Viologen-based ionic conjugated mesoporous polymer as the electron conveyer for efficient polysulfide trapping and conversion.

The commercialization of lithium-sulfur (Li-S) batteries has been hindered by the shuttle effect and sluggish redox kinetics of lithium polysulfides (LiPSs). Herein, we reported a viologen-based ionic conjugated mesoporous polymer (TpV-Cl), which acts as the cathode host for modifying Li-S batteries. The viologen component serves as a reversible electron conveyer, leading to a comprehensive enhancement in the adsorption of polysulfides and improved conversion rate of polysulfides during the electrochemical process. As a result, the S@TpV-PS cathode exhibits outstanding cycling performance, achieving 300 cycles at 2.0 C (1 C = 1675 mA g-1) with low decay rate of 0.032% per cycle. Even at a high sulfur loading of 4.0 mg cm-2, S@TpV-PS shows excellent cycling stability with a Coulombic efficiency of up to 98%. These results highlight the significant potential of S@TpV-PS in developing high-performance Li-S batteries.

[Variation of stem radius of Larix principis-rupprechtii and its influencing factors in the semi-humid Liupan Mountains, China]. / å ­ç›˜å±±åŠæ¹¿æ¶¦åŒºåŽåŒ—è½å¶æ¾æ ‘å¹²åŠå¾„å˜åŒ–ç‰¹å¾åŠå ¶å½±å“å› ç´ .

We measured stem radius of Larix principis-rupprechtii at the semi-humid Liupan Mountains using the automatic band dendrometer over the growing season in 2016. We examined the diurnal and seasonal variations of stem radius, determined the main stem growth period, and analyzed the response of stem radius to environmental factors during the main stem growth period. The aim was to accurately understand the effects of short-term environmental variation on tree growth. The results showed that stem radius had a clear diurnal variation, with the phases of daytime shrin-kage, nighttime recovery, and increment. The seasonal variation of stem radius could be divided into three distinct stages, including stem relatively stable, stem continuous increasing, and stem swell-shrinking fluctuation. Under the meteorological, soil moisture and topographic conditions of 2016, main stem growth period of L. principis-rupprechtii started from 14th May and ended on the 31th July, with the maximum radius growth rate occurred on 8th June. The environmental factors influencing the daily radius shrinkage at different phases (shrinkage phase, daily, cycle) were gene-rally the same, including temperature (including the air and soil temperature), solar radiation intensity, saturation vapor pressure deficit and soil water content. Temperature had the highest contribution (50.3%-71.0%). However, the influencing factors of daily radius increment varied at different phases. Precipitation (with a contribution of 86.9%) and maximum air temperature (13.1%) were the influencing factors at the radius increment phase. Precipitation (50.3%), saturation vapor pressure deficit (29.9%), relative humidity (12.7%) and solar radiation intensity (7.1%) were the factors at stem cycle. Precipitation and solar radiation intensity were the factors at diurnal scale. Radius increment was more sensitive to environmental variation at the time of stem cycle than that at diurnal scale.

Novel Insights on Notch signaling pathways in liver fibrosis.

Liver fibrosis is characterized by an increased and altered deposition of extracellular matrix (ECM) proteins that make up excessive tissue scarring and promote chronic liver injury. Activation of hepatic stellate cells (HSCs) is a pivotal cellular event in the progression of liver fibrosis. However, the mechanisms involved in the development of liver fibrosis are only now beginning to be unveiled. The Notch pathway is a fundamental and highly conserved pathway able to control cell-fate, including cell proliferation, differentiation, apoptosis, regeneration and other cellular activities. Recently, the deregulation of Notch cascade has been found involved in many pathological processes, including liver fibrosis. These data give evidence for a role for Notch signaling in liver fibrosis. In addition，more and more date are available on the role of Notch pathways in the process. Therefore, this review focuses on the current knowledge about the Notch signaling pathway, which dramatically takes part in HSC activation and liver fibrosis, and look ahead on new perspectives of Notch signaling pathway research. Furthermore, we will summarize this new evidence on the different interactions in Notch signaling pathway-regulated liver fibrosis, and support the potentiality of putative biomarkers and unique therapeutic targets.

Inhibition of IRF3 expression reduces TGF-beta1-induced proliferation of hepatic stellate cells

Therapeutic management of liver fibrosis remains an unresolved clinical problem. Activation of hepatic stellate cell (HSC) is a pivotal event in the progression of liver fibrosis. Recent reports have showed that inhibition of activated HSC proliferation contributes to the reversal of liver fibrosis. Interferon regulatory factor 3 (IRF3), one member of the interferon regulatory factor (IRF) family, is recently proven to be a critical modulator in cardiac fibrosis. And accumulating evidence demonstrated that IRF3 plays a crucial role in liver diseases, such as hepatic steatosis, liver inflammation, and alcoholic liver injury. However, the understanding of the function of IRF3 in liver fibrosis remains limited. Our results identified the role of IRF3 in regulating human HSC (LX-2 cell) cell proliferation and apoptosis. The present study indicated that the expression of IRF3 was significantly increased in HSCs in response to TGF-β1 stimulation. Moreover, a stable and unlimited source of human HSC, the LX-2 cell line, transfected with IRF3-siRNA significantly decreases the expression level of type I collagen (Col1a1) and α-smooth muscle actin (α-SMA) in activated LX-2 cells. On the contrary, overexpression of IRF3 gives rise to an upregulation of Col1a1 and α-SMA in LX-2 cells, and further promoted HSC proliferation. Moreover, the inhibition of IRF3 significantly suppressed TGF-β1-induced HSC proliferation and increased its apoptosis. Of note, the present study indicated IRF3 may regulate LX-2 cell proliferation by via AKT signaling pathway. In summary, these observations suggest IRF3 may function as a novel regulator to modulate TGF-β1-induced LX-2 proliferation, at least in part, via AKT signaling pathway (AU)

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Inhibition of IRF3 expression reduces TGF-ß1-induced proliferation of hepatic stellate cells.

Therapeutic management of liver fibrosis remains an unresolved clinical problem. Activation of hepatic stellate cell (HSC) is a pivotal event in the progression of liver fibrosis. Recent reports have showed that inhibition of activated HSC proliferation contributes to the reversal of liver fibrosis. Interferon regulatory factor 3 (IRF3), one member of the interferon regulatory factor (IRF) family, is recently proven to be a critical modulator in cardiac fibrosis. And accumulating evidence demonstrated that IRF3 plays a crucial role in liver diseases, such as hepatic steatosis, liver inflammation, and alcoholic liver injury. However, the understanding of the function of IRF3 in liver fibrosis remains limited. Our results identified the role of IRF3 in regulating human HSC (LX-2 cell) cell proliferation and apoptosis. The present study indicated that the expression of IRF3 was significantly increased in HSCs in response to TGF-ß1 stimulation. Moreover, a stable and unlimited source of human HSC, the LX-2 cell line, transfected with IRF3-siRNA significantly decreases the expression level of type I collagen (Col1a1) and α-smooth muscle actin (α-SMA) in activated LX-2 cells. On the contrary, overexpression of IRF3 gives rise to an upregulation of Col1a1 and α-SMA in LX-2 cells, and further promoted HSC proliferation. Moreover, the inhibition of IRF3 significantly suppressed TGF-ß1-induced HSC proliferation and increased its apoptosis. Of note, the present study indicated IRF3 may regulate LX-2 cell proliferation by via AKT signaling pathway. In summary, these observations suggest IRF3 may function as a novel regulator to modulate TGF-ß1-induced LX-2 proliferation, at least in part, via AKT signaling pathway.

New surprises of suppressor of cytokine signalling in liver fibrosis.

INTRODUCTION: Liver fibrosis is a progressive condition with serious clinical complications arising from abnormal proliferation and amassing of tough fibrous scar tissue. Macrophages are found in secreting chemokines that recruit fibroblasts and other inflammatory cells, and inflammatory cytokines that activate the hepatic stellate cell (HSC) play an essential event during liver fibrogenesis. The potential of macrophages acts in both pro- and anti-fibrotic capacities followed by related genes of inflammation in coordination with epigenetic modifications in liver fibrogenesis. AREAS COVERED: In this review, we focus on the role of suppressor of cytokine signalling (SOCS) proteins in transcriptional regulation at the level of the chromatin structure and the interaction of SOCS with microRNAs during liver fibrosis. Moreover, we will discuss the different signalling pathways that interact with SOCS-regulated HSC activation. EXPERT OPINION: Although the exact role of SOCS proteins in liver fibrosis has not been fully elucidated, recognition of SOCS proteins and its regulation by these multiple mechanisms may offer new potential targets of liver fibrosis, and provide new understandings of the development of future therapeutic strategies.