the expression of PD-L1 by inhibiting the phosphorylation of STAT3 in glioblastoma.

ACT001, which is derived from an ancient anti-inflammatory drug, has been shown to cross the blood-brain barrier in preclinical studies and has demonstrated anti-glioblastoma (GBM) activity in clinical trials. However, its pharmacological potential for anti-GBM immune response modulation remains unclear. The chemical structure of ACT001 indicates that it may bind to STAT3 and thus modulate antitumor immune response. Methods: Bioinformatics and immunohistochemistry (IHC) were used to assess STAT3 and PD-L1 expression in gliomas. Western blotting, RT-PCR and immunofluorescence were used to detect PD-L1 and p-STAT3 expression in glioma cells exposed to ACT001. Chromatin immunoprecipitation, an ACT001-Biotin probe, and a dual-luciferase reporter assay were used to detect direct modulation. The in vivo efficacy of ACT001 was evaluated in GL261 murine glioma model. Survival analyses were conducted using the log-rank (Mantel-Cox) test. Results: Bioinformatic analysis of 1,837 samples from 4 public glioma datasets showed that STAT3 mRNA expression was correlated with the degree of malignancy and therapeutic resistance and that STAT3 mRNA expression was related to immunosuppression, leukocyte infiltration, and PD-L1 expression. IHC staining of 53 tissue samples confirmed that relatively high phosphorylated STAT3 and PD-L1 protein expression was associated with a relatively advanced World Health Organization (WHO) glioma grade. Next, we confirmed that ACT001 treatment reduced PD-L1 expression and STAT3 phosphorylation. An ACT001-biotin probe was used to verify that ACT001 bound to STAT3. We also demonstrated that STAT3 bound to the PD-L1 promoter. The inhibition of PD-L1 expression and STAT3 phosphorylation by ACT001 could be rescued by STAT3 overexpression. Additionally, ACT001 inhibited GBM growth and decreased PD-L1 expression in vivo. The expression of the M2 markers CD206 and CD163 was decreased, while that of the antitumor immune markers iNOS and IFNγ was increased by ACT001 in vivo. Conclusion: Our results demonstrate that STAT3 plays a key role in immunosuppression of glioma and is inhibited by ACT001. ACT001 inhibits PD-L1 transcription and modulates anti-tumor immune response in glioma bearing mice. These findings will help us to understand the mechanism of ACT001 in GBM therapy.

Molecular and clinical characterization of Galectin-9 in glioma through 1,027 samples.

In recent years, research on glioma immunotherapy have grown rapidly. However, the autoimmune-like side effects that are caused by blocking immunological checkpoints hinder their clinical application in gliomas currently. Galectin-9, a ligand for T-cell immunoglobulin mucin 3, has shed a new light on the treatment of malignant glioma. However, the potential mechanism of Galectin-9 is still under discussion. In this study, first, we methodically gathered 1,027 glioma patients with RNA-seq and 986 patients with survival data to explore the role and mechanism of Galectin-9 in gliomas. Second, we analyzed glioma samples from 50 patients in the Department of Neurosurgery, Tianjin Medical University General Hospital. Finally, we found that Galectin-9 was strongly upregulated in glioblastoma multiforme compared with normal brain tissues and lower-grade glioma. Patients with Galectin-9 overexpression had a significantly shorter overall survival. Moreover, the tissue microarray data displayed that the expression of Galectin-9 in the core of tumor is higher than that in the border and was correlated with the shorter survival in glioma patients. Galectin-9 is more highly expressed in the mesenchymal subtype of glioblastoma multiforme than in the other subtypes. Simultaneously, Galectin-9 was closely associated with the immune response and lymphocyte activation, especially T-cell activation. To further determine the underlying role of Galectin-9 in the immune response, we selected seven immune metagenes. Through cluster analysis and correlation analysis, we discovered that Galectin-9 was highly correlated with immune checkpoint molecules and M2 tumor-associated macrophages. In summary, Galectin-9 serves as a potential therapeutic target to treat glioblastoma multiforme.

Identification of Key Pathways and Genes in the Orai2 Mediated Classical and Mesenchymal Subtype of Glioblastoma by Bioinformatic Analyses.

BACKGROUND: Ca2+ release-activated Ca2+ channels (CRAC) are the main Ca2+ entry pathway regulating intracellular Ca2+ concentration in a variety of cancer types. Orai2 is the main pore-forming subunit of CRAC channels in central neurons. To explore the role of Orai2 in glioblastoma (GBM), we investigated the key pathways and genes in Orai2-mediated GBM by bioinformatic analyses. METHODS: Via The Cancer Genome Atlas (TCGA), French, Sun, and Gene Expression Omnibus (GEO) (GDS3885) datasets, we collected 1231 cases with RNA-seq data and analyzed the functional annotation of Orai2 by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Univariate and multivariate survival analyses were applied to 823 patients with survival data. RESULTS: We discovered that Orai2 was markedly upregulated in GBM compared to normal brain samples and lower-grade gliomas (LGG). Survival analysis found that higher expression of Orai2 was independently associated with a worse prognosis of patients with the classical and mesenchymal subtypes of GBM. Simultaneously, Orai2 expression was higher in tumors of the classical and mesenchymal subtypes than other subtypes and was significantly correlated with classical- and mesenchymal-related genes. GO and KEGG pathway analysis revealed that genes significantly correlated with Orai2 were involved in the JNK pathway. Through screening transcriptomic data, we found a strong association between Orai2 and apoptosis, stemness, and an epithelial-mesenchymal transition- (EMT-) like phenotype. CONCLUSION: As a prognostic factor, Orai2 is obviously activated in the classical and mesenchymal subtypes of GBM and promotes glioma cell self-renewal, apoptosis, and EMT-like by the JNK pathway. These findings indicate that Orai2 could be a candidate prognostic and therapeutic target, especially for the classical and mesenchymal subtypes of GBM.

Notch1 signaling pathway promotes invasion, self-renewal and growth of glioma initiating cells via modulating chemokine system CXCL12/CXCR4.

BACKGROUND: Glioma initiating cells (GICs), also known as glioma stem cells (GSCs), play an important role in the progression and recurrence of glioblastoma multiforme (GBM) due to their potential for self-renewal, multiple differentiation and tumor initiation. In the recent years, Notch1 has been found to be overexpressed in GICs. However, the regulatory mechanism of Notch1 in the self-renewal and invasion ability of GICs remains unclear. This study aims to explore the effect of Notch pathway on self-renewal and invasion of GICs and the underlying mechanisms. METHODS: Bioinformatic analysis and immunohistochemistry (IHC) were performed to evaluate the expression of Notch1 and Hes1 in GBM samples. Immunofluorescent (IF) staining was performed to observe the distribution of Notch1 and CXCR4 in GBM and GICs. Both pharmacological intervention and RNA interference were employed to investigate the role of Notch1 in GICs self-renewal, invasion and tumor growth in vitro or in vivo. The crosstalk effect of Notch1 and CXCL12/CXCR4 system on GIC self-renewal and invasion was explored by sphere formation assay, limiting dilution assay and Transwell assay. Western blots were used to verify the activation of Notch1/CXCR4/AKT pathway in self-renewal, invasion and tumor growth of GICs. Luciferase reporter assay was used to testify the potential binding site of Notch1 signaling and CXCR4. The orthotopic GICs implantations were established to analyze the role and the mechanism of Notch1 in glioma progression in vivo. RESULTS: Notch1 signaling activity was elevated in GBM tissues. Notch1 and CXCR4 were both upregulated in GICs, compared to Notch1 positive glioma cells comprised a large proportion in the CD133+ glioma cell spheres, CXCR4 positive glioma cells which usually expressed Notch1 both and dispersed in the periphery of the sphere, only represent a small subset of CD133+ glioma cell spheres. Furthermore, downregulation of the Notch1 pathway by shRNA and MK0752 significantly inhibited the PI3K/AKT/mTOR signaling pathway via the decreased expression of CXCR4 in GICs, and weakened the self-renewal, invasion and tumor growth ability of GICs. CONCLUSIONS: These findings suggest that the cross-talk between Notch1 signaling and CXCL12/CXCR4 system could contribute to the self-renewal and invasion of GICs, and this discovery could help drive the design of more effective therapies in Notch1-targeted treatment of GBMs.

NKCC1 promotes EMT-like process in GBM via RhoA and Rac1 signaling pathways.

Glioblastoma is the most common and lethal primary intracranial tumor. As the key regulator of tumor cell volume, sodium-potassium-chloride cotransporter 1 (NKCC1) expression increases along with the malignancy of the glioma, and NKCC1 has been implicated in glioblastoma invasion. However, little is known about the role of NKCC1 in the epithelial-mesenchymal transition-like process in gliomas. We noticed that aberrantly elevated expression of NKCC1 leads to changes in the shape, polarity, and adhesion of cells in glioma. Here, we investigated whether NKCC1 promotes an epithelial-mesenchymal transition (EMT)-like process in gliomas via the RhoA and Rac1 signaling pathways. Pharmacological inhibition and knockdown of NKCC1 both decrease the expressions of mesenchymal markers, such as N-cadherin, vimentin, and snail, whereas these treatments increase the expression of the epithelial marker E-cadherin. These findings indicate that NKCC1 promotes an EMT-like process in gliomas. The underlying mechanism is the facilitation of the binding of Rac1 and RhoA to GTP by NKCC1, which results in a significant enhancement of the EMT-like process. Specific inhibition or knockdown of NKCC1 both attenuate activated Rac1 and RhoA, and the pharmacological inhibitions of Rac1 and RhoA both impair the invasion and migration abilities of gliomas. Furthermore, we illustrated that NKCC1 knockdown abolished the dissemination and spread of glioma cells in a nude mouse intracranial model. These findings suggest that elevated NKCC1 activity acts in the regulation of an EMT-like process in gliomas, and thus provides a novel therapeutic strategy for targeting the invasiveness of gliomas, which might help to inhibit the spread of malignant intracranial tumors.

Jagged1 is Clinically Prognostic and Promotes Invasion of Glioma-Initiating Cells by Activating NF-κB(p65) Signaling.

BACKGROUND/AIMS: Jagged1 is the ligands of the Notch signaling and has been shown to promote glioma-initiating cells (GICs) in glioblastoma. The role of Jagged1 in GICs invasion and underlying molecular mechanisms remain unclear. METHODS: Survival data from R2 genomics analysis, the Cancer Genome Atlas (TCGA), the Chinese Glioma Genome Atlas (CGGA) and visualization platform database were used to evaluate the effects of Jagged1 on overall patient survival. we investigated Jagged1 induced the GICs cells' invasion by matrix degradation assays and Transwell cell invasion assays in vitro, then we further explored the underlying molecular mechanisms using Co-immunoprecipitation (co-IP) analysis. RESULTS: High expression of Jagged1 in human glioma was associated with poor survival. Clinical data analysis showed that the Jagged1 was positively correlated with NF-κB(p65). Jagged1-induced invasion of GICs cells through activation of NF-κB(p65) pathway. In vivo, knockdown of Jagged1 could suppress the tumorigenicity of GICs cells through NF-κB(p65) signaling. CONCLUSION: Insights gained from these findings suggest that Jagged1 plays an important oncogenic role in GICs malignancy by activation of NF-κB(p65) signaling, and Jagged1 could be employed as an effective therapeutic target for GICs.

Autophagy suppresses self-renewal ability and tumorigenicity of glioma-initiating cells and promotes Notch1 degradation.

Autophagy is a vital process that involves degradation of long-lived proteins and dysfunctional organelles and contributes to cellular metabolism. Glioma-initiating cells (GICs) have the ability to self-renew, differentiate into heterogeneous types of tumor cells, and sustain tumorigenicity; thus, GICs lead to tumor recurrence. Accumulating evidence indicates that autophagy can induce stem cell differentiation and increase the lethality of temozolomide against GICs. However, the mechanism underlying the regulation of GIC self-renewal by autophagy remains uncharacterized. In the present study, autophagy induced by AZD8055 and rapamycin treatment suppressed GIC self-renewal in vitro. We found that autophagy inhibited Notch1 pathway activation. Moreover, autophagy activated Notch1 degradation, which is associated with maintenance of the self-renewal ability of GICs. Furthermore, autophagy abolished the tumorigenicity of CD133 + U87-MG neurosphere cells in an intracranial model. These findings suggest that autophagy regulating GICs self-renewal and tumorigenicity is probably bound up with Notch1 degradation. The results of this study could aid in the design of autophagy-based clinical trials for glioma treatments, which may be of great value.

Tumour cell dormancy as a contributor to the reduced survival of GBM patients who received standard therapy.

Glioblastoma multiforme (GBM) is a fatal cancer with varying life expectancy, even for patients undergoing the same standard therapy. Identification of differentially expressed genes in GBM patients with different survival rates may benefit the development of effective therapeutic strategies. In the present study, key pathways and genes correlated with survival in GBM patients were screened with bioinformatic analysis. Included in the study were 136 eligible patients who had undertaken surgical resection of GBM followed by temozolomide (TMZ) chemoradiation and long-term therapy with TMZ. A total of 383 differentially expressed genes (DEGs) related to GBM survival were identified. Gene Ontology and pathway enrichment analysis as well as hub gene screening and module analysis were performed. As expected, angiogenesis and migration of GBM cells were closely correlated with a poor prognosis. Importantly, the results also indicated that cell dormancy was an essential contributor to the reduced survival of GBM patients. Given the lack of specific targeted genes and pathways known to be involved in tumour cell dormancy, we proposed enriched candidate genes related to the negative regulation of cell proliferation, signalling pathways regulating pluripotency of stem cells and neuroactive ligand-receptor interaction, and 3 hub genes (FTH1, GRM1 and DDIT3). Maintaining persistent cell dormancy or preventing tumour cells from entering dormancy during chemoradiation should be a promising therapeutic strategy.

Bioinformatic analyses reveal the key pathways and genes in the CXCR4 mediated mesenchymal subtype of glioblastoma.

Glioblastoma multiforme (GBM) is one of the most lethal types of tumour, despite severe treatment methods. The Cancer Genome Atlas has categorised GBMs into proneural, neural, classical and mesenchymal subtypes; the mesenchymal subgroup has the worst prognosis. CXCR4 has been reported as selectively overexpressed in the mesenchymal subtype and positively associated with MES markers. However, to the best of our knowledge the underlying mechanisms regarding how CXCR4 may regulate mesenchymal GBM are still unknown. The present study aimed to investigate the critical pathways mediated by CXCR4 in mesenchymal GBM using bioinformatic analyses. The results suggested that CXCR4 is a predictor of poor prognosis and may serve as a biomarker of the mesenchymal subtype in patients with GBM. In addition, CXCR4 mediated the mitogen­activated protein kinase signaling pathway, which was identified specifically in patients with mesenchymal GBM. CXCR4 associated genes or pathways may be a 'basket trial' option for the management of melanoma, prostate cancer and mesenchymal GBM.

The interactome and spatial redistribution feature of Ca2+ receptor protein calmodulin reveals a novel role in invadopodia-mediated invasion.

Numerous studies have shown that calmodulin (CaM) is a major regulator of calcium-dependent signaling, which regulates cell proliferation, programmed cell death, and autophagy in cancer. However, limited information is available on mechanisms underlying the effect of CaM on the invasive property of glioblastoma multiforme (GBM) cells, especially with respect to invadopodia formation. In this study, we find that CaM serves as a prognostic factor for GBM, and it is strongly associated with the invasive nature of this tumor. Results of preliminary experiments indicated that CaM concentration was significantly correlated with the invasive capacity of and invadopodia formation by different GBM cell lines. CaM inhibition via a small hairpin RNA or a pharmacological inhibitor significantly disrupted invadopodia formation and MMP activity and downregulated vimentin expression. Moreover, CaM knockdown exerted a strong anti-invasive effect on GBM in vivo. Interestingly, epidermal growth factor treatment promoted CaM redistribution from the nucleus to the cytoplasm, eventually activating invadopodia-associated proteins by binding to them via their cytosolic-binding sites. Moreover, CaM inhibition suppressed the activation of invadopodia-associated proteins. Thus, our findings provide a novel therapeutic strategy to impede GBM invasion by inhibiting invadopodia formation, and shed light on the spatial organization of CaM signals during GBM invasion.

Three-dimensional hydrogel is suitable for targeted investigation of amoeboid migration of glioma cells.

Glioblastoma (GBM) invasion and migration are key biological behaviors leading to refractoriness to current therapies and infiltration into the non­tumor brain parenchyma. GBM cell migration is strongly dependent on tumor architecture in vivo, which is absent in traditional two­dimensional (2D) monolayer culture. The present study applied a three­dimensional (3D) hydrogel model to rebuild the tumor architecture in vitro. Treatment with NSC23766, a specific inhibitor of Ras­related C3 botulinum toxin substrate 1 (Rac1), inhibited the mesenchymal invasiveness however triggered the amoeboid motility called mesenchymal­amoeboid transition (MAT). Notably, NSC23766 stimulated U87 GBM cell migration in the 3D hydrogel. However, this compound inhibited cell motility in 2D monolayer culture without tumor architecture for MAT, suggesting the advantage of 3D hydrogel to investigate tumor cell invasion. Due to the inverse interaction of Rac1 and Ras homolog family member A (RhoA) signaling in the transition between mesenchymal and amoeboid morphology, simultaneous treatment of NSC23766 and Y27632 (selective Rho associated coiled­coil containing protein kinase 1 inhibitor), abolished U87 GBM cell migration through inhibiting MAT and amoeboid­mesenchymal transition. In addition, Y27632 induced integrin expression which gave rise to the focal adhesion to facilitate the mesenchymal invasion. The results of the present study demonstrated that the 3D hydrogel was a preferable model in vitro to study tumor cell invasion and migration. The combined inhibition of Rac1 and RhoA signaling would be a promising strategy to suppress GBM invasion.

Chemical modification of bagasse-based mesoporous carbons for chromium(III) ion adsorption.

AIMS: Modified bagasse-based mesoporous carbons were prepared for the efficient chromium(III) ion adsorption and removal from aqueous solutions. METHODS: Mesoporous carbons were prepared from bagasse with H3PO4 activation and subsequently oxidized with nitric acid and modified with ethylenediamine. RESULTS: The results showed that the modified carbon was rich in mesopores, oxygen and nitrogen-containing groups, and the Cr(III) adsorption capacity was greatly improved after modification, which was found to be higher than both pristine and oxidized carbons. The Cr(III) adsorption capacity on modified carbon was significantly influenced by the solution pH, and the optimum pH was 6 with the maximum Cr(III) adsorption capacity up to 24.61mg/g, which was almost 3 times higher than that for pristine carbon. Thermodynamic results manifested the adsorption was spontaneous and endothermic. Kinetic rates fitted the pseudo-second-order model very well. XPS study indicated the amino group was a key factor of the high efficient adsorption.