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Telecom fraud detection is a challenging task since the fact that fraudulent behaviors are hidden in the vast amount of telecom records. More concerning, the ongoing coronavirus pandemic (COVID-19) accelerated the use of mobile internet, providing more criminal opportunities for fraudsters. However, current telecom fraud detection mostly focuses on individual sequences representation, rarely noticing the collaboration of fraudsters, making it exhibit unsatisfactory performance in the face of gang crimes. To address this problem, we propose to extract collaborative networks from user call logs with an emphasis on unveiling collaborative fraud. We employ eight months of telecom datasets in China with 6,106 users and 5.0 million call logs between 1.25 million telephone recipients. Through our study, we find that the social structure of fraudsters evolute rapidly while the normal users remain stable relatively. In addition, we find that mining collaborative fraud strategies help to detect fraudsters with less distinct fraud characteristics. To this end, we propose a novel model named COllaborative-REsistant Dynamic Graph Neural Network (CORE-DGNN), to enhance the dynamic GNN aggregation process. Specifically, we first use co-recipients to obtain the collaborative network under each time slice. Then, we design a multi-frequency graph neural network to adaptively aggregate the features of node neighbors at different frequencies to address the problem of heterophily in collaborative networks. Finally, a self-attentive temporal convolutional network is designed to aggregate node embedding features across multiple time spans. Comprehensive experiments on two real-world telecom fraud datasets show that our approach outperforms several state-of-the-art algorithms. [ABSTRACT FROM AUTHOR]

Objectives: To retrospectively compare multilevel volumetric changes in both hard and soft tissues between antral pseudocyst (AP) removal and retainment before maxillary sinus floor augmentation (MSFA) and immediate implant placement. Material and methods: Twenty‐six patients with 38 implants placed from 2016 to 2021 were included and divided according to a cohort design as follows: 13 removing the cyst (RC group) and 13 "leaving alone" the cyst (LC group). 3D radiographic parameters (primary outcome), 2D parameters and clinical records (secondary outcome) involving both hard and soft tissues were evaluated for four periods (T1: immediate postoperative, T2: 6‐month, T3: 12‐month, and T4: 2‐ to 5‐ year follow‐up). Possible confounding factors, including sinus anatomical features and implant distribution, were also analyzed to eliminate their disturbance. Results: The 3D volumetric change rate of bone grafts in the RC group (−9.32% ± 10.01%) from T2 to T3 was significantly lower than that in the LC group (−19.8% ± 10.59%) (p <.05). The change rate of apical bone height (ABH), endo‐sinus bone gain (ESBG) and other 2D parameters were not significantly different between the two groups. 5.3% implants in RC group and 9.1% implants in LC group failed during follow‐ups. 0% postoperative complications were observed in RC group. The Schneiderian membrane of RC group was significantly thinner than that of LC group at two measuring points in sinus. Conclusion: The present study demonstrated that compared to AP retainment, AP removal before MSFA and immediate implant placement can obtain higher bone graft volumetric stability and favorable prognosis. [ABSTRACT FROM AUTHOR]

Objectives: To retrospectively evaluate whether repositioning the bone window leads to a better outcome of three‐dimensional sinus augmentation in lateral sinus floor elevation (LSFE) with simultaneous implant placement. Methods: 34 patients with a total of 40 implants (14: test group, 26: control group) receiving LSFE with simultaneous implant placement were included in this retrospective research. CBCT images were taken before surgery, immediately and 6 months after surgery. The two‐dimensional augmentation parameters, including apical bone height (ABH), endo‐sinus bone gain (ESBG), and palatal/buccal bone height (PBH/BBH), and three‐dimensional parameters, including augmentation volume (AV) and palatal/buccal augmentation volume (PAV/BAV), were measured. The lateral defect length (LDL) and lateral window length (LWL) were also measured to evaluate the lateral antrostomy recovery. Results: At the 6‐month follow‐up, the reduction rates at ABH, ESBG, and BBH of the test group (ABH: 10.41% ± 30.30%, ESBG: 2.55% ± 8.91%, BBH: 2.50% ± 8.65%) were significantly lower than those of the control group (ABH: 25.10% ± 22.02%, ESBG: 11.47% ± 9.79%, BBH: 7.10% ± 5.37%; p <.05). In addition, the test group showed better three‐dimensional augmentation stability on the buccal side (BAV reduction: 15.51% ± 10.86% vs. 27.15% ± 12.61%; p <.05). Moreover, the LDL/LWL ratio of the test group was significantly lower than that of the control group (p <.05). Conclusion: Within the limitations of this study, repositioning of the bone window in LSFE with simultaneous implant placement could contribute to endo‐sinus augmentation stability on the buccal side at the 6‐month follow‐up. Moreover, it would also facilitate recovery of the lateral antrostomy defect. [ABSTRACT FROM AUTHOR]

The development of telecom technology not only facilitates social interactions but also inevitably provides the breeding ground for telecom fraud crimes. However, telecom fraud detection is a challenging task as fraudsters tend to commit co-fraud and disguise themselves within the mass of benign ones. Previous approaches work by unearthing differences in calling sequential patterns between independent fraudsters, but they may ignore synergic fraud patterns and oversimplify fraudulent behaviors. Fortunately, graph-like data formed by traceable telecom interaction provides opportunities for graph neural network (GNN)-based telecom fraud detection methods. Therefore, we develop a latent synergy graph (LSG) learning-based telecom fraud detector, named LSG-FD, to model both sequential and interactive fraudulent behaviors. Specifically, LSG-FD introduces (1) a multi-view LSG extractor to reconstruct synergy relationship-oriented graphs from the meta-interaction graph based on second-order proximity assumption; (2) an LSTM-based calling behavior encoder to capture the sequential patterns from the perspective of local individuals; (3) a dual-channel based graph learning module to alleviate the disassortativity issue (caused by the camouflages of fraudsters) by incorporating the dual-channel frequency filters and the learnable controller to adaptively aggregate high- and low-frequency information from their neighbors; (4) an imbalance-resistant model trainer to remedy the graph imbalance issue by developing a label-aware sampler. Experiment results on the telecom fraud dataset and another two widely used fraud datasets have verified the effectiveness of our model. [ABSTRACT FROM AUTHOR]

To date, the wide application of cell-based biomaterials in tissue engineering and regeneration is remarkably hampered by immune rejection. Reducing the immunogenicity of cell-based biomaterials has become the latest direction in biomaterial research. Recently, genetically modified cell-based biomaterials with immunomodulatory genes have become a feasible solution to the immunogenicity problem. In this review, recent advances and future challenges of genetically modified immunomodulatory cell-based biomaterials are elaborated, including fabrication approaches, mechanisms of common immunomodulatory genes, application and, more importantly, current preclinical and clinical advances. The fabrication approaches can be categorized into commonly used (e.g., virus transfection) and newly developed approaches. The immunomodulatory mechanisms of representative genes involve complicated cell signaling pathways and metabolic activities. Wide application in curing multiple end-term diseases and replacing lifelong immunosuppressive therapy in multiple cell and organ transplantation models is demonstrated. Most significantly, practices of genetically modified organ transplantation have been conducted on brain-dead human decedent and even on living patients after a series of experiments on nonhuman primates. Nevertheless, uncertain biosecurity, nonspecific effects and overlooked personalization of current genetically modified immunomodulatory cell-based biomaterials are shortcomings that remain to be overcome. [Display omitted] • Cell-based biomaterials can be genetically modified with immunomodulatory genes. • Immunomodulatory genes help alleviate immune rejection of cell-based biomaterials. • Fabrication processes include common and newly developed methods. • Clinical/preclinical practices of gene-edited biomaterial transplantation. • Challenges: antigen elimination, systemic administration, individualization. [ABSTRACT FROM AUTHOR]

Gain-of-function mutations in the low-density lipoprotein receptor-related protein 5 (LRP5) can cause high-bone-mass (HBM) phenotype, with 19 identified mutations so far. The A242T mutation in LRP5 has been found in 9 families, making it one of the most prevalent mutations. However, the correlation between the A242T mutation and HBM phenotype remains unverified in animal models. This study aimed to investigate the bone properties in a new transgenic mouse model carrying the LRP5 A241T missense mutation, equivalent to A242T in humans. Heterozygous Lrp5 A241T mice were generated using CRISPR/Cas9 genome editing. Body weight increased with age from 4 to 16 weeks, higher in males than females, with no difference between Lrp5 A241T mice and wild-type control. Micro-CT showed slightly longer femur and notably elevated trabecular bone mass of the femur and fifth lumbar spine with higher bone mineral density, bone volume fraction, and trabecular thickness in Lrp5 A241T mice compared to wild-type mice. Additionally, increased cortical bone thickness and volume of the femur shaft and skull were observed in Lrp5 A241T mice. Three-point bending tests of the tibia demonstrated enhanced bone strength properties in Lrp5 A241T mice. Histomorphometry confirmed that the A241T mutation increased bone formation without affecting osteoblast number and reduced resorption activities in vivo. In vitro experiments indicated that the LRP5 A241T mutation enhanced osteogenic capacity of osteoblasts with upregulation of the Wnt signaling pathway, with no significant impact on the resorptive activity of osteoclasts. In summary, mice carrying the LRP5 A241T mutation displayed high bone mass and quality due to enhanced bone formation and reduced bone resorption in vivo , potentially mediated by the augmented osteogenic potential of osteoblasts. Continued investigation into the regulatory mechanisms of its bone metabolism and homeostasis may contribute to the advancement of novel therapeutic strategies for bone disorders. • HBM caused by LRP5 A241T mutation was confirmed in the mouse model. • Mice carrying LRP5 A241T mutation exhibit significant bone formation in vivo. • LRP5 A241T mutation enhances the osteogenic activity of osteoblasts via the Wnt signaling pathway. [ABSTRACT FROM AUTHOR]

[Display omitted] Various modifications have been performed on biomaterials to improve their applications in tissue engineering and regenerative medicine. However, the challenges of immunogenicity and biocompatibility existed since the application of biomaterials. As a method to solve this problem, the decellularization process removes most living cells from biomaterials to minimize their immunogenicity; and preserves the native structures and compositions that favour cell growth and the subsequent construction of functional tissue. On the other hand, genetic modification of biomaterials aims to achieve specific functions (low immunogenicity, osteogenesis, etc.) or analyse the genetic mechanisms underlying some diseases (cardiac dysfunction, liver fibrosis, etc.). The combination of decellularization and gene modification is highly superior to biomaterials; thus, we must obtain a deeper understanding of these novel biomaterials. In this review, we summarize the fabrication approaches and current applications of genetically modified decellularized biomaterials and then discuss their disadvantages and corresponding future perspectives. [ABSTRACT FROM AUTHOR]

Nanomaterial-based cell sheet technology has been reported to be an effective method in regenerative medicine and tissue engineering. Here, we summarized several types of nanomaterials used to harvest cell sheets. Currently, the technology is divided into four categories according to the mechanisms: light-induced cell sheet technology, thermo-responsive cell sheet technology, magnetic-controlled cell sheet technology, and reactive oxygen species (ROS)-induced cell sheet technology. Furthermore, some studies have been conducted to show that nanomaterial-based cell sheets produce satisfying outcomes in the regeneration of bone, skeletal muscle, cardiac tissue, and tendon, as well as angiogenesis and osseointegration. Nevertheless, some shortcomings still exist, such as comprehensive preparation, unclear safety, and cell quality. Thus, future studies should aim to produce more types of nanomaterials to solve this problem. [Display omitted] • Mechanisms of four types of cell sheet detachment have been discussed. • Applications of nanomaterials-based cell sheet technology have been listed. • Advantages and disadvantages of nanomaterials have been summarized. • Potential nanomaterials for cell sheet technology have been illustrated. [ABSTRACT FROM AUTHOR]

Genetically modified cell sheet technology is emerging as a promising biomedical tool to deliver therapeutic genes for regenerative medicine and tissue engineering. Virus-based gene transfection and non-viral gene transfection have been used to fabricate genetically modified cell sheets. Preclinical and clinical studies have shown various beneficial effects of genetically modified cell sheets in the regeneration of bone, periodontal tissue, cartilage and nerves, as well as the amelioration of dental implant osseointegration, myocardial infarction, skeletal muscle ischemia and kidney injury. Furthermore, this technology provides a potential treatment option for various hereditary diseases. However, the method has several limitations, such as safety concerns and difficulties in controlling transgene expression. Therefore, recent studies explored efficient and safe gene transfection methods, prolonged and controllable transgene expression and their potential application in personalized and precision medicine. This review summarizes various types of genetically modified cell sheets, preparation procedures, therapeutic applications and possible improvements. [ABSTRACT FROM AUTHOR]

• A case of early-onset periodontitis with VitD deficiency and VitD receptor mutation was reported. • Vitamin D could promote early osteogenic differentiation of periodontal ligament stem cells (PDLSCs). • Vitamin D could inhibit TNF-α-induced inflammation of PDLSCs. Periodontitis is a chronic periodontal disease that contributes to tooth loss. In recent years, many animal studies have reported that vitamin D (VitD) deficiency results in chronic periodontitis. However, no studies have reported cases of early-onset periodontitis with VitD deficiency. This study reports a 5-year-old male patient with early-onset periodontitis, VitD deficiency and VitD receptor (VDR) mutation. The patient was treated with VitD and calcium, and received systematic periodontal treatment. During the 12-year treatment, the periodontal conditions of this patient were stable. Our in vitro study found that VitD could promote the expression of alkaline phosphatase (ALP), runt-related transcription factor 2 (Runx2), bone morphogenetic protein 2 (BMP2), bone gamma-carboxyglutamate protein (BGLAP), and VDR in the early osteogenic differentiation of periodontal ligament stem cells (PDLSCs). Meanwhile, VitD could downregulate mRNA expression levels of Interleukin-6 (IL-6), Interleukin-8 (IL-8), Interleukin-1β (IL-1β) and protein levels of IL-6 in the tumor necrosis factor-α (TNF-α) -induced inflammation of PDLSCs. Therefore, sufficient VitD supply can be a potential treatment for VitD deficiency induced early-onset periodontitis. [ABSTRACT FROM AUTHOR]