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For tailoring the mechanical and magnetic properties of dual-phase high-entropy alloys (HEAs), it is crucial to understand the effect of each phase on the overall properties. In this paper, the effects of individual FCC and BCC phases on the mechanical and magnetic properties of the FeCoNi(CuAl)0.8 HEA are investigated by nanoindentation and first-principles calculations. The nano-hardness of the BCC phase is 8.73 GPa, which is nearly double the 4.60 GPa of the FCC phase, which ascribes to spherical nanoprecipitates that are only observed in the BCC phase leading to precipitation hardening. First-principles calculations on the electronic structure show that calculated saturation magnetization (Ms) of the BCC phase is 0.81 T, higher than 0.77 T of the FCC phase. An approximate yield strength and Ms can be estimated by summing the volume-fraction-weighted contributions from each phase, and are in good agreement with experimental values. It indicates that the overall mechanical and magnetic properties of the dual-phase HEAs can be tailored by tuning the volume fraction of the individual phase. Our findings are helpful to design prospective dual-phase HEAs with both good mechanical properties and soft magnetic performance by adjusting the content of each phase. [ABSTRACT FROM AUTHOR]

Purpose: To define and predict early recurrence (ER) in patients with gastric cancer (GC) who underwent radical gastrectomy after neoadjuvant chemotherapy (NAC). Methods: The present study included 573 patients who underwent NAC followed by curative resection for GC between January 2014 and December 2019. The patients were randomly divided into the training (n = 382) and validation (n = 191) cohorts in a 2:1 ratio. The optimal cut-off value of recurrence-free survival for defining ER was determined based on post-recurrence survival (PRS). Risk factors for ER were identified by logistic regression. A nomogram was further constructed and evaluated. Results: The optimal cut-off value for defining ER was 12 months. Overall, 136 patients (23.7%) experienced ER and had significantly shorter median PRS (4 vs. 13 months, P < 0.001). In the training cohort, factors independently associated with ER included age (P = 0.026), Lauren classification (P < 0.001), preoperative carcinoembryonic antigen (P = 0.029), ypN staging (P < 0.001), major pathological regression (P = 0.004), and postoperative complications (P < 0.001). A nomogram integrating these factors exhibited higher predictive accuracy than the ypTNM stage alone in both the training and validation cohorts. Moreover, the nomogram enabled significant risk stratification in both cohorts; only the high-risk patients could benefit from adjuvant chemotherapy (ER rate: 53.9% vs. 85.7%, P = 0.007). Conclusion: A nomogram involving preoperative factors can accurately predict the risk of ER and guide individualized treatment strategies for GC patients following NAC, which may assist in clinical decision-making. [ABSTRACT FROM AUTHOR]

Aim: Vitamin D3 has been implicated in multiple reproductive events, whereas the effect of its bioactive metabolite 1α, 25 dihydroxyvitamin D3 (1,25(OH) 2D3) on transcriptome profile of the placenta is unclear. The aim of this article is to determine transcriptome‐wide profile caused by 1,25(OH) 2D3 in human placental trophoblast cells. Methods: We performed RNA sequencing after stimulation of HTR‐8/SVneo cells with 0.1, 1, 10, and 100 nM 1,25(OH)2D3 for 24 h, identified differentially expressed genes by edgeR package (version 3.38.4), and analyzed Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways by webtool Metascape. Also, common genes and specific genes in different concentrations of 1,25(OH) 2D3 were identified. Results: There were 180, 158, 161, and 174 differentially expressed genes after 0.1, 1, 10, and 100 nM 1,25(OH) 2D3 stimulation, respectively. KEGG pathway analysis displayed that "lipid and atherosclerosis" were significantly enriched at 0.1 and 1 nM 1,25(OH)2D3, while "cytokine‐cytokine receptor interaction," "TGF‐beta signaling pathway" and "hippo signaling pathway" were significantly enriched in 1, 10, and 100 nM 1,25(OH)2D3. CYP24A1 was a significantly expressed common gene. UCP3 was significantly expressed in low concentrations and might affect energy metabolism. TCF24, EIF3CL, ABCD2, EPHA7, CRLF1, and SECTM1 were specific genes at physiological concentration. Similarly, SPDYE1, IQUB, IL18R1, and ZNF713 were considered as specific genes at supraphysiological concentration. Conclusions: 1,25(OH)2D3 mainly affected the expression of CYP24A1 gene in HTR‐8/SVneo cells. Specific genes accounted for the majority of differentially expressed genes at different concentrations. However, their functions need to be further confirmed. [ABSTRACT FROM AUTHOR]

Let A (n , d) be the size of the maximum binary code of length n and minimum Hamming distance d. A (n , d , w) is defined similarly for binary code with constant weight w. Obviously, finding the value of A (n , d) is equivalent to finding the maximum independent set of the d − 1 th-power of n -dimensional hypercube. Based on this, this paper obtains that A (3 m , 2 m) = 4 , A (m (m + 1) 2 , 2 m − 2 , m) = m + 1 , A (2 m + 1 − 2 , 2 m − 1) = 2 m + 1 , and explores the structure of the maximum code of length 2 m + 2 and minimum Hamming distance 2 m + 1 , where m is an integer. [ABSTRACT FROM AUTHOR]

Background and Aims. MicroR-23b-3p (miR-23b-3p) has been found to be abnormally expressed in a variety of malignant tumors and to play a role in tumor inhibition or promotion. However, the regulatory mechanism of miR-23b-3p in COAD remains unclear. The purpose of this study was to investigate the clinical significance of miR-23b-3p expression in COAD cells and to explore its role and regulatory mechanism in the growth of COAD. Materials and Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure miR-23b-3p expression in COAD tissues and cell lines. After transfecting miR-23b-3p mimics into two human COAD cell lines (SW620 and LoVo), the cell counting kit-8 (CCK-8), colony formation, and 5-ethynyl-2′-deoxyuridine (EdU) assays were used to detect cell proliferation, the Transwell assay was used to measure cell migration and invasion capacity, and flow cytometry was used to evaluate cell apoptosis in vitro. In addition, a luciferase reporter assay was used to determine whether miR-23b-3p targets NFE2L3. The downstream regulatory mechanisms of miR-23b-3p action in COAD cells were also investigated. For in vivo tumorigenesis assay, COAD cells stably overexpressing miR-23b-3p were injected subcutaneously into the flank of nude mice to obtain tumors. Results. Significantly decreased expression of miR-23b-3p was detected in COAD tissues and cell lines. Exogenous miR-23b-3p expression inhibited cell proliferation, migration, and invasion and promoted cell apoptosis of COAD cells in vitro. Nuclear factor erythroid 2 like 3 (NFE2L3) was identified as a direct target gene of miR-23b-3p. In addition, reintroduction of NFE2L3 partially abolished the anticancer effects of miR-23b-3p on COAD cells. Furthermore, miR-23b-3p overexpression hindered the growth of COAD cells in vivo. Conclusion. miR-23b-3p inhibited the oncogenicity of COAD cells in vitro and in vivo by directly targeting NFE2L3, suggesting the importance of the miR-23b-3p/NFE2L3 pathway in the development of COAD. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC) is a common malignancy worldwide with a high mortality rate. lncRNA SFTA1P is highly expressed in HCC. We aimed to study the role of SFTA1P in HCC and its relationship with miR-4766-5p. Materials and Methods: The levels of SFTA1P in HCC tissues and cell lines were determined. Relationship between SFTA1P and clinical features and prognosis was studied. The influence of SFTA1P on HCC cell viability, migration, invasion and apoptosis was studied in vitro. Rescue experiments were conducted after the binding site between SFTA1P and miR-4766-5p confirmed by dual-luciferase assay. The protein expression of AKT, p-AKT, mTOR and p-mTOR in HCC cells with knockdown of SFTA1P was determined by Western blotting. A tumor study in nude mice was conducted in order to assess the effects of SFTA1P on tumor growth characteristics. Results: SFTA1P was up-regulated in HCC tissues and cell lines. SFTA1P expression was closely related to tumor size, vascular invasion and TNM stage. Knockdown of SFTA1P inhibited HCC cell viability, migration and invasion and promoted cell apoptosis. MiR-4766-5p was a target of SFTA1P and knockdown of SFTA1P could decrease the protein expression of p-AKT and p-mTOR. Rescue experiments showed that miR-4766-5p mimics could attenuate the promoting role of SFTA1P on HCC cell viability, invasion and migration, and inhibiting role on cell apoptosis. Moreover, we used nude mice models and also found that the knockdown of SFTA1P reduced tumor volume and weight. Conclusion: lncRNA SFTA1P could promote tumor development in HCC by down-regulating miR-4766-5p expression via PI3K/AKT/mTOR signaling pathway. It may be a potential therapeutic target for HCC. [ABSTRACT FROM AUTHOR]