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Abstract Video Anomaly Detection (VAD) has been an active research field for several decades. However, most existing approaches merely extract a single type of feature from videos and define a single paradigm to indicate the extent of abnormalities. A coarse‐to‐fine three‐level prediction is built by integrating different levels of spatio‐temporal representations, better highlighting the difference between normal and abnormal behaviors. First, an object‐level trajectory prediction is proposed to model human historical position using a graph transformer network. Subsequently, skeleton‐level prediction is achieved by incorporating the positional information from the trajectory prediction. More importantly, based on the predicted skeleton, a skeleton‐guided pixel‐level region prediction is performed. A novel Skeleton Conditioned Generative Adversarial Network (SCGAN) is designed to explore the correlation between skeleton‐level and pixel‐level motion prediction. Benefiting from SCGAN, the prediction of human regions is contributed by both coarse‐grained and fine‐grained motion features. This three‐level prediction, namely Progressive Prediction Video Anomaly Detection (P3VAD), enlarges the prediction error on irregular motion patterns. Besides, a pixel‐level analysis method is proposed to achieve Background‐bias Elimination (BE) and denoise the predicted region. Experimental results validate the effectiveness of P3VAD on the four benchmark datasets (ShanghaiTech, CUHK Avenue, IITB‐Corridor, and ADOC).

Abstract Considerable progress has been made in the development of drug delivery systems for diabetic wounds. However, underlying drawbacks, such as low delivery efficiency and poor tissue permeability, have rarely been addressed. In this study, a multifunctional biohybrid nanorobot platform comprising an artificial unit and several biological components is constructed. The artificial unit is a magnetically driven nanorobot surface modified with antibacterial 2‐hydroxypropyltrimethyl ammonium chloride chitosan, which enables the entire platform to move and has excellent tissue penetration capacity. The biological components are two‐step engineered extracellular vesicles that are first loaded with mangiferin, a natural polyphenolic compound with antioxidant properties, and then glycoengineered on the surface to enhance cellular uptake efficiency. As expected, the platform is more easily absorbed by endothelial cells and fibroblasts and exhibits outstanding dermal penetration performance and antioxidant properties. Encouraging results are also observed in infected diabetic wound models, showing improved wound re‐epithelialization, collagen deposition, angiogenesis, and accelerated wound healing. Collectively, a biohybrid nanorobot platform that possesses the functionalities of both artificial units and biological components serves as an efficient delivery system to promote diabetic wound repair through dual‐enhanced cell and tissue penetration and multistep interventions.

Abstract Background The current study aims to explore the relationship between tumor necrosis factor‐α (TNF‐α) polymorphism and the risk of primary nephrotic syndrome (PNS). Methods A total of 250 PNS patients were selected for this study, as well as 300 volunteers serving as the control group. TNF‐α polymorphism were assessed using the polymerase chain reaction‐restriction fragment length polymorphism method. In addition, a meta‐analysis was conducted to analyze previously published literature on this topic. Results No significant differences were observed in the genotypes frequency or alleles frequency among the study populations. Meta‐analysis results revealed a positive association between TNF‐α rs1800629 polymorphism and allele contrast in African populations (p = 0), homozygote comparison (p = .007), heterozygote comparison (p = .026), recessive genetic model (p = .011), and dominant genetic model (p = .000). Conclusions TNF‐α rs1800629 polymorphism does not appear to confer any increased risk for PNS.

Abstract Resistance training could counter hypertension and improve muscle quality (MQ), but current evidence about the correlation between MQ and hypertension is limited. The authors aimed to explore this correlation using the data of participants aged 20–59 from NHANES 2011–2014 via a cross‐sectional study. The MQ was quantified as handgrip strength (kg)/lean soft tissue mass (kg) of the dominant arm. Weighted multivariate logistic regression models were mainly utilized to investigate the MQ—hypertension association; linear trend tests and subgroup analysis were also conducted. Moreover, the authors employed weighted multivariate linear regression models to uncover the association between blood pressure (BP) and MQ. Four thousand four hundred and sixty‐nine individuals were enrolled, and 1167 were hypertensive. Hypertensive participants had a lower MQ than normotensive participants. In the totally adjusted model, each unit elevation in MQ was related to a 7% reduction in hypertension prevalence (p =.002). There was a decreasing trend in hypertension prevalence and in systolic BP as the MQ increased from the bottom to the top quartile across all three models (p for trend ≤.01), with a 28% difference (OR: 0.72, 95% CI: 0.54, 0.95) in hypertension prevalence and a 1.88 mm Hg (95% CI: −3.56, −0.20) difference in SBP between the top and bottom quartiles in the fully adjusted model. Subgroup analysis further confirmed the MQ—hypertension inverse association. In conclusions, the MQ was negatively associated with hypertension prevalence and systolic BP, which suggests the MQ may be a protective factor for hypertension and need to be improved.

Abstract Mitochondrial dysfunction alters cellular metabolism, increases tissue oxidative stress, and may be principal to the dysregulated signaling and function of CD4+ T lymphocytes in the elderly. In this proof of principle study, it is investigated whether the transfer of functional mitochondria into CD4+ T cells that are isolated from old mice (aged CD4+ T cells), can abrogate aging‐associated mitochondrial dysfunction, and improve the aged CD4+ T cell functionality. The results show that the delivery of exogenous mitochondria to aged non‐activated CD4+ T cells led to significant mitochondrial proteome alterations highlighted by improved aerobic metabolism and decreased cellular mitoROS. Additionally, mito‐transferred aged CD4+ T cells showed improvements in activation‐induced TCR‐signaling kinetics displaying markers of activation (CD25), increased IL‐2 production, enhanced proliferation ex vivo. Importantly, immune deficient mouse models (RAG‐KO) showed that adoptive transfer of mito‐transferred naive aged CD4+ T cells, protected recipient mice from influenza A and Mycobacterium tuberculosis infections. These findings support mitochondria as targets of therapeutic intervention in aging.

Abstract Studies show that birds cognize human disturbance as a potential predation risk. However, the responses of breeding birds to long‐term continuous disturbance by research activities and whether researcher disturbance affects the fitness of target species remain poorly understood. In this study, we used field observation data collected over 6 years to assess the potential impacts of research activities on nest‐site selection and nest success of the Emei Shan Liocichla (Liocichla omeiensis), a vulnerable babbler species endemic to Southwest China. Our results showed that Emei Shan Liocichlas tended to nest in taller nesting plants or the higher parts of nesting plants to increase nest‐site height following researcher disturbance. The average height of Emei Shan Liocichla nests increased by 52.2% over the 6‐year study period, from 129.8 ± 9.2 cm in 2009 (n = 11) to 197.5 ± 12.1 cm in 2015 (n = 18). While some pairs adopted a different strategy, placing their nests in Rosaceae plants with thorns instead of the bamboo Chimonobambusa szechuanensis (the favored nesting plant of the Emei Shan Liocichla) under high interference pressure, which made it more difficult for researchers to approach their nests. There were no significant differences both in clutch size and nest success between the low‐ and high‐disturbance groups. The study revealed the behavioral response pattern of breeding Emei Shan Liocichlas to researcher disturbance, which will contribute to conservation of this threatened songbird and the knowledge of reproductive strategies of birds. Developing specific guidelines for fieldwork and strengthening visitor management within its core habitat of Emei Shan Liocichla during breeding period should be considered.

Background The association between sodium‐glucose cotransporter 2 inhibitors (SGLT2i) and atrial fibrillation (AF) recurrence after catheter ablation among patients with diabetes and AF remains unclear. Methods and Results Patients with AF undergoing initial catheter ablation with a history of diabetes from the China AF registry were included. Patients using SGLT2i were identified and matched by propensity score with non‐SGLT2i patients in a 1:3 ratio. The main outcome was AF recurrence during the 18‐month follow‐up. A total of 138 patients with diabetes with SGLT2i therapy and 387 without SGLT2i were analyzed. AF recurrence occurred in 37 patients (26.8%) in the SGLT2i group and 152 patients (39.3%) in the non‐SGLT2i group during a total of 593.3 person‐years follow‐up. The SGLT2i group was associated with lower AF recurrence compared with the non‐SGLT2i group (hazard ratio, 0.63 [95% CI, 0.44–0.90], P=0.007). A total of 4 studies were analyzed in our meta‐analysis demonstrating that SGLT2i was associated with lower AF recurrence after catheter ablation (odds ratio, 0.61 [95% CI, 0.54–0.69]; P

Background The knowledge gap regarding whether the correlation between atrial fibrillation (AF) and dementia in observational studies is causation or driven by other shared risk factors remains substantially unfilled. Methods and Results We performed a comprehensive 2‐sample Mendelian randomization study to evaluate the causal effect of AF on overall dementia and its subtypes, including vascular dementia, Alzheimer dementia, Lewy body dementia, and frontotemporal dementia. The primary results in inverse variance–weighted analyses were further validated by various Mendelian randomization sensitivity analyses. Additionally, we conducted multivariable Mendelian randomization to examine 10 candidate mediators of the causal association of AF and dementia. Genetic predisposition to AF was modestly associated with an increased risk of overall dementia (odds ratio, 1.140 [95% CI, 1.023–1.271]; P=0.018) and strongly associated with vascular dementia (odds ratio, 1.350 [95% CI, 1.076–1.695]; P=0.010). Genetically predicted AF indicated neutral effects on Alzheimer dementia, Lewy body dementia, and frontotemporal dementia. In multivariable Mendelian randomization analysis, the total effect of AF on overall dementia was remarkably attenuated by adjusting for genetic effect for ischemic stroke (odds ratio, 1.068 [95% CI, 0.953–1.197]; P=0.259) and low cardiac output (odds ratio, 1.046 [95% CI, 0.926–1.181]; P=0.475), indicating that the causal association of genetically predicted AF with dementia was potentially mediated by ischemic stroke and low cardiac output. The causal effect of genetically predicted AF on dementia was independent of cerebral small‐vessel disease and brain volume phenotypes. Conclusions Our findings provided novel evidence supporting the causal effect of genetically predicted AF on dementia mediated by ischemic stroke and low cardiac output. Future clinical trials are warranted to evaluate the potential role of appropriate AF management in dementia prevention.

Abstract Tendon‐to‐bone interface has a hierarchical structure and gradient component that are conducive to distributing the stresses to achieve movement. Conventional biomaterials lack the capacity to induce synchronous repair of multiple tissues, resulting in the failure of the interface repair. Biomimetic strategies have attracted enormous attention in the field of complex structure regeneration because they can meet the different physiological requirements of multiple tissues. Herein, a biomimetic ink mimicking tendon/bone tissues is developed by combining tendon/bone‐related cells and Mo‐containing silicate (MS) bioceramics. Subsequently, biomimetic multicellular scaffolds are fabricated to achieve the simulation of the hierarchical structure and cellular composition of tendon‐to‐bone interfaces by the spatial distribution of the biomimetic inks via 3D bioprinting, which is of great significance for inducing the regeneration of complex structures in the interface region. In addition, attributed to the desirable ionic microenvironment created by MS bioceramics, the biomimetic scaffolds possess the dual function of inducing tendon/bone‐related cells tenogenic and osteogenic differentiation in vitro, and promote the integrated regeneration of tendon‐to‐bone interfaces in vivo. The study offers a feasible strategy to construct biomimetic multicellular scaffolds with bifunction for inducing multi‐lineage tissue regeneration, especially for regenerating soft‐to‐hard tissue interfaces.

Abstract Osteoarthritis (OA) is a degenerative disease that often causes cartilage lesions and even osteochondral damage. Osteochondral defects induced by OA are accompanied by an inflammatory arthrosis microenvironment with overproduced reactive oxygen species (ROS), resulting in the exacerbation of defects and difficulty regenerating osteochondral tissues. Therefore, it is urgently needed to develop osteochondral scaffolds that can not only promote the integrated regeneration of cartilage and subchondral bone, but also possess ROS‐scavenging ability to protect tissues from oxidative stress. Herein, zinc‐cobalt bimetallic organic framework (Zn/Co‐MOF) functionalized bioceramic scaffolds are designed for repairing osteochondral defects under OA environment. By functionalizing Zn/Co‐MOF on the 3D‐printed beta‐tricalcium phosphate (β‐TCP) scaffolds, the Zn/Co‐MOF functionalized β‐TCP (MOF‐TCP) scaffolds with broad‐spectrum ROS‐scavenging ability are successfully developed. Benefiting from its catalytic active sites and degradation products, Zn/Co‐MOF endows the scaffolds with excellent antioxidative and anti‐inflammatory properties to protect cells from ROS invasion, as well as dual‐bioactivities of simultaneously inducing osteogenic and chondrogenic differentiation in vitro. Furthermore, in vivo results confirm that MOF‐TCP scaffolds accelerate the integrated regeneration of cartilage and subchondral bone in severe osteochondral defects. This study offers a promising strategy for treating defects induced by OA as well as other inflammatory diseases.

Abstract The conventional selective harmonic elimination method of random pulse width modulation (RPWM) is only suitable for the two‐level inverter. Furthermore, when the harmonics below 6 kHz are selectively eliminated, it is easy to cause a low average switching frequency of the inverter, which leads to the increase of load current distortion rate. This paper proposes an RPWM selective voltage harmonic elimination method for a single‐phase five‐level MPUC (modified packed U‐cells) inverter based on cell division. The MPUC inverter is supposed to be divided into three series cells, and the carrier stacking strategy is used to realize the coordinated control between each cell. In the process of RPWM, the average switching frequency can be controlled within a certain range by selecting the random number. This method is divided into normal mode and master–slave mode. In the normal mode, the selective harmonic elimination is realized by the method of cancelling the front and back terms of Fourier series in each cell. In the master–slave mode, the master cell is mainly used for fundamental power output, and the slave cell is mainly used for RPWM selective harmonic elimination. The effectiveness of the proposed method is verified by the simulation and experimental results.

Abstract Conductive polymer hydrogels are attractive due to their combination of high theoretical capacitance, intrinsic electrical conductivity, fast ion transport, and high flexibility for supercapacitor electrodes. However, it is challenging to integrate conductive polymer hydrogels into an all‐in‐one supercapacitor (A‐SC) simultaneously with large stretchability and superior energy density. Here, a self‐wrinkled polyaniline (PANI)‐based composite hydrogel (SPCH) with an electrolytic hydrogel and a PANI composite hydrogel as the core and sheath, respectively, was prepared through a stretching/cryopolymerization/releasing strategy. The self‐wrinkled PANI‐based hydrogel exhibited large stretchability (∼970%) and high fatigue resistance (∼100% retention of tensile strength after 1200 cycles at a 200% strain) ascribing to the formation of the self‐wrinkled surfaces and the intrinsic stretchability of hydrogels. Upon cutting off the edge connections, the SPCH could directly work as an intrinsically stretchable A‐SC maintaining high energy density (70 µW h cm−2) and stable electrochemical outputs under a stretchability of 500% strain and a full‐scale bending of 180°. After 1000 cycles of 100% strain stretching and releasing processes, the A‐SC device could deliver highly stable outputs with high capacitance retention of 92%. This study might provide a straightforward method for fabricating self‐wrinkled conductive polymer‐based hydrogels for A‐SCs with highly deformation‐tolerant energy storage.

Abstract Natural tissues are composed of ordered architectural organizations of multiple tissue cells. The spatial distribution of cells is crucial for directing cellular behavior and maintaining tissue homeostasis and function. Herein, an artificial bone bioceramic scaffold with star‐, Tai Chi‐, or interlacing‐shaped multicellular patterns is constructed. The “cross‐talk” between mesenchymal stem cells (MSCs) and macrophages can be effectively manipulated by altering the spatial distribution of two kinds of cells in the scaffolds, thus achieving controllable modulation of the scaffold‐mediated osteo‐immune responses. Compared with other multicellular patterns, the Tai Chi pattern with a 2:1 ratio of MSCs to macrophages is more effective in activating anti‐inflammatory M2 macrophages, improving MSCs osteogenic differentiation, and accelerating new bone formation in vivo. In brief, the Tai Chi pattern generates a more favorable osteo‐immune environment for bone regeneration, exhibiting enhanced immunomodulation and osteogenesis, which may be associated with the activation of BMP‐Smad, Oncostatin M (OSM), and Wnt/β‐catenin signaling pathways in MSCs mediated by macrophage‐derived paracrine signaling mediators. The study suggests that the manipulation of cell distribution to improve tissue formation is a feasible approach that can offer new insights for the design of tissue‐engineered bone substitutes with multicellular interactions.

Abstract Electrocardiogram is a powerful tool for differentiating acute ST‐segment elevation myocardial infarction (STEMI) and pericarditis. However, an unusual ECG presentation of the simultaneous occurrence of the two conditions has not been reported previously. In this article, we report a case of ECG evolution of acute anterior STEMI following pericarditis with pericardial effusion (PE) and find that QRS complex widening in ECG lead with maximal ST‐segment elevation is also applicable for identifying STEMI even in patients with prior pericarditis. Undoubtedly, our case can help prevent emergency physicians from making incorrect diagnoses and administering inappropriate treatments.

Background. Adiponectin is a recognized antiatherogenic molecule; this study was aimed at clarifying the effects of adiponectin variants on lipid and adiponectin levels. Methods. By searching PubMed and Cochrane databases for studies published before March 31, 2022, a total of 86,610 individuals were included in the analysis. Results. Variants of rs2241766 and rs266729 were associated with decreased adiponectin and high-density lipoprotein cholesterol (HDL-C), as well as increased triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels. In contrast, the rs1501299 variant was correlated with increased adiponectin and HDL-C, as well as decreased TG, TC, and LDL-C levels. Subgroup analysis indicated that the significant effect of the rs2241766 and rs266729 variants on lipid profile was predominant in Chinese, while the significant effect of the rs1501299 variant on lipid profile was primarily in Caucasians. Moreover, a stronger effect of the rs2241766 and rs1501299 variants on LDL-C levels was observed in males, while a considerable effect of the rs266729 variant on LDL-C levels was observed in children. Conclusions. The present study indicated that Chinese with the rs2241766 and rs266729 variants were at high risk of dyslipidemia, atherosclerosis, or coronary artery disease (CAD). Males with the rs2241766 variant were at high risk of CAD. Children with the rs266729 variant had a high risk to develop dyslipidemia, atherosclerosis, and even early onset of CAD in the future. These findings are beneficial to clinical physicians to choose different management strategies for cardiovascular disease (CVD) prevention.

Abstract Background Hepatocellular carcinoma (HCC) is the fourth fatal malignant tumour type worldwide. However, the exact molecular mechanism involved in HCC progression remains unclear. Methods Three pairs of HCC and matched portal vein tumour thrombus (PVTT) tissue samples were analysed by isobaric tags for relative and absolute quantification (iTRAQ) assay to investigate the differentially expressed proteins. Real‐time quantitative PCR, immunostaining, and immunoblotting were performed to detect cofilin 1 (CFL1) in HCC and non‐tumour tissues. CCK8 and EdU, and Transwell assays, respectively, determined cell proliferation, migration, and invasion of HCC cells. Further, subcutaneous and tail vein injection were performed in nude mice for investigating HCC growth and lung metastasis in vivo. Regulatory effect of hypoxia‐inducible factor‐1α (HIF‐1α) on CFL1 was confirmed by chromatin immunoprecipitation (ChIP) assay. Finally, interaction between CFL1 and phospholipase D1 (PLD1) was studied using immunoprecipitation (IP) assay. Results The iTRAQ analysis identified expression of CFL1 to be significantly upregulated in PVTT than in HCC tissues. Increased expression of CFL1 was closely associated with unfavourable clinical features, and was an independent risk predictor of overall survival in HCC patients. The knockdown of CFL1 inhibited cell growth viability, invasiveness, and epithelial‐mesenchymal transformation (EMT) in HCC cells. Furthermore, CFL1 silencing significantly suppressed the growth and lung metastasis of HCC cells in nude mice. Next, HIF‐1α directly regulated CFL1 transcription by binding to the hypoxia‐responsive element (HRE) in the promoter. Moreover, we disclosed the interaction between CFL1 and PLD1 in HCC cells using IP assay. Mechanistically, CFL1 maintained PLD1 expression by repressing ubiquitin‐mediated protein degradation, thereby activating AKT signalling in HCC cells. Notably, the CFL1/PLD1 axis was found mediating the hypoxia‐induced activation of the AKT pathway and EMT. Conclusion The analysis suggests that hypoxia‐induced CFL1 increases the proliferation, migration, invasion, and EMT in HCC by activating the PLD1/AKT pathway.

Abstract Objective Deductive reasoning is a complex and poorly understood concept in the field of psychology. Many cognitive neuroscience studies have been published on deductive reasoning but have yielded inconsistent findings. Methods In this study, we analyzed collected data from 38 articles using a recently proposed activation likelihood estimation (ALE) approach and used conjunction analysis to better determine the intersection of the results of meta‐analyses. Results First, the left hemispheres in the inferior parietal lobule (Brodmann area 40 [BA40]), middle frontal gyrus (BA6), medial frontal gyrus (BA8), inferior frontal gyrus (BA45/46), caudate, and insula (BA47) were revealed to be significant brain regions via simple‐effect analysis (deductive reasoning versus baseline). Furthermore, IFG, insula, and cingulate (the key neural hubs of the cingulo‐opercular network) were highlighted in overlapped functional connectivity maps. Conclusion The findings of the current study are consistent with the view that deductive reasoning requires a succession of stages, which included decoding of linguistic information, conversion and correction of rules, and transformation of inferential results into conclusive outputs, all of which are putatively processed via a distributed network of brain regions encompassing frontal/parietal cortices, as well as the caudate and other subcortical structures, which suggested that in the process of deductive reasoning, the coding and integration of premise information is indispensable, and it is also crucial to the execution and monitoring of the cognitive processing of reasoning.

In this paper, we consider two kinds of time-delay slow-fast modified Leslie-Gower models. For the first system, we prove the existence and uniqueness of relaxation oscillation cycle through the geometric singular perturbation theory and entry-exit function. For the second system, we put forward a conjecture that the relaxation oscillation of the system is unique. Numerical simulation also verifies our results for the systems.

Lymphocyte‐specific protein 1 (LSP1) has been reported to regulate cell biology in several human cancers including lymphoma and breast cancer. However, the functions of LSP1 in human hepatocellular carcinoma (HCC) are still unknown. In this study, we found that LSP1 expression was downregulated in HCC tissues and cell lines, and lower LSP1 expression was correlated with poor clinicopathological features including large tumor size, high Edmondson–Steiner grading and advanced tumor–node–metastasis (TNM) stage. Additionally, we demonstrated that patients with high LSP1 expression had significantly better overall survival and disease‐free survival. Moreover, LSP1 was found to be an independent factor for predicting the prognosis of HCC patients. In vitro and in vivo assays showed that overexpressing LSP1 inhibited HCC growth by inducing both apoptosis and growth arrest. Mechanistically, we found that expression of phosphorylated extracellular regulated protein kinases 1 and 2 (ERK1/2) was downregulated after LSP1 overexpression, indicating LSP1 could suppress HCC growth by inhibiting the ERK pathway in HCC cells. Taken together, these results indicate that LSP1 may serve as a prognostic marker and a potential therapeutic target in human HCC.

BackgroundStructural remodeling of human atria plays a key role in sustaining atrial fibrillation (AF), but insufficient quantitative analysis of human atrial structure impedes the treatment of AF. We aimed to develop a novel 3‐dimensional (3D) structural and computational simulation analysis tool that could reveal the structural contributors to human reentrant AF drivers. Methods and ResultsHigh‐resolution panoramic epicardial optical mapping of the coronary‐perfused explanted intact human atria (63‐year‐old woman, chronic hypertension, heart weight 608 g) was conducted during sinus rhythm and sustained AF maintained by spatially stable reentrant AF drivers in the left and right atrium. The whole atria (107×61×85 mm3) were then imaged with contrast‐enhancement MRI (9.4 T, 180×180×360‐μm3 resolution). The entire 3D human atria were analyzed for wall thickness (0.4–11.7 mm), myofiber orientations, and transmural fibrosis (36.9% subendocardium; 14.2% midwall; 3.4% subepicardium). The 3D computational analysis revealed that a specific combination of wall thickness and fibrosis ranges were primarily present in the optically defined AF driver regions versus nondriver tissue. Finally, a 3D human heart–specific atrial computer model was developed by integrating 3D structural and functional mapping data to test AF induction, maintenance, and ablation strategies. This 3D model reproduced the optically defined reentrant AF drivers, which were uninducible when fibrosis and myofiber anisotropy were removed from the model. ConclusionsOur novel 3D computational high‐resolution framework may be used to quantitatively analyze structural substrates, such as wall thickness, myofiber orientation, and fibrosis, underlying localized AF drivers, and aid the development of new patient‐specific treatments.

Aim. To detect the expression of dual oxidase (DUOX) 2 in Barrett esophagus, gastric cancer, and colorectal cancer (CRC). Materials and Methods. The endoscopic biopsies were collected from patients with Barrett esophagus, while the curative resection tissues were obtained from patients with gastric cancer, CRC, or hepatic carcinoma. The DUOX2 protein and mRNA levels were detected with immunohistochemistry (IHC) and real-time quantitative PCR (qPCR). The correlation of DUOX2 expression with clinicopathological parameters of tumors was identified. Results. Low levels of DUOX2 mRNA were detected in Barrett esophagus and the adjacent normal tissues, and there was no difference between these two groups. DUOX2 protein was found in Barrett esophagus and undetectable in the normal epithelium. The DUOX2 mRNA and protein levels in the gastric cancer and CRC were increased compared to the adjacent nonmalignant tissues. The elevated DUOX2 in the gastric cancer was significantly associated with smoking history. In CRC tissues, the DUOX2 protein expression level in stages II–IV was significantly higher than that in stage I. In both hepatic carcinoma and the adjacent nonmalignant tissue, the DUOX2 was virtually undetectable. Conclusion. DUOX2 in Barrett esophagus, gastric cancer, and CRC may be involved in the tumorigenesis of these tissues.