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COVID-19 has caused enormous negative effects all over the world since the first confirmed case appeared in 2019. Social media has become an important way for people to get news about the epidemic due to convenience. However, rumors and fake news on social media destroy the trust of people. So how to improve the media trust and provide more useful information for people has become a great challenge for social media users. This paper will focus on the news post on Weibo in post-epidemic era, and discuss the factors that influence the media trust.

Background. Physical activity presents significant protection against death from cancer in the general population, so the global recommendations on physical activity for health are recommended by the WHO. While the recommendation is a guideline for general population, whether all cancer patients could get benefits from physical activity and whether the cancer patients who did not meet the requirement of the recommendation could get benefits from the physical activity, compared with the cancer patients with no physical activity, are unclear. Accordingly, we conducted a meta-analysis to identify whether the physical activity, even if low level of physical activity, could reduce the mortality of various cancer patients. Method. We conducted a systematic search of PubMed, Embase, and Cochrane Library for published cohorts and case-control studies of cancer survivors with physical activity comparing with no physical activity and reported outcomes of mortality through October 15, 2018. Two investigators independently reviewed the included studies and extracted relevant data. The effect estimate of interest was the hazard ratios (HRs). Results. There are 21811 participants in total in the nine studies, and 2386 cancer deaths in this meta-analysis. Among them, 1 was a case-control study and 8 were cohort studies. The meta-analysis results showed that physical activity was associated with a significantly reduced risk of mortality in cancer survivors, with a pooled HR and 95% CI of 0.66 (0.58∼0.73), reducing mortality by 34% and also suggested that low level of physical activity could reduce the mortality with an HR and 95% CI of 0.60 (0.50∼0.69). Conclusion. The results of this meta-analysis demonstrated that postdiagnosis physical activity, no matter the level of physical activity, could significantly reduce the mortality by 34%, compared with the no physical activity. At the same time, the results also suggested that cancer survivors undergoing low level of physical activity had a 40% reduction in mortality, which means that the cancer patients with poor ECOG need to do physical activity as much as they can, even if the amount of physical activity was low.

Trauma, infection, cancer, and congenital diseases can lead to bone defects. The combination of 3D printing with biomaterials is of great significance in the treatment of bone defects. In addition, pulse electromagnetic fields (PEMFs) can promote bone regeneration. The main purpose of this study was to evaluate the effects of 3D-printed scaffolds using β-tricalcium phosphate (β-TCP) as the raw material combined with a PEMF on the proliferation and differentiation of rat adipose stem cells (rADSCs) and on the repair of critical defects of the rat skull. The Cell Counting Kit-8 assay was performed to assess the proliferation of rADSCs. Alkaline phosphatase (ALP) activity, ALP staining, and the detection of osteogenic-related gene expression were performed to assess the differentiation of rADSCs. Micro-computed tomography and hematoxylin-eosin staining were used to assess the repair of rat skull defects. The results showed that the combination of the scaffold and PEMF could significantly promote the proliferation and differentiation of rADSCs and the repair of a critical defect in the rat skull. Therefore, the combination of β-TCP and PEMF with 3D printing technology can provide better treatment of clinical bone defect patients.

Antenna pattern distortion incorporating the systematic differences among array elements is one of the most important factors that decrease the accuracy of radar direction of arrival estimation. In this letter, a new antenna pattern measurement (APM) method based on a fully-digital radar receiver and a portable signal source is presented. Compared with previous methods, the proposed method not only improves the measurement accuracy, but also reduces the complexity and time cost of measurement. APM results of a compact high-frequency (HF) antenna measured in two modes are depicted, both showing that two independent measurements at the same site are highly consistent. Moreover, the method is further verified by a comparison of radar measured radial current velocity with acoustic Doppler current profiler data.

Bone homeostasis is a dynamic balance maintained by bone formation and resorption. An increase in the number and activity of osteoclasts leads to excessive bone resorption, which in turn results in bone disease, including osteoporosis. Therefore, inhibiting the differentiation and activity of osteoclasts is important for maintaining bone mass. Several studies have revealed that the use of a low‑frequency pulsed electromagnetic field (PEMF) is an effective method to treat osteoporosis. However, its exact mechanism remains to be fully clarified. Therefore, the present study was designed to examine the effects that PEMF exerts on receptor activator of nuclear factor‑κB ligand (RANKL)‑induced osteoclastogenesis and intracellular reactive oxygen species (ROS) production in RAW264.7 cells. The viability of cells was determined using a Cell Counting Kit‑8 assay, and gene and protein expression were investigated via reverse transcription‑quantitative polymerase chain reaction and western blot analyses. Furthermore, microscopy was performed to detect the levels of intracellular ROS and tartrate‑resistant acid phosphatase (TRAP). Following the culture of RAW264.7 cells with RANKL (50 ng/ml) for 4 days (3 h/day) under PEMF (75 Hz, 1 mt) exposure, it was observed that PEMF had an inhibitory effect on RANKL‑induced osteoclastic differentiation. Multinucleated osteoclast formation, the activity of TRAP and the expression of osteoclastogenesis‑associated genes, including cathepsin K, nuclear factor of activated T cells cytoplasmic 1 and TRAP, were significantly reduced by PEMF. Furthermore, PEMF effectively decreased the generation of intracellular ROS during osteoclastic differentiation. In addition, the results demonstrated that ROS are the key factor in osteoclast differentiation and formation. Reducing intracellular ROS with diphenylene‑iodonium chloride significantly inhibited RANKL‑induced osteoclast differentiation. Taken together, the results of the present study demonstrated that PEMF may inhibit RANKL‑induced osteoclastogenesis by scavenging intracellular ROS. These results may provide the groundwork for future PEMF clinical applications in osteoclast‑associated bone disease.

Recent investigations suggest microRNAs (miRs) exert functions in fibroblast osteogenesis in ankylosing spondylitis (AS), an inflammatory rheumatic disease. But the mechanism of miR-214-3p in osteogenic differentiation in AS is not clearly understood yet. In this study, fibroblasts were obtained from the capsular ligament of patients with AS and femoral neck fracture and cultured for osteogenic induction and identified. The roles of miR-214-3p and bone morphogenic protein 2 (BMP2) in AS fibroblast osteogenesis were assessed via gain- and loss-of-function, alizarin red S staining, and alkaline phosphatase (ALP) detection. Levels of miR-214-3p, BMP2, osteogenic differentiation-related proteins, and BMP–TGFβ axis-related proteins were further measured. Consequently, miR-214-3p was downregulated in AS fibroblasts, with enhanced ALP activity and calcium nodules, which were reversed by miR-214-3p overexpression. BMP2 was a target gene of miR-214-3p and promoted AS fibroblast osteogenesis by activating BMP–TGFβ axis, while miR-214-3p inhibited AS fibroblast osteogenesis by targeting BMP2. Together, miR-214-3p could prevent AS fibroblast osteogenic differentiation by targeting BMP2 and blocking BMP–TGFβ axis. This study may offer a novel insight for AS treatment.

Additional file 1: Table S1. Primer sequence

Monitoring small drones is significant for security requirements, but it is challenging because of small drones' low radar cross section (RCS) and hovering ability. In order to analyze the effect of radar waveform on the echo spectra and optimize the waveform design, an analytical expression of the rotor's temporal RCS is desired. Integral model, a widely used radar echo model of the rotor's temporal RCS, does not involve the electromagnetic scattering, thus it cannot be applied to all frequency bands. The method of moments (MoM) is a strictly numerical method based on the Maxwell's equations, but cannot obtain the analytical expression. Hence, this paper proposes a new method combing the integral model and MoM to model the rotor's temporal RCS in very high frequency (VHF) band. The linear frequency modulation (LFM) signal which has a high Doppler tolerance and a large gain bandwidth product is adopted in optimizing waveform parameters design. Based on the new method, the analytical expression of LFM echo is also derived. Moreover, the spectral spread over range and Doppler dimension caused by the rotating rotors is analyzed in detail. A criterion for optimizing the LFM waveform parameters for small drone detection is presented. Field experiments confirm the validity of the echo model and waveform parameters optimization criterion, and the full Acrylonitrile Butadiene Styrene small drone is successfully detected in VHF band. In addition, experiments are implemented to verify the applicability of the echo model and waveform parameters optimization method to other drones with different size.

The aim of this study was to investigate the effect of Curcumae Rhizoma-Sparganii Rhizoma (CR-SR) medicated serum on the changes of epithelial-mesenchymal transition (EMT) in the triple-negative breast cancer (TNBC). The EMT model was developed by using the TNBC MDA-MB-468 cells, which were treated with TGF-β1. The migration and invasion abilities of TGF-β1-treated MDA-MB-468 cells were detected by wound healing assay and transwell assay. Protein expression levels of E-cadherin and vimentin were determined by western blot. CR-SR medicated serum repressed the phenotypic transition in the TGF-β1-induced MDA-MB-468 cells. Moreover, CR-SR medicated serum inhibited TGF-β1-induced cell proliferation, migration and invasion. Besides, CR-SR medicated serum could reduce TGF-β1-induced up-regulation of the phosphorylation levels of Smad3, and reduce the expression of several transcription factors (Snail1, Snail2 and Twist1). CR-SR medicated serum might suppress TGF-β1-induced EMT in TNBC by decreasing the phosphorylated Smad3 (p-Smad3) pathway in vitro.

DNA damage response plays a critical role in tumor growth, but little is known about its potential role in bone metabolism. We employed selective inhibitors of Chk1 and examined their effects on the proliferation and migration of mammary tumor cells as well as the development of osteoblasts and osteoclasts. Further, using a mouse model of bone metastasis we evaluated the effects of Chk1 inhibitors on bone quality. Chk1 inhibitors blocked the proliferation, survival, and migration of tumor cells in vitro and suppressed the development of bone-resorbing osteoclasts by downregulating NFATc1. In the mouse model, Chk1 inhibitor reduced osteolytic lesions and prevented mechanical weakening of the femur and tibia. Analysis of RNA-seq expression data indicated that the observed effects were mediated through the regulation of eukaryotic translation initiation factor 2 alpha, stress to the endoplasmic reticulum, S100 proteins, and bone remodeling-linked genes. Our findings suggest that targeting Chk1 signaling without adding DNA damaging agents may protect bone from degradation while suppressing tumor growth and migration.

Keap1 is a negative controller of the transcription factor Nrf2 for its activity. The Keap1/Nrf2 signaling pathway has been considered as a master regulator of cytoprotective genes, and exists in many cell types including osteoblasts and osteoclasts. Our previous study shows Nrf2 deletion decreases bone formation. Recent studies show hyperactivation of Nrf2 causes osteopenia in Keap1−/− mice, and Keap1−/− osteoblasts have significantly less proliferative potential than Keap1+/− osteoblasts. We aimed to examine if moderate Nrf2 activation by disruption of Keap1 impacts bone metabolism. We examined bone phenotype of Keap1 heterozygotic mice (Ht) in comparison with Keap1 wild type (WT) mice. Deletion or knockdown of Keap1 enhanced the gene expression of Nrf2, ALP and wnt5a in cultured primary osteoblasts compared to WT control. In male mice, compared with their age-matched littermate WT controls, Keap1 Ht mice showed significant increase in bone formation rate (+30.7%, P = 0.0029), but did not change the ultimate force (P

Keap1 is a negative controller of the transcription factor Nrf2 for its activity. The Keap1/Nrf2 signaling pathway has been considered as a master regulator of cytoprotective genes, and exists in many cell types including osteoblasts and osteoclasts. Our previous study shows Nrf2 deletion decreases bone formation. Recent studies show hyperactivation of Nrf2 causes osteopenia in Keap1

Additional file 1: Table S1. Primer sequence

BACKGROUND A low frequency pulsed electromagnetic field (PEMF) has been confirmed to play an important role in promoting the osteogenic differentiation of human bone marrow stem cells (BMSCs). Adipose-derived stem cells (ASCs) possess some attractive characteristics for clinical application compared to BMSCs, such as abundant stem cells from lipoaspirates, faster growth, less discomfort and morbidity during surgery. ASCs can become adipocytes, osteoblasts, chondrocytes, myocytes, neurocytes, and other cell types. Thus, ASCs might be a good alternative in clinical work involving treatment with PEMF. MATERIAL AND METHODS Human ASCs (hASCs)were divided into a control group (without PEMF exposure) and an experimental group (PEMF for two hours per day). We examined the effect of PEMF on promoting cell proliferation and osteogenic differentiation from several aspects: CCK-8 proliferation assay, RNA extraction, qRT-PCR detection, western blotting, and immunofluorescence staining experiments. RESULTS PEMF could promote cell proliferation of human ASCs (hASCs) at an early stage as determined by CCK-8 assay. A specific intensity (1 mT) and frequency (50 Hz) of PEMF promoted osteogenic differentiation in hASCs in alkaline phosphatase (ALP) staining experiments. In addition, bone-related gene expression increased after two weeks of PEMF exposure, the protein expression of OPN, OCN, and RUNX-2 also increased after a longer period (three weeks) of PEMF treatment as determined by western blotting and immunofluorescence staining. CONCLUSIONS We found for the first time that PMEF has a role in stimulating cell proliferation of hASCs at an early period, subsequently promoting bone-related gene expression and inducing the expression of related proteins to stimulate osteogenic differentiation.

This review aims to assess the effect of Wuqinxi exercise for primary osteoporosis. Literature search was conducted on the seven databases until June 2015. No statistical differences were found between the Wuqinxi versus no intervention, Wuqinxi plus antiosteoporosis medications versus antiosteoporosis medications on lumbar spine bone mineral density (BMD). However, Wuqinxi significantly improved lumbar spine BMD compared with antiosteoporosis medications (MD= 0.02g/cm(2); 95% CI: 0.01-0.03; P

The aim of this study was to investigate the effect of Curcumae Rhizoma-Sparganii Rhizoma (CR-SR) medicated serum on the changes of epithelial-mesenchymal transition (EMT) in the triple-negative breast cancer (TNBC). The EMT model was developed by using the TNBC MDA-MB-468 cells, which were treated with TGF-β1. The migration and invasion abilities of TGF-β1-treated MDA-MB-468 cells were detected by wound healing assay and transwell assay. Protein expression levels of E-cadherin and vimentin were determined by western blot. CR-SR medicated serum repressed the phenotypic transition in the TGF-β1-induced MDA-MB-468 cells. Moreover, CR-SR medicated serum inhibited TGF-β1-induced cell proliferation, migration and invasion. Besides, CR-SR medicated serum could reduce TGF-β1-induced up-regulation of the phosphorylation levels of Smad3, and reduce the expression of several transcription factors (Snail1, Snail2 and Twist1). CR-SR medicated serum might suppress TGF-β1-induced EMT in TNBC by decreasing the phosphorylated Smad3 (p-Smad3) pathway in vitro.

Osteosarcoma remains the most prevalent primary malignant bone tumor in children and young adults globally. Therefore, novel and highly effective antitumor agents are urgently required. Elemene is a natural plant compound extracted from the medicinal Chinese herb, Rhizomazedoariae, which has been employed as an antitumor agent for the treatment of a number of tumors, including osteosarcoma. However, the mechanisms underlying its antitumor effect are currently unclear. The human osteosarcoma cell lines, MG‑63 and U2OS, were employed in the present study. MTT, migration, transwell invasion and terminal deoxynucleotidyltransferase‑mediated deoxy‑UTP‑fluorescein nick end‑labeling assays were performed to evaluate cell viability, migration, invasion and apoptosis, respectively. Western blotting and immunohistochemistry analyses were performed to measure the levels of renin‑angiotensin system (RAS) components. In order to evaluate the effect of elemene on tumor weight and volume, MG‑63 and U2OS cells were injected into mice. Treatment of osteosarcoma cell lines, MG‑63 and U2OS, with elemene led to the inhibition of cell viability, migration and invasion, as well as induction of cell apoptosis. In addition, elemene treatment downregulated the expression of a number of RAS components. The growth of osteosarcoma cell‑transplanted tumors in nude mice and angiotensin II expression were inhibited by elemene treatment. The results of the present study indicate that the antitumor effects of elemene may partly be due to downregulation of the RAS signaling pathway, and that RAS may be a putative pharmacological target for osteosarcoma therapy.

Background: Angio-Associated Migratory Cell Protein (AAMP) is a 52 kDa protein expressed in a variety of human cell lines. Previous studies have demonstrated that AAMP is involved in endothelial cell adhesion, migration, and tube formation and plays roles in signalling pathways, such as RhoA-ROCK Methods: In this study, we knocked down the expression of AAMP in HECV cells using hammerhead ribozymes and assessed the influence of AAMP on endothelial cells. In order to explore potential mechanisms, Wnt/β catenin inhibitors (FH535 or IWP2) were also used in a number of the functional assays and the immunofluorescent staining patterns of several key molecules were explored. Results: Knockdown of AAMP expression was observed in the HECV cell line following transfection with the ribozyme transgene. Cellular migration and attachment, assessed using ECIS methods, and tubule formation were significantly inhibited by the knockdown of AAMP. Additionally, cell growth and cell matrix adhesion was also substantially reduced following AAMP knockdown, though this did not reach significance. Cell aggregation levels showed no statistical difference between AAMP knockdown cells and control cells. Interestingly, immunofluorescence staining showed AAMP knockdown cells had a reduced expression of VE-cadherin. Some overlap of function was seen between AAMP knockdown and the FH535 inhibitor. Conclusion: AAMP appears to influence endothelial cell migration and tubule formation and potentially, to a lesser effect, cell matrix adhesion and growth and also affects the expression of VE-cadherin. This data suggests that AAMP may play a role in angiogenesis. Assays performed with the FH535 inhibitor suggest a potential relationship between AAMP and Wnt/β catenin signalling.

Angio-associated migratory cell protein (AAMP), which belongs to the immunoglobulin superfamily, was found to be expressed in different human cell lines and exhibited a predominant cytosolic localization in epithelial cells. Previous studies show that the specific gene product is functional in cell migration and angiogenesis and can also be used as a marker of poor prognosis in invasive gastrointestinal stromal tumours and ductal carcinoma in situ (DCIS) of the breast. However, the cellular role of AAMP in breast cancer is still unclear. The aim of the current study was to provide new insights into the implication of AAMP in breast cancer.We knocked-down the expression of AAMP through transfection of MCF-7 and MDA-MB-231 breast cancer cells with a hammerhead ribozyme transgene (MCF-7(AAMPrib) and MDA-MB-231(AAMPrib)) and examined the impact on cell function using in vitro assays. Additionally, AAMP expression was examined in a cohort of breast specimens (normal, n=28; cancer, n=102) using quantitative-real-time polymerase chain reaction (Q-PCR) and immunohistochemical methods.AAMP knock-down dramatically reduced cell adhesion and cell growth of MCF-7 cells (p0.05), and suppressed cell invasion of MDA-MB-231 cells (p0.05). Increased expression of AAMP in breast cancer was observed compared with that in normal tissues (p0.05). High levels of AAMP transcripts were associated with disease progression, metastasis, and poor prognosis of the patients. Disease-free and overall survival time of patients with lower levels of AAMP were significantly longer compared to those of patients with high levels (p0.05).AAMP has a significant influence on the biological functions of breast cancer cells and its high expression correlates with poor prognosis and metastasis.