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Hazardous dye substances discharged from the textile and dyestuff industries not only threaten local the surrounding ecosystems but are also hard to degraded. We report the preparation of process for a photocatalytic membrane device that can degrade dye pollution under visible light. This filtration membrane, with a well-organized multilayer structure, simultaneously achieves continuous and flow-through separation of degradation products. Cellulose nanofibers (CNFs) were used as a template for nanosheet C 3 N 4 (NS C 3 N 4 ) preparation; the performance for the photocatalytic degradation of dyes improved as the morphology changed from bulking to nanosheet. NS C 3 N 4 was then attached to the surface of a prepared CNF membrane via vacuum filtration. This device exhibited high efficiency (the degradation rates of both Rhodamine B and Methylene blue both reached 96%), high flux (above 160 L·h −1 ·m −2 ·bar −1 ) and excellent stability (maintaining steady flux and high separation were maintained after 4 h). This easy-preparation, easy-scale-up, and low-cost process provides a new method of fabricating photocatalytic membrane devices for dye wastewater treatment.

The effects of CeO2, ZrO2, Nb2O5, and ZnO catalysts supported on carbon nanotubes (CNT) relative to cellulose hydrothermal hydrogenolysis in the presence of Ni/CNT and pressured H2 was studied in this work. The catalysts were characterized by inductively coupled plasma – optical emission spectrometry, X-ray diffraction, X-ray photoelectron spectrometry, transmission electron microscopy, NH3 temperature programmed desorption (TPD), and CO2-TPD. Glucose and its isomers were detected by mass spectrometry. The results showed that redox active CeO2/CNT with strong Lewis acid and strong Lewis base sites was active in C-C bong cracking, isomerization, dehydrogenation, and hydrodeoxygenation reaction, yielding 36.3% ethylene glycol and 17.2% 1,2-propylene glycol. The ZnO/CNT with Bronsted base accelerated isomerization, retro-aldol condensation, and dehydrogenation, yielding 20.7% 1,2-propylene glycol, 17.8% ethylene glycol, and 12.7% tetrahydrofuran dimethanol. The Nb2O5/CNT and ZrO2/CNT were inert to C-C bond cracking, whereas H+ in hot compressed water and the Bronsted acid in Nb2O5/CNT accelerated dehydration, yielding more sorbitol and sorbitans. The results provide reference for catalyst selection and product regulation in cellulose hydrogenolysis.

Despite encouraging progresses in the development of novel therapies, cancer remains the dominant cause of disease-related mortality and has become a leading economic and healthcare burden worldwide. Scutellariae radix (SR, Huangqin in Chinese) is a common herb used in traditional Chinese medicine, with a long history in treating a series of symptoms resulting from cancer, like dysregulated immune response and metabolic abnormalities. As major bioactive ingredients extracted from SR, flavonoids, including baicalein, wogonin, along with their glycosides (baicalin and wogonoside), represent promising pharmacological and anti-tumor activities and deserve extensive research attention. Emerging evidence has made great strides in elucidating the multi-targeting therapeutic mechanisms and key signaling pathways underlying the efficacious potential of flavonoids derived from SR in the field of cancer treatment. In this current review, we aim to summarize the pharmacological actions of flavonoids against various cancers in vivo and in vitro. Moreover, we also make a brief summarization of the endeavor in developing a drug delivery system or structural modification to enhance the bioavailability and biological activities of flavonoid monomers. Taken together, flavonoid components in SR have great potential to be developed as adjuvant or even primary therapies for the clinical management of cancers and have a promising prospect.

Autophagy is essential for the maintenance of hepatic homeostasis, and autophagic malfunction has been linked to the pathogenesis of substantial liver diseases. As a popular source of drug discovery, natural products have been used for centuries to effectively prevent the progression of various liver diseases. Emerging evidence has suggested that autophagy regulation is a critical mechanism underlying the therapeutic effects of these natural products. In this review, relevant studies are retrieved from scientific databases published between 2011 and 2022, and a novel scoring system was established to critically evaluate the completeness and scientific significance of the reviewed literature. We observed that numerous natural products were suggested to regulate autophagic flux. Depending on the therapeutic or pathogenic role autophagy plays in different liver diseases, autophagy-regulative natural products exhibit different therapeutic effects. According to our novel scoring system, in a considerable amount of the involved studies, convincing and reasonable evidence to elucidate the regulatory effects and underlying mechanisms of natural-product-mediated autophagy regulation was missing and needed further illustration. We highlight that autophagy-regulative natural products are valuable drug candidates with promising prospects for the treatment of liver diseases and deserve more attention in the future.

Ethanol production from NaOH-Pretreated solid state fermented sweet sorghum bagasse with an engineered strain of Z. mobilis TSH-ZM-01 was optimized. Results showed that: (1) residual solid removal during ethanol fermentation was unnecessary and 24 h fermentation duration was optimal for ethanol production; (2) ethanol yield of 179.20 g/kg of solid state fermented sweet sorghum bagasse achieved under the optimized process conditions of cellulase loading of 0.04 g/g-glucan, xylanase loading of 0.01 g/g-xylan, liquid to solid ratio of 9:1 and pre-hydrolysis duration for 72 h.

The treatment of ulcerative colitis (UC) presents an ongoing clinical challenge. Emerging research has implicated that the cGAS-STING pathway promotes the progression of UC, but conflicting results have hindered the development of STING as a therapeutic target. In the current study, we aim to comprehensively elucidate the origins, downstream signaling and pathogenic roles of myeloid STING in colitis and colitis-associated carcinoma (CAC). mice were constructed for inducible myeloid-specific deletion of STING. RNA-sequencing, flow cytometry, and multiplex immunohistochemistry were employed to investigate immune responses in DSS-induced colitis or AOM/DSS-induced carcinogenesis. Colonic organoids, primary bone marrow derived macrophages and dendritic cells, and splenic T cells were used for studies. We observed that myeloid STING knockout in adult mice inhibited macrophage maturation, reduced DC cell activation, and suppressed pro-inflammatory Th1 and Th17 cells, thereby protecting against both acute and chronic colitis and CAC. However, myeloid STING deletion in neonatal or tumor-present mice exhibited impaired immune tolerance and anti-tumor immunity. Furthermore, we found that TFAM-associated mtDNA released from damaged colonic organoids, rather than bacterial products, activates STING in dendritic cells in an extracellular vesicle-independent yet endocytosis-dependent manner. Both IRF3 and NF-κB are required for STING-mediated expression of IL-12 family cytokines, promoting Th1 and Th17 differentiation and contributing to excessive inflammation in colitis. Detection of the TFAM-mtDNA complex from damaged intestinal epithelium by myeloid STING exacerbates colitis through IL-12 cytokines, providing new evidence to support the development of STING as a therapeutic target for UC and CAC.

The effects of CeO2, ZrO2, Nb2O5, and ZnO catalysts supported on carbon nanotubes (CNT) relative to cellulose hydrothermal hydrogenolysis in the presence of Ni/CNT and pressured H2 was studied in this work. The catalysts were characterized by inductively coupled plasma – optical emission spectrometry, X-ray diffraction, X-ray photoelectron spectrometry, transmission electron microscopy, NH3 temperature programmed desorption (TPD), and CO2-TPD. Glucose and its isomers were detected by mass spectrometry. The results showed that redox active CeO2/CNT with strong Lewis acid and strong Lewis base sites was active in C-C bong cracking, isomerization, dehydrogenation, and hydrodeoxygenation reaction, yielding 36.3% ethylene glycol and 17.2% 1,2-propylene glycol. The ZnO/CNT with Bronsted base accelerated isomerization, retro-aldol condensation, and dehydrogenation, yielding 20.7% 1,2-propylene glycol, 17.8% ethylene glycol, and 12.7% tetrahydrofuran dimethanol. The Nb2O5/CNT and ZrO2/CNT were inert to C-C bond cracking, whereas H+ in hot compressed water and the Bronsted acid in Nb2O5/CNT accelerated dehydration, yielding more sorbitol and sorbitans. The results provide reference for catalyst selection and product regulation in cellulose hydrogenolysis.

Inducing the senescence of activated hepatic stellate cells (HSCs) has emerged as a promising therapeutic strategy for liver fibrosis, with potential connections to the Yes-associated protein (YAP)-controlled cGAS-STING pathway. However, the regulatory role of cytoskeletal dynamics on HSC senescence and its potential as a target for natural products have remained poorly understood. We employed preclinical and transcriptome analyses, experimental systems, Tmem173 mice and liver-specific STING knockdown mice to demonstrate the anti-fibrotic effects and mechanism of ligustilide (LIG). LIG selectively bound to monomeric globular actin (G-actin), thereby preventing its polymerization into polymeric filamentous actin (F-actin), which disturbed its interaction with intermediate filament component lamin A/C and initially destroyed the nuclear membrane. Moreover, the disruption of nuclear membrane caused YAP leakage from nuclear, which in turn suppressed lamin A/C and created a deleterious feedback loop that exacerbated nuclear membrane destabilization. Consequently, nuclear double stranded DNA (dsDNA) leakage caused by the above damage cascade ultimately triggered the activation of the cGAS-STING signaling pathway, promoting senescence-associated secretory phenotypes (SASPs) release and inducing HSC senescence. Moreover, the induction of HSC senescence and anti-fibrotic effects of LIG were completely abrogated in both whole-body STING knockout and liver-specific STING knockdown mice. By interacting with G-actin, LIG disrupted the cytoskeleton to compromise nuclear integrity with the involvement of YAP and further stimulated the cGAS-STING pathway, leading to the release of SASPs and HSC senescence, which ultimately mitigated liver fibrosis.

The liver possesses extensive regenerative capacity. Nevertheless, the most proximal events driving the transition from quiescent to proliferative hepatocytes remain largely elusive. Using the combination of spatiotemporal metabolomics and transcriptomics, our study mapped out the temporal-spatial landscape of metabolic reprogramming, epigenetic remodeling, and transcriptomic rewiring from 3 to 12 hours post-partial hepatectomy. Specifically, we identified a profound metabolic shift towards hyperactive fatty acid oxidation (FAO) and suppressed phospholipid biosynthesis during the preparation phase of liver regeneration, which were surprisingly reversed afterwards. FAO-dependent accumulation of Acetyl-CoA particularly remodeled H3K27ac landscape. These metabolic reprograming and epigenetic regulation were spatially specific, aligning with the zonation of hepatocyte proliferation. Blocking FAO in etomoxir-treated or hepatocyte-specific Cpt1a knockout mice, suppressing Acetyl-CoA biosynthesis, and inhibiting histone acetyltransferase all resulted in lethal liver regeneration deficiency. CUT&Tag analysis further revealed that the reshaping of H3K27ac profiles favored the transcription of genes associated with cell cycle transition and mitosis, and rewired the metabolic gene network. Collectively, we highlight a previously underappreciated role of FAO in epigenetic remodeling that is essential for the initiation of liver regeneration, offering exciting opportunity for the rescue of regeneration-deficient livers.

With the development of high-performance electrode materials, sodium-ion batteries have been extensively studied and could potentially be applied in various fields to replace the lithium-ion cells, owing to the low cost and natural abundance. As the key anode materials of sodium-ion batteries, hard carbons still face problems, such as poor cycling performance and low initial Coulombic efficiency. Owning to the low synthesis cost and the natural presence of heteroatoms of biomasses, biomasses have positive implications for synthesizing the hard carbons for sodium-ion batteries. This minireview mainly explains the research progress of biomasses used as the precursors to prepare the hard-carbon materials. The storage mechanism of hard carbons, comparisons of the structural properties of hard carbons prepared from different biomasses, and the influence of the preparation conditions on the electrochemical properties of hard carbons are introduced. In addition, the effect of doping atoms is also summarized to provide an in-depth understanding and guidance for the design of high-performance hard carbons for sodium-ion batteries.