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Bacterial contamination of medical devices not only constitutes a serious threat to the health of patients, but also promotes the evolution of bacterial drug-resistance. Here, a new strategy to fabricate a highly efficient self-cleaning antibacterial coating is reported. Briefly, a nano-topological structure is formed on the substrate surface by the deposition of a gold nanoparticle layer (GNPL), and then antimicrobial peptide mimetics (AMPMs) with optimized structure and catalase (CAT) are modified on the surface. The optimized AMPMs not only inhibit the growth of over 99% of

The development of a fast and safe reactive oxygen species (ROS)-responsive vector is generally limited by the intracellular unstable ROS concentration, and a relatively long time is still needed for the complete intracellular release of drugs or genes induced by ROS. In this work, a gene transfection platform based on ROS-responsive silicon nanowire arrays (SN) is developed, to promote the gene transfection efficiency for several cell lines. Briefly, the surface of the ROS generating system, gold nanoparticle modified SN (SN-Au), is grafted with poly[(2-acryloyl)ethyl(

Low surface energy materials with micro-nano structures have been widely developed to prevent non-specific adhesion of biomolecules. Herein we put forward a new approach based on the antifouling and self-assembly properties of fluorine components, to construct a non-specific protein resistance surface with selective protein adsorption property. Briefly, the antifouling surface (SN-F) was obtained by a simple one-step modification on silicon nanowire arrays (SiNWAs) with fluorine coupling agent 1 H,1 H,2 H,2 H-perfluorodecyltrimethoxysilane (FAS). And protein was fluorinated by conjugation with an amphiphilic fluoro-copolymer, produced from 2-methacrylamido glucopyranose (MAG) and trifluoroethyl methacrylate (TFEMA) via RAFT polymerization. The properties of the materials were characterized by

Natural killer cells are the first line of host immune surveillance and play major roles in the defence against infection and tumours. Hepatic NK cells exhibit unique phenotypic and functional characteristics compared to circulating and spleen NK cells, such as higher levels of cytolytic activity and cytotoxicity mediators against tumour cells. However, the activities of NK cells may be reversed during tumour progression. Recent studies demonstrated that hepatic NK cells were exhausted in hepatocellular carcinoma (HCC) and exhibited impaired cytolytic activity and decreased production of effector cytokines. The present review discusses current knowledge on the role of exhausted NK cells in promoting HCC development and the mechanisms contributing to tumour immune escape, including an imbalance of activating and inhibitory receptors on NK cells, abnormal receptor-ligand interaction, and cross-talk with immune cells and other stromal cells in the tumour environment. We provide a fundamental basis for further study of innate immunity in tumour progression and serve the purpose of exploring new HCC treatment strategies.

Background Despite titanium (Ti) implants have been commonly used in the medical device field due to their superior biocompatibility, implant-associated bacterial infection remains a major clinical complication. Nanosilver, an effective antibacterial agent against a wide spectrum of bacterial strains, with a low-resistance potential, has attracted much interest too. Incorporation of nanosilver on Ti implants may be a promising approach to prevent biofilm formation. Purpose The objective of the study was to investigate the antibacterial effects and osteoinductive properties of nanosilver/poly (dl-lactic-co-glycolic acid)-coated titanium (NSPTi). Methods Gram-positive methicillin-resistant Staphylococcus aureus (MRSA) and the Gram-negative opportunistic pathogen Pseudomonas aeruginosa (PAO-1) were used to evaluate the antibacterial activity of NSPTi implants through the analysis of bacterial colonization in vitro and in vivo. Furthermore, we examined the osteoinductive potential of NSPTi implants by investigating the proliferation and differentiation of MC3T3-E1 preosteoblast cells. In vivo, the osteoinductive properties of NSPTi implants were assessed by radiographic evaluation, H&E staining, and Masson's trichrome staining. Results In vitro, bacterial adhesion to the 2% NSPTi was significantly inhibited and

Exosomes are extracellular vesicles released from numerous types of cells that are involved in multiple tumors development. Exosomes contribute to the modulation of tumor microenvironment (TME) through intercellular communication. As essential immune stromal cells in the TME, tumor-associated macrophages (TAMs) participate in tumor development by mediating angiogenesis, metastasis, chemoresistance, and immune escape. Due to communication with multiple cells in the TME, they exhibit plasticity and heterogeneity during the progress of polarization from monocytes to macrophages. Previous studies suggest that targeting TAMs is a promising therapeutic strategy; however, the detailed mechanism by which TAMs regulate tumor development still remains unclear. In this review, we provide an overview of the roles of exosomes as messengers in the communication between tumor cells and polarization of TAMs; we also describe the effects of their interaction on tumor development. Finally, we comprehensively discussed the potential application of exosomes as the promising tumor immunotherapy strategy.

Background Cancer stem cells (CSCs) have been proposed to be responsible for tumor recurrence and chemo-resistance. Previous studies suggested that miR-153 played essential roles in lung cancer. However, the molecular mechanism of miR-153 in regulating the stemness of non-small cell lung cancer (NSCLC) remains poorly understood. In this study, we investigated the role of miR-153 in regulation of the stemness of NSCLC. Methods The stemness property of lung stem cancer cells was detected by sphere formation assay, immunofluorescence, and Western blot. Luciferase reporter assay was performed to investigate the direct binding of miR-153 to the 3′-UTR of JAG1 mRNA. Animal study was conducted to evaluate the effect of miR-153 on tumor growth in vivo. The clinical relevance of miR-153 in NSCLC was evaluated by Rt-PCR and Kaplan-Meier analysis. Results MiR-153 expression was decreased in lung cancer tissues. Reduced miR-153 expression was associated with lung metastasis and poor overall survival of lung cancer patients. Jagged1, one of the ligands of Notch1, is targeted by miR-153 and inversely correlates with miR-153 in human lung samples. More importantly, we found that miR-153 inhibited stem cell-like phenotype and tumor growth of lung adenocarcinoma through inactivating the Jagged1/Notch1 axis. Conclusion MiR-153 suppresses the stem cell-like phenotypes and tumor growth of lung adenocarcinoma by targeting Jagged1 and provides a potential therapeutic target in lung cancer therapy.

Additional file 1: Figure S1. Uncropped full-length blot images for Fig. 2b, 4a, b. The cropped blots were marked with red frame.

In the field of security monitoring, flame detection system is used to realize large-scale, high-precision and real-time monitoring. Traditional flame detection systems have many problems, such as higher cost, less flexibility, low precision, small scale and poor real-time performance. In this paper, a novel flame detection system based on embedded GPU is proposed to achieve a high-precision and real-time flame detection. The flame detection algorithm is optimized to meet the requirements of high precision, and the hardware acceleration of the flame detection algorithm is realized by using OpenVX framework to satisfy real-time processing restriction. The experimental results show that the system can achieve accurate real-time monitoring of the flame on many occasions. Compared with the use of the PC server, embedded system can reduce the cost of system, increase the scope and flexibility of the monitoring. Furthermore, the powerful parallel computing ability of GPU enables the system to meet the real-time requirements, so the system has a certain practical value.

Power-gating-aware design has been an active area of research in the last decade, aiming at reducing power dissipation while meeting a desired system throughput. In this study, an algorithm integrating both scheduling and binding processes is developed with the functional unit (FU) power-gating technique, to achieve maximum leakage energy reduction under both performance and resource constraints. Firstly, the possible leakage energy reductions of all idle intervals are analyzed by evaluating the operation mobilities. Secondly, a min-cost flow-based algorithm is conducted to evaluate the total leakage energy saving from power-gating FUs, and operations are scheduled to the clock cycles with maximization of the leakage energy saving. Finally, all operations are bound to FUs following the min-cost flow solution of the network derived from the final scheduling result. Experimental results show the effectiveness of our algorithm in leakage energy reduction.

Baicalin is a flavonoid compound isolated from Scutellaria baicalensis, a Chinese traditional medicinal herb, and is used as an anti-inflammatory, antibacterial, anxiolytic and hepatoprotective drug. Accumulating evidence has demonstrated that baicalin exhibits potent antitumor properties by suppressing cell growth, arresting cell cycle progression and inducing differentiation or apoptosis in leukemia cell lines. However, whether or not the extrinsic pathway is involved in baicalin-induced apoptosis of leukemia cells and the mechanisms underlying the antitumor activity of baicalin remain unclear. In the present study, the effect of baicalin on the expression of caspase-8, Fas cell surface death receptor (Fas) and Fas ligand in HL-60 cells was assessed, and it was demonstrated that the Fas-mediated extrinsic pathway was also involved in baicalin-triggered cell apoptosis, in addition to the intrinsic pathway. Furthermore, baicalin was able to inhibit the proliferation of HL-60 cells by arresting the cell cycle at the G0/G1 phase, and by down-regulating Myc proto-oncogene protein (c-Myc) along with its target gene, human telomerase reverse transcriptase. In summary, the results of the present study demonstrated that baicalin was able to inhibit the growth of HL-60 cells through blockade of the G0/G1 phase of the cell cycle, and significantly induce the apoptosis of cells by activating the intrinsic and extrinsic pathways. The inhibition of HL-60 cell growth was also demonstrated to be mediated by telomerase inhibition through suppression of c-Myc. The results of the present study highlight the possibility of baicalin as a promising regimen for the treatment of AML.

Honokiol [3,5-di-(2-propenyl)-1,1-biphenyl-2,2-diol; HNK], a natural bioactive molecular compound isolated from the Magnolia officinalis, exhibits potent antitumor activity against a variety of human cancer cell lines. However, few studies have reported the antineoplastic effects of HNK on glioblastoma cells. It remains unknown how apoptosis is induced by HNK in glioblastoma cells and through which associated pathway this compound acts. The present study confirmed that HNK inhibited proliferation of glioblastoma cells by inducing a slight G0/G1 phase cell cycle arrest and apoptosis. We demonstrated for the first time that HNK triggered apoptosis of glioblastoma cells through both caspase-independent and caspase-dependent pathways, the latter including the extrinsic pathway and intrinsic pathway. Moreover, the inhibition of STAT3 signaling, ERK1/2 as well as activation of the p38 MAPK signaling pathway may be involved in apoptosis induced by HNK in U87 cells. Our findings suggest that HNK treatment could be a promising therapeutic strategy in human glioblastoma.

Oridonin, obtained from the traditional Chinese herbal medicine rabdosia rubescens, exerts potent antitumor activities in cancer cells. Valproic acid (VPA), as a potent histone deacetylase inhibitor (HDACI), also plays an important role in inhibition of proliferation of tumor cells. However, there are no reports so far on the cooperation between oridonin and VPA for anti-leukemic effect. Therefore, in the present study, we undertook experiments to determine whether lower concentration of oridonin in conjunction with lower concentration of VPA would produce even more encouraging synergistic effect than each of them alone, and to clarify its molecular mechanism. The results demonstrated that the lower concentration of oridonin in combination with lower concentration of VPA synergistically inhibited the proliferation of HL-60 cells, and induced obvious caspase-dependent apoptosis through activation of the intrinsic apoptosis pathway, which is involved in the downregulation of Bcl-2/Bax ratio, release of cytochrome c to cytosol and caspase-9 activation, as well as through the extrinsic apoptosis pathway mediated by Fas/FasL and caspase-8 activation. In addition, MAPK signaling pathway was also involved in apoptosis induced by oridonin plus VPA. Furthermore, the combination treatment in vivo remarkably reduced the xenograft tumor size and triggered tumor cell apoptosis. Taken together, the novel combination of oridonin plus VPA exerted synergistic anti-proliferative and apoptosis-inducing effects on human myeloid leukemia cells, and may serve as a potential promising anti-leukemia strategy.

Hexamethylene bisacetamide (HMBA) and natural flavanoid baicalin both exert potent antileukemic activity. However, there is currently no data on the anti-leukemic effects of baicalin in combination with HMBA. In the present study, we demonstrated that the combination of baicalin and HMBA synergistically inhibited the proliferation of acute myeloid leukemia (AML) cell lines. In addition, a slight G0/G1 phase arrest and significant apoptosis were observed. The combination treatment triggered apoptosis through the intrinsic pathway, which involved loss of MMP, decreased Bcl‑2/Bax ratio and Bcl‑XL/Bax ratio, caspase‑9 activation, as well as through the extrinsic pathway mediated by Fas and caspase‑8 activation. On the other hand, combination of baicalin and HMBA showed little toxic effect on peripheral blood mononuclear cells from healthy volunteers. Our results raise the possibility that the novel combination of baicalin and HMBA may be a promising regimen for the treatment of AML.