Industry convergence is a popular term that has been widely referenced in the context of rural tourism development in China. All levels of government (local, regional, national) in China have repeatedly addressed the significance of industry convergence in their tourism plans and related policies. Despite its popularity, limited studies at present have explored this concept. Using Huai'an as a case, this study applied a path analysis and reported the industry convergence process in a destination. The findings of this study can provide both theoretical and practical implications that are useful for tourism planners and policy makers.

BackgroundAlthough N6-methyladenosine (m6A) RNA methylation is the most abundant reversible methylation of mRNA, which plays a critical role in regulating cancer processing, few studies have examined the role of m6A in nonsmall-cell lung cancer-derived cancer stem-like cells (CSCs).MethodsCSCs were enriched by culturing NSCLC cells in a serum-free medium, and stem factors, including CD24, CD44, ALDH1, Nanog, Oct4, and Sox2 were detected by Western blot. ALKBH5 expression was measured by employing a tissue array. Global m6A methylation was measured after ALKBH5 knockdown. Malignances of CSCs were detected by performing CCK-8 assay, invasion assay, cell cycle analysis, and tumor formation in vitro and in vivo.Resultsm6A demethylase ALKBH5 is highly expressed in CSCs derived from NSCLC. Knockdown of ALKBH5 increased global m6A level, and also increased E-cadherin, decreased stem hallmarkers, Nanog and Oct4, and inhibited stemness of CSCs. In lung carcinoma, ALKBH5 is found to be positively correlated with p53 by using Gene Expression Profiling Interactive Analysis (GEPIA) online tool. P53 transcriptionally regulates ALKBH5 and subsequently regulates the global m6A methylation level. Knockdown of p53 or inhibition of p53’s transcriptional activity by addition of its specific inhibitor PFT-α decreased expression of ALKBH5 and CSCs’ malignancies, including proliferation, invasion, and tumor formation ability, indicating that p53 may partially regulate CSC’s malignancies via ALKBH5. Furthermore, we also found p53 transcriptionally regulates PRRX1, which is consistent with our previous report.ConclusionCollectively, our findings indicate the pivotal role of ALKBH5 in CSCs derived from NSCLC and highlight the regulatory function of the p53/ALKBH5 axis in modulating CSC progression, which could be a promising therapeutic target for NSCLC.

In the process of physical fitness training, it is an important subject of scientific physical fitness training to adjust and control the physical load intensity in real-time, accurately and effectively according to the physiological load inside the human body so as to make it consistent with the predetermined goal of the training plan. Aiming at the current demand of smartphone popularization and athlete training monitoring, this paper designs an intelligent monitoring system of physical fitness based on the Internet of Things technology. By selecting such factors as vertical jump, fast leg raising, sitting forward, height, chest circumference, percentage of body constitution, YOYO intermittent endurance running and so on, using RFID technology to mark different athletes, and after using the particle swarm optimization method of BP network to establish the evaluation model of the athletes' physical condition. Through simulation, the physical condition of athletes is accurately predicted, which provides a new scientific and technological means to improve the efficiency of physical training and make physical training scientific. INDEX TERMS Physical fitness, intelligent monitoring, The Internet of Things, BP neural network, particle swarm.

Defects in DNA repair pathways are emerging hallmarks of cancer. Accurate DNA repairs and replications are essential for genomic stability. Cancer cells require residual DNA repair capabilities to repair the damage from replication stress and genotoxic anti-tumor agents. Defective DNA repair also promotes the accumulation of genomic changes that eventually lead to tumorigenesis, tumor progression, and therapeutic resistance to DNA-damaging anti-tumor agents. Rad51 recombinase is a critical effector of homologous recombination, which is an essential DNA repair mechanism for double-strand breaks. Rad51 has been found to be upregulated in many malignant solid tumors, and is correlated with poor prognosis. In multiple tumor types, Rad51 is critical for tumor metabolism, metastasis and drug resistance. Herein, we initially introduced the structure, expression pattern of Rad51 and key Rad51 mediators involved in homologous recombination. Additionally, we primarily discussed the role of Rad51 in tumor metabolism, metastasis, resistance to chemotherapeutic agents and poly-ADP ribose polymerase inhibitors.