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Abstract Mobile edge computing (MEC) has risen as an effective approach to support ubiquitous and prosperous mobile applications. Due to the strict delay requirements and the increasingly complex application environments, the computation efficiency and security have become the bottleneck that restricts the MEC system. Here, a blockchain‐enabled task offloading scheme is proposed, where the sensitive computation tasks of user terminals (UTs) can be offloaded to a blockchain‐assisted base station (BS). The MEC‐assisted BS helps UTs compute tasks while the blockchain consensus protocol ensures the security of the task offloading and computing process. To manage the allocation of computing resources between task offloading and blockchain consensus, the task offloading and resource allocation are formulated as a joint optimization problem. The aim of the problem is to minimize the energy consumption of UTs while guaranteeing the delay requirement. By transforming the original problem into a Markov decision process, a collective reinforcement learning algorithm is proposed to solve the problem in an online fashion. In the simulations, the convergence and the performance of the proposed scheme are evaluated. The simulation results show the effectiveness of the scheme.

Abstract Pyroptosis possesses potent antitumor immune activity, making pyroptosis inducer development a promising direction for tumor immunotherapy. Persistent luminescence nanoparticles (PLNPs) are highly sensitive optical probes extensively employed in tumor diagnosis and therapy. However, a pyroptosis inducer based on PLNPs has not been reported yet. Herein, polyethylene glycol–poly lactic acid‐co‐glycolic acid (PEG–PLGA: PP) modified biodegradable CaS:Eu2+ (CSE@PP) PLNPs are synthesized as a pyroptosis inducer for tumor immunotherapy for the first time. The synthesized CSE@PP possesses biowindow persistent luminescence (PersL) and pH‐responsive degradation properties, allowing it to remain stable under neutral pH but degrade when exposed to weak acid (pH < 6.5). During degradation within the tumor, CSE@PP constantly releases H2S and Ca2+ while its PersL gradually fades away. Thus, the PersL signal can self‐monitor H2S and Ca2+ release. Furthermore, the released H2S and Ca2+ result in mitochondrial dysfunction and the inactivation of reactive oxygen species scavenging enzymes, synergistic facilitating intracellular oxidative stress, which induces caspase‐1/GSDM‐D dependent pyroptosis and subsequent antitumor immune responses. In a word, it is confirmed that CSE@PP can self‐monitor H2S and Ca2+ release and pyroptosis‐mediated tumor Immunotherapy. This work will facilitate biomedical applications of PLNPs and inspire pyroptosis‐induced tumor immunotherapy.

Abstract Immunosuppression is a major hallmark of tumor progression in non‐small cell lung cancer (NSCLC). Cluster of differentiation 147 (CD147), an important pro‐tumorigenic factor, is closely linked to NSCLC immunosuppression. However, the role of CD147 di‐methylation in the immunosuppressive tumor microenvironment (TME) remains unclear. Here, di‐methylation of CD147 at Lys148 (CD147‐K148me2) is identified as a common post‐translational modification (PTM) in NSCLC that is significantly associated with unsatisfying survival outcomes among NSCLC sufferers, especially those in the advanced stages of the disease. The methyltransferase NSD2 catalyzes CD147 to generate CD147‐K148me2. Further analysis demonstrates that CD147‐K148me2 reestablishes the immunosuppressive TME and promotes NSCLC progression. Mechanistically, this modification promotes the interaction between cyclophilin A (CyPA) and CD147, and in turn, increases CCL5 gene transcription by activating p38‐ZBTB32 signaling, leading to increased NSCLC cell‐derived CCL5 secretion. Subsequently, CD147‐K148me2‐mediated CCL5 upregulation facilitates M2‐like tumor‐associated macrophage (TAM) infiltration in NSCLC tissues via CCL5/CCR5 axis‐dependent intercellular crosstalk between tumor cells and macrophages, which is inhibited by blocking CD147‐K148me2 with the targeted antibody 12C8. Overall, this study reveals the role of CD147‐K148me2‐driven intercellular crosstalk in the development of NSCLC immunosuppression, and provides a potential interventional strategy for PTM‐targeted NSCLC therapy.

Abstract The accuracy and reliability of circuit board fault detection are significantly influenced by the uncertainty inherent in the VI curve. Here, an ensemble neural network is proposed, which combines the neural network‐based prediction interval and ensemble approaches, to improve the accuracy of fault detection using the VI curve. First, a loss function with multiple objectives is formulated by integrating curve fitting and prediction interval. The aim is to achieve the curve fitting between current and voltage while simultaneously determining the optimal upper and lower bounds of the prediction interval. Second, an ensemble approach is employed to reduce model uncertainty and derive the ultimate current predictions and intervals. These predictions and intervals are then used in a comparative approach to automatically detect faults in circuit boards. Finally, the effectiveness of the proposed algorithm in improving the accuracy of fault detection is verified on experimental circuit boards.

Background. This research investigated whether glucose fluctuation (GF) can exacerbate cognitive impairment in streptozotocin-induced diabetic rats and explored the related mechanism. Methods. After 4 weeks of feeding with diets containing high fats plus sugar, the rat model of diabetes mellitus (DM) was established by intraperitoneal injection of streptozotocin (STZ). Then, GF was triggered by means of alternating satiety and starvation for 24 h. The weight, blood glucose level, and water intake of the rats were recorded. The Morris water maze (MWM) test was carried out to appraise the cognitive function at the end of week 12. Moreover, the morphological structure of hippocampal neurons was viewed through HE and Nissl staining, and transmission electron microscopy (TEM) was performed for ultrastructure observation. The protein expression levels of Nrf2, HO-1, NQO-1, Bax, Bcl-2, and Caspase-3 in the hippocampal tissues of rats were measured via Western blotting, and the mRNA expressions of Nrf2, HO-1, and NQO-1 were examined using qRT-PCR. Finally, Western blotting and immunohistochemistry were conducted to detect BDNF levels. Results. It was manifested that GF not only aggravated the impairment of spatial memory in rats with STZ-induced type 2 DM but also stimulated the loss, shrinkage, and apoptosis of hippocampal neurons. Regarding the expressions in murine hippocampal tissues, GF depressed Nrf2, HO-1, NQO-1, Bcl-2, and BDNF but boosted Caspase-3 and Bax. Conclusions. GF aggravates cognitive impairment by inhibiting the Nrf2 signaling pathway and inducing oxidative stress and apoptosis in the hippocampal tissues.

Abstract Stromal antigen 2 (STAG2), a subunit of the cohesin complex, is recurrently mutated in various tumors. However, the role of STAG2 in DNA repair and its therapeutic implications are largely unknown. Here it is reported that knockout of STAG2 results in increased double‐stranded breaks (DSBs) and chromosomal aberrations by reducing homologous recombination (HR) repair, and confers hypersensitivity to inhibitors of ataxia telangiectasia mutated (ATMi), Poly ADP Ribose Polymerase (PARPi), or the combination of both. Of note, the impaired HR by STAG2‐deficiency is mainly attributed to the restored expression of KMT5A, which in turn methylates H4K20 (H4K20me0) to H4K20me1 and thereby decreases the recruitment of BRCA1‐BARD1 to chromatin. Importantly, STAG2 expression correlates with poor prognosis of cancer patients. STAG2 is identified as an important regulator of HR and a potential therapeutic strategy for STAG2‐mutant tumors is elucidated.

Abstract Background Immune checkpoint inhibitor (ICI) monotherapy and neoadjuvant immunochemotherapy have shown promising results in esophageal carcinoma. However, it is still unclear whether more courses of immunochemotherapy are therapeutically better. We aimed to investigate the safety and efficacy of three courses of neoadjuvant treatment for patients with locally advanced esophageal squamous cell carcinoma (ESCC). Methods Patients with locally advanced ESCC received three courses of camrelizumab plus nab‐paclitaxel and capecitabine before undergoing surgery. Additionally, patients received safety, computed tomography (CT), and endoscopy (with endoscopic ultrasonography and mucosal biopsy) assessments before and in the second and third courses of treatment. We used the CT and endoscopic assessment results from the second and third courses for comparison. Results From May 2020 to December 2021, 47 patients were enrolled at Sun Yat‐sen University Cancer Center. In our study, 43 patients completed three courses of preoperative chemotherapy combined with anti‐Programmed cell death‐1 (PD‐1) therapy and radical surgical resection. The toxicity of the third course of immunochemotherapy was mild and well tolerated without increased treatment‐related adverse events (TRAEs) and mortality compared with that of the second course of treatment. In terms of efficacy, an additional course of treatment after the second course of treatment was effective, with increased CT and endoscopy T (clinical T stage) downstaging rates by 16.3% and 25.9%, N (clincial N stage) downstaging rates by 7.0% and 11.1%, and objective response rates (ORRs) by 13.6% and 22.0%, respectively. Conclusions Regardless of downstaging or ORR, three courses of immunochemotherapy appear to be superior to two courses of treatment without increasing TRAEs.

Abstract Near‐infrared (NIR) fluorescence imaging poses significant superiority over traditional medical imaging for tumor resection, thus having attracted widely attention. However, for tiny tumor residues, it requires relative high sensitivity to determine. Here, based on persistent luminescence nanoparticles (PLNPs), an ultrasensitive nanoprobe with extraordinary tumor imaging result is developed to guide surgical removal. Persistent luminescence (PersL) is quenched in normal tissue by the outer layer of MnO2, and is recovered due to the degradation of MnO2 in tumor microenvironment, significantly improving the sensitivity of tumor imaging. Combined with the absence of background fluorescence in imaging of PLNPs, ultrahigh sensitivity is achieved. In orthotopic breast cancer model, the intraoperative tumor‐to‐normal tissue (T/NT) signal ratio of the nanoprobe is 58.8, about 9 times that of downconversion nanoparticles. The T/NT ratio of residual tumor (

Abstract Background To investigate the impact of station 3A lymph node dissection (LND) on overall survival (OS) and disease‐free survival (DFS) in completely resected right‐side non‐small‐cell lung cancer (NSCLC) patients. Methods A total of 1661 cases with completely resected right‐side NSCLC were included. Propensity score matching (PSM) was performed to minimize selection bias, and a logistic regression model was conducted to investigate the risk factors associated with station 3A lymph node metastasis (LNM). The Kaplan–Meier method and Cox proportional hazards model were used to evaluate the impact of station 3A LND on survival. Results For the entire cohort, 503 patients (30.3%) underwent station 3A LND. Of those, 11.3% (57/503) presented station 3A LNM. Univariate and multivariate logistic analyses showed that station 10 LNM, tumor location, and the number of resected lymph nodes were independent risk factors associated with station 3A LNM. Before PSM, patients with station 3A LND had worse 5‐year OS (p = 0.002) and DFS (p = 0.011), and more drainage on postoperative day 1 (p = 0.041) than those without. After PSM, however, station 3A LND was not associated with the 5‐year OS (65.7% vs. 63.6%, p = 0.432) or DFS (57.4% vs. 56.0%, p = 0.437). The multivariate analysis further confirmed that station 3A LND was not a prognostic factor (OS, p = 0.361; DFS, p = 0.447). Conclusions Station 3A LND could not improve long‐term outcomes and it was unnecessary to dissect station 3A lymph nodes during surgery of right‐side NSCLC.

Abstract Background The mechanism underlying colorectal cancer (CRC) initiation and progression remains elusive, and overall survival is far from satisfactory. Previous studies have shown that PDGFA‐associated protein 1 (PDAP1) is upregulated in several cancers including CRC. Here, we aimed to identify the cause and consequence of PDAP1 dysregulation in CRC and evaluate its role as a potential therapeutic target. Methods Multi‐omics data analysis was performed to identify potential key players in CRC initiation and progression. Immunohistochemistry (IHC) staining was applied to determine the expression pattern of PDAP1 in CRC tissues. Pdap1 conditional knockout mice were used to establish colitis and CRC mouse models. RNA sequencing, a phosphoprotein antibody array, western blotting, histological analysis, 5‐bromo‐2′‐deoxyuridine (BrdU) incorporation assay, and interactome analysis were applied to identify the underlying mechanisms of PDAP1. A human patient‐derived xenograft (PDX) model was used to assess the potential of PDAP1 as a therapeutic target. Results PDAP1 was identified as a potential key player in CRC development using multi‐omics data analysis. PDAP1 was overexpressed in CRC cells and correlated with reduced overall survival. Further investigation showed that PDAP1 was critical for the regulation of cell proliferation, migration, invasion, and metastasis. Significantly, depletion of Pdap1 in intestinal epithelial cells impaired mucosal restitution in dextran sulfate sodium salt‐induced colitis and inhibited tumor initiation and growth in colitis‐associated cancers. Mechanistic studies showed that c‐Myc directly transactivated PDAP1, which contributed to the high PDAP1 expression in CRC cells. PDAP1 interacted with the juxtamembrane domain of epidermal growth factor receptor (EGFR) and facilitated EGFR‐mitogen‐activated protein kinase (MAPK) signaling activation, which resulted in FOS‐related antigen 1 (FRA‐1) expression, thereby facilitating CRC progression. Notably, silencing of PDAP1 could hinder the growth of patient‐derived xenografts that sustain high PDAP1 levels. Conclusions PDAP1 facilitates mucosal restitution and carcinogenesis in colitis‐associated cancer. c‐Myc‐driven upregulation of PDAP1 promotes proliferation, migration, invasion, and metastasis of CRC cells via the EGFR‐MAPK‐FRA‐1 signaling axis. These findings indicated that PDAP1 inhibition is warranted for CRC patients with PDAP1 overexpression.

Abstract Background Persistent Müllerian duct syndrome (PMDS) is an autosomal recessive congenital abnormality in which Müllerian derivatives, uterus, cervix, upper two‐thirds of the vagina, and fallopian tubes persist in otherwise normally virilized males. Mutations in anti‐Müllerian hormone (AMH) and AMH receptor type II (AMHR2) genes have been identified as causative. However, functional experimental analysis of AMHR2 or AMH variants that cause PMDS is still lacking. Materials and Methods A Chinese Han family affected by PMDS was identified. To assess the history and clinical manifestations of PMDS, physical, operational, ultrasonographical, pathological, and other examinations were performed on family members. The variant screening was conducted using trio whole‐exome sequencing (trio WES) and Sanger sequencing. Complementation‐based NanoLuciferase Binary Technology (NanoBiT) was used to examine the interaction between AMH and AMHR2 variants in vivo. The effect of the two variants on the transcriptional activity of the TGFβ/BMP pathway was evaluated using a luciferase assay. Results Classic phenotypic manifestations of PMDS in a pair of identical twins were described and confirmed by genetic sequence analysis. Molecular studies revealed two novel variants c.118G > C [p.(Gly40Arg)], c.1222G > C [p.(Ala408Pro)] in the AMHR2 gene. The AMHR2 p.Gly40Arg variant reduces its ability to bind to AMH, while the p.Ala408Pro variant alters the kinase domain structure. Both variants significantly reduce TGFβ/BMP signaling. Conclusion Two missense AMHR2 variants associated with PMDS were identified. These findings provide novel insights toward better clinical evaluation and further understanding of the molecular basis of PMDS.

The emergence of memristors with potential applications in data storage and artificial intelligence has attracted wide attentions. Memristors are assembled in crossbar arrays with data bits encoded by the resistance of individual cells. Despite the proposed high density and excellent scalability, the sneak‐path current causing cross interference impedes their practical applications. Therefore, developing novel architectures to mitigate sneak‐path current and improve efficiency, reliability, and stability may benefit next‐generation storage‐class memory (SCM). Moreover, conventional digital computers face the von‐Neumann bottleneck and the slowdown of transistors’ scaling, imposing a big challenge to hardware artificial intelligence. Memristive crossbar features colocation of memory and processing units, as well as superior scalability, making it a promising candidate for hardware accelerating machine learning and neuromorphic computing. Herein, first, crossbar architecture is introduced. Then, for storage, the origin of sneak‐path current is reviewed and techniques to mitigate this issue from the angle of materials and circuits are discussed. Computing wise, the applications of memristive crossbars in both machine learning and neuromorphic computing are surveyed, focusing on the structure of unit cells, the network topology, and the learning types. Finally, a perspective on future engineering and applications of memristive crossbars is discussed.

The loss of auditory sensory hair cells (HCs) is the most common cause of sensorineural hearing loss (SNHL). As the main sound transmission structure in the cochlea, it is necessary to maintain the normal shape and survival of HCs. In this review, we described and summarized the signaling pathways that regulate the development and survival of auditory HCs in SNHL. The role of the mitogen-activated protein kinase (MAPK), phosphoinositide-3 kinase/protein kinase B (PI3K/Akt), Notch/Wnt/Atoh1, calcium channels, and oxidative stress/reactive oxygen species (ROS) signaling pathways are the most relevant. The molecular interactions of these signaling pathways play an important role in the survival of HCs, which may provide a theoretical basis and possible therapeutic interventions for the treatment of hearing loss.

The RFPA3D is used to establish a fine finite element model of 6.63 million elements, which realizes the fine simulation of the stability of the Xiluodu arch dam under layered, overall, multiworking conditions and multistress fields, and the cracking and failure process under overload. The structural design scheme of the arch dam and the corresponding foundation treatment design are evaluated. The model fully reflects the measures of dam shape structure design, angle fitting structure design, and foundation concrete replacement in the Xiluodu arch dam technical design stage. The RFPA3D adopts the mesoelement elastic damage model, which considers the Mohr–Coulomb criterion of shear fracture and the maximum tensile failure criterion, and assumes that the mechanical properties of the element satisfy Weibull distribution to consider its heterogeneity. The simulation results show that, under normal load conditions, the dam foundation surface after comprehensive reinforcement has better overall stability, the stress and deformation of the dam body have good symmetry, and the overload factor of crack initiation under overload calculation K1 = 2P0 (P0 is normal water load), the nonlinear deformation overload factor K2 = 3.5–4P0, and the limit load factor K3 = 7.5–8.0P0, dam safety can be satisfied. The RFPA3D is used to establish a superlarge fine model to study the overall stability of the high arch dam, which provides an effective method for analysis and research of other large hydraulic projects in the world.

Abstract To solve the problems of fast‐charging of lithium‐ion batteries in essence, development of new electrode materials with higher lithium‐ion diffusion coefficients is the key. In this work, a novel flower‐like Ni@SnNi structure is synthesized via a two‐step process design, which consists of the fabrication of Ni cores by spray pyrolysis followed by the formation of SnNi shells via a simple oxidation–reduction reaction. The obtained Ni@SnNi composite exhibits an initial capacity of ≈693 mA h g−1 and a reversible capacity of ≈570 mA h g−1 after 300 charge/discharge cycles at 0.5 C, and maintains 450 mA h g−1 even at a high rate of 3 C. Further, it is proved that a Ni@SnNi composite possesses high lithium‐ion diffusion coefficient (≈10−8), which is much higher than those (≈10−10) reported previously, which can be mainly attributed to the unique flower‐like Ni@SnNi structure. In addition, the full cell performance (Ni@SnNi‐9h/graphite vs LiCoO2) with a capacity ratio of 1.13 (anode/cathode) is also tested. It is found that even at 2 C rate charging/discharging, the capacity retention at 100 cycles is still close to 89%. It means that Ni@SnNi‐9h is a promising anode additive for lithium‐ion batteries with high energy density and power density.

Abstract The OMPs A (OmpA)—of Edwardsiella anguillarum and OmpU of V. vulnificus have been proven to be good antigens. In this study, after construction of a vector, a new recombinant Omp (rOMP) containing both OmpA and OmpU was expressed and purified. Then, the Japanese eels (Anguilla japonica) were intraperitoneally (i.p.) injected with the phosphate‐buffered saline (PBS group), formalin‐killed‐cell (FKC group) or the recombinant Omp (rOMP group). The stimulation index of the whole blood cells in eels from FKC group was significantly higher than the eels from PBS and rOMP groups at 28 dpi; serum titers of anti‐E. anguillarum and anti‐V. vulnificus antibody of eels from FKC and rOMP group increased significantly at 21 and 28 dpi; in the rOMP group, eels serum titer stayed at a high level on 42 dpi. The activities of lysozyme in skin mucus, liver, kidney, and serum in three groups exhibited considerable changes. The relative percent survival (RPS) rate of eels from rOMP group were 100% and 83% when challenged with V. vulnificus or E. anguillarum. These results indicated that inoculation of rOMP would protect Japanese eels against the infection by E. anguillarum and V. vulnificus.

miR-362 is a recently discovered member of the microRNA family, and it modulates a variety of physical activities and plays an important role in the occurrence and development of many tumors. However, the biological functions of hsa-miR-362-5p in non-small-cell lung carcinoma (NSCLC) are unknown. Transwell assay and colony formation were used to determine the migration, invasion, and proliferation of NSCLC cells in vitro. A subcutaneous tumor model in nude mice was established to detect NSCLC tumor growth in vivo. The direct binding of miR-362 to the 3′UTR of Semaphorin 3A (Sema3A) was confirmed by luciferase reporter assay. In this study, we found that the level of miR-362 was higher in NSCLC tissues than in adjacent normal tissues and that the level of miR-362 expression was also elevated in five NSCLC cell lines (A549, 95-D, H1299, H292, and H460) relative to a human normal lung epithelial cell line (BEAS2B). Furthermore, miR-362 promoted NSCLC cell invasion, migration, and colony formation in vitro and tumor formation in vivo. Next, we identified the miR-362 target gene Sema3A, which is significantly correlated with metastasis. Sema3A expression was increased in normal tissues relative to NSCLC tissues. This result is consistent with the fact that miR-362 expression is negatively correlated with Sema3A expression in clinical tissue samples and indicated that miR-362 can regulate Sema3A expression in NSCLC cells and consequently affect NSCLC invasion, migration, and colony formation. Taken together, these findings on the newly identified miR-362/Sema3A axis elucidate the molecular mechanism of NSCLC invasion and migration and could lead to a potential therapeutic target in NSCLC treatment.

Betatrophin and irisin are two recently identified hormones which may participate in regulating pancreatic β-cell function. However, the associations of these two hormones with β-cell function remain unclear. The present study aims to demonstrate the associations of circulating betatrophin and irisin levels with β-cell function, assessed by the area under the curve (AUC) of C-peptide, and the possible correlation between these two hormones in previously diagnosed type 2 diabetes mellitus (T2DM) patients. In total, 20 age-, sex-, and body mass index- (BMI-) matched normal glucose tolerance (NGT) subjects and 120 previously diagnosed T2DM patients were included in this study. Partial correlation analysis was used to evaluate the relationships between these two hormones and indexes of β-cell function and insulin resistance. Our results showed that betatrophin levels were significantly elevated, while irisin levels were significantly decreased, in patients with T2DM compared with NGT subjects. However, partial correlation analysis showed that betatrophin levels did not correlate with β-cell function-related variables or insulin resistance-related variables before or after controlling multiple covariates, while irisin correlated positively with insulin sensitivity but is not associated with β-cell function-related variables. Besides, no correlation was observed between betatrophin and irisin levels. Hence we concluded that betatrophin and irisin were not associated with β-cell function in previously diagnosed T2DM patients.

The safe landing of a Moon lander and the performance of the precise instruments it carries may be affected by too heavy impact on touchdown. Accordingly, landing characteristics have become an important research focus. Described in this paper are model tests carried out using simulated lunar soils of different relative densities (called “simulant” lunar soils below), with a scale reduction factor of 1/6 to consider the relative gravities of the Earth and Moon. In the model tests, the lander was simplified as an impact column with a saucer-shaped footpad with various impact landing masses and velocities. Based on the test results, the relationships between the footpad peak feature responses and impact kinetic energy have been analyzed. Numerical simulation analyses were also conducted to simulate the vertical impact process. A 3D dynamic finite element model was built for which the material parameters were obtained from laboratory test data. When compared with the model tests, the numerical model proved able to effectively simulate the dynamic characteristics of the axial forces, accelerations, and penetration depths of the impact column during landing. This numerical model can be further used as required for simulating oblique landing impacts.

A dam ant colony optimization (D-ACO) analysis of the overall stability of high arch dams on complicated foundations is presented in this paper. A modified ant colony optimization (ACO) model is proposed for obtaining dam concrete and rock mechanical parameters. A typical dam parameter feedback problem is proposed for nonlinear back-analysis numerical model based on field monitoring deformation and ACO. The basic principle of the proposed model is the establishment of the objective function of optimizing real concrete and rock mechanical parameter. The feedback analysis is then implemented with a modified ant colony algorithm. The algorithm performance is satisfactory, and the accuracy is verified. The m groups of feedback parameters, used to run a nonlinear FEM code, and the displacement and stress distribution are discussed. A feedback analysis of the deformation of the Lijiaxia arch dam and based on the modified ant colony optimization method is also conducted. By considering various material parameters obtained using different analysis methods, comparative analyses were conducted on dam displacements, stress distribution characteristics, and overall dam stability. The comparison results show that the proposal model can effectively solve for feedback multiple parameters of dam concrete and rock material and basically satisfy assessment requirements for geotechnical structural engineering discipline.

In this paper, case study on outlet cracking is first conducted for the Goupitan and Xiaowan arch dams. A nonlinear FEM method is then implemented to study effects of the outlets on integral stability of the Xiluodu arch dam under two loading conditions, i.e., normal loading and overloading conditions. On the basis of the case study and the numerical modelling, the outlet cracking mechanism, risk, and corresponding reinforcement measures are discussed. Furthermore, the numerical simulation reveals that (1) under the normal loading conditions, the optimal distribution of the outlets will contribute to the tensile stress release in the local zone of the dam stream surface and decrease the outlet cracking risk during the operation period. (2) Under the overloading conditions, the cracks initiate around the outlets, then propagate along the horizontal direction, and finally coalesce with those in adjacent outlets, where the yield zone of the dam has a shape of butterfly. Throughout this study, a dam outlet cracking risk control and reinforcement principle is proposed to optimize the outlet design, select the appropriate concrete material, strengthen the temperature control during construction period, design reasonable impounding scheme, and repair the cracks according to their classification.

The concern for workers’ safety in construction industry is reflected in many studies focusing on static safety risk identification and assessment. However, studies on real-time safety risk assessment aimed at reducing uncertainty and supporting quick response are rare. A method for real-time safety risk assessment (RTSRA) to implement a dynamic evaluation of worker safety states on construction site has been proposed in this paper. The method provides construction managers who are in charge of safety with more abundant information to reduce the uncertainty of the site. A quantitative calculation formula, integrating the influence of static and dynamic hazards and that of safety supervisors, is established to link the safety risk of workers with the locations of on-site assets. By employing the hidden Markov model (HMM), the RTSRA provides a mechanism for processing location data provided by the real-time location system (RTLS) and analyzing the probability distributions of different states in terms of false positives and negatives. Simulation analysis demonstrated the logic of the proposed method and how it works. Application case shows that the proposed RTSRA is both feasible and effective in managing construction project safety concerns.