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Objective We evaluated the effectiveness and safety of adding tirofiban or argatroban after early neurological deterioration (END) in patients with branch atheromatous disease (BAD) receiving dual antiplatelet therapy and compared the outcomes with those of patients who continued dual antiplatelet therapy alone. Methods This retrospective study focused on 135 consecutive patients with BAD and END between June 2020 and June 2022. The primary and secondary efficacy endpoints were a modified Rankin scale (mRS) score ≤ 2 at 90 days after stroke and a National Institutes of Health Stroke Scale (NIHSS) score on day 7 after END. Safety outcomes included other bleeding and mortality events. Results A total of 65, 33, and 37 patients were included in the dual antiplatelet therapy (DAPT), argatroban, and tirofiban groups, respectively. There was a statistically significant difference in the clinical outcome (mRS 0–2) among the three groups (P = 0.001). Post-hoc test analysis showed that the proportion of good outcomes in the tirofiban group was significantly higher than that in the argatroban and DAPT group (P = 0.011, P

Background Patients with single subcortical infarction (SSI) in the middle cerebral artery (MCA) will often suffer from early neurological deterioration (END) despite receiving intravenous thrombolytic therapy (IVT). In this study, the predictors for END were studied in patients with single subcortical infarction in the MCA after IVT. Methods Patients with SSIs in the territory of the middle cerebral artery with IVT between June 2020 and June 2022 were included in this study. END was defined as an ≥ 2 increase in the total National Institutes of Health Stroke Scale (NIHSS) score or ≥ 1 in the motor NIHSS score within the first 72 hours of admission. In addition to the analysis of the predictors of END in SSI patients who received IVT in the territory of MCA, proximal and distal SSI patients were also analyzed. Results A total of 174 patients with SSI in the territory of the MCA who received IVT were evaluated. In multivariable logistic regression analysis, the presence of pSSI (odds ratio, 5.98;95% CI, 2.13–16.78; P = 0.001), lower TT (odds ratio, 0.694; 95% CI, 0.511 ~ 0.943; P = 0.019), and higher red blood cells (odds ratio,2.047; 95% CI, 1.120 ~ 3.741; P = 0.020) were positively associated with END in patients with proximal SSI (pSSI). In patients with pSSI, there was a positive correlation between AST and blood sugar. Meanwhile, no variable related to END was found in the distal SSI (dSSI) group. Conclusions The presence of pSSI, lower TT, and higher red blood cells are associated with END in patients with SSI in the territory of the MCA who received IVT. The frequency and predictors of SSI in the territory of the MCA were different between proximal and distal SSI.

ObjectivesNo standard treatment exists for branch atheromatous disease (BAD), and patients' conditions often worsen after thrombolytic therapy. We evaluated the safety and effectiveness of tirofiban after early neurological deterioration (END) development in patients receiving intravenous alteplase.Materials and methodsBleeding incidence, National Institute of Health Stroke Scale (NIHSS) score, and modified Rankin scale (mRS) score were assessed for patients with BAD receiving alteplase within 4.5 h of stroke onset.ResultsAmong 193 patients, 119 (61.64%) did not experience exacerbation after thrombolytic treatment, 74 (38.34%) had END, 34 were treated with tirofiban after END, and 40 received standard treatment. On day 7 or at discharge, no cases of symptomatic cerebral hemorrhage were noted, and no patient died during the 90-day follow-up. Fifty-two of 74 patients (70.27%) had a good mRS score at 90 days. Among patients with END who received tirofiban, 27 (79.41%) had a good mRS score at 90 days, which was significantly better than that of the 18 cases that did not receive tirofiban after exacerbation (45%; P < 0.001). NIHSS scores were significantly lower 24 h, 48 h, and 7 days after tirofiban treatment in patients with exacerbation after thrombolytic therapy than in those without tirofiban treatment.ConclusionsPatients with BAD have elevated risks of END after thrombolytic therapy. Compared with conventional oral antiplatelet aggregation drugs, tirofiban rescue therapy resulted in significantly better NIHSS and mRS scores without increased symptomatic cerebral hemorrhage rates.

The sodium channel epithelial 1 subunit gamma (SCNN1G) is mainly responsible for sodium entry and absorption. The dysfunction of SCNN1G has been widely studied in kidney-related diseases and chronic heart failure. However, its role in cancer remains unclear. Here, we found that SCNN1G was aberrantly downregulated in head and neck squamous cell cancer (HNSCC) tissues, which showed an efficifent diagnostic value according to the ROC curve analysis. The lower expression of SCNN1G was significantly correlated with lymphatic metastasis and a worse outcome of HNSCC patients. Ectopic overexpressing SCNN1G inhibited the invasive and migratory abilities of HNSCC cells, while knocking down SCNN1G showed an opposite effect. A positive correlation between SCNN1G and CDH1 expression was observed, which suggested that SCNN1G might impede HNSCC metastasis via strengthing cell-cell adherin. In addition, RAS signaling and ion channel transport signaling were enriched by SCNN1G in HNSCC using GSEA analysis, indicating that these signaling pathways might be the underlying mechanisms for SCNN1G as well. In addition, six sorts of immune infiltrate subtype cells were associated with SCNN1G expression. Our findings support that SCNN1G inactivation contributes to the metastasis of HNSCC. SCNN1G could serves as a valuable diagnostic and prognostic marker for HNSCC.

Acetyl-CoA acyltransferase 1 (ACAT1) is a key enzyme catalyzing the production of mitochondrial ketone bodies. We have shown that ACAT1 is down-regulated in kidney renal clear cell carcinoma (KIRC) previously.To investigate the reasons for downregulation of ACAT1 in KIRC and explore the underlying mechanisms involved in metastatic inhibition regulated by ACAT1.The Gene Expression Omnibus (GEO) database was queried for meta-analysis of ACAT1 mRNA expression in KIRC. The UALCAN website was used to compare the methylation levels of the ACAT1 promoter region in KIRC and normal tissues. RT-qPCR was used to quantitate ACAT1 transcription levels. The GCBI and Tarbase V.8 databases were used to predict miRNAs that may target the mRNA of ACAT1. The correlation between mRNA expression of ACAT1, MMP7 (matrix metallopeptidase 7), CDH1 (E-cadherin), EpCAM (epithelial cell adhesion molecule), and VIM (vimentin) was analyzed. Extracellular MMP7 protein was quantitated using an ELISA assay.The methylation level of the ACAT1 promoter region in KIRC was significantly higher than that in the normal kidney tissues. The ACAT1 mRNA expression in the KIRC cell lines was restored after treatment with 5-aza-dC (p 0.05). MiR-21-5p is a conserved microRNA targeting ACAT1. It is expressed at a significantly higher level in KIRC than in normal tissues (p 0.001). MiR-21-5p miRNA expression negatively correlates with ACAT1 mRNA expression. The expression of miR-21-5p is higher at the T3-T4 stages and in the histologic grades G3-G4. Patients with high miR-21-5p expression tended to have lower overall survival, suggesting that miR-21-5p could serve as a potentially valuable diagnostic biomarker for KIRC (AUC = 0.957; p 0.001). A mimetic of miR-21-5p inhibited the expression of ACAT1 mRNA and protein. In addition, ACAT1 mRNA expression positively correlates with CDH1 and EpCAM but is negatively correlated with VIM. Overexpression of ACAT1 suppresses the secretion of MMP7 in KIRC cells.Expression of ACAT1 in KIRC is controlled at two levels, firstly by the hypermethylation of the ACAT1 promoter region and secondly by overexpression of miR-21-5p. Downregulation of ACAT1 expression correlates with epithelial-mesenchymal transition (EMT).

The dysregulation of epigenetic modification and energy metabolism cooperatively contribute to the tumorigenesis of nasopharyngeal carcinoma (NPC). However, the detailed mechanisms underlying their joint contribution to NPC development and progression remain unclear. Here, we investigate the role of Acy1 Coenzyme A Acyltransferases1 (ACAT1), a key enzyme in the metabolic pathway of ketone bodies, in the proliferation and metastasis of NPC and to elucidate the underlying molecular mechanisms. Ketogenesis, plays a critical role in tumorigenesis. Previously, we reported two enzymes involved in ketone body metabolism mediate epigenetic silencing and act as tumor suppressor genes in NPC. Here, we identify another key enzyme, Acetyl-CoA acetyltransferase 1 (ACAT1), and show that its transcriptional inactivation in NPC is due to promoter hypermethylation. Ectopic overexpression of ACAT1 significantly suppressed the proliferation and colony formation of NPC cells in vitro. The migratory and invasive capacity of NPC cells was inhibited by ACAT1. The tumorigenesis of NPC cells overexpressing ACAT1 was decreased in vivo. Elevated ACAT1 in NPC cells was accompanied by an elevated expression of CDH1 and a reduced expression of vimentin and SPARC, strongly indicating that ACAT1 is involved in regulating epithelial-mesenchymal transition (EMT). We also found that ACAT1 contributes to increased intracellular levels of β-hydroxybutyrate (β-HB). Exogenously supplied β-HB significantly inhibits the growth of NPC cells in a dose-dependent manner. In summary, ACAT1 may function as a tumor suppressor via modulation of ketogenesis and could thus serve as a potential therapeutic target in NPC. In summary, our data suggest that regulation of ketogenesis may serve as adjuvant therapy in NPC.

Background: Prevention and treatment of stroke are very important to reduce the incidence of stroke-related disability and the associated death. This study aimed to investigate the current ability of community doctors in stroke management in the Jinjiang district of Chengdu, China, and the effect of intensive training on stroke prevention and management ability of these doctors.Methods: A self-designed questionnaire was used to investigate the current status of stroke management by community doctors in the Jinjiang district. Subsequently, a series of intensive stroke management training courses for community doctors was designed according to the relevant guidelines for cerebrovascular accident prevention and treatment in China. All community doctors were trained, and their ability to treat and prevent stroke was reassessed using the self-designed questionnaire.Results: Of the 450 questionnaires issued, 370 (74%) and 389 (77.8%) community doctors were enrolled before and after intensive training, respectively. The results showed that the stroke management ability of community doctors improved after intensive training (p < 0.05), including pre-hospital identification and management of stroke, and management of its risk factors.Conclusions: The stroke management ability of community doctors in the Jinjiang district of Chengdu can be improved by promoting intensive training.

The formation of macromolecules is an indispensable step in the process leading to the appearance of life on Earth. As their constituents were widely distributed over geological time and space on the surface of the primitive Earth, clay minerals are regarded as an essential factor influencing the formation of macromolecules due to their high reactivity and their close association with organic matter that could be the precursors of macromolecules. Over the years, many researchers have studied the roles of clay minerals in macromolecules formation through the condensation of amino acids (AAs) in aqueous systems in order to understand the thermal evolution of organic matter (OM) in pristine oceans. However, the condensation of AAs in non-aqueous systems has received limited attention. In particular, the stability and evolution of AAs in volcanic eruption environments that are rich in clay minerals have rarely been investigated. In this work, the influence of clay mineral on the thermal evolution of AAs was studied. Two types of clay-AA complexes, i.e., clay-AA interlayer complexes and clay-AA external complexes (where AAs exist outside the interlayer structure) were used. An expandable clay mineral, montmorillonite (Mt), was chosen as the typical clay mineral, and L-arginine (Arg) and glycine (Gly) were used as the model AAs for the preparation of clay-AA complexes. In situ diffuse-reflectance infrared Fourier transform spectroscopy (in situ DRIFT) was used to monitor the thermal evolution behaviors of the clay-AA complexes, such as the formation of macromolecules with peptide bonds, and thermogravimetry (TG) and TG coupled with Fourier transform infrared spectroscopy (TG-FTIR) analyses were used to investigate the decomposition of the produced macromolecules. The results show that Mt strongly affects macromolecules formation during the thermal evolution of AAs, which is mainly due to that the inherent solid acidity of the different structural sites of Mt varies. When AAs are present on the external surfaces of Mt, the interaction between AAs and clay minerals substantially decreases the initial formation temperature of the macromolecules with peptide bonds (for Arg) and strongly affects the types of condensation products (for Gly). When AAs exist in the interlayer structure of Mt, the interlayer structure has a steric effect on the thermal evolution of these monomers, which, together with the effects of the molecular structure of Arg, enhances the initial temperature of condensation and increases the thermal decomposition temperature of the formed macromolecules. Regardless of whether AAs exist in the interlayer sites or on the external surfaces of clay minerals, clay-OM association is able to protect macromolecules, postponing their thermal decomposition. The present work indicates that macromolecules with peptide bonds could readily form via the condensation of AAs under dry high-temperature conditions, which implies that non-aqueous thermal conditions resulting from volcanic activities might be a favorable geological setting for prebiotic chemical evolution on the early Earth.

This work investigated changes in the chemical composition, structure and porosity of hollow spherical allophane under alkaline conditions, which are significant not only for understanding its fate in natural environment but also for its functional applications. Hollow spherical allophane with a silicon/aluminium (Si/Al) molar ratio of 0.77 was hydrothermally synthesised followed by treatment with dilute sodium hydroxide (NaOH) solutions with different concentrations (indicated by pH values). The allophane and its alkali-treated products were then characterized using a combination of techniques, such as Fourier-transform infrared spectroscopy, nuclear magnetic resonance and nitrogen physisorption analysis. Allophane showed a weak structural stability in alkaline conditions. At pH ≤ 11.0, the framework of allophane particles was almost intact; its polymerised silicates showed only slight dissolution. At a higher pH (> 11.0), desilication and dealumination enhanced, resulting in the destruction of the imogolite local structure (ImoLS) along the edges of defect pores and the formation of amorphous materials. Most of the defect pores increased in size, becoming accessible to nitrogen and the textural parameters of the micropores reached their maximum values at a pH of 12.5. However, the damage to some secondary pores and the collapse of some hollow spherules reduced total pore volume (Vtotal). At a pH of 13.0, most of the hollow spherules were observed to have collapsed, resulting in remarkable decrease in the textural parameters. However, some unbroken and/or mildly broken allophane particles might remain, deduced from the relatively high BET specific surface area (SSA) and Vtotal and the considerable proportion of micropores for Allo13.0. These results reveal the dissolution behaviour of allophane in alkaline conditions and the mechanism underlying this behaviour, providing essential insights into the mineral's potential applications.

Background Cadherin-5 (CDH5) is aberrantly expressed in a variety of human cancers and plays an important role in angiogenesis. The present study provides further insight into the role of miR-27a-3p in the regulation of CDH5 expression in renal clear cell carcinoma (ccRCC). Methods Thedysregulation of CDH5 expression in ccRCC and its association with clinicopathological characteristics were analyzed using the TCGA database. A meta-analysis was performed to verify the alteration of CDH5 expression in ccRCC using the GEO database. Quantitative RT-PCR and immunohistochemical staining were applied to assess the transcriptional and protein levels of CDH5. TargetScan and Tarbase were employed to predict the miRNAs with the potential to target mRNA of CDH5. Results The mRNA level of CDH5 in ccRCCwas significantly higher than in normal tissue. CDH5 mRNA expression could therefore serve as a potential diagnostic biomarker for ccRCC (AUC = 0.844). However, the reduced CDH5 transcription levels were significantly correlated with patients in the T3-4 stage, lymph node, and distant metastasis, as well as with a worse clinical outcome. We further observed that CDH5, at the protein level, was almost absent in ccRCC samples. In addition, a few databases screen showed that mir-27a-3p is a highly conserved miRNA targeting CDH5. The expression of mir-27a-3p was significantly elevated in ccRCC tissues in contrast to normal tissues. Importantly, it was positively associated with the T3-4 stage and M stage, respectively, suggesting that the expression level of mir-27a-3p could serve as a diagnostic biomarker for ccRCC (AUC = 0.775). Conclusion Our data suggest that thereduced translational level of CDH5 in ccRCC was related to the overexpression of mir-27a-3p. The higher mir-27a-3p and lower CDH5 expression significantly correlated with advanced clinical stages for ccRCC patients.

Background: Cadherin-5 (CDH5) is aberrantly expressed in a variety of human cancers and plays an important role in angiogenesis. But its role in renal clear cell carcinoma (ccRCC) remains to be understood. Methods: The dysregulation of CDH5 expression in ccRCC and its association with clinicopathological characteristics were analyzed using the TCGA database. A meta-analysis was performed to verify the alteration of CDH5 expression in ccRCC using the GEO database. Quantitative RT-PCR and immunohistochemical staining were applied to assess the transcriptional and protein levels of CDH5. TargetScan and Tarbase were employed to predict the miRNAs with the potential to target mRNA of CDH5.Results: The mRNA level of CDH5 in ccRCC was significantly higher than in normal tissue. CDH5 mRNA expression could therefore serve as a potential diagnostic biomarker for ccRCC (AUC=0.844). However, the reduced CDH5 transcription levels were significantly correlated with patients in the T3-4 stage, lymph node and distant metastasis, as well as with a worse clinical outcome. We further observed that CDH5, at the protein level, was almost absent in ccRCC samples. In addition, a few databases screen showed that mir-27a-3p, is a highly conserved miRNA targeting CDH5. The expression of mir-27a-3p was significantly elevated in ccRCC tissues in contrast to normal tissues. Importantly, it was positively associated with the T3-4 stage and M stage, respectively, suggesting that the expression level of mir-27a-3p could serve as a diagnostic biomarker for ccRCC (AUC=0.775).Conclusion: Our data suggest that the reduced translational levels of CDH5 in ccRCC was related to the overexpression of mir-27a-3p. The higher mir-27a-3p and lower CDH5 expression significantly correlated with advanced clinical stages for ccRCC patients.

Background Acy1 Coenzyme A Acyltransferases1 (ACAT1) is a key enzyme in the metabolism of ketone bodies, but its expression and biological function in the pathogenesis of NPC remains underexplored. Methods The mRNA and protein expression levels of ACAT1 in NPC and normal control tissues were analyzed by qPCR and immunohistochemistry staining, respectively. GEO database was applied for meta-analysis of ACAT1 mRNA expression and DNA promoter methylation. The role of ACAT1 in NPC proliferation was examined by CCK8 and colony formation assays in vitro and tumorigenicity in vivo. The wound healing and transwell assays were used for analyzing the migratory and invasive ability. cDNA microarray analysis was performed to identify the genes involved in epithelial-mesenchymal transition and dysregulated by ACAT1. These changes were further confirmed by western blot. Results We found that ACAT1 is inactivated in NPC cell lines and primary tissues. DNA microarray data showed higher methylation in the CpG island region of ACAT1 in NPC than normal tissues. The demethylating reagent 5-aza-dC significantly restored the transcription of ACAT1 in NPC cell lines, suggesting that ACAT1 was inactivated by DNA promoter hypermethylation. Ectopic overexpression of ACAT1 remarkably suppressed the proliferation and colony formation of NPC cells in vitro. As well, the tumorigenesis of NPC cells overexpressing ACAT1 was decreased in vivo. In addition, the migratory and invasive capacities of NPC cells was inhibited by ACAT1 overexpression. Importantly, the higher level of ACAT1 was accompanied by an increased expression of CDH1, EPCAM, and a decreased expression of vimentin and SPARC. This strongly indicates that ACAT1 is able to affect the epithelial-mesenchymal transition in NPC, thereby controlling cellular motility. In addition, we found that ACAT1 expression increases the intracellular level of β-HB. Moreover, exogenous β-HB remarkably inhibits the growth of NPC cells in a dose-dependent manner. Conclusions We have discovered that the ketone body metabolism enzyme ACAT1 is epigenetically downregulated in NPC and acts as a potential tumor suppressor in NPC. Our findings highlight the possibility of using the modulation of ketone body metabolism as effective adjuvant therapy for NPC.

Background: This study aimed to investigate the recognition of stroke-related knowledge in a community population (including high-risk groups for stroke) in Jinjiang District of Chengdu and to strengthen the publicity of the impact of stroke-related knowledge on community residents’ stroke recognition by carrying out stroke-health education activities. Methods: By conducting an epidemiological survey, nine communities in Jinjiang District were sampled, and a questionnaire on stroke-related knowledge was designed to investigate the community residents in Jinjiang District of Chengdu City. We carried out stroke health education activities with the theme of “understanding stroke” and evaluated the impact.Results: There were 1685 valid questionnaires, and the awareness level of stroke risk among community residents in Jinjiang District of Chengdu was 11.4%. Participants with three or more risk factors were aware that the risk of stroke was only 40.3%. The recognition rate of stroke warning symptoms among community residents was 29.8–59.5%. Among them, the recognition rate of common stroke symptoms; such as limb weakness, language disorder, and imbalance; was more than 50%, and the cognitive proportion of rare symptoms including monocular or binocular blurred vision, and severe headache with no known cause was only about 1%. When faced with five sudden stroke warning symptoms, the proportion of participants who chose to make an emergency call (120, in China) was about 41.5%. Nearly 10% of the respondents chose to consult a doctor, take medicine, or wait. After strengthening publicity and education, there was a significant improvement in the identification of stroke risk factors, stroke warning symptoms, and stroke management. The number of respondents who chose to dial 120 increased from 59.2% to 82.7%. Conclusions: The recognition of stroke-related knowledge among community residents in Jinjiang District of Chengdu was low. Strengthening publicity and education on stroke-related knowledge and post-stroke treatment can significantly improve patients’ cognition of stroke-related knowledge and enhance community residents’ awareness of giving priority to dialing 120 after the onset of stroke symptoms.

Background: This study aimed to investigate stroke recognition in a community population (including high-risk groups of stroke) in Jinjiang District of Chengdu and strengthen the publicity of the impact of stroke-related knowledge on community residents’ stroke recognition. Methods: By conducting an epidemiological survey, nine communities in Jinjiang District were sampled, and a questionnaire on stroke-related knowledge was designed to investigate the community residents in Jinjiang District of Chengdu City. We carried out stroke health education activities with the theme of “understanding stroke” and evaluated the impact. Results: There were 1685 valid questionnaires, and the awareness level of stroke risk among community residents in Jinjiang District of Chengdu was 11.4%. The proportion of people who recognized that there was a risk of stroke increased with the increase in the number of risk factors (P < 0.001). Participants with three or more risk factors were aware that the risk of stroke was only 40.3%. The recognition rate of stroke warning symptoms among community residents was 29.8–59.5%. Among them, the recognition rate of common stroke symptoms such as limb weakness, language disorder, and imbalance was more than 50%, and the cognitive proportion of rare symptoms including monocular or binocular blurred vision and severe headache with no known cause was only about 1%. When faced with five sudden stroke warning symptoms, the proportion of participants who chose to make an emergency call (120, in China) was about 41.5%. Nearly 10% of the respondents chose to consult a doctor, take medicine, or wait. After strengthening publicity and education, there was a significant improvement in the identification of stroke risk factors, stroke warning symptoms, and stroke management. The number of respondents who chose to dial 120 increased from 59.2% to 82.7%. Conclusions: The recognition of stroke among community residents in Jinjiang District of Chengdu is low. Strengthening publicity and education on stroke-related knowledge and post-stroke treatment can significantly improve patients’ cognition of stroke-related knowledge and enhance community residents’ awareness of giving priority to dialing 120 after the onset of stroke symptoms. Key words: stroke, community residents, warning symptoms, intensive education

Despite the focus of many studies on the preparation, characterization, and potential applications of solvent-free nanofluids based on diverse nanomaterials, fewer studies have focused on how to control the macroscopic liquid-like behaviour of solvent-free nanofluids. The present study prepared a halloysite-based solvent-free nanofluid and developed a facile method of tuning the fluidity of this nanofluid by preheating halloysite (Hal) at different temperatures. The effects of preheating on the structure and surface functional groups of halloysite and further on the fluidity of the obtained nanofluids were explored. Heating Hal at 110 °C resulted in little changes to its surface functional moieties, and the obtained nanofluid (Hal110-F) did not exhibit a markedly different fluidity compared with Hal-F at room temperature, though Hal-F and Hal110-F had different melting temperatures and exhibited different fluidities at a lower temperature. While for Hal heated at 700 °C, the corresponding nanofluid (Hal700-F) exhibited a lower fluidity than Hal-F and Hal110-F due to the remarkable calcination-induced changes in the species/amount of surface functional moieties of Hal700. This method for controlling the fluidity of the nanofluids via a facile core pretreatment was believed to be versatile for most, if not all, solvent-free nanofluids.

Halloysite is a hydrated polymorph of kaolinite but possesses a distinctive nanosized tubular structure and surface reactivity. The microstructure and mechanical performance of geopolymers derived from calcined halloysite via acid-activation were investigated in this study. The acid-activation products were characterized using a combination of techniques including X-ray diffraction (XRD), Fourier-transform infrared spectroscopy (FTIR), nuclear magnetic resonance (NMR), scanning electron microscopy (SEM), and transmission electron microscopy (TEM). Acid-activation of halloysite calcined at 450 °C by 6 mol/L and 10 mol/L phosphoric acid solution produced metavariscite crystals. When the phosphoric acid concentration was increased to 14 mol/L, the acid-activation product became more compact due to the formation of geopolymer that were mainly composed of Al–O–P networks. Calcination of halloysite at 750 °C led to an active form of halloysite, which was favored by geopolymerization. Higher phosphoric acid concentration led to the incorporation of more Si and P in the geopolymer matrix with Si–O–P–O–Al networks, and thus greater compressive strength. Halloysites calcined at 1000 °C barely reacted with phosphoric acid, due to the nanocrystalline formation and the decreased Si–OH content in the calcined halloysite, which had low reactivity unfavorable for geopolymerization. These results indicated that the microstructure and mechanical performance of halloysite-based geopolymers are highly dependent on the precalcination temperature of halloysite and the phosphoric acid concentration. Suitable precalcination temperature and high concentration of phosphoric acid facilitate high degree of geopolymerization, which is conducive to the formation of an acid-activated halloysite-based geopolymer with excellent mechanical performance.

In this work, halloysite-CeOx (x = 1.5–2.0) nanocomposites were prepared using a redox-precipitation method, and the As(III) removal performance of the obtained materials was evaluated. These composites were formed by supporting CeO2 nanoparticles on the chemically modified halloysite substrate. The modification of halloysite using a facile NaOH treatment dramatically increased the inner-surface and inner hydroxyl groups. These increased groups significantly enhanced the dispersion of the coating of CeO2 nanoparticles due to electrostatic interactions. The specific surface area and pore volume of the optimized Hal0.01Ce composite was 91.1 m2/g and 0.16 cm3/g, respectively. This composite exhibited an excellent As(III) adsorption capacity (209.3 mg/g CeO2), which was much higher than the unmodified halloysite-CeOx composite (158.5 mg/g CeO2) and unsupported CeO2 nanoparticles (61.9 mg/g). The As(III) adsorption mechanisms on this composite involved the formation of surface complexes and oxidation of partial As(III) followed by As(V) adsorption. In addition, the Hal0.01Ce composite also possessed selective adsorption for As(III) in the presence of coexisting ions and maintained 91.4% of the As(III) removal efficiency after three regeneration cycles. These results demonstrate that this composite can be used as a potential candidate for As(III) removal from contaminated water.