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With the impacts of COVID-19 epidemic, e-learning has become a popular research issue. Therefore, how to upgrade the interactivity of e-learning, and allow learners to quickly access personalized and popular learning information from huge digital materials, is very important. However, chatbots are mostly used in automation, as well as simple occasions of general standard question and answer. But to solve the different problems of e-learners in the learning process, chatbots are used to filter the blind spots of learners and to provide further relevant information, so that e-learning can improve in efficiency and interactivity. This study utilizes AI, two-stage Bayesian algorithm, and crawler technology to provide customized learning materials according to learner's current learning situation. The experimental results show that this research system can indeed correctly understand and judge the blind spots of digital learners, and effectively find the relevant e-learning and video information. The accuracy rate reaches nearly 90%.

Objective To understand the pathogenesis of bisphosphonate⁃related osteonecrosis of the jaws (BRONJ) and to investigate its differential diagnosis, clinical manifestations, treatment and prevention. Methods By analyzing the clinical data of 4 patients with BRONJ in the retrospective study with reviewing related literatures in the world to make a summary of it. Results Cases of 4 patients mainly presented recurring pain, discharging of pus and disposure and necrosis of the bone. 3 patients received surgical and antibiotics treatments, one of them had local infection which was under control by oral antibiotic. The other 2 patients had no infection and recurrence. Conclusion BRONJ is caused by jaw necrosis due to bisphosphonate inhibition of osteoclast function. For the reason that none of the treat⁃ ments is unified and satisfied, we should focus on the risk factors in prevention. Appropriate surgery treatment could be well controlled the process of the BRONJ which should be popularization in our study.

Background: CD24+CK19+/CD24+SOX9+ resident liver cells are activated and expanded after chronic liver injury in a ductular reaction. However, the sources and functions of these cells in liver damage remain disputed. Results: The current study combined genetic lineage tracing with in vitro small-molecule-based reprogramming to define liver progenitor cells (LPCs) derived from hepatic parenchymal and non-parenchymal tissues. tdTom+ hepatocytes were isolated from ROSA26tdTomato mice following AAV8-Tbg-Cre-mediated recombination, EpCAM+ biliary epithelial cells (BECs) from wild-type intrahepatic bile ducts and ALB/GFP−EpCAM− cells were isolated from AlbCreERT/R26GFP mice. A cocktail of small molecules was used to convert the isolated cells into LPCs. These in vitro cultured LPCs with CD24 and SOX9 expression regained the ability to proliferate. Transcriptional profiling showed that the in-vitro cultured LPCs derived from the resident LPCs in non-parenchymal tissues expressed Lipocalin-2 (Lcn2) at high levels. Accordingly, endogenous Cd24a+Lcn2+ LPCs were identified by integration of sc-RNA-sequencing and pathological datasets of liver dysfunction which indicates that LPCs produced by ductular reactions might also originate from the resident LPCs. Transplantation of in-vitro cultured Cd24a+Lcn2+ LPCs into CCl4-induced fibrotic livers exacerbated liver damage and dysfunction, possibly due to LCN2-dependent macrophage inflammatory response. Conclusions: CD24+LCN2+ LPCs constituted the expanding ductular reaction and contributed to macrophage-mediated inflammation in chronic liver damage. The current findings highlight the roles of LPCs from distinct origins and expose the possibility of targeting LPCs in the treatment of chronic hepatic diseases. [ABSTRACT FROM AUTHOR]

Intraoperatively, a Foley catheter and a rectal tube were placed in the fistula and the rectum to help identify the duplicated colon and the native colon respectively (Figure 1D). (B) The plain radiograph showing duplicated bowel gas pattern of the colon and rectum. Duplicated bowel gas pattern of the colon and rectum was revealed at the plain radiograph (Figure 1B). [Extracted from the article]

Background: Metastasis to long distance organs is the main reason leading to morality of tongue squamous cell carcinoma (TSCC); however, the molecular mechanisms are still unknown. High mobility group AT-hook 2 (HMGA2) is highly expressed in multiple metastatic carcinomas, in which it contributes to cancer progression, metastasis and poor prognosis by upregulating Snail expression and inducing epithelial mesenchymal transition (EMT). This study focuses on investigating the role and mechanism of regulation of HMGA2 in the metastasis of TSCC. Methods: HMGA2 mRNA and protein expression were examined in TSCC specimens by quantitative real-time polymerase chain reaction, western blotting and immunohistochemistry (IHC). Western blotting, IHC and immunofluorescence were also used to measure the expression and localization of EMT marker E-Cadherin and Vimentin both in TSCC cells and tissues. Knockdown assay was performed in vitro in TSCC cell lines using small interfering RNAs and the functional assay was carried out to determine the role of HMGA2 in TSCC cell migration and invasion. Results: TSCC mRNA and protein expression were significantly up-regulated in tumor tissues when compared to adjacent non-tumor tissues, and the overexpression of HMGA2 was closely correlated with lymph nodes metastasis. Clinicopathological analysis indicated that HMGA2 expression was associated with clinical stage (P = 0.001), lymph node metastasis (P = 0.000), histological differentiation (P = 0.002) and survival (P = 0.000). Silencing the HMGA2 expression in Cal27 and UM1 resulted in the inhibition of cell migration and invasion, meanwhile down-regulation of HMGA2 impaired the phenotype of EMT in TSCC cell lines and tissues. The Multivariate survival analysis indicates that HMGA2 can be an independent prognosis biomarker in TSCC. Conclusion: Our findings demonstrate that HMGA2 promotes TSCC invasion and metastasis; additionally, HMGA2 is an independent prognostic factor which implied that HMGA2 can be a biomarker both for prognosis and therapeutic target of TSCC. [ABSTRACT FROM AUTHOR]