Solid proton electrolytes play a crucial role in various electrochemical energy storage and conversion devices. However, the development of fast proton conducting solid proton electrolytes at ambient ...conditions remains a significant challenge. In this study, a novel acidified nitrogen self‐doped porous carbon material is presented that demonstrates exceptional superprotonic conduction for applications in solid‐state proton battery. The material, designated as MSA@ZIF‐8‐C, is synthesized through the acidification of nitrogen‐doped porous carbon, specifically by integrating methanesulfonic acid (MSA) into zeolitic imidazolate framework‐derived nitrogen self‐doped porous carbons (ZIF‐8‐C). This study reveals that MSA@ZIF‐8‐C achieves a record‐high proton conductivity beyond 10−2 S cm−1 at ambient condition, along with good long‐term stability, positioning it as a cutting‐edge alternative solid proton electrolyte to the default aqueous H2SO4 electrolyte in proton batteries.
A new family of solid proton electrolytes is prepared through the integration of acidic molecular species into nitrogen self‐doped porous carbon. These new solid proton electrolytes exhibit record‐high proton conduction beyond 10−2 S cm−1 at ambient condition and hold great promise as an electrolyte for solid‐state proton batteries.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
The long term effect of biochar application on soil microbial biomass is not well understood. We measured soil microbial biomass carbon (MBC) and nitrogen (MBN) in a field experiment during a winter ...wheat growing season after four consecutive years of no (CK), 4.5 (B4.5) and 9.0 t biochar ha(-1) yr(-1) (B9.0) applied. For comparison, a treatment with wheat straw residue incorporation (SR) was also included. Results showed that biochar application increased soil MBC significantly compared to the CK treatment, and that the effect size increased with biochar application rate. The B9.0 treatment showed the same effect on MBC as the SR treatment. Treatments effects on soil MBN were less strong than for MBC. The microbial biomass C∶N ratio was significantly increased by biochar. Biochar might decrease the fraction of biomass N mineralized (KN), which would make the soil MBN for biochar treatments underestimated, and microbial biomass C∶N ratios overestimated. Seasonal fluctuation in MBC was less for biochar amended soils than for CK and SR treatments, suggesting that biochar induced a less extreme environment for microorganisms throughout the season. There was a significant positive correlation between MBC and soil water content (SWC), but there was no significant correlation between MBC and soil temperature. Biochar amendments may therefore reduce temporal variability in environmental conditions for microbial growth in this system thereby reducing temporal fluctuations in C and N dynamics.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Recent spatial gene expression technologies enable comprehensive measurement of transcriptomic profiles while retaining spatial context. However, existing analysis methods do not address the limited ...resolution of the technology or use the spatial information efficiently. Here, we introduce BayesSpace, a fully Bayesian statistical method that uses the information from spatial neighborhoods for resolution enhancement of spatial transcriptomic data and for clustering analysis. We benchmark BayesSpace against current methods for spatial and non-spatial clustering and show that it improves identification of distinct intra-tissue transcriptional profiles from samples of the brain, melanoma, invasive ductal carcinoma and ovarian adenocarcinoma. Using immunohistochemistry and an in silico dataset constructed from scRNA-seq data, we show that BayesSpace resolves tissue structure that is not detectable at the original resolution and identifies transcriptional heterogeneity inaccessible to histological analysis. Our results illustrate BayesSpace's utility in facilitating the discovery of biological insights from spatial transcriptomic datasets.
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GEOZS, IJS, IMTLJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBMB, UL, UM, UPUK, ZAGLJ
Fibronectin type III domain-containing 5 (FNDC5) protein induces browning of subcutaneous fat and mediates the beneficial effects of exercise on metabolism. However, whether FNDC5 is associated with ...hepatic steatosis, autophagy, fatty acid oxidation (FAO), and lipogenesis remains unknown. Herein, we show the roles and mechanisms of FNDC5 in hepatic steatosis, autophagy, and lipid metabolism. Fasted FNDC5
mice exhibited severe steatosis, reduced autophagy, and FAO, and enhanced lipogenesis in the liver compared with wild-type mice. Energy deprivation-induced autophagy, FAO, and AMPK activity were attenuated in FNDC5
hepatocytes, which were restored by activating AMPK with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR). Inhibition of mammalian target of rapamycin (mTOR) complex 1 with rapamycin enhanced autophagy and FAO and attenuated lipogenesis and steatosis in FNDC5
livers. FNDC5 deficiency exacerbated hyperlipemia, hepatic FAO and autophagy impairment, hepatic lipogenesis, and lipid accumulation in obese mice. Exogenous FNDC5 stimulated autophagy and FAO gene expression in hepatocytes and repaired the attenuated autophagy and palmitate-induced steatosis in FNDC5
hepatocytes. FNDC5 overexpression prevented hyperlipemia, hepatic FAO and autophagy impairment, hepatic lipogenesis, and lipid accumulation in obese mice. These results indicate that FNDC5 deficiency impairs autophagy and FAO and enhances lipogenesis via the AMPK/mTOR pathway. FNDC5 deficiency aggravates whereas FNDC5 overexpression prevents the HFD-induced hyperlipemia, hepatic lipid accumulation, and impaired FAO and autophagy in the liver.
Background/Aims: Angiotensin (Ang) II plays vital roles in vascular inflammation and remodeling in hypertension. Phenotypic transformation of vascular smooth muscle cells (VSMCs) is a major ...initiating factor for vascular remodeling. The present study was designed to determine the roles of NLRP3 inflammasome activation in Ang II-induced VSMC phenotypic transformation and vascular remodeling in hypertension. Methods: Primary VSMCs from the aorta of NLRP3 knockout (NLRP3-/-) mice and wild-type (WT) mice were treated with Ang II for 24 h. Subcutaneous infusion of Ang II via osmotic minipump for 2 weeks was used to induce vascular remodeling and hypertension in WT and NLRP3-/- mice. Results: NLRP3 gene deletion attenuates Ang II-induced NLRP3 inflammasome activation, phenotypic transformation from a contractile phenotype to a synthetic phenotype and proliferation in primary mice VSMCs. Ang II-induced hypertension and vascular remodeling in WT mice were attenuated in NLRP3-/- mice. Furthermore, Ang II-induced NLRP3 inflammasome activation, phenotypic transformation and proliferating cell nuclear antigen (PCNA) upregulation were inhibited in the media of aorta of NLRP3-/- mice. Conclusions: NLRP3 inflammasome activation contributes to Ang II-induced VSMC phenotypic transformation and proliferation as well as vascular remodeling and hypertension.
Proliferation of vascular smooth muscle cells (VSMCs) plays crucial roles in vascular remodelling and stiffening in hypertension. Vascular adventitial fibroblasts are a key regulator of vascular wall ...function and structure. This study is designed to investigate the roles of adventitial fibroblasts-derived extracellular vesicles (EVs) in VSMC proliferation and vascular remodelling in normotensive Wistar-Kyoto rat (WKY) and spontaneously hypertensive rat (SHR), an animal model of human essential hypertension. EVs were isolated from aortic adventitial fibroblasts of WKY (WKY-EVs) and SHR (SHR-EVs). Compared with WKY-EVs, miR155-5p content was reduced, while angiotensin-converting enzyme (ACE) content was increased in SHR-EVs. WKY-EVs inhibited VSMC proliferation of SHR, which was prevented by miR155-5p inhibitor. SHR-EVs promoted VSMC proliferation of both strains, which was enhanced by miR155-5p inhibitor, but abolished by captopril or losartan. Dual luciferase reporter assay showed that ACE was a target gene of miR155-5p. MiR155-5p mimic or overexpression inhibited VSMC proliferation and ACE upregulation of SHR. WKY-EVs reduced ACE mRNA and protein expressions while SHR-EVs only increased ACE protein level in VSMCs of both strains. However, the SHR-EVs-derived from the ACE knockdown-treated adventitial fibroblasts lost the roles in promoting VSMC proliferation and ACE upregulation. Systemic miR155-5p overexpression reduced vascular ACE, angiotensin II and proliferating cell nuclear antigen levels, and attenuated hypertension and vascular remodelling in SHR. Repetitive intravenous injection of SHR-EVs increased blood pressure and vascular ACE contents, and promoted vascular remodelling in both strains, while WKY-EVs reduced vascular ACE contents and attenuated hypertension and vascular remodelling in SHR. We concluded that WKY-EVs-mediated miR155-5p transfer attenuates VSMC proliferation and vascular remodelling in SHR via suppressing ACE expression, while SHR-EVs-mediated ACE transfer promotes VSMC proliferation and vascular remodelling.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Exploitation of key protected wild plant resources makes great sense, but their limited populations become the major barrier. A particular strategy for breaking this barrier was inspired by the ...exploration of a resource‐saving fungal endophyte Penicillium sp. DG23, which inhabits the key protected wild plant Schisandra macrocarpa. Chemical studies on the cultures of this strain afforded eight novel indole diterpenoids, schipenindolenes A−H (1–8), belonging to six diverse skeleton types. Importantly, semisyntheses suggested some key nonenzymatic reactions constructing these molecules and provided targeted compounds, in particular schipenindolene A (Spid A, 1) with low natural abundance. Remarkably, Spid A was the most potent HMG‐CoA reductase (HMGCR) degrader among the indole diterpenoid family. It degraded statin‐induced accumulation of HMGCR protein, decreased cholesterol levels and acted synergistically with statin to further lower cholesterol. Mechanistically, transcriptomic and proteomic profiling suggested that Spid A potentially activated the endoplasmic reticulum‐associated degradation (ERAD) pathway to enhance the degradation of HMGCR, while simultaneously inhibiting the statin‐activated expression of many key enzymes in the cholesterol and fatty acid synthesis pathways, thereby strengthening the efficacy of statins and potentially reducing the side effects of statins. Collectively, this study suggests the potential of Spid A for treating cardiovascular disease.
The plant Schisandra macrocarpa was explored for the extraction of novel compounds from its fungal endophyte Penicillium sp. DG23. Of the indole diterpenoids and derivatives identified, biological evaluation highlighted schipenindolene A as a potent HMGCR degrader that further lowered cholesterol with statin (HMGCR inhibitor) by activating the endoplasmic reticulum‐associated degradation pathway and inhibiting the compensatory effects of statin.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Molecularly imprinted polymer nanozyme (MIL-101(Co,Fe)@MIP) with bimetallic active sites and high-efficiency peroxidase-like (POD-like) activity were synthesized for the ratiometric fluorescence and ...colorimetric dual-mode detection of vanillin with high selectivity and sensitivity. Compared with the monometallic nanozyme, the POD-like activity of bimetallic nanozyme was greatly enhanced by changing the electronic structure and surface structure. Ratiometric fluorescence and colorimetric dual-mode detection of vanillin in aqueous solution was realized by vanillin entering specific imprinted cavities and blocking the molecular channels on the surface of MIL-101(Co,Fe)@MIP and the dual-mode visual detection was also realized. The limits of detection were as low as 104 nM and 198 nM, respectively. The method proposed in this paper was applied to the real samples of ice cream and candy. And the recoveries were between 93.3% and 105.5%, which also reached a satisfactory degree. The further detection of dexamethasone and prednisone, two drugs belonging to glucocorticoid, proved that the nanozyme analysis method based on MIL-101(Co,Fe)@MIP could be developed into a sensing platform.
•The bimetallic active sites molecularly imprinted polymer was innovatively synthesized.•MIL-101(Co,Fe)@MIP nanozyme has high-efficiency peroxidase-like activity.•The method of ratiometric fluorescence and colorimetric dual-mode sensing platform was built.•The visual detection was realized.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Inflammation is involved in pathogenesis of hypertension. NLRP3 inflammasome activation is a powerful mediator of inflammatory response via caspase-1 activation. The present study was designed to ...determine the roles and mechanisms of NLRP3 inflammasome in phenotypic modulation and proliferation of vascular smooth muscle cells (VSMCs) in hypertension. Experiments were conducted in spontaneously hypertensive rats (SHR) and primary aortic VSMCs. NLRP3 inflammasome activation was observed in the media of aorta in SHR and in the VSMCs from SHR. Knockdown of NLRP3 inhibited inflammasome activation, VSMC phenotypic transformation and proliferation in SHR-derived VSMCs. Increased NFκB activation, histone acetylation and histone acetyltransferase expression were observed in SHR-derived VSMCs and in media of aorta in SHR. Chromatin immunoprecipitation analysis revealed the increased histone acetylation, p65-NFκB and Pol II occupancy at the NLRP3 promoter in vivo and in vitro. Inhibition of NFκB with BAY11-7082 or inhibition of histone acetyltransferase with curcumin prevented the NLRP3 inflammasome activation, VSMC phenotype switching and proliferation in VSMCs from SHR. Moreover, curcumin repressed NFκB activation. Silencing of NLRP3 gene ameliorated hypertension, vascular remodeling, NLRP3 inflammasome activation and phenotype switching in the aorta of SHR. These results indicate that NLRP3 inflammasome activation response to histone acetylation and NFκB activation contributes to VSMC phenotype switching and proliferation and vascular remodeling in hypertension.
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