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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%.

Heat shock proteins (HSPs), which function as chaperones, are activated in response to various environmental stressors. In addition to their role in diverse aspects of protein production, HSPs protect against harmful protein-related stressors. Calycosin exhibits numerous beneficial properties. This study aims to explore the protective effects of calycosin in the heart under heat shock and determine its underlying mechanism. H9c2 cells, western blot, TUNEL staining, flow cytometry, and immunofluorescence staining were used. The time-dependent effects of heat shock analyzed using western blot revealed increased HSP expression for up to 2 h, followed by protein degradation after 4 h. Hence, a heat shock damage duration of 4 h was chosen for subsequent investigations. Calycosin administered post-heat shock demonstrated dose-dependent recovery of cell viability. Under heat shock conditions, calycosin prevented the apoptosis of H9c2 cells by upregulating HSPs, suppressing p-JNK, enhancing Bcl-2 activation, and inhibiting cleaved caspase 3. Calycosin also inhibited Fas/FasL expression and activated cell survival markers (p-PI3K, p-ERK, p-Akt), indicating their cytoprotective properties through PI3K/Akt activation and JNK inhibition. TUNEL staining and flow cytometry confirmed that calycosin reduced apoptosis. Moreover, calycosin reversed the inhibitory effects of quercetin on HSF1 and Hsp70 expression, illustrating its role in enhancing Hsp70 expression through HSF1 activation during heat shock. Immunofluorescence staining demonstrated HSF1 translocation to the nucleus following calycosin treatment, emphasizing its cytoprotective effects. In conclusion, calycosin exhibits pronounced protective effects against heat shock-induced damages by modulating HSP expression and regulating key signaling pathways to promote cell survival in H9c2 cells. [ABSTRACT FROM AUTHOR]

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]