Algorithm of face anti-spoofing based on pseudo-negative features generation.

Introduction: Despite advancements in face anti-spoofing technology, attackers continue to pose challenges with their evolving deceptive methods. This is primarily due to the increased complexity of their attacks, coupled with a diversity in presentation modes, acquisition devices, and prosthetic materials. Furthermore, the scarcity of negative sample data exacerbates the situation by causing domain shift issues and impeding robust generalization. Hence, there is a pressing need for more effective cross-domain approaches to bolster the model's capability to generalize across different scenarios. Methods: This method improves the effectiveness of face anti-spoofing systems by analyzing pseudo-negative sample features, expanding the training dataset, and boosting cross-domain generalization. By generating pseudo-negative features with a new algorithm and aligning these features with the use of KL divergence loss, we enrich the negative sample dataset, aiding the training of a more robust feature classifier and broadening the range of attacks that the system can defend against. Results: Through experiments on four public datasets (MSU-MFSD, OULU-NPU, Replay-Attack, and CASIA-FASD), we assess the model's performance within and across datasets by controlling variables. Our method delivers positive results in multiple experiments, including those conducted on smaller datasets. Discussion: Through controlled experiments, we demonstrate the effectiveness of our method. Furthermore, our approach consistently yields favorable results in both intra-dataset and cross-dataset evaluations, thereby highlighting its excellent generalization capabilities. The superior performance on small datasets further underscores our method's remarkable ability to handle unseen data beyond the training set.

Sensing platform for the highly sensitive detection of catechol based on composite coupling with conductive Ni3(HITP)2 and nanosilvers.

Catechol, which has a high toxicity and low degradability, poses significant risks to both human health and the environment. Tracking of catechol residues is essential to protect human health and to assess the safety of the environment. We constructed sensing platforms to detect catechol based on the conductive metal-organic frameworks [Ni3(HITP)2] and their nanosilver composites. The reduction process of catechol at the Ni3(HITP)2/AgNP electrode is chemically irreversible as a result of the difference in compatibility of the oxidation stability and conductivity between the Ni3(HITP)2/AgNS and Ni3(HITP)2/AgNP electrodes. The electrochemical results show that the Ni3(HITP)2/AgNS electrode presents a lower detection limit of 0.053 µM and better sensitivity, reproducibility and repeatability than the Ni3(HITP)2/AgNP electrode. The kinetic mechanism of the catechol electrooxidation at the surface of the electrode is controlled by diffusion through a 2H+/2e- process. The transfer coefficient is the key factor used to illustrate this process. During the electrochemical conversion of phenol to ketone, more than half of ΔG is used to change the activation energy. We also studied the stability, anti-interference and reproducibility of these electrode systems.

Effective degradation of phenol by activating PMS with bimetallic Mo and Ni Co-doped g C3N4 composite catalyst: A Fenton-like degradation process promoted by non-free radical 1O2.

The application of bimetal supported graphite phase carbon nitride in activated peroxymonosulfate (PMS) process has become a research hotspot in recent years. In this study, 8-g C3N4/Mo/Ni composite catalyst material was successfully prepared by doping Mo and Ni in graphite phase carbon nitride. The bimetallic active sites were formed in the catalyst, and PMS was activated by the metal valence Mo6+/Mo4+ and Ni2+/Ni(0) through redox double cycle to effectively degrade phenol. When pH was neutral, the degradation rate of 20 mg/L phenol solution with 8-g C3N4/Mo/Ni (0.35 g/L) and PMS (0.6 mM) could reach 95% within 20 min. The degradation rate of 8-g C3N4/Mo/Ni/PMS catalytic system could reach more than 90% within 20min under the condition of pH range of 3-11 and different anions. Meanwhile, the degradation effects of RhB, MB and OFX on different pollutants within 30min were 99%, 100% and 82%, respectively. Electron spin resonance and quenching experiments showed that in 8-g C3N4/Mo/Ni/PMS system, the degradation mechanism was mainly non-free radicals, and the main active species in the degradation process was 1O2. This study provides a new idea for the study of bimetal supported graphite phase carbon nitride activation of PMS and the theoretical study of degradation mechanism.

Designed fabrication of MoS2 hollow structures with different geometries and the comparative investigation toward capacitive properties.

Hollow MoS2 cubes and spheres were synthesized by a one-step hydrothermal method with the hard template method. The structure and morphology were characterized, and their electrochemical properties were studied. It is concluded that the specific capacitance of the hollow MoS2 cubes (335.7 F g-1) is higher than that of the hollow MoS2 spheres (256.1 F g-1). The symmetrical supercapacitors were assembled, and the results indicate that the specific capacitance of the device composed of hollow MoS2 spheres (32.9 F g-1) is slightly lower than that of the hollow MoS2 cube (37.4 F g-1) device. Furthermore, the symmetrical supercapacitor (MoS2-cube//MoS2-cube) provides a maximum energy density of 4.93 W h kg-1, which is greater than that of the symmetrical capacitor (MoS2-sphere//MoS2-sphere, 3.65 W h kg-1). This may indicate that hollow molybdenum disulfide cubes with substructures have more efficient charge transfer capabilities and better capacitance characteristics than hollow spheres. After 8000 cycles, the coulombic efficiency of the two symmetrical capacitors is close to 100%. The capacity retention of the MoS2 sphere device (95.2%) is slightly higher than that of the MoS2 cube device (90.1%). These results show that the pore structure, specific surface, and active site of MoS2 with different hollow structures have a greater impact on its electrochemical properties.

Enhanced Adsorption of Aromatic Volatile Organic Compounds on a Perchloro Covalent Triazine Framework through Multiple Intermolecular Interactions.

Volatile organic compounds (VOCs) may have short- and long-term adverse health effects. Especially, aromatic VOCs including benzene, toluene, ethylbenzene, and xylene (BTEX) are important indoor air pollutants. Developing highly efficient porous adsorbents with broad applicability remains a major challenge. In this study, a perchlorinated covalent-triazine framework (ClCTF-1-400) is prepared for adsorbing BTEX. ClCTF-1-400 is confirmed as a partially oxidized/chlorinated microporous covalent triazine framework through a variety of characterization. It is found that ClCTF-1-400 is reversible VOCs absorbent with very high absorption capacities, which can adsorb benzene (693 mg g-1 ), toluene (621 mg g-1 ), ethylbenzene (603 mg g-1 ), o-xylene (500 mg g-1 ), m-xylene (538 mg g-1 ), and p-xylene (592 mg g-1 ) at 25 °C and their saturated vapor pressure (≈ 1 kPa). ClCTF-1-400 is of higher adsorption capacities for all selected VOCs than activated carbon and other reported adsorbents. The adsorption mechanism is also inferred through theoretical calculation and in-site Fourier Transform Infrared (FTIR) spectroscopy. The observed excellent BTEX adsorption performance is attributed to the multiple weak interactions between the ClCTF-1-400 frameworks and aromatic molecules through multiple weak interactions (CH… π and CCl… π). The breakthrough experiment demonstrates ClCTF-1-400 has the potential for real VOCs pollutant removal in air.

EIF3H stabilizes CCND1 to promotes intrahepatic cholangiocarcinoma progression via Wnt/ß-catenin signaling.

Cholangiocarcinoma (CCA) is a group of tumors that arise along the human biliary duct tree, ranking second in primary hepatic malignancies. Intrahepatic CCA (iCCA) represents about 10%-20% of CCAs. There is an increasing body of evidence suggesting that iCCAs' incidence and mortality have been increasing globally over the past few decades. In this study, we found that the EIF3H expression level in iCCA tissues was significantly increased compared to the adjacent non-cancerous tissues by immunohistochemistry analysis (IHC). A similar tendency of EIF3H mRNA and protein level was confirmed in iCCA cell lines using RT-qPCR and Western blot. EIF3H has been identified as a critical molecule that plays a pro-neoplasmic role in iCCA both in vivo and in vitro, such as proliferation, migration, and anti-apoptosis. Mechanistically, we found that EIF3H knockdown can promote the degradation of CCND1 and the proteolysis of CCND1 is mediated by ubiquitin-proteasome system (UPS). Thus, we come to the conclusion that EIF3H promotes proliferation and migration of iCCAs, inhibiting apoptosis of iCCA cells at the same time by stabilizing the CCND1 protein structure. Our findings provide insights into the mechanism of tumorigenesis role of EIF3H in iCCAs and a potential therapeutic target for iCCA treatment.

One-Stage Posterior Vertebral Column Resection in the Treatment of Adolescent Thoracic and Lumbar Tuberculosis Complicated With Severe Kyphotic Deformity.

BACKGROUND: Our study aims to investigate the clinical outcome of 1-stage posterior vertebral column resection (PVCR) for adolescent thoracic and lumbar tuberculosis with severe kyphotic deformity (Cobb angle≥60°). METHODS: Between January 2008 and January 2016, we recorded 16 (9 male, 7 female) adolescent cases of thoracic and lumbar tuberculosis complicated with severe kyphotic deformity treated by 1-stage PVCR (average age: 15.38 ± 1.54 years; range: 13-18 years). The Cobb angle of kyphosis was 64.56° ± 3.41°. According to the American Spinal Injury Association (ASIA) classification, all patients were classified preoperatively. The lesions involved T4-T11 in 10 cases and T12-L2 in 6 cases. RESULTS: The mean follow-up time was 19.06 ± 11.42 months (range: 12-48 months). Based on ASIA classification, postoperative grades were significantly increased compared with preoperative grades (P < 0.05), The mean Cobb angle was significantly corrected to 20.25° ± 13.83° at 1 week after surgery, when compared with preoperative Cobb angle (P < 0.05). There was no significant difference in Cobb angle between 1-week after operation and the last follow-up (20.69° ± 13.83°) (P > 0.05). All the patients achieved bony fusion at a mean time of 14 months (range: 10-20 months) postoperatively. No fixation loosening, displacement, or fracture was observed during follow-up. CONCLUSIONS: One-stage PVCR is an effective surgical method for the treatment of adolescent thoracic and lumbar spinal tuberculosis with severe kyphotic deformity, which can completely remove the lesion, effectively correct the kyphosis deformity, and prevent related complications.

The development of a nomogram and the prognostic prediction value of patients with esophageal squamous cell carcinoma undergoing radical radiotherapy.

AIM: This study aimed to explore the role of the developed nomogram in the prognosis of esophageal squamous cell carcinoma (ESCC). METHODS: A total of 181 ESCC patients were randomly divided into a training cohort (n = 141) and a validation cohort (n = 40). Significant factors impacting overall survival (OS) were identified in the training set and integrated into the nomogram based on Cox proportional hazards regression. RESULTS: In the training cohort, the median OS in the high group (≥222) was 49.9 months and the median OS in the low group (<222) was 14.4 months. Multivariate analysis revealed that age, Karnofsky performance status score, tumor stage, chemotherapy, BMI, cervical esophageal carcinoma index and neutrophil to lymphocyte ratio were predictors of OS. CONCLUSION: The developed nomogram can effectively predict the survival prognosis of ESCC patients.

Safety and efficacy of nivolumab plus recombinant human endostatin in previously treated advanced non-small-cell lung cancer.

Background: Evidence of the efficacy of immune checkpoint inhibitors (ICIs) plus antiangiogenic drugs in previously treated patients with advanced non-small-cell lung cancer (NSCLC) is still insufficient, so we investigated the safety and efficacy of nivolumab plus recombinant human (rh)-endostatin in such patients. Methods: Patients without epithelial growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK) targetable mutations in advanced NSCLC who did not respond to previous treatment were enrolled. Eligible patients received nivolumab (3 mg/kg, i.v. drip, day 1) every 2 weeks and rh-endostatin (210 mg, continuous i.v. infusion for 168 h) every 4 weeks until disease progression or discontinuation. The primary endpoint was the objective response rate (ORR). The secondary endpoints included disease control rate (DCR), duration of response (DOR), clinical benefit response rate (CBR), progression-free survival (PFS), overall survival (OS) and safety. Results: A total of 34 patients received a median of 4 cycles of therapy. In all, 14 patients achieved confirmed partial response (PR) with an ORR of 41.2% [14/34; 95% confidence interval (CI): 23.7-58.6%], DCR of 64.7% (22/34; 95% CI: 47.8-81.6%), CBR of 44.1% (95% CI: 26.5-61.7%), and a DOR of 6.9 (95% CI: 4.4-9.4) months. Median follow-up was 12.2 (range, 2.3-18.1) months. Median PFS (mPFS) was 6.8 (95% CI: 1.1-12.1) months, median OS (mOS) was 17.1 (95% CI: 6.6-27.6) months, and 12-month survival rate of 64.4% (95% CI: 46.2-82.6%). In all, 18 (18/34, 52.9%) patients experienced at least one treatment-related adverse event (TRAE), and Grade 3 TRAEs occurred in 4 (4/34, 11.8%) of them. Conclusions: This study is first to assess nivolumab plus rh-endostatin in previously treated patients with advanced NSCLC. In view of its favorable efficacy and safety profile, this combination represents a promising treatment regimen in this patient population.

Preoperative prediction for lymph node metastasis in early gastric cancer by interpretable machine learning models: A multicenter study.

BACKGROUND: The presence of lymph node metastasis plays a decisive role in the selection of treatment options in patients with early gastric cancer. However, there is currently no established protocol to predict the risk of lymph node metastasis before/after endoscopic resection. The aim of this study was to develop and validate several machine learning algorithms for clinical practice. METHODS: A total of 2,348 patients with early gastric cancer were selected from 5 major tertiary medical centers. We applied 6 machine learning algorithms to develop lymph node metastasis prediction models for clinical feature variables. The partial dependence plots were used to explain the prediction of the models. The area under the receiver operating characteristic curve and area under the precision recall curve were measured to assess the detection performance. The R shiny interactive web application was used to translate the prediction model in a clinical setting. RESULTS: The incidence of lymph node metastasis in patients with early gastric cancer was 13.63% (320/2348) and significantly higher in young women, in the lower third of the stomach, with a size >2 cm, depressed type, poorly/nondifferentiated, lymphovascular invasion, nerve invasion, and submucosal infiltration. In terms of age, there is a nonlinear and younger trend. XGBOOST displayed the best predictive performance at the initial and postendoscopy evaluation. In addition, the machine learning algorithm was converted to a user-friendly web tool for patients and clinicians. CONCLUSION: XGBOOST can predict the risk of lymph node metastasis with best accuracy in patients with early gastric cancer. Our online web application may help determine the optimal best surgical option for patients with early gastric cancer.

Clinical observation of pulmonary lymphoepithelioma-like carcinoma.

BACKGROUND: Lymphoepithelioma-like carcinoma (LELC) of the lung is a rare type of non-small cell lung cancer (NSCLC), and researches of it are still not enough. METHODS: In this study, we retrospectively analyzed 36 patients with LELC diagnosed in the Fifth Affiliated Hospital of Sun Yat-sen University and Zhaoqing First People's Hospital from January 2014 to June 2021, to investigate the clinical manifestations, tumor markers, treatment, and prognosis of LELC. Clinical data including age, gender, smoking history, family history of cancers, Epstein-Barr virus (EBV) encoding RNA (EBER) status, gene mutations, programmed death-ligand 1 (PD-L1) expression, treatment, and prognosis. RESULTS: There was a total of 36 participants in this study, 16 males and 20 females, the median age was 57 years (37-76 years). A total of 22 cases (61.1%) were advanced (stage III and IV), and EBER was 94.4% positive. Most patients were treated with surgery, platinum chemotherapy, or radiotherapy. At the time of 31 June 2021, 33 participants had survived, and the longest survival time was 72 months. Lung LELC was more common in old participants (≥59 years) and was not associated with smoking history. Expression of PD-L1 was positive in the majority (27 cases, 75%) and participants with positive PD-L1 expression tended to have longer progression-free survival (PFS) and overall survival (OS) time than those with negative PD-L1 expression. CONCLUSIONS: Pulmonary LELC usually occurs in non-smoking patients and is associated with EBV infection. Common treatments for tumors include multimodal therapy. The expression of PD-1 may be related to the prognosis of LELC, but more studies are needed to support further optimization of the treatment of LELC.

Transcription factor CDX2 up-regulates proto-oncogenic miR-744 via a promoter activation mechanism in non-small-cell lung cancer.

BACKGROUND: The role of caudal-related homeobox 2 (CDX2) in the pathogenesis of non-small cell lung cancer (NSCLC) is unclear. The purpose of this study was to investigate the mRNA (message RNA) expression of CDX2 in NSCLC, and to determine its relationship with miR-744 (microRNA744) and its potential as a biomarker of NSCLC. METHODS: MiR-744 is overexpressed in A549, H460, and H1299 cell lines. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression. A chromatin immunoprecipitation (ChIP) essay was performed to determine the CDX2 binding sites. We then conducted a luciferase reporter essay to analyze interaction between MiR-744 and 3'UTRs (the 3' untranslated sequences). The migration and Boyden chamber method were used to study cell mobility. RESULTS: In this study, we found that ectopic CDX2 increased the expression of miR-744, while the attenuation of CDX2 reduced the expression of miR-744 by qRT-PCR. Chromatin immunoprecipitation experiments confirmed that CDX2 directly binds to the promoter of miR-744. The luciferase reporter assay further verified the binding sites of -347 to -358 bp in the most likely promoter like sequence of miR-744. CDX2-induced up-regulation of miR-744 can significantly promote the migration and invasion of NSCLC cells, while overexpression CDX2 is sufficient to rescue the migration and invasion capacity of these cells following knockdown of miR-744. CONCLUSIONS: In summary, our results confirmed for the first time the regulatory mechanism of CDX2 on miR-744 transcription and provided a potential mechanism for CDX2 as an oncogene in lung cancer.

Treatment Patterns and Survival of Patients With Advanced Non-Small Cell Lung Cancer Guided by Comprehensive Genomic Profiling: Real-World Single-Institute Study in China.

Although the National Comprehensive Cancer Network and the Chinese Society of Clinical Oncology guidelines recommend comprehensive genomic profiling of lung adenocarcinoma, it has not been widely applied in Chinese hospitals. This observational study aimed to determine real-world evidence of whether comprehensive genomic profiling can benefit the survival of patients with lung cancer. We investigated the frequency of genomic alterations, treatment strategies, and clinical outcomes in 233 patients with advanced non-small cell lung carcinoma who were routinely screened using a 508-gene panel. The most prevalent drivers were mutations of EGFR (51%), KRAS (9%), PIK3CA (7%), ALK (7%), MET (6%), and BRAF (5%). Mutations in tumor suppressor genes included TP53, KEAP1, RB1, PTEN, and APC. Median overall survival (OS) was significantly shorter among patients harboring KRAS (mutant, n = 17; WT, n = 154) and TP53 (mutant, n = 103; WT n =68) mutations (11.3 vs. 24.0 months; P = 0.16 and 18.7 vs. 28.7 months; P = 0.018, respectively). The OS was longer among patients with tumors harboring EGFR (P = 0.069) and ALK (P = 0.51) mutations. Most patients (65.4%) with the driver gene-positive (EGFR, ALK, and ROS1) tumors were received TKI treatment, whereas those with driver gene wild tumors (53.1%) chose platinum-based therapy. Univariate and multivariate analyses associated a shorter OS among patients with tumors harboring concomitant TP53 and EGFR mutations. These findings provide additional evidence from real-world on the potential importance of targeted therapies as a treatment option in NSCLC patients harboring clinically actionable mutation.

lncRNA GABPB1 intronic transcript 1 upregulates pigment epithelium-derived factor via miR-93 to suppress cell proliferation in hepatocellular carcinoma.

Liver cancer ranks in the top 10 most common malignancies for both mortality rate and incidence worldwide. Hepatocellular carcinoma (HCC) is the most common subtype of liver cancer. It has been reported that long non-coding RNA GABPB1 intronic transcript 1 (IT1) is downregulated in lung cancer and predicts poor survival. However, its role in live cancer remains unclear. Therefore, the present study aimed to investigate the role of GABPB1-IT1 in HCC. A total of 64 patients with HCC (40 males and 24 females; range, 43-67 years old; mean age=55.1±5.1 years) were enrolled at the 96604 Military Hospital of the Chinese People's Liberation Army between May 2012 and May 2014. The expression levels of GABPB1-IT1 and microRNA (miR)-93 in tumor and adjacent normal tissues were measured using quantitative PCR. A dual luciferase activity assay was performed to analyze the interaction between miR-93 and GABPB1-IT1. A Cell Counting Kit-8 assay was used to analyze the effect of miR transfection on the proliferation of SNU-398 cells. It was demonstrated that GABPB1-IT1 can interact with miR-93 in HCC cells, while overexpression of GABPB1-IT1 and miR-93 in HCC cells did not affect the expression of each other. GABPB1-IT1 was downregulated in HCC tissues compared with paired non-tumor tissues and predicted poor survival. Notably, overexpression of GABPB1-IT1 in HCC cells led to upregulation of pigment epithelium-derived factor (PEDF), a target of miR-93. In addition, overexpression of GABPB1-IT1 reduced the enhancing effects of miR-93 on HCC cell proliferation. Therefore, GABPB1-IT1 may upregulate PEDF through miR-93 to suppress cell proliferation in HCC.

Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial­to­mesenchymal transition through the Wnt/ß­catenin pathway.

Mounting evidence indicates that there exists an association between heparanase (HPSE) and several physiological and pathological mechanisms in humans. However, the dynamics of the mechanisms involved in the regulation of HPSE expression in pancreatic cancer (PC) remain unclear. The aim of the present study was to assess the levels of HPSE in PC tissues and cell lines by western blotting and reverse transcription­quantitative PCR (RT­qPCR) analysis. Wound healing and Transwell assays were conducted to examine the effects of HPSE on migration and invasion in sh­NC and sh­HPSE PC cell lines. In addition, tumor growth was assessed in a mouse xenograft model in vivo. The expression levels of epithelial­to­mesenchymal transition (EMT)­related biomarkers and the involvement of the Wnt/ß­catenin pathway were assessed by analyzing the results of western blot and RT­qPCR assays. The results indicated that the expression of HPSE was substantially higher in PC tissues and cell lines, whereas experimental knockdown of HPSE suppressed the rates of migration and invasion of PC cells. Western blotting was used to assess the expression of EMT biomarkers and determine the function of HPSE in EMT. Furthermore, our results indicated that downregulation of HPSE expression decreased the expression of Wnt/ß­catenin associated proteins. In conclusion, HPSE appears to be a good candidate as a molecular target for the treatment of PC based on the finding of the present study.

Upregulation of DUSP14 Affects Proliferation, Invasion and Metastasis, Potentially via Epithelial-Mesenchymal Transition and Is Associated with Poor Prognosis in Pancreatic Cancer.

BACKGROUND: There is a growing number of evidence which report the relationship of the dual-specificity phosphatases 14 (DUSP14) with physiological and pathological mechanisms in the human body. However, it is still not known what if any role DUSP14 plays in pancreatic cancer. MATERIALS AND METHODS: The study evaluates the levels of DUSP14 in the pancreatic cancer tissues and cell lines using Western blotting and qRT-PCR to assess the levels of the DUSP14 and epithelial-mesenchymal transition (EMT) biomarkers. After the DUSP14 was blocked, the following assays were performed: colony formation, assessments of scratch wound and transwell to examine the effects of DUSP14 on the proliferation, migration and invasion of the pancreatic cancer. RESULTS: Results showed that there was a significant increase in the level of DUSP14 expression both in the pancreatic cancer tissues and cell lines. Experimental downregulation of DUSP14 induced the inhibition of the capacity of proliferation, migration and invasion of the pancreatic cancer cells. Western blotting analyses showed changes in the levels of expression of the EMT biomarkers, which helped to determine the function of DUSP14 in EMT. CONCLUSION: In conclusion, we suggest that DUSP14 is a novel molecular target that can be used for the treatment of pancreatic cancer.

Tracking the important role of JUNB in hepatocellular carcinoma by single-cell sequencing analysis.

Hepatocellular carcinoma (HCC) is the most commonly diagnosed liver cancer, accounting for ~90% of all primary malignancy of the liver. Although various medical treatments have been used as systemic therapies, patient survival time may be extended by only a few months. Moreover, the underlying mechanisms of HCC development and progression remain poorly understood. In the present study, the single-cell transcriptome of one in vivo HCC tumor sample, two in vitro HCC cell lines and normal peripheral blood mononuclear cells were analysed in order to identify the potential mechanism underlying the development and progression of HCC. Interestingly, JunB proto-oncogene was identified to serve a role in the immune response and in development and progression of HCC, potentially contributing to the development of novel therapeutics for HCC patients.

Nanospace-confined preparation of uniform nitrogen-doped graphene quantum dots for highly selective fluorescence dual-function determination of Fe3+ and ascorbic acid.

N-Doped graphene quantum dots (N-GQDs) combine the advantages of N-doped carbon and quantum dot materials, displaying enhanced performance in electrocatalysis, drug delivery, sensing and so on. In this work, novel hydrotropic N-GQDs with controlled size are obtained for the first time via a nanospace-confined preparation strategy, in which HNO3 vapour serves as scissors for quickly cutting the N-doped carbon nanolayer in the confined nanospace of reusable mesoporous molecular sieves. The as-prepared N-GQDs exhibit a uniform lateral size of about 2.4 nm, high photostability and yellow fluorescence, which is strongly quenched upon addition of ferric ions due to the coordination between ferric ions and N/O-rich groups of the N-GQDs surface. Significantly, the fluorescence response to Fe3+ is linear in the 0.5 to 40 µM concentration range and the N-GQDs showed good selectivity and satisfying recovery for ferric ion detection in tap water. Noteworthily, the quenched fluorescence by Fe3+ can be recovered by adding ascorbic acid (AA), which efficiently destroyed the coordination between Fe3+ and N-GQDs. Based on this principle, the N-GQDs were used to successfully construct an AA sensor, exhibiting a wide linearity range (between 0.5 and 90 µM) with a low detection of limit (80 nM at S/N = 3) and better selectivity towards AA compared with other common physiological substances. Finally, the constructed fluorescence sensor was employed successfully for AA determination in fish blood with satisfactory recovery ranging from 95.3 to 106.2%. The results indicate that N-GQDs synthesized by the nanospace-confined strategy are promising in biosensor fabrication.

Long non-coding RNA CRNDE sponges miR-384 to promote proliferation and metastasis of pancreatic cancer cells through upregulating IRS1.

OBJECTIVE: Colorectal neoplasia differentially expressed (CRNDE), a vital cancer-related long non-coding RNA (lncRNA), has been brought to reports for playing quintessential functions in the growth and progression of several human malignancies. Nevertheless, the expression as well as the functional mechanisms of CRNDE in pancreatic cancer is not known so for. This study aimed at investigating the biological and clinical importance of CRNDE in human pancreatic cancer. MATERIALS AND METHODS: The expression levels of CRNDE in pancreatic cancer tissues as well as cell lines were identified with the help of quantitative real-time PCR (qRT-PCR). Furthermore, the analysis of the relationship between CRNDE expression and clinicopathologic characteristics of patients with pancreatic cancer was also performed. Novel target of CRNDE was identified with the use of bioinformatics analysis and confirmed by a dual-luciferase reporter assay. Colorectal neoplasia differentially expressed was knocked down using siRNA in pancreatic cancer cells. Thereafter, cell proliferation, migration and invasion were examined. Tumour xenograft was created to explore the function of CRNDE in tumorigenesis in vivo. RESULTS: Upregulation of the expression of CRNDE was found in pancreatic cancer tissues as well as cell lines, in comparison with the adjacent non-tumour tissues and human pancreatic duct epithelial cells. High expression of CRNDE was correlated with poor clinicpathological characteristics and shorter overall survival. We identified miR-384 as a direct target for CRNDE. Moreover, the CRNDE knockdown considerably inhibited pancreatic cancer cell proliferation, migration and invasion not only in vitro but also in vivo. In addition, CRNDE positively regulated IRS1 expression through sponging miR-384. CONCLUSIONS: Colorectal neoplasia differentially expressed performed an oncogenic function in cell proliferation as well as metastasis of pancreatic cancer. Our results suggest that CRNDE is likely to serve as an efficient therapeutic approach in respect of pancreatic cancer treatment.

Latent Transforming Growth Factor ß Binding Protein 2 (LTBP2) as a Novel Biomarker for the Diagnosis and Prognosis of Pancreatic Carcinoma.

BACKGROUND Latent transforming growth factor b binding protein 2 (LTBP2) is proven to be associated with ECM and involved in the advancement of several kinds of cancer. The present study evaluated the diagnosis and prognosis of pancreatic carcinoma (PC) using LTBP2 as a biomarker. MATERIAL AND METHODS Protein levels of LTBP2 were evaluated in 111 pairs of pancreatic ductal adenocarcinoma (PDAC) tissues and adjacent nontumor tissues via immunohistochemistry. ELISA method was used to quantify the serum concentration of LTBP2. The subjects in this study included 141 PDAC patients, 20 patients with benign pancreatic disease, and 20 healthy volunteers. RESULTS IHC results showed that LTBP2 levels were significantly elevated in the PDAC tissues as compared with the adjacent nontumor tissues (P<0.05). Sixty-one of the 111 (54.9%) PDAC tissues showed high expression of the protein. LTBP2 overexpression was significantly correlated with poor differentiation (P=0.018) and advanced TNM stage (P=0.036). Moreover, Kaplan-Meier analysis showed that high levels of LTBP2 predicted worse overall survival (P=0.001) and disease-free survival (P=0.001). Multivariate Cox regression analysis indicated that high expression of LTBP2 was an autonomous prognostic factor for poor overall and disease-free survival (P=0.001; P=0.002). Receiver operating characteristic (ROC) curve analyses of showed that LTBP-2 had an area under the curve (AUC) of 0.846 (95% confidence intervals: 0.757-0.934) and cut-off value of 19.12. CONCLUSIONS LTBP2 is a novel biomarker for the diagnosis of PC and may be a potential target for PDAC clinical therapy.