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The poor interfacial stability and undesirable cycling performance caused by their dramatic volume change hinder the large-scale commercial application of SiOx materials for high-energy-density lithium-ion batteries. Herein, a simple two-step carbonization process is employed to prepare highly pyrrolic-nitrogen-doped carbon modified SiOx anode materials (SiOx@NC). The designed SiOx@NC materials exhibit high electron conductivity and favorable electrochemical kinetics. As expected, the SiOx@NC electrode delivers a high specific capacity of 1003.46 mA h g−1 after 200 cycles at 500 mA g−1. The NCM622‖‖SiOx@NC full cell also demonstrates excellent cycling stability and rate performance. [ABSTRACT FROM AUTHOR]

On the basis of the previous research, the Traditional Chinese Medicine theory was used to improve the drug composition for gastrointestinal acute radiation syndrome (GI-ARS). The purpose of this study was to study the therapeutic mechanism of Liangxue-Guyuan-Yishen decoction (LGYD) on GI-ARS and to provide a new scheme for the treatment of radiation injury. Here, we investigated the effects of LGYD on intestinal stem cells (ISCs) in a GI-ARS rat model. Rat health and survival and the protective efficacy of LGYD on the intestines were analyzed. The active principles in LGYD were detected using liquid chromatography-mass spectrometry (LC–MS). ISC proliferation, intestinal epithelial tight junction (TJ) protein expression and regulatory pathways were explored using immunohistochemistry, western blotting (WB) and reverse transcription quantitative polymerase chain reaction (RT-qPCR), respectively. Involvement of the WNT and MEK/ERK pathways in intestinal recovery was screened using network pharmacology analysis and validated by WB and RT-qPCR. LGYD administration significantly improved health and survival in GI-ARS rats. Pathological analysis showed that LGYD ameliorated radiation-induced intestinal injury and significantly promoted LGR5+ stem cell regeneration in the intestinal crypts, upregulated TJ protein, and accelerated crypt reconstruction in the irradiated rats. LC–MS revealed ≥13 constituents that might contribute to LGYD's protective effects. Collectively, LGYD can promote crypt cell proliferation and ISCs after radiation damage, the above effect may be related to WNT and MEK/ERK pathway. [ABSTRACT FROM AUTHOR]

Silicon oxide-based (SiO x -based) materials show great promise as anodes for high-energy lithium-ion batteries due to their high specific capacity. However, their practical application is hindered by the inevitable volumetric expansion during the lithiation/delithiation process. Constructing high-performance binders for SiO x -based anodes has been regarded as an efficient strategy to mitigate their volume expansion and preserve structural integrity. In this work, we propose a green water-solution PAA-LS binder composed of poly(acrylic acid) (PAA) and sodium lignosulfonate (LS) with fast self-healing properties. The designed binder can be restored due to the strong affinity between Fe 3+ -catechol coordination bonds, thereby effectively alleviating the volumetric strain of SiO x -based anodes. Notably, with an optimized LS content of 0.5%, the SiO x @PAA-LS electrode exhibits excellent performance, delivering a high capacity of 997.3 mAh g -1 after 450 cycles at 0.5 A g -1 . Furthermore, the SiO x ||NCM622 full cell also demonstrates superior cycling stability, maintaining a discharge capacity of 147.58 mAh g -1 after 100 cycles at 0.5 A g -1 , with an impressive capacity retention rate of 82.72%.

Components of normal tissue architecture serve as barriers to tumor progression. Inflammatory and wound-healing programs are requisite features of solid tumorigenesis, wherein alterations to immune and non-immune stromal elements enable loss of homeostasis during tumor evolution. The precise mechanisms by which normal stromal cell states limit tissue plasticity and tumorigenesis, and which are lost during tumor progression, remain largely unknown. Here we show that healthy pancreatic mesenchyme expresses the paracrine signaling molecule KITL, also known as stem cell factor, and identify loss of stromal KITL during tumorigenesis as tumor-promoting. Genetic inhibition of mesenchymal KITL in the contexts of homeostasis, injury, and cancer together indicate a role for KITL signaling in maintenance of pancreas tissue architecture, such that loss of the stromal KITL pool increased tumor growth and reduced survival of tumor-bearing mice. Together, these findings implicate loss of mesenchymal KITL as a mechanism for establishing a tumor-permissive microenvironment., Competing Interests: Conflict of interest disclosure statement: M.H. Sherman is a paid consultant for Autobahn Labs.