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Activated carbon (AC) is widely used to removing hazardous pollutants from air and water, owing to its exceptional adsorption properties. However, the high affinity of water molecules with the surface oxygen-containing functional groups can adversely affect the adsorption performance of AC. In this study, a facile and efficient method is presented for fabrication of hydrophobic AC through surface monolayer silanation. Compared to initial AC, the hydrophobic AC improves the water contact angle from 29.7° to 123.5° while maintaining high specific surface area and enhances the removal capacity of multi-phase pollutants (emulsified oil and toluene). Additionally, the hydrophobic AC exhibits excellent adsorption capability to harmful algal bloom species (Chlorella) (97.56%) and algal organic matter (AOM) (96.23%) owing to electrostatic interactions and surface hydrophobicity. The study demonstrates that this method of surface monolayer silanation can effectively weaken the effect of water molecules on AC adsorption capacity, which has significant potential for practical use in air and water purification, as well as in the control of harmful algal blooms.
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Previous studies have proven that long intergenic non-coding RNA regulator of reprogramming (Linc-ROR) plays opposing roles in different cancer types. This work intended to investigate its functions and underlying mechanisms in gastric carcinoma (GCa) progression. RT-qPCR was utilized for gene expression measurement. GCa cell viability, apoptosis, migration, and invasion were detected by functional assays, including CCK-8, flow cytometry, and Transwell assays. ChIP assay and Dual-luciferase reporter assay were utilized to affirm the associations between genes. Linc-ROR expression dramatically declined in GCa tissues and cell lines. Linc-ROR upregulation suppressed GCa cell proliferation, migration, and invasion but accelerated GCa cell apoptosis. As for Linc-ROR-associated molecular mechanisms in GCa, SOX2 associated with Linc-ROR promoter region to activate Linc-ROR transcription in GCa cells; Linc-ROR upregulated ANXA10 level in GCa cells by competitively binding to miR-580-3p. As revealed by rescue assays, Linc-ROR-induced inhibition on malignant biological behaviors of GCa cells could be partially abated by ANXA10 deletion or miR-580-3p upregulation. SOX2-activated Linc-ROR serves as a cancer suppressor to restrain GCa progression in vitro via the miR-580-3p/ANXA10 pathway, suggesting a promising diagnostic and therapeutic target for GCa patients.
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Carcinoma , MicroRNAs , RNA Longo não Codificante , Neoplasias Gástricas , Humanos , Anexinas/genética , Anexinas/metabolismo , Linhagem Celular Tumoral , Proliferação de Células/genética , MicroRNAs/genética , MicroRNAs/metabolismo , Fatores de Transcrição SOXB1/genética , Fatores de Transcrição SOXB1/metabolismo , Regulação para Cima , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Neoplasias Gástricas/genética , Neoplasias Gástricas/metabolismoRESUMO
BACKGROUND: The triglyceride-glucose (TyG) index is known as a reliable alternative marker of insulin resistance (IR), which has been regarded as a predictor of cardiovascular disease (CVD). However, whether TyG index can predict the risk and occurrence of CVD in non-diabetic population remains uncertain. The aim of this study was to explore the association between the TyG index and cardiovascular risk factors and to clarify the prognostic value of the TyG index for CVD, coronary heart disease (CHD) and stroke in non-diabetic general population in Eastern China. METHODS: A total of 6095 cases without diagnosed diabetes and CVD were included. The TyG index was calculated as ln (fasting triglyceride [mg/dL] × fasting glucose [mg/dL]/2) and the participants were divided into 4 groups according to the TyG index quartiles (Q1, Q2, Q3, Q4). The primary outcome was CVD, including CHD and stroke. Cox proportional hazards regression analysis was used to investigate the association between the TyG index and the risk of CVD. RESULTS: During the 10-year follow-up, 357 (5.9%) participants of CVD, 224 (3.7%) participants of CHD and 151 (2.5%) participants of stroke were observed. The incidence of CVD increased with the TyG index quartiles. Multivariate Cox regression analysis showed that the hazard ratios [95% confidence interval (CI)] in Q4 group were respectively 1.484 (1.074-2.051) for CVD, 1.687 (1.105-2.575) for CHD and 1.402 (0.853-2.305) for stroke compared to Q1 group. Moreover, adding the TyG index to models with traditional risk factors yielded a significant improvement in discrimination and reclassification of incident CVD and CHD. CONCLUSIONS: The TyG index is associated with cardiovascular risk factors and can be used as a useful, low-cost predictive marker for CVD and CHD risk in non-diabetic population.
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Doenças Cardiovasculares , Acidente Vascular Cerebral , Humanos , Triglicerídeos , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/epidemiologia , Glucose , Glicemia , Estudos Prospectivos , Fatores de Risco , Biomarcadores , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/epidemiologiaRESUMO
INTRODUCTION: The PER2 (Period circadian regulator 2) gene is related to the circadian clock, and it has been deemed as a suppressor gene in osteosarcoma and lung carcinoma. However, the part of PER2 in CRC (colorectal cancer) needs to be further determined. METHODS: First, we collected clinical samples to detect PER2 expression in CRC. Then, we used cell transfection to knock down PER2 expression in CRC cell lines and performed a series of functional experiments to elucidate the effects of PER2 on CRC cells. We next verified whether PER2 affects the epithelial-mesenchymal transformation (EMT) process in CRC by conducting quantitative real-time PCR and western blotting. RESULTS: In the research, we revealed that the expression of PER2 decreased in CRC clinical samples. In addition, knocking down PER2 expression caused CRC cells to acquire malignant biological features. Finally, we found that PER2 knockdown may activate the Snail/Slug axis through inhibiting p53, therefore promote the activation of the EMT pathway. CONCLUSION: In conclusion, low PER2 expression reinforces migration and activates EMT in CRC, suggesting that PER2 is closely related to CRC development and could be used as a potential treatment site in the clinic.
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Neoplasias Colorretais , Transição Epitelial-Mesenquimal , Linhagem Celular Tumoral , Movimento Celular , Neoplasias Colorretais/genética , Neoplasias Colorretais/patologia , Transição Epitelial-Mesenquimal/genética , Regulação Neoplásica da Expressão Gênica , HumanosRESUMO
BACKGROUND: Metabolic reprogramming has been reported in various kinds of cancers and is related to clinical prognosis, but the prognostic role of pyrimidine metabolism in gastric cancer (GC) remains unclear. METHODS: Here, we employed DEG analysis to detect the differentially expressed genes (DEGs) in pyrimidine metabolic signaling pathway and used univariate Cox analysis, Lasso-penalizes Cox regression analysis, Kaplan-Meier survival analysis, univariate and multivariate Cox regression analysis to explore their prognostic roles in GC. The DEGs were experimentally validated in GC cells and clinical samples by quantitative real-time PCR. RESULTS: Through DEG analysis, we found NT5E, DPYS and UPP1 these three genes are highly expressed in GC. This conclusion has also been verified in GC cells and clinical samples. A prognostic risk model was established according to these three DEGs by Univariate Cox analysis and Lasso-penalizes Cox regression analysis. Kaplan-Meier survival analysis suggested that patient cohorts with high risk score undertook a lower overall survival rate than those with low risk score. Stratified survival analysis, Univariate and multivariate Cox regression analysis of this model confirmed that it is a reliable and independent clinical factor. Therefore, we made nomograms to visually depict the survival rate of GC patients according to some important clinical factors including our risk model. CONCLUSION: In a word, our research found that pyrimidine metabolism is dysregulated in GC and established a prognostic model of GC based on genes differentially expressed in pyrimidine metabolism.
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BACKGROUND: Nanoscale drug delivery systems have emerged as broadly applicable approach for chemo-photothermal therapy. However, these nanoscale drug delivery systems suffer from carrier-induced toxicity, uncontrolled drug release and low drug carrying capacity issues. Thus, to develop carrier-free nanoparticles self-assembled from amphiphilic drug molecules, containing photothermal agent and anticancer drug, are very attractive. RESULTS: In this study, we conjugated camptothecin (CPT) with a photothermal agent new indocyanine green (IR820) via a redox-responsive disulfide linker. The resulting amphiphilic drug-drug conjugate (IR820-SS-CPT) can self-assemble into nanoparticles (IR820-SS-CPT NPs) in aqueous solution, thus remarkably improving the membrane permeability of IR820 and the aqueous solubility of CPT. The disulfide bond in the IR820-SS-CPT NPs could be cleaved in GSH rich tumor microenvironment, leading to the on demand release of the conjugated drug. Importantly, the IR820-SS-CPT NPs displayed an extremely high therapeutic agent loading efficiency (approaching 100%). Besides, in vitro experimental results indicated that IR820-SS-CPT NPs displayed remarkable tumor cell killing efficiency. Especially, the IR820-SS-CPT NPs exhibited excellent anti-tumor effects in vivo. Both in vitro and in vivo experiments were conducted, which have indicated that the design of IR820-SS-CPT NPs can provide an efficient nanotherapeutics for chemo-photothermal therapy. CONCLUSION: A novel activatable amphiphilic small molecular prodrug IR820-SS-CPT has been developed in this study, which integrated multiple advantages of GSH-triggered drug release, high therapeutic agent content, and combined chemo-photothermal therapy into one drug delivery system.
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Camptotecina/administração & dosagem , Camptotecina/química , Sistemas de Liberação de Medicamentos/métodos , Nanopartículas/química , Terapia Fototérmica/métodos , Pró-Fármacos/química , Animais , Antineoplásicos/farmacologia , Linhagem Celular Tumoral , Liberação Controlada de Fármacos , Feminino , Humanos , Verde de Indocianina , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Fototerapia , SolubilidadeRESUMO
BACKGROUND Ultrasound (US) is the preferred imaging method for cryptorchidism, but most guidelines indicate that its value is questionable. The aim of this study was to evaluate the clinical value of ultrasonic mobility and testicular atrophy index (TAI) based on threedimensional US (3DUS) in preoperative and postoperative assessment of the undescended testis. MATERIAL AND METHODS Data from 158 children with unilateral extraperitoneal cryptorchidism were collected and their diagnoses were surgically confirmed. They were divided into different age groups and into 2 ultrasonic mobility groups: the mobile group (MG) and the restricted group (RG). Differences in sonographic characteristics between different groups were compared. Three-dimensional ultrasound performed with virtual organ computer-aided analysis (VOCAL) was used to determined preoperative and postoperative TAI and the reliability of TAI was analyzed. RESULTS Measurement of testicular volume with the VOCAL method was significantly more reliable than that done with the two-dimensional Lambert method. In all age groups, preoperative testicular volumes were smaller than that in the contralateral scrotal testis and postoperatively, they increased steadily. Both preoperative and postoperative TAI were higher in the RG than in the MG. In the MG, postoperative TAI decreased significantly in all age groups. In the RG, in contrast, effective volume growth was only achieved in patients who had undergone surgery before they reached age 1 year. CONCLUSIONS TAI values determined with 3DUS using the VOCAL technique objectively reflect recovery of testicular volume following surgery for undescended testicle. Ultrasonic mobility evaluation is beneficial for clinical management of the condition.
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Criptorquidismo , Ecocardiografia Tridimensional , Cuidados Pós-Operatórios , Cuidados Pré-Operatórios , Testículo , Criança , Criptorquidismo/diagnóstico por imagem , Criptorquidismo/cirurgia , Humanos , Masculino , Tamanho do Órgão , Estudos Retrospectivos , Testículo/diagnóstico por imagem , Testículo/cirurgiaRESUMO
BACKGROUND: The metabolic score for insulin resistance (METS-IR) is a simple, convenient, and reliable marker for resistance insulin (IR), which has been regarded as a predictor of cardiovascular disease (CVD) and cardiovascular events. However, few studies examined the relationship between METS-IR and prognosis after coronary artery bypass graft (CABG). This study aimed to investigate the potential value of METS-IR as a prognostic indicator for the major adverse cardiovascular events (MACE) in patients after CABG. METHOD: 1100 CABG patients were enrolled in the study, including 760 men (69.1%) and 340 women (30.9%). The METS-IR was calculated as Ln [(2 × FPG (mg/dL) + fasting TG (mg/dL)] × BMI (kg/m2)/Ln [HDL-C (mg/dL)]. The primary endpoint of this study was the occurrence of major adverse cardiovascular events (MACE), including a composite of all-cause death, non-fatal myocardial infarction (MI), coronary artery revascularization, and stroke. RESULT: The following-up time of this study was 49-101 months (median, 70 months; interquartile range, 62-78 months). During the follow-up period, there were 243 MACEs (22.1%). The probability of cumulative incidence of MACE increased incrementally across the quartiles of METS-IR (log-rank test, p < 0.001). Multivariate Cox regression analysis demonstrated a hazard ratio (95% CI) of 1.97 (1.36-2.86) for MACE in quartile 4 compared with participants in quartile 1. The addition of the METS-IR to the model with fully adjusting variables significantly improved its predictive value [C-statistic increased from 0.702 to 0.720, p < 0.001, continuous net reclassification improvement (NRI) = 0.305, < 0.001, integrated discrimination improvement (IDI) = 0.021, p < 0.001]. CONCLUSION: METS-IR is an independent and favorable risk factor for predicting the occurrence of MACE and can be used as a simple and reliable indicator that can be used for risk stratification and early intervention in patients after CABG.
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Hot corrosion is one of the crucial failure modes of Ni-based superalloy components operating at high temperatures, which inevitably affects the subsequent mechanical properties of the alloys. In this research, damaged Inconel 718 alloy components with a pre-made trapezoid groove are repaired using laser additive manufacturing technique, and the change mechanisms of the microstructure and tensile properties of the repaired Inconel 718 alloy due to the hot corrosion in the salt mixture of 87.5 wt.% Na2SO4 + 5 wt.% NaCl + 7.5 wt.% NaNO3 at 650 °C for different durations are investigated. The results show that oxidation and Cr-depletion occur on the repaired components due to the hot corrosion, and the corrosion products are mainly composed of Cr2O3, Fe3O4, and Ni3S2. The tensile strength and elongation of the as-repaired specimens are 736.6 MPa and 12.5%, respectively. After being hot corroded for 50 h, the tensile strength increases to 1022.9 MPa and elongation decreases to 1.7%. However, after being hot corroded for 150 h, both tensile strength and elongation of the repaired specimens drop to 955.8 MPa and 1.2%, respectively. The mechanical performance alteration is highly related to thermal effects instead of the molten salt attack.
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According to Ming's classification, gastric cancer (GC) can be divided into two types: expanding and infiltrative. The two types are readily recognizable by histology: expanding carcinomas grow en masse and by expansion, resulting in the formation of discrete tumour nodules, whereas in infiltrative carcinoma, tumour cells invade individually. Both types show varying degrees of cell maturation. The two types of carcinomas have vastly different pathological and clinical features. However, little is known concerning the mechanisms underlying these differences since no GC cell line models are available. For comprehensive and insightful analyses of mechanisms and treatment methods, new cell lines derived from expanding- and infiltrative-type gastric tumours are urgently needed. In the present study, we established an expanding-type GC cell line from a 72-year-old male patient. Different in vitro and in vivo methods were used to characterize the phenotypes of this cell line. This GC cell line was named XGC-2 and had an ~60 h doubling time. The cell line displayed strong colony formation and tumourigenicity in nude mice and had complicated chromosomal abnormalities. XGC-2 cells showed some markers of epithelial-to-mesenchymal transition (EMT), with decreased E-cadherin expression levels and increased vimentin expression levels. The XGC-2 cell line may be useful for future studies of GC development, progression, metastasis and therapy.
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Carcinoma/patologia , Linhagem Celular Tumoral/patologia , Neoplasias Gástricas/patologia , Idoso , Animais , Caderinas/biossíntese , Diferenciação Celular/genética , Transição Epitelial-Mesenquimal , Regulação Neoplásica da Expressão Gênica , Humanos , Masculino , Camundongos , Vimentina/biossíntese , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
MicroRNAs are critical in various human cancers, including gastric cancer (GC). However, the mechanism underlying the GC development remains elusive. In this study, we demonstrate that miR-448 is increased in GC samples and cell lines. Overexpression of miR-448 facilitated the proliferation of GC cells by stimulating glycolysis. Mechanistically, we identified KDM2B, a reader for methylated CpGs, as the target of miR-448 that represses glycolysis and promotes oxidative phosphorylation. Overexpression of miR-448 reduced both the mRNA and protein levels of KDM2B, whereas KDM2B re-expression abrogated the miR-448-mediated glycolytic activities. Furthermore, we discovered Myc as a key target of KDM2B that controls metabolic switch in GC. Importantly, a cohort of 81 GC tissues revealed that miR-448 level closely associated with a battery of glycolytic genes, in which KDM2B showed the strongest anti-correlation coefficient. In addition, enhanced miR-448 level was significantly associated with poor clinical outcomes of GC patients. Hence, we identified a previously unappreciated mechanism by which miR-448 orchestrate epigenetic, transcriptional and metabolic networks to promote GC progression, suggesting the possibility of therapeutic intervention against cancer metabolic pathways.