18 research outputs found
Suppressing Anion Repulsion for Enhancing Li-Mediated Nitrogen Reduction
No full textElectrochemical lithium-mediated nitrogen reduction (Li-NRR) presents a sustainable alternative to Haber-Bosch for ammonia synthesis. Efficiency and stability are critically governed by the solid electrolyte interphase (SEI), which regulates reactant transport and suppresses side reactions. While anion-derived SEI formed under anion-rich solvation is beneficial, conventional electric double layer (EDL) repel anion at the cathode, limiting favorable SEI formation. Therefore, this study introduces cationic ionomer additives that form a positively charged ionic interfacial layer, mitigating anion repulsion and reducing interfacial solvent accumulation. An imidazolium (C3H4N2)-functionalized cation ionomer enables the formation of a tailored EDL, achieving a Faradaic efficiency and ammonia yield of 92 +/- 3% and 58 +/- 4 nmol s-1 cm-2, markedly surpassing the conventional EDL (63 +/- 7%, 28 +/- 9 nmol s-1 cm-2). A significant decrease in anion repulsion was confirmed via computational and in situ spectroscopic analyses. The demonstrated applicability across various lithium salts clearly reveals the overall effectiveness of this cationic ionomer-based EDL engineering in Li-NRR.
Universal hydrogel adhesives with robust chain entanglement for bridging soft electronic materials
No full textEnsuring stable integration of diverse soft electronic components for reliable operation under dynamic conditions is crucial. However, integrating soft electronics, comprising various materials like polymers, metals, and hydrogels, poses challenges due to their different mechanical and chemical properties. This study introduces a dried-hydrogel adhesive made of poly(vinyl alcohol) and tannic acid multilayers (d-HAPT), which integrates soft electronic materials through moisture-derived chain entanglement. d-HAPT is a thin (similar to 1 mu m) and highly transparent (over 85% transmittance in the visible light region) adhesive, showing robust bonding (up to 3.6 MPa) within a short time (<1 min). d-HAPT demonstrates practical application in wearable devices, including a hydrogel touch panel and strain sensors. Additionally, the potential of d-HAPT for use in implantable electronics is demonstrated through in vivo neuromodulation and electrocardiographic recording experiments while confirming its biocompatibility both in vitro and in vivo. It is expected that d-HAPT will provide a reliable platform for integrating soft electronic applications.
Follow the Footprints: Self-supervised Traversability Estimation for Off-road Vehicle Navigation based on Geometric and Visual Cues
No full textIn this study, we address the off-road traversability estimation problem,
that predicts areas where a robot can navigate in off-road environments. An
off-road environment is an unstructured environment comprising a combination of
traversable and non-traversable spaces, which presents a challenge for
estimating traversability. This study highlights three primary factors that
affect a robot's traversability in an off-road environment: surface slope,
semantic information, and robot platform. We present two strategies for
estimating traversability, using a guide filter network (GFN) and footprint
supervision module (FSM). The first strategy involves building a novel GFN
using a newly designed guide filter layer. The GFN interprets the surface and
semantic information from the input data and integrates them to extract
features optimized for traversability estimation. The second strategy involves
developing an FSM, which is a self-supervision module that utilizes the path
traversed by the robot in pre-driving, also known as a footprint. This enables
the prediction of traversability that reflects the characteristics of the robot
platform. Based on these two strategies, the proposed method overcomes the
limitations of existing methods, which require laborious human supervision and
lack scalability. Extensive experiments in diverse conditions, including
automobiles and unmanned ground vehicles, herbfields, woodlands, and farmlands,
demonstrate that the proposed method is compatible for various robot platforms
and adaptable to a range of terrains. Code is available at
https://github.com/yurimjeon1892/FtFoot.Comment: Accepted to IEEE International Conference on Robotics and Automation
(ICRA) 202
Focal stimulation of retinal ganglion cells using subretinal 3D microelectrodes with peripheral electrodes of opposite current
No full textSubretinal prostheses have been developed to stimulate survived retinal ganglion cells (RGCs), indirectly following the physiological visual pathways. However, current spreading from the prosthesis electrode causes the activation of unintended RGCs, thereby limiting the spatial resolution of artificial vision. This study proposes a strategy for focal stimulation of RGCs using a subretinal electrode array, in which six hexagonally arranged peripheral electrodes surround a stimulating electrode. RGCs in an in-vitro condition were subretinally stimulated using a fabricated electrode array coated with iridium oxide, following the three different stimulation configurations (with no peripheral, six electrodes of opposite current, and six ground). In-vitro experiments showed that the stimulation with six electrodes of opposite current was most effective in controlling RGC responses with a high spatial resolution. The results suggest that the effective utilization of return electrodes, such as by applying an opposite current to them, could help reduce current spreading beyond the local area targeted for stimulation and elicit RGC responses only in the vicinity of the stimulating electrode. © 2023, Korean Society of Medical and Biological Engineering.FALSEsciescopuskc
Overcoming the therapeutic limitations of EZH2 inhibitors in Burkitt’s lymphoma: a comprehensive study on the combined effects of MS1943 and Ibrutinib
No full textEnhancer of zeste homolog 2 (EZH2) and Bruton’s tyrosine kinase (BTK) are both key factors involved in the development and progression of hematological malignancies. Clinical studies have demonstrated the potential of various EZH2 inhibitors, which target the methyltransferase activity of EZH2, for the treatment of lymphomas. However, despite their ability to effectively reduce the H3K27me3 levels, these inhibitors have shown limited efficacy in blocking the proliferation of lymphoma cells. To overcome this challenge, we employed a hydrophobic tagging approach utilizing MS1943, a selective EZH2 degrader. In this study, we investigated the inhibitory effects of two drugs, the FDA-approved EZH2 inhibitor Tazemetostat, currently undergoing clinical trials, and the novel drug MS1943, on Burkitt’s lymphoma. Furthermore, we assessed the potential synergistic effect of combining these drugs with the BTK inhibitor Ibrutinib. In this study, we evaluated the effects of combination therapy with MS1943 and Ibrutinib on the proliferation of three Burkitt’s lymphoma cell lines, namely RPMI1788, Ramos, and Daudi cells. Our results demonstrated that the combination of MS1943 and Ibrutinib significantly suppressed cell proliferation to a greater extent compared to the combination of Tazemetostat and Ibrutinib. Additionally, we investigated the underlying mechanisms of action and found that the combination therapy of MS1943 and Ibrutinib led to the upregulation of miR29B-mediated p53-upregulated modulator of apoptosis PUMA, BAX, cleaved PARP, and cleaved caspase-3 in Burkitt’s lymphoma cells. These findings highlight the potential of this innovative therapeutic strategy as an alternative to traditional EZH2 inhibitors, offering promising prospects for improving treatment outcomes in Burkitt’s lymphoma
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Optimizing anesthesia and delivery approaches for dosing into lungs of mice
No full textBiophysical Changes of Leukocyte Activation (and NETosis) in the Cellular Host Response to Sepsis
No full textImage_1_Overcoming the therapeutic limitations of EZH2 inhibitors in Burkitt’s lymphoma: a comprehensive study on the combined effects of MS1943 and Ibrutinib.jpeg
No full textEnhancer of zeste homolog 2 (EZH2) and Bruton’s tyrosine kinase (BTK) are both key factors involved in the development and progression of hematological malignancies. Clinical studies have demonstrated the potential of various EZH2 inhibitors, which target the methyltransferase activity of EZH2, for the treatment of lymphomas. However, despite their ability to effectively reduce the H3K27me3 levels, these inhibitors have shown limited efficacy in blocking the proliferation of lymphoma cells. To overcome this challenge, we employed a hydrophobic tagging approach utilizing MS1943, a selective EZH2 degrader. In this study, we investigated the inhibitory effects of two drugs, the FDA-approved EZH2 inhibitor Tazemetostat, currently undergoing clinical trials, and the novel drug MS1943, on Burkitt’s lymphoma. Furthermore, we assessed the potential synergistic effect of combining these drugs with the BTK inhibitor Ibrutinib. In this study, we evaluated the effects of combination therapy with MS1943 and Ibrutinib on the proliferation of three Burkitt’s lymphoma cell lines, namely RPMI1788, Ramos, and Daudi cells. Our results demonstrated that the combination of MS1943 and Ibrutinib significantly suppressed cell proliferation to a greater extent compared to the combination of Tazemetostat and Ibrutinib. Additionally, we investigated the underlying mechanisms of action and found that the combination therapy of MS1943 and Ibrutinib led to the upregulation of miR29B-mediated p53-upregulated modulator of apoptosis PUMA, BAX, cleaved PARP, and cleaved caspase-3 in Burkitt’s lymphoma cells. These findings highlight the potential of this innovative therapeutic strategy as an alternative to traditional EZH2 inhibitors, offering promising prospects for improving treatment outcomes in Burkitt’s lymphoma.</p
Image_2.jpeg
No full textEnhancer of zeste homolog 2 (EZH2) and Bruton’s tyrosine kinase (BTK) are both key factors involved in the development and progression of hematological malignancies. Clinical studies have demonstrated the potential of various EZH2 inhibitors, which target the methyltransferase activity of EZH2, for the treatment of lymphomas. However, despite their ability to effectively reduce the H3K27me3 levels, these inhibitors have shown limited efficacy in blocking the proliferation of lymphoma cells. To overcome this challenge, we employed a hydrophobic tagging approach utilizing MS1943, a selective EZH2 degrader. In this study, we investigated the inhibitory effects of two drugs, the FDA-approved EZH2 inhibitor Tazemetostat, currently undergoing clinical trials, and the novel drug MS1943, on Burkitt’s lymphoma. Furthermore, we assessed the potential synergistic effect of combining these drugs with the BTK inhibitor Ibrutinib. In this study, we evaluated the effects of combination therapy with MS1943 and Ibrutinib on the proliferation of three Burkitt’s lymphoma cell lines, namely RPMI1788, Ramos, and Daudi cells. Our results demonstrated that the combination of MS1943 and Ibrutinib significantly suppressed cell proliferation to a greater extent compared to the combination of Tazemetostat and Ibrutinib. Additionally, we investigated the underlying mechanisms of action and found that the combination therapy of MS1943 and Ibrutinib led to the upregulation of miR29B-mediated p53-upregulated modulator of apoptosis PUMA, BAX, cleaved PARP, and cleaved caspase-3 in Burkitt’s lymphoma cells. These findings highlight the potential of this innovative therapeutic strategy as an alternative to traditional EZH2 inhibitors, offering promising prospects for improving treatment outcomes in Burkitt’s lymphoma.</p
IgG hexamers initiate complement-dependent acute lung injury
No full textAntibodies can initiate lung injury in a variety of disease states such as autoimmunity, in reactions to transfusions, or after organ transplantation, but the key factors determining in vivo pathogenicity of injury-inducing antibodies are unclear. Harmful antibodies often activate the complement cascade. A model for how IgG antibodies trigger complement activation involves interactions between IgG Fc domains driving the assembly of IgG hexamer structures that activate C1 complexes. The importance of IgG hexamers in initiating injury responses was not clear, so we tested their relevance in a mouse model of alloantibody- and complement-mediated acute lung injury. We used 3 approaches to block alloantibody hexamerization (antibody carbamylation, the K439E Fc mutation, or treatment with domain B from staphylococcal protein A), all of which reduced acute lung injury. Conversely, Fc mutations promoting spontaneous hexamerization made a harmful alloantibody into a more potent inducer of acute lung injury and rendered an innocuous alloantibody pathogenic. Treatment with a recombinant Fc hexamer "decoy" therapeutic protected mice from lung injury, including in a model with transgenic human FCGR2A expression that exacerbated pathology. These results indicate an in vivo role of IgG hexamerization in initiating acute lung injury and the potential for therapeutics that inhibit or mimic hexamerization to treat antibody-mediated diseases.</p
