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Nowadays, with the continuous development of the times, multimedia technology(MT) is rapidly infiltrating people's lives, and people are paying more and more attention to multimedia teaching, which has been well applied in vocal music(VM) teaching. Since VM is a highly practical and relatively abstract subject, it is necessary to organically combine theory with practice. In addition, nowadays people have higher and higher requirements for music aesthetics, and the enrollment scale of VM majors is increasing, making traditional teaching methods no longer able to meet the needs of vocal talents. Because the network MT can well solve the problems in the traditional classroom and make up for the shortcomings, it has played an important role in improving classroom efficiency, improving the quality of teaching and teaching effects. At the same time, the use of modern methods for VM teaching can also provide teachers with more convenience. Therefore, under this background, it is necessary to combine modern education methods with VM teaching mode(VMTM) to realize the transformation of VMTM. This article uses questionnaire survey method and data analysis method to make use of the advantages of computer network MT to make VM teaching simpler and more intuitive, so as to achieve better VM teaching effects. According to the survey results, most interviewees believe that the application of computer network MT in the VMTM has certain effects and brings a lot of vitality to the development of the course.

Due to the characteristics of high recurrence and metastasis, it is still difficult to cure lung cancer. Cancer stem cells (CSCs) are a group of tumor cells with self-renewal ability and differentiation potential, which are responsible for lung cancer recurrence. Therefore, targeting CSCs may provide a new strategy for lung cancer treatment. Thymoquinone (TQ), the main active ingredient isolated from black seed oil, has shown significant anti-cancer effects in various cancers. However, the effect of TQ on lung cancer stem cells (LCSCs) has never been clarified. In the present study, we successfully separated and enriched lung cancer tumorsphere cells. Our data showed that TQ significantly inhibited the stem-like properties of LCSCs. In addition, we found TQ promoted Yes-associated protein (YAP) phosphorylation and ubiquitination, and the inhibitory effects of TQ on LCSCs could be enhanced by silencing YAP. Taken together, these results suggest that TQ, functions by targeting YAP, may be a potential therapeutic agent against lung cancer. [ABSTRACT FROM AUTHOR]

A hypergraph $\mathcal{F}$ is non-trivial intersecting if every pair of edges in it have a nonempty intersection, but no vertex is contained in all edges of $\mathcal{F}$. Mubayi and Verstraëte showed that for every $k \ge d+1 \ge 3$ and $n \ge (d+1)k/d$ every $k$ -graph $\mathcal{H}$ on $n$ vertices without a non-trivial intersecting subgraph of size $d+1$ contains at most $\binom{n-1}{k-1}$ edges. They conjectured that the same conclusion holds for all $d \ge k \ge 4$ and sufficiently large $n$. We confirm their conjecture by proving a stronger statement. They also conjectured that for $m \ge 4$ and sufficiently large $n$ the maximum size of a $3$ -graph on $n$ vertices without a non-trivial intersecting subgraph of size $3m+1$ is achieved by certain Steiner triple systems. We give a construction with more edges showing that their conjecture is not true in general. [ABSTRACT FROM AUTHOR]

A k‐uniform hypergraph with n vertices is an (n,k,ℓ)$$ \left(n,k,\ell \right) $$‐omitting system if it has no two edges with intersection size ℓ$$ \ell $$. If in addition it has no two edges with intersection size greater than ℓ$$ \ell $$, then it is an (n,k,ℓ)$$ \left(n,k,\ell \right) $$‐system. Rödl and Šiňajová proved a sharp lower bound for the independence number of (n,k,ℓ)$$ \left(n,k,\ell \right) $$‐systems. We consider the same question for (n,k,ℓ)$$ \left(n,k,\ell \right) $$‐omitting systems. Our proofs use adaptations of the random greedy independent set algorithm, and pseudorandom graphs. We also prove related results where we forbid more than two edges with a prescribed common intersection size leading to some applications in Ramsey theory. For example, we obtain good bounds for the Ramsey number rk(F,t)$$ {r}_k\left(F,t\right) $$, where F is the k‐uniform Fan. The behavior is quite different than the case k=2$$ k=2 $$ which is the classical Ramsey number r(3,t)$$ r\left(3,t\right) $$. [ABSTRACT FROM AUTHOR]

The triangle covering number of a graph is the minimum number of vertices that hit all triangles. Given positive integers s,t and an n‐vertex graph G with ⌊n2∕4⌋+t edges and triangle covering number s, we determine (for large n) sharp bounds on the minimum number of triangles in G and also describe the extremal constructions. Similar results are proved for cliques of larger size and color critical graphs. This extends classical work of Rademacher, Erdős, and Lovász–Simonovits whose results apply only to s≤t. Our results also address two conjectures of Xiao and Katona. We prove one of them and give a counterexample and prove a modified version of the other conjecture. [ABSTRACT FROM AUTHOR]

A conjecture of Chung and Graham states that every K4‐free graph on n vertices contains a vertex set of size ⌊n∕2⌋ that spans at most n2∕18 edges. We make the first step toward this conjecture by showing that it holds for all regular graphs. [ABSTRACT FROM AUTHOR]

Background: Dapagliflozin is commonly used to treat type 2 diabetes mellitus (T2DM). However, research into the specific anti-T2DM mechanisms of dapagliflozin remains scarce., Objective: This study aimed to explore the underlying mechanisms of dapagliflozin against T2DM., Methods: Dapagliflozin-associated targets were acquired from CTD, SwissTargetPrediction, and SuperPred. T2DM-associated targets were obtained from GeneCards and DigSee. VennDiagram was used to obtain the overlapping targets of dapagliflozin and T2DM. GO and KEGG analyses were performed using clusterProfiler. A PPI network was built by STRING database and Cytoscape, and the top 30 targets were screened using the degree, maximal clique centrality (MCC), and edge percolated component (EPC) algorithms of CytoHubba. The top 30 targets screened by the three algorithms were intersected with the core pathway-related targets to obtain the key targets. DeepPurpose was used to evaluate the binding affinity of dapagliflozin with the key targets., Results: In total, 155 overlapping targets of dapagliflozin and T2DM were obtained. GO and KEGG analyses revealed that the targets were primarily enriched in response to peptide, membrane microdomain, protein serine/threonine/tyrosine kinase activity, PI3K-Akt signaling pathway, MAPK signaling pathway, and AGE-RAGE signaling pathway in diabetic complications. AKT1, PIK3CA, NOS3, EGFR, MAPK1, MAPK3, HSP90AA1, MTOR, RELA, NFKB1, IKBKB, ITGB1, and TP53 were the key targets, mainly related to oxidative stress, endothelial function, and autophagy. Through the DeepPurpose algorithm, AKT1, HSP90AA1, RELA, ITGB1, and TP53 were identified as the top 5 anti-targets of dapagliflozin., Conclusion: Dapagliflozin might treat T2DM mainly by targeting AKT1, HSP90AA1, RELA, ITGB1, and TP53 through PI3K-Akt signaling., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Triple-negative breast cancer (TNBC) has long been considered a major clinical challenge due to its aggressive behavior and poor prognosis. Cancer stem cells (CSCs) are known as the main cells responsible for tumor origination, progression, recurrence and metastasis. Here, we report that M2-type tumor-associated macrophages (TAMs) contribute to cancer stemness in TNBC cells via the secretion of VEGFA. Reciprocally, elevated VEGFA expression by TAM-educated TNBC cells acts as a regulator of macrophage polarization, therefore constitute a feed-back loop between TNBC cells and TAMs. Mechanistically, VEGFA facilitates the CSC phenotype via the NRP-1 receptor and downstream GAPVD1/Wnt/β-catenin signaling pathway in TNBC cells. Our study underscores the crosstalk between TNBC cells and TAMs mediated by VEGFA and further clarifies the role and underlying mechanisms of the VEGFA/NRP-1/GAPVD1 axis in regulating cancer stemness. We also document an immunosuppressive function of VEGFA in the tumor microenvironment (TME). Therefore, the present study indicates crosstalk between TNBC cells and TAMs induced by VEGFA and provides a potential implication for the combination of immunotherapy and VEGFA-targeted agents in TNBC therapy., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

The role of microRNAs (miRNAs) in regulating gene expression is currently an area of intense interest. Previous studies have shown that miRNA-372 plays crucial roles in gastric tumorigenesis by targeting the mRNA of tumor necrosis factor, α-induced protein 1 (TNFAIP1). The present study showed that miR-373 is upregulated in gastric adenocarcinoma tissue and gastric carcinoma cell lines when compared to normal gastric tissues. The overexpression of miR-373 in the gastric cancer cells increased cell proliferation. A bioinformatics search revealed a conserved target site within the 3' untranslated region (UTR) of TNFAIP1, an immediate-early response gene of the endothelium induced by TNF-α. The overexpression of miR-373 caused the suppression of a luciferase reporter containing the TNFAIP1 3'UTR in the HEK293 cells and reduced the levels of TNFAIP1 protein in the AGS cells. The mRNA levels of TNFAIP1 in the gastric cancer and normal gastric tissues were negatively correlated with the expression levels of miR-373 in these tissues. Moreover, the knockdown of TNFAIP1 had a similar effect to the overexpression of miR-373. The overexpression of TNFAIP1 may partly rescue the inhibition of proliferation caused by the inhibitor, miR-373-ASO. Taken together, these findings demonstrate an oncogenic role for miR-373, similar to that of miR-372, in controlling cell growth through the downregulation of TNFAIP1.

Caudatin has been reported to trigger apoptosis in several types of cancer cell lines. In the present study, we investigated whether caudatin has therapeutic value in gastric cancer and examined the effects of caudatin on the expression of β-catenin in human gastric carcinoma cell lines. Here, we showed that caudatin treatment resulted in a dose- and time‑dependent inhibition of proliferation of the gastric carcinoma cell lines. Cell cycle analysis demonstrated that caudatin induced G0/G1 arrest and downregulated CDK2 levels. In contrast, the expression of the p21 protein was increased. AGS cells treated with caudatin exhibited typical characteristics of apoptosis, which were accompanied by activation of caspase‑3, ‑8, ‑9 and PARP. Western blot analysis and immunocytochemical staining showed that caudatin induced a reduction in β‑catenin expression and this reduction was due to proteosome-mediated degradation. This reduction in β‑catenin activation was due to the downregulation of its downstream targets cyclinD1 and c‑MYC in all gastric carcinoma cell lines. Furthermore, we demonstrated that gastric adenocarcinoma tissues and AGS cells exhibited abnormal expression of miR‑372. Additionally, caudatin downregulated the expression of oncomir miR‑372 and miR‑21, and upregulated tumor suppressor let‑7a miRNA expression. These data revealed that inhibition of Wnt/β‑catenin signaling is a novel mechanism of action for caudatin during therapeutic intervention in gastric cancers.

Aberrant microRNA (miRNA) expression has been investigated in gastric cancer, which is one of the most common malignancies. However, the roles of miRNAs in gastric cancer remain largely unknown. In the present study, we found that microRNA-372 (miR-372) directly targets tumor necrosis factor, α-induced protein 1 (TNFAIP1), and is involved in the regulation of the NFκB signaling pathway. Furthermore, overexpression of TNFAIP1 induced changes in AGS cells similar to those in AGS cells treated with miR-372-ASO. Collectively, these findings demonstrate an oncogenic role for miR-372 in controlling cell growth and apoptosis through downregulation of TNFAIP1. This novel molecular basis provides new insights into the etiology of gastric cancer.