CR3 and Dectin-1 Collaborate in Macrophage Cytokine Response through Association on Lipid Rafts and Activation of Syk-JNK-AP-1 Pathway

Copyright: © 2015 Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Acknowledgments We are grateful to the Second Core Laboratory of Research Core Facility at the National Taiwan University Hospital for confocal microscopy service and providing ultracentrifuge. We thank Dr. William E. Goldman (University of North Carolina, Chapel Hill, NC) for kindly providing WT and ags1-null mutant of H. capsulatum G186A. Funding: This work is supported by research grants 101-2320-B-002-030-MY3 from the Ministry of Science and Technology (http://www.most.gov.tw) and AS-101-TP-B06-3 from Academia Sinica (http://www.sinica.edu.tw) to BAWH. GDB is funded by research grant 102705 from Welcome Trust (http://www.wellcome.ac.uk). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD

Hypothermic manipulation of bone cement can extend the handling time during vertebroplasty

BACKGROUND: Polymethylmethacrylate (PMMA) is commonly used for clinical applications. However, the short handling time increases the probability of a surgeon missing the crucial period in which the cement maintains its ideal viscosity for a successful injection. The aim of this article was to illustrate the effects a reduction in temperature would have on the cement handling time during percutaneous vertebroplasty. METHODS: The injectability of bone cement was assessed using a cement compressor. By twisting the compressor, the piston transmits its axial load to the plunger, which then pumps the bone cement out. The experiments were categorized based on the different types of hypothermic manipulation that were used. In group I (room temperature, sham group), the syringes were kept at 22°C after mixing the bone cement. In group 2 (precooling the bone cement and the container), the PMMA powder and liquid, as well as the beaker, spatula, and syringe, were stored in the refrigerator (4°C) overnight before mixing. In group 3 (ice bath cooling), the syringes were immediately submerged in ice water after mixing the bone cement at room temperature. RESULTS: The average liquid time, paste time, and handling time were 5.1 ± 0.7, 3.4 ± 0.3, and 8.5 ± 0.8 min, respectively, for group 1; 9.4 ± 1.1, 5.8 ± 0.5, and 15.2 ± 1.2 min, respectively, for group 2; and 83.8 ± 5.2, 28.8 ± 6.9, and 112.5 ± 11.3 min, respectively, for group 3. The liquid and paste times could be increased through different cooling methods. In addition, the liquid time (i.e. waiting time) for ice bath cooling was longer than for that of the precooling method (p < 0.05). CONCLUSIONS: Both precooling (i.e. lowering the initial temperature) and ice bath cooling (i.e. lowering the surrounding temperature) can effectively slow polymerization. Precooling is easy for clinical applications, while ice bath cooling might be more suitable for multiple-level vertebroplasty. Clinicians can take advantage of the improved injectability without any increased cost

Autophagy regulation in heme-induced neutrophil activation is associated with microRNA expression on transfusion-related acute lung injury

AbstractTransfusion-related acute lung injury (TRALI) is the leading cause of death after transfusion therapy. The pathogenesis of TRALI is associated with neutrophil activation in the lungs, causing endothelial damage and capillary leakage, and thus neutrophil extravasation. Heme-related molecules derived from the hemolysis of red blood cell components have been recognized as a stimulator, inducing neutrophil activation at TRALI. To investigate post-transcriptional changes of the neutrophil at TRALI, we performed heme-related molecules induced reactive oxygen species production in the neutrophil as a model. Neutrophils were isolated from heparinized peripheral blood and stimulated with heme-related molecules. After stimulation, reactive oxygen species production, degranulation, phagocytosis activity, and miRNA expression profile of neutrophil were analyzed by luminol assay, flow cytometry, and real-time polymerase chain reaction. The expression of miRNA targeting NADPH oxidase and autophagy in the neutrophil activation of TRALI was explored. The expression profile of miRNAs will be a useful predictor of disease severity and for the grading of patients for transfusion

Myeloid cells, BAFF, and IFN-γ establish an inflammatory loop that exacerbates autoimmunity in Lyn-deficient mice

Autoimmunity is traditionally attributed to altered lymphoid cell selection and/or tolerance, whereas the contribution of innate immune cells is less well understood. Autoimmunity is also associated with increased levels of B cell–activating factor of the TNF family (BAFF; also known as B lymphocyte stimulator), a cytokine that promotes survival of self-reactive B cell clones. We describe an important role for myeloid cells in autoimmune disease progression. Using Lyn-deficient mice, we show that overproduction of BAFF by hyperactive myeloid cells contributes to inflammation and autoimmunity in part by acting directly on T cells to induce the release of IFN-γ. Genetic deletion of IFN-γ or reduction of BAFF activity, achieved by either reducing myeloid cell hyperproduction or by treating with an anti-BAFF monoclonal antibody, reduced disease development in lyn−/− mice. The increased production of IFN-γ in lyn−/− mice feeds back on the myeloid cells to further stimulate BAFF release. Expression of BAFF receptor on T cells was required for their full activation and IFN-γ release. Overall, our data suggest that the reciprocal production of BAFF and IFN-γ establishes an inflammatory loop between myeloid cells and T cells that exacerbates autoimmunity in this model. Our findings uncover an important pathological role of BAFF in autoimmune disorders

Design of a bionic-inspired exoskeleton robot for lower limb assist

The design of an intelligent exoskeleton robot with pneumatic artificial muscles for human lower limb motion assist using electromyography (EMG) is presented. There are four topics addressed in this paper. Decoding electromyography is the first topic. When muscles are active, they produce an electrical activity. EMG is a record of this electrical activity that reflects human’s movement. Through regression analysis a model is obtained to extract motion commands from EMG. It would be an advantage to employ EMG as a control signal for the exoskeleton control. Second, the pneumatic artificial muscle, air muscle for short, is a simple and powerful actuator. When actuated with compressed air, it contracts and provides a pulling force. As a result of its behavior in a similar way to a biological muscle, air muscle is adapted for a bionic actuator of the assist robot. The force models of air muscles are investigated by experiments in a workbench. Third, for the control of a bionic-inspired robot, the multimodal sensory feedback including EMG and inertial sensors is necessary. By using EMG as a force-proportional measurement between human and robot, a control system combined a sensor-fusion approach and a compliant mechanism enables exoskeleton to carry out human-robot collaboration. Finally, a prototype of power-assist exoskeleton robot for lower limb is completed and evaluated by experiments successfully