With the continuous improvement of roads in China, the number of vehicles, complexity of traffic and personalized needs of vehicle owners are also increasing gradually, which makes the routing planning particularly important. As a result, it is more and more important to develop appropriate routing planning algorithms to meet the needs of vehicles. However, most of the existing algorithms only solve the problem for a certain condition, rather than meeting the multiple conditions. In view of the above-mentioned problems, this paper describes the multi-condition vehicle routing planning algorithm and the current development status quo in detail by referring to the materials, analyzes the process of each algorithm and points out its advantages and disadvantages. Finally, the future trend of the vehicle routing planning algorithm under multiple conditions is predicted.
The article analyzes the application of association rules at libraries both at home and abroad on the application of related documents in libraries, and analyzes them from the application of association rules in digital library personalized recommendation services, library resource configuration management and reader behavior analysis. The status of application, and put forward the prospects for its future development.
Overexpression of adenosine triphosphate-binding cassette (ABC) transport protein is emerging as a critical contributor to anticancer drug resistance. The eukaryotic translation initiation factor (eIF) 4F complex, the key modulator of mRNA translation, is regulated by the phosphoinositide 3-kinase-AKT‑mammalian target of rapamycin pathway in anticancer drug‑resistant tumors. The present study demonstrated the roles of ABC translation protein alterations in the acquisition of the Adriamycin (ADM)‑resistant phenotype of MCF‑7 human breast cells. Quantitative polymerase chain reaction and western blot analysis were applied to examine the differences in mRNA and protein levels, respectively. It was found that the expression of the ABC sub‑family B member 1, ABC sub‑family C member 1 and ABC sub‑family G member 2 transport proteins were upregulated in MCF‑7/ADR cells. An MTT assay was used to detect the cell viability, from the results MCF‑7/ADR cells were less sensitive to ADM, tamoxifen (TAM) and taxol (TAX) treatment compared with MCF‑7 cells. We predicted that the 3'‑untranslated region of eukaryotic translation initiation factor 4‑γ 1 (eIF4G) contains a potential miRNA binding site for microRNA (miR)‑503 through using computational programs. These binding sites were confirmed by luciferase reporter assays. eIF4G mRNA degradation was accelerated in cells transfected with miR‑503 mimics. Furthermore, it was demonstrated that eIF4G and ABC translation proteins were significantly downregulated in MCF‑7/ADR cells after transfection with miR‑503. It was found that miR‑503 mimics could sensitize the cells to treatment with ADM, TAM and TAX. These findings demonstrated for the first time that eIF4G acted as a key factor in MCF‑7/ADR cells, and may be an efficient agent for preventing and reversing multi‑drug resistance in breast cancer.
In the internet age, whether a book has the value of reading, online comments play an important role.The data set in this paper is 4,000 comments obtained by the web crawler in Douban Reading.Based on the improved support vector machine (SVM) algorithm, a sentiment analysis has been given to these comments.The experimental results show that the improved SVM algorithm has a good effect on the rate and accuracy of sentiment polarity analysis of book reviews.
The triggering receptor expressed on myeloid cells-1 (TREM-1) is a pro-inflammatory immune receptor potentiating acute lung injury (ALI).However, the mechanism of TREM-1-triggered inflammation response remains poorly understood.Here, we showed that TREM-1 blocking attenuated NOD-, LRRand pyrin domain-containing 3 (NLRP3) inflammasome activation and glycolysis in LPS-induced ALI mice.Then, we observed that TREM-1 activation enhanced glucose consumption, induced glycolysis, and inhibited oxidative phosphorylation in macrophages.Specifically, inhibition of glycolysis with 2-deoxyglucose diminished NLRP3 inflammasome activation of macrophages triggered by TREM-1.Hypoxia-inducible factor-1α (HIF-1α) is a critical transcriptional regulator of glycolysis.We further found that TREM-1 activation facilitated HIF-1α accumulation and translocation to the nucleus via the phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway.Inhibiting mTOR or HIF-1α also suppressed TREM-1-induced metabolic reprogramming and NLRP3/caspase-1 activation.Overall, the mTOR/HIF-1α/glycolysis pathway is a novel mechanism underlying TREM-1-governed NLRP3 inflammasome activation.Therapeutic targeting of the mTOR/HIF-1α/glycolysis pathway in TREM-1-activated macrophages could be beneficial for treating or preventing inflammatory diseases, such as ALI.
Rationale: Dysregulation of arachidonic acid (ARA) metabolism results in inflammation; however, its role in acute lung injury (ALI) remains elusive.In this study, we addressed the role of dysregulated ARA metabolism in cytochromes P450 (CYPs) /cyclooxygenase-2 (COX-2) pathways in the pathogenesis of lipopolysaccharide (LPS)-induced ALI in mice.Methods: The metabolism of CYPs/COX-2-derived ARA in the lungs of LPS-induced ALI was investigated in C57BL/6 mice.The COX-2/sEH dual inhibitor PTUPB was used to establish the function of CYPs/COX-2 dysregulation in ALI.Primary murine macrophages were used to evaluate the underlying mechanism of PTUPB involved in the activation of NLRP3 inflammasome in vitro.Results: Dysregulation of CYPs/COX-2 metabolism of ARA occurred in the lungs and in primary macrophages under the LPS challenge.Decrease mRNA expression of Cyp2j9, Cyp2j6, and Cyp2j5 was observed, which metabolize ARA into epoxyeicosatrienoic acids (EETs).The expressions of COX-2 and soluble epoxide hydrolase (sEH), on the other hand, was significantly upregulated.Pre-treatment with the dual COX-2 and sEH inhibitor, PTUPB, attenuated the pathological injury of lung tissues and reduced the infiltration of inflammatory cells.Furthermore, PTUPB decreased the pro-inflammatory factors, oxidative stress, and activation of NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in LPS-induced ALI mice.PTUPB pre-treatment remarkably reduced the activation of macrophages and NLRP3 inflammasome in vitro.Significantly, both preventive and therapeutic treatment with PTUPB improved the survival rate of mice receiving a lethal dose of LPS. Conclusion:The dysregulation of CYPs/COX-2 metabolized ARA contributes to the uncontrolled inflammatory response in ALI.The dual COX-2 and sEH inhibitor PTUPB exerts anti-inflammatory effects in treating ALI by inhibiting the NLRP3 inflammasome activation.
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