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In this article, three dimensional elastic-plastic curved crack tip opening displacement under quasi-static loads has been mainly studied, and three dimensional curved crack tip opening displacement has been calculated as a practical application of a second order perturbation method, where the effects of quasi-static applied stresses and quasi-static normal and shear stresses on the boundaries of plasticity area are synthetically taken into considerations. Three dimensional curved elastic-plastic crack tip opening displacement has been calculated by numerical solutions, diagrams have been constructed to analyse the transformation relationships between curved crack tip opening displacement and three dimensional crack body geometrical measurement. Curved crack tip opening displacement will decrease when three dimensional crack body thickness increases. When crack body thickness increases evenly, three dimensional curved crack tip opening displacement will continuously decrease, furthermore, the decrease extent will be more and more slightly, and tend to plane strain state ultimately. Curved crack tip opening displacement will increase when external loads increase with the same crack body thickness. A new theoretical model where curved crack tip opening displacement was calculated has been established in three dimensional crack body.

MicroRNAs (miRNAs) are a class of short (approximately 22 nucleotides), non-coding and endogenous RNA molecules that play pivotal roles in the occurrence and development of cancer. The present study aimed to investigate key miRNAs involved in papillary thyroid carcinoma (PTC). Two independent datasets (GSE73182 and GSE113629) were obtained from the GEO database. The differentially expressed miRNAs (DEmiRNAs) between PTC tissues and normal thyroid tissues were analyzed by GEO2R with the Limma R package. Key miRNAs in PTC were identified by the VennDiagram R package. The targets of the key miRNAs were predicted by miRWalk and were functionally enriched by clusterProfiler R package. Five miRNAs including hsa-miR-146b-5p, hsa-miR-15a-5p, hsa-miR-21-5p, hsa-miR-221-3p and hsa-miR-222-3p were identified as key miRNAs in PTC. The expression levels of these key miRNAs were upregulated in PTC. This finding was also confirmed in the other dataset. Target prediction of miRNAs indicated that hsa-miR-146b-5p, hsa-miR-15a-5p, hsa-miR-21-5p, hsa-miR-221-3p and hsa-miR-222-3p exhibited 2, 41, 3, 14 and 8 target genes, respectively. Enrichment analysis indicated that these key miRNAs were mainly involved in nine biological processes, such as regulation of MAP kinase activity, JNK cascade signaling and regulation of protein serine/threonine kinase activity) and in 28 pathways, including the mitogen associated protein kinase, the sphingolipid, ErbB, Ras and the C-type lectin receptor signaling pathways. In conclusion, the present study identified several key miRNAs in PTC, which serve as potential targets for PTC diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Background: The dysfunction of cell apoptosis is an important event in the progression of cancer, and the growth of cancer cells is negatively regulated by cell apoptosis. In different types of cancers, inhibition of cellular apoptosis is often observed in the cancerous tissue, and increased resistance to apoptosis is a hallmark of cancer. Although previous studies have shown that 12-lipoxygenase (12-LOX)/12-hydroxyeicosatetraenoic acid (12-HETE) is activated and upregulated in different types of cancers, the consequences of 12-LOX/12-HETE upregulation and its precise roles in the survival of ovarian carcinoma cells are still unknown.Methods: MTT assays, caspase activity assays, lactate dehydrogenase (LDH) assays, and Western blot analysis were the methods used in this study.Results: In our study, we found that 12-HETE, a major metabolic product of arachidonic acid using 12-LOX catalysis, inhibited cell apoptosis in a dose-dependent manner and that the effects of 12-HETE on cell apoptosis were mediated by the integrin-linked kinase (ILK) pathway. Moreover, the downstream target of 12-HETE-activated ILK was nuclear factor kappa-B (NF-κB) in ovarian carcinoma. The inhibitory effects of 12-HETE on cell apoptosis were attenuated by the inhibition of the NF-κB pathway.Conclusion: These results indicate that 12-HETE participates in the inhibition of cell apoptosis by activating the ILK/NF-κB pathway, implying an important underlying mechanism that promotes the survival of ovarian cancer cells. [ABSTRACT FROM AUTHOR]