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OBJECTIVE: The aim of this study was to analyze the biological effects of circ-0079593 and its potential mechanism in the progression of melanoma. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was carried out to detect circ-0079593 expression in melanoma tissue samples and cell lines, and the relationship between circ-0079593 expression and prognosis of patients with melanoma was analyzed based on collected clinical information. Then, the melanoma cell line stably overexpressing circ-0079593 was constructed using lentiviral stable transfection technique, and then, Cell Counting Kit-8 (CCK-8) and transwell assays were carried out to detect the proliferation rate, migration, as well as invasion abilities of melanoma cells, respectively. In addition, the potential binding targets of circ-0079593 were searched through bioinformatics analysis, and the results were verified by Dual-Luciferase assay. RESULTS: It was found that, in comparison with the normal control group, circ-0079593 showed a significantly high expression in melanoma tissues and cell lines, which predicted a poor prognosis of melanoma patients. In vitro experiments showed that the overexpression of circ-0079593 remarkably enhanced proliferation rate, as well as invasion ability of melanoma cells. Moreover, bioinformatics data analysis revealed that there exist binding sites of microRNA-433 both in circ-0079593 and EGFR. Meanwhile, the results of the Luciferase assay confirmed that circ-0079593 probably bound to microRNA-433, as an endogenous competitive RNA (ceRNA), to regulate EGFR expression. At last, cell reverse experiments demonstrated that the overexpression of microRNA-433 could attenuate the capacity of melanoma cells to proliferate and migrate, while simultaneous overexpression of circ-0079593 partially restored those cell functions. CONCLUSIONS: In melanoma, circ-0079593 may serve as a cancer-promoting gene to accelerate the rates of cell proliferation and migration, which may exert its effects by elevating EGFR expression by binding to microRNA-433. [ABSTRACT FROM AUTHOR]

The response of a ballistic two-dimensional electron gas (2DEG) confined to a Hall cross and subjected to a locally inhomogeneous magnetic field which is created by two parallel or antiparallel magnetized cylindrical dots deposited above the 2DEG is investigated. The Hall and bend resistances are calculated as a function of the magnetization of the magnetic dots for different positions of the dots on the Hall bar. The Hall and bend resistances are different for parallel and antiparallel magnetized dots and depend on the relative position of the magnetic dots on the Hall bar. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Deregulated expression of miRNAs contributes to the development of acute myeloid leukemia (AML). miR-504-3p, one of these miRNAs, has been found have upregulated expression in various human malignancies. Our present study aimed to detect the expression of miR-504-3p and its biological effect in AML. PATIENTS AND METHODS: Real-time quantitative PCR was applied to evaluate the expression level of miR-504-3p in AML cell lines and the serum from AML cases. The correlations between miR-504-3p and AML patients' clinicopathological characteristics, as well as AML patients' overall survival, were statistically assessed. Moreover, we investigated the effect of miR-504-3p knockdown on AML cells by CCK-8, Transwell assays and flow cytometry, in vitro. The Western blot, RT-PCR and luciferase reporter assay were performed to evaluate the relationship between miR-504-3p and its downstream target genes. Finally, the biological function of MTHFD2 was also analyzed. RESULTS: The expression levels of miR-504-3p were significantly down-regulated in the serum of AML patients and cell lines, and its low expression was positively associated with advanced clinical stages and poor prognosis of AML patients. Functional assays indicated that overexpression of miR-504-3p leads to AML cell growth arrest, invasion and migration inhibition, and elevated rates of apoptosis. We also found that miR-504-3p regulated the expression of MTHFD2 by binding to its 3'-UTR, and knockdown of MTHFD2 significantly suppressed AML cells proliferation, migration and invasion, and promoted apoptosis. CONCLUSIONS: Our findings provide important evidence that supports the role of miR-504- 3p as a tumor suppressor in AML via the inhibition of MTHFD2 expression. [ABSTRACT FROM AUTHOR]

The objective of the study described here is to fundamentally elucidate the biological response of 3D printed Ti-6Al-4V alloy mesh structures that were surface modified to introduce titania nanotubes with an average pore size of ∼80 nm via an electrochemical anodization process from the perspective of enhancing bioactivity. The bioactivity of the mesh structures were analyzed through immersion test in simulated body fluid, which confirmed the nucleation and growth of fine globular nanoscale apatite on the nanoporous titania-modified (anodized) mesh structure surface, and agglomerated apatite with fine flakes of apatite crystals on as-fabricated mesh structure surface, that were rich in calcium and phosphorous. The cellular activity of bioactive anodized mesh structure was explored in terms of cell–material interactions involving adhesion, proliferation, synthesis of extracellular and intracellular proteins, differentiation, and mineralization. Cells adhered with a sheet-like morphology on as-fabricated mesh structure, whereas, on anodized mesh structure, numerous filopodia-like cellular extensions interacting with nanotube pores were observed. The formation of a bioactive nanoscale apatite, cell–nanotube interactions as imaged via electron microscopy, higher expression of proteins (actin, vinculin, fibronectin, and alkaline phosphatase (ALP)), and calcium content points toward the determining role of anodized mesh structure in modulating osteoblasts functions. The unique combination of nanoporous bioactive titania and interconnected porous architecture of anodized titanium alloy mesh structure provided a multimodal roughness surface ranging from nano to micro to macroscale, which helps in attaining strong primary and secondary fixation of the implant device along with the pathway for supply of nutrients and oxygen to cells and tissue. [ABSTRACT FROM AUTHOR]

The leaching kinetics of 20CaO·13Al2O3·3MgO·3SiO2(Q phase) was studied in this paper. The effects of agitation speed, leaching temperature, concentration of sodium carbonate, particle size and liquid–solid ratio on alumina leaching ratio of Q phase were investigated. The results indicate that the agitation speed did not influence alumina leaching ratio when it was higher than 400 r min−1, and the effect of liquid film diffusion on the leaching process was eliminated. The alumina leaching ratio would not increase by changing the liquid–solid ratio, when the concentration of sodium carbonate was excessive. The leaching process of Q phase was better as both the temperature and the concentration of sodium carbonate were higher and the particle size was smaller. The effect of concentration of sodium carbonate on alumina leaching ratio was not obvious. The leaching kinetics followed the shrinking unreacted core model, the reaction order of leaching process of Q phase was 0.47, and it can be described by surface chemical reaction. The activation energy was 41.63 ± 10 kJ mol−1, and the frequency factor was 1.472 × 103. [ABSTRACT FROM AUTHOR]

We report a real-time method to determine the size, i.e. diameter, and refractive index of single gold nanoparticles using an optofluidic chip, which consists of a quasi-Bessel beam optical chromatography. The tightly focused (~ 0.5 μm) quasi-Bessel beam with low divergence (NA ~ 0.04) was used to trap sub-100 nm gold nanoparticles within a long trapping distance of 140 μm. In the experiment, 60 to 100 nm gold nanoparticles were separated efficiently with at least 18 μm. The diameter and refractive index (real and imaginary) of single gold nanoparticles were measured at high resolutions with respect to the trapping distance, i.e. 0.36 nm/μm, 0.003/μm and 0.0016/μm, respectively. [ABSTRACT FROM AUTHOR]

Titanium alloys (Ti-6Al-4V and Ti-6Al-7Nb) are widely used for implants, which are characterized by high elastic modulus (∼110 GPa) with (α + β) structure and that may induce undesirable stress shielding effect and immune responses associated with the presence of toxic elements. In this regard, we have combined the attributes of a new alloy design and the concept of additive manufacturing to fabricate 3D scaffolds with an interconnected porous structure. The new alloy is a β-type Ti-24Nb-4Zr-8Sn (Ti2448) alloy with significantly reduced modulus. In the present study, we explore the biological response of electron beam melted low modulus Ti2448 alloy porous mesh structure through the elucidation of bioactivity and osteoblast functions. The cellular activity was explored in terms of cell-to-cell communication involving proliferation, spreading, synthesis of extracellular and intracellular proteins, differentiation, and mineralization. The formation of fine apatite-like crystals on the surface during immersion test in simulated body fluid confirmed the bioactivity of the scaffold surface, which provided the favorable osteogenic microenvironment for cell-material interaction. The combination of unique surface chemistry and interconnected porous architecture provided the desired pathway for supply of nutrients and oxygen to cells and a favorable osteogenic micro-environment for incorporation (on-growth and in-growth) of osteoblasts. The proliferation and differentiation of pre-osteoblasts and their ability to form a well mineralized bone-like extracellular matrix (ECM) by secreting bone markers (ALP, calcium, etc.) over the struts of the scaffold point toward the determining role of unique surface chemistry and 3D architecture of the Ti2448 alloy mesh structure in modulating osteoblasts functions. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 859-870, 2017. [ABSTRACT FROM AUTHOR]