Multiple-Beam Steering Using Graphene-Based Coding Metasurfaces.

Recently, the coding metasurface has gained significant attention due to its exceptional potential in controlling electromagnetic (EM) waves with the rapid development of wireless communication systems. Meanwhile, graphene shows tremendous promise for the implementation of reconfigurable antennas due to its high tunable conductivity and its unique property that makes it a very suitable material for realizing steerable coded states. In this paper, we first propose a simple structured beam reconfigurable millimeter wave (MMW) antenna using a novel graphene-based coding metasurface (GBCM). Different from the previous method, its coding state can be manipulated by altering the sheet impedance of graphene instead of bias voltage. Then, we design and simulate several most popular coding sequences, including dual-, quad-and single-beam-generated implement, 30° beam deflection, as well as a random coding sequence for radar cross-section (RCS) reduction. The theoretical and simulation results show that graphene has great potential for MMW manipulation applications, which lay a foundation for the subsequent development and fabrication of GBCM.

Analysis of Landscape Ecological Planning Based on the High-Order Multiwavelet Neural Network Algorithm.

Landscape architecture has both natural and social properties, which is the embodiment of people protecting the natural environment. Since the industrial revolution, the modern industry has developed rapidly. It has increased the living standard of people and consumed a lot of natural resources such as forest and energy. The ecological environment has been greatly damaged, and the landscape of gardens has been affected. Therefore, it is of great significance to find a method to evaluate the landscape ecology and plan the landscape ecology. This paper proposes a new high-order wavelet neural network algorithm combining wavelet analysis and artificial neural network. A model of ecological evaluation of landscape based on high-order wavelet neural network algorithm is proposed to evaluate the landscape ecology and provide reference data for the ecological planning of the landscape. The results show that the training times of the wavelet neural network to achieve the target accuracy are 3600 times less than those of the BP neural network. The MSE and MAE of the WNN are 0.0639 and 0.1501, respectively. The average error of the model to the comprehensive evaluation index of the landscape ecology is 0.005. The accuracy of the model to evaluate the sustainability of landscape land resources is 98.67%. The above results show that the model based on the wavelet neural network can effectively and accurately complete the evaluation of landscape ecology and then provide a decision-making basis for landscape ecological planning, which is of high practicability.

miR-342-5p inhibits expression of Bmp7 to regulate proliferation, differentiation and migration of osteoblasts.

BACKGROUND: Fracture healing is a complex process, and patients with fracture will undergo non-union or compromised regeneration. MicroRNA (miR)-342-5p is a Notch downstream molecule, and its roles in fracture healing remain unclear. We aimed to explore the functional roles of miR-342-5p in osteoblasts as well as the underlying mechanisms. METHODS: The expression of miR-342-5p in differentiation of MC3T3-E1 cells or hMSCs was examined by quantitative reverse transcription PCR (qRT-PCR). The effects of aberrantly expressed miR-342-5p on cell proliferation, apoptosis, migration, and expressions of proteins associated with proliferation and osteogenic differentiation were determined by Cell Counting Kit-8, trypan blue staining, flow cytometry, Transwell assay, Western blot and qRT-PCR assays, respectively. The downstream factor and the target genes of miR-342-5p as well as the involvements of the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway were finally assessed. RESULTS: miR-342-5p level was decreased during differentiation of MC3T3-E1 cells or hMSCs. After cell transfection, miR-342-5p overexpression significantly reduced cell viability, induced apoptosis, inhibited proliferation, migration and differentiation, and down-regulated Bmp7 expression. Subsequent experiments showed the effects of miR-342-5p inhibition on MC3T3-E1 cells were abrogated by Bmp7 knockdown. Additionally, COL4A6 and Bmp2 were predicated as target genes of miR-342-5p. Finally, phosphorylated levels of MEK and ERK were increased by miR-342-5p inhibition via up-regulating Bmp7 expression. CONCLUSION: miR-342-5p inhibition promoted proliferation, migration and differentiation of osteoblasts via regulating Bmp7, along with activation of the MEK/ERK pathway.

Lipopolysaccharides-mediated injury to chondrogenic ATDC5 cells can be relieved by Sinomenine via downregulating microRNA-192.

Sinomenine (SIN) is an isoquinoline derived from Caulis Sinomenii that has been used to treat rheumatoid arthritis and osteoarthritis for several decades in China. This study aims to reveal the effects of SIN on mouse chondrogenic ATDC5 cells growth and inflammation. SIN was used to treat ATDC5 cells injured by lipopolysaccharides (LPS). The following parameters were determined for evaluating the treatment effects of SIN: cell viability, apoptosis, reactive oxygen species generation, and pro-inflammatory cytokines release. Besides, the expression of LPS-sensitive miRNA (miR-192) and the activation of NF-κB and MAPK signaling were studied to explain SIN's function. SIN with concentration of 30 µM significantly attenuated LPS-induced cell damage via increasing cell viability, inhibiting apoptosis and reactive oxygen species generation, and declining IL-6 and TNF-α release. miR-192 was downregulated by SIN treatment. Restoration of miR-192 expression by miRNA transfection could significantly impede SIN's protective action. Besides, the inhibitory effects of SIN on the activation of NF-κB and MAPK signaling were attenuated by miR-192 overexpression. Furthermore, GDF11 was found to be a target gene of miR-192. LPS-mediated injury to chondrogenic ATDC5 cells can be relieved by SIN via downregulating miR-192 and subsequently repressing the activation of NF-κB and MAPK signaling.

Long noncoding RNA CHRF exacerbates IL-6-induced inflammatory damages by downregulating microRNA-146a in ATDC5 cells.

Osteoarthritis (OA) is a frequent chronic musculoskeletal disorder which lacks applicably effective therapeutic strategy. In this study, we attempted to investigate whether long noncoding RNA (lncRNA) cardiac hypertrophy-related factor (CHRF) participated in mediating interleukin-6 (IL-6)-induced in vitro inflammatory damages as well as the regulatory mechanisms. ATDC5 cells were stimulated with IL-6, and then cellular damages were evaluated on the basis of cell viability by CCK-8, apoptotic cells by observation with flow cytometry, apoptosis-associated proteins by western blot analysis, and accumulation of inflammatory factors by quantitative reverse transcription polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and western blot analysis. Then, effects of lncRNA CHRF on IL-6-treated cells were evaluated. We further explored the downstream factor of lncRNA CHRF and demonstrated whether lncRNA CHRF functioned through the downstream factor. Afterwards, crucial signaling cascades were anatomized. We found that IL-6 reduced cell viability, elevated apoptosis, induced upregulation of inflammatory factors, as well as upregulated lncRNA CHRF and down-regulated miR-146a expression. Then, we found lncRNA CHRF overexpression aggravated IL-6-induced alterations, and lncRNA CHRF knockdown showed the opposite effects. Furthermore, miR-146a was identified to be negatively regulated by lncRNA CHRF, and its overexpression abrogated the roles of lncRNA CHRF in IL-6-treated cells. IL-6-induced the accumulation of IκBα, p65, JAK1, and STAT3 at phosphorylated level was further facilitated by lncRNA CHRF whereas repressed by miR-146a. In conclusion, lncRNA CHRF aggravated the IL-6-induced inflammatory damages in ATDC5 cells. We further outlined a possible mechanism that through downregulating miR-146a, lncRNA CHRF evoked the activation of NF-κB and JAK1/STAT3 signaling cascades.

MicroRNA-493-5p inhibits proliferation and metastasis of osteosarcoma cells by targeting Kruppel-like factor 5.

Osteosarcoma, including spinal osteosarcoma, has properties of high degree of malignancy, high rate of recurrence, and high incidence of metastasis. microRNAs can exert oncogenic or tumor suppressive roles in cancer cells. This study explored the effects of microRNA-493-5p (miR-493-5p) on osteosarcoma cell viability, migration, invasion, and apoptosis, as well as the underlying possible mechanism. First, the expression of miR-493-5p in osteosarcoma tissues and cells was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Then, the effects of miR-493-5p overexpression (or suppression) on osteosarcoma cell viability, migration, invasion, and apoptosis, as well as Kruppel-like factor 5 (KLF5) expression, were assessed using the Cell Counting Kit-8 assay, two-chamber transwell assay, Annexin V-FITC/PI apoptosis detection kit, qRT-PCR, and western blotting, respectively. Finally, the roles of KLF5 in miR-493-5p suppression-induced U20S cell viability, migration, and invasion enhancement, as well as the PI3K/AKT pathway activation, were evaluated. We found that miR-493-5p had lower expression in tumor tissues of spinal osteosarcoma and osteosarcoma cells. Overexpression of miR-493-5p inhibited osteosarcoma U20S cell viability, migration, and invasion, but induced cell apoptosis. On the contrary, suppression of miR-493-5p-promoted U20S cell viability, migration, and invasion. KLF5 was a direct target gene of miR-493-5p, which participated in the effects of miR-493-5p on U20S cell viability, migration, invasion, and apoptosis. Furthermore, suppression of the miR-493-5p activated PI3K/AKT pathway in U20S cells by upregulating KLF5. In conclusion, we revealed that miR-493-5p exerted tumor suppressive roles in spinal osteosarcoma and osteosarcoma cells. Overexpression of miR-493-5p inhibited proliferation and metastasis of osteosarcoma cells by downregulating KLF5 and inactivating the PI3K/AKT signaling pathway.

Kaempferol protects chondrogenic ATDC5 cells against inflammatory injury triggered by lipopolysaccharide through down-regulating miR-146a.

Kaempferol is a kind of bioflavonoid exerts diverse pharmacological activities, including anti-apoptotic and anti-inflammatory activities. Kaempferol has been recognized as an effective agent for alleviating the clinical symptoms of osteoarthritis (OA). This study aimed to provide evidence that Kaempferol has potential in the management of OA. Lipopolysaccharide (LPS) stimulation induced a significant cell death and inflammatory injury in ATDC5 cells, as evidenced by the decreased cell viability, the induced apoptosis, the activated caspase-3, and the excessive production of IL-6, IL-8 and TNF-α. Precondition of cells with Kaempferol prevented apoptosis and the release of proinflammatory cytokines triggered by LPS. miR-146a was down-regulated by Kaempferol treatment, and Decorin was up-regulated by miR-146a overexpression. Consistently, both silence of miR-146a and Decorin exhibited Kaempferol-like effects towards ATDC5 cells stimulated by LPS. Moreover, Decorin silence activated PI3K/AKT/mTOR signaling pathway. In rat model of OA, the expression of miR-146a and Decorin in cartilage tissues was repressed by Kaempferol. Also, the activated PI3K/AKT/mTOR signaling pathway in OA animal model was enhanced by Kaempferol administration. These data suggested that Kaempferol exerted potential anti-OA effects through down-regulation of miR-146a, and thus repressing the expression of Decorin.

RETRACTED: MicroRNA-19a promotes cell viability and migration of chondrocytes via up-regulating SOX9 through NF-κB pathway.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. Given the comments of Dr Elisabeth Bik regarding this article "The Western blots and other figures in this paper have an interesting layout that appears to be shared with many other papers … In almost all papers, Western blot panels within the same figure, and across figures and papers, appear to share the same background, while the bands are regularly spaced, all have similar rounded edges without the usual smudges and specks, and with some bands showing a recognizable "jumping sardine" shape", the journal requested the authors to provide the raw data. However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article.