Authors: Huang, Qian
Article Type: Research Article
Abstract: Ethnic identity is an important reason for national unity. The formation of ethnic groups is mostly due to external and internal reasons, with a complex mechanism structure. When people’s environment is destroyed, this value identity will be stronger, national cohesion and solidarity will grow sharply, an unprecedented high. Minority languages are characterized by a wide variety, cultural generation, and dynamic evolution. The languages are complex and diverse, and are deeply influenced by their cultural heritage. This has led to the fact that for a long time, minority languages have been learned almost exclusively by people of their own ethnic group. …This has led to a steady decline in the number of minority language speakers. However, the birth of the Internet of Things (IoT) has created an opportunity for the development of minority languages. Foreign minority languages have the following status (1) rapid decline (2) many endangered languages (3) low willingness to learn. In order to further investigate the current situation of minority language protection, the team conducted a survey in the minority cluster A. The results of the survey are as follows: most of the villagers are in love with the ethnic language and must inherit and promote the ethnic language, which is the wealth of a nation, but there are also a few residents who think that Mandarin should be used to replace the ethnic language. This reflects that most of the residents love the national language, but their young people as the inherited generation lose their love for the national language and are not willing to inherit and promote it. To solve this problem, an Internet of Things (IoT)-based ethnic language data system has been constructed so that the data system for ethnic minority language protection built through IoT technology can become the last line of defense for protecting ethnic languages, while allowing ethnic languages to be known and understood by more people through IoT technology, fostering the love and reverence of ethnic minority people for ethnic languages, and enhancing other ethnic groups’ sense of identity and support for ethnic languages. We propose to protect minority languages. Ultimately, we propose recommendations for the preservation of minority languages. (1) Increase publicity for minority language preservation. (2) Construct laws and regulations related to minority language protection. (3) Conduct in-depth research on minority language work and build an information base. (4) Promote minority language education. Show more
Keywords: Ethnic identity, Internet of Things, foreign minority, current situation of language protection
DOI: 10.3233/JCM-226899
Citation: Journal of Computational Methods in Sciences and Engineering, vol. 23, no. 5, pp. 2677-2686, 2023
Authors: Wang, Chaofeng | Song, Dezhi | Huang, Qian | Liu, Qian
Article Type: Research Article
Abstract: Cancer has become a leading cause of morbidity and mortality in recent years. Its high prevalence has had a severe impact on society. Researchers have achieved fruitful results in the causative factors, pathogenesis, treatment strategies, and cancer prevention. Semaphorin 3F (SEMA3F), a member of the signaling family, was initially reported in the literature to inhibit the growth, invasion, and metastasis of cancer cells in lung cancer. Later studies showed it has cancer-inhibiting effects in malignant tumors such as breast, colorectal, ovarian, oral squamous cell carcinoma, melanoma, and head and neck squamous carcinoma. In contrast, recent studies have reported that SEMA3F …is expressed more in hepatocellular carcinoma than in normal tissue and promotes metastasis of hepatocellular carcinoma. We chose lung, breast, colorectal, and hepatocellular carcinomas with high clinical prevalence to review the roles and molecular mechanisms of SEMA3F in these four carcinomas. We concluded with an outlook on clinical interventions for patients targeting SEMA3F. Show more
Keywords: SEMA3F, cancer, anti-oncogene
DOI: 10.3233/CBM-230085
Citation: Cancer Biomarkers, vol. 38, no. 2, pp. 131-142, 2023
Authors: Shi, Xiao-Ping | Tugusheva, Katherine | Bruce, James E. | Lucka, Adam | Chen-Dodson, Elizabeth | Hu, Binghua | Wu, Guo-Xin | Price, Eric | Register, Robert B. | Lineberger, Janet | Miller, Ron | Tang, Mei-Jy | Espeseth, Amy | Kahana, Jason | Wolfe, Abigail | Crouthamel, Ming-Chih | Sankaranarayanan, Sethu | Simon, Adam | Chen, Lin | Lai, Ming-Tain | Pietrak, Beth | DiMuzio, Jillian | Li, Yueming | Xu, Min | Huang, Qian | Garsky, Victor | Sardana, Mohinder K. | Hazuda, Daria J.
Article Type: Research Article
Abstract: Abnormal production and accumulation of amyloid-β peptide (Aβ) plays a major role in the pathogenesis of Alzheimer's disease (AD). β-secretase (BACE1) is responsible for the cleavage at the β-site in amyloid β protein precursor (AβPP/APP) to generate the N-terminus of Aβ. Here we report the stepwise identification and characterization of a novel APP-β-site mutant, “NFEV” (APP_NFEV) in vitro and in cells. In vitro, the APP_NFEV exhibits 100-fold enhanced cleavage rate relative to the “wild-type” substrate (APPwt) and 10-fold increase relative to the Swedish-type mutation variant (APPsw). In cells, it was preferably cleaved among 24 APP β-site mutations tested. More importantly, …the APP_NFEV mutant failed to generate any detectable Aβ peptides in BACE1-KO mouse fibroblast cells. The production of Aβ peptides was restored by co-transfecting human BACE1, demonstrating that BACE1 is the only enzyme responsible for the processing of APP_NFEV in these cells. Analysis of APP_NFEV cleavage products secreted in the media revealed that in cells BACE1 cleaves APP_NFEV at the position between NF and EV, identical to that observed in vitro. A BACE inhibitor blocked the processing of the APP_NFEV β-site in vitro and in cells. Our data indicates that the "NFEV" mutant is not only an enhanced substrate for BACE1 in vitro, but also a specific substrate for BACE1 in cells. Show more
Keywords: Alzheimer's disease, BACE, β-secretases, APP
DOI: 10.3233/JAD-2005-7207
Citation: Journal of Alzheimer's Disease, vol. 7, no. 2, pp. 139-148, 2005
