Photoredox-Enabled Deconstructive [5 + 1] Annulation Approach to Isoquinolones from Indanones in Water

We disclose a deconstructive [5 + 1] annulation protocol for the synthesis of isoquinolones through a nitrogen insertion into abundant indanones. This method exploits photoredox-catalyzed ring-opening of oxime esters. The reaction proceeds smoothly with water as the reaction medium and tolerates a range of functional groups on diverse thiophenols, amines, or indanones. Moreover, the representative isoquinolones exhibit promising antifungal activities

Binding capacity and co-migration potential of Pb(II), Cu(II), and Cd(II) on colloids in road runoff

To evaluate the co-migration potential between heavy metal ions and road runoff colloids, the influence of contact time, temperature, initial concentration of metal ions, pH, humic acid (HA), and polymetallic coexistence on the binding capacity of heavy metals onto runoff colloids were investigated. The adsorption of heavy metals by runoff colloids was extremely rapid, approximately 80% of the equilibrium adsorption capacity was achieved in the first 30 min. The binding capacity exhibited an increasing trend with the initial concentration of metal ions increasing, and the maximum adsorption capacities of Pb(II), Cu(II), and Cd(II) achieved 159.13, 56.06, and 78.35 mg/g at 298 K, respectively. The adsorption capacity of Cu(II) and Cd(II) by runoff colloids increased with temperature increasing, while it displayed a converse trend for Pb(II). Neutral pH facilitated the combination of metal ions and runoff colloids. The presence of humic acid increased the binding capacity of Pb(II), Cu(II), and Cd(II) onto runoff colloids by 72.19, 63.31, and 13.83mg/g, respectively. Compared to the monometallic systems, the binding capacity of Pb(II), Cu(II), and Cd(II) by runoff colloids decreased by 18.44%, 22.35%, and 56.06% in polymetallic systems, respectively. Pb(II) bounded with colloids in the road runoff should be controlled preferentially to avoid their migrations to aquatic environments.</p

Image_3_Neutrophil autophagy induced by monosodium urate crystals facilitates neutrophil extracellular traps formation and inflammation remission in gouty arthritis.tif

Neutrophil extracellular traps (NETs) are composed of chromatin filaments coated with granular and cytosolic proteins, which contribute to the pathogenesis and progression of immune-related diseases. NETs are frequently observed in gouty arthritis, but the related mechanisms remain poorly understood. The aim of our study was to systematically elucidate the molecular mechanisms of self-remitting effects in gouty arthritis, and the causative relationship between neutrophil autophagy and NETs. The air pouch and paw edema model were used to simulate gouty arthritis in mice. Neutrophil infiltration and the formation of NETs were found in gouty arthritis. Interestingly, monosodium urate (MSU) crystals could induce the formation of NETs, degrade inflammatory factors, and alleviate the inflammatory response in gouty arthritis. In addition, MSU crystals resulted in profound molecular alterations in neutrophils using RNA-seq analysis, including autophagy activation. MSU crystals could activate neutrophil autophagy in vitro, and autophagy activators and inhibitors could regulate the formation of NETs. Furthermore, we explored the mechanism of autophagy-induced NETs. Autophagy related protein 7 (ATG7) produced by neutrophils stimulated with MSU crystals worked synergistically with p53 to enter the nucleus, promoting peptidyl arginine deiminase 4 (PAD4) expression, and inducing the formation of NETs. Finally, we substantiated that neutrophil autophagy regulates the severity of gouty arthritis via the formation of NETs in PAD4 -/- mice. Our results indicated that the autophagy of neutrophils regulates the formation of NETs and degrades inflammatory factors. Regulating autophagy and interfering with the formation of NETs represents a potential therapeutic approach against gouty arthritis during clinical practice.</p

From Tea to Health: Exploring <i>Abrus mollis</i> for Liver Protection and Unraveling Its Potential Mechanisms

Abrus mollis Hance is a characteristic medicinal herb which is used in Guangdong and Guangxi provinces of China for making soup, medicinal meals, and herbal tea to treat dampheat jaundice and rib discomfort. Current phytochemical study on A. mollis led to the isolation of four new flavones, mollisone A-D (1–4), and thirty two known compounds (5–36). Their structures were characterized by an extensive analysis of spectroscopic data including IR, UV, HR-ESI-MS, and 1D and 2D NMR, as well as electronic circular dichroism calculation. In addition, in order to initially understand their biological activities for traditional applications, in vitro antioxidant and hepatoprotective tests were carried out, whose results illustrated that 25 compounds had significant free radical scavenging ability, and compounds 13 and 16 exhibited protective activities on D-GalN-induced LO2 cell damage than the positive control. Moreover, network pharmacological analysis revealed that the hepatoprotective activity of A. mollis involved multitargets and multipathways such as PI3K/Akt, MAPK, and JAK-STAT pathways and various biological processes such as positive regulation of phosphorylation and regulation of kinase activity. These results suggested that this species could serve as a potential hepatoprotective agent for functional food or medicinal use

One-Step Synthesis of Uniform Double-Shelled Polystyrene/Poly(<i>o</i>‑toluidine) Composite Hollow Spheres

Uniform double-shelled polystyrene/poly­(<i>o</i>-toluidine) (PS/POT) composite hollow spheres with tunable shell thickness of the POT layer have been successfully synthesized by a simple method. POT was directly coated onto the surface of negatively charged PS template spheres, which were synthesized by soap-free emulsion polymerization. Surprisingly, the resultant spheres show a double-shelled hollow structure with PS as an inner wall and POT as an exterior shell. In comparison to conventional methods, the benefits of this route are that neither organic solvents nor high-temperature calcinations were used to remove the PS template. The surface morphology, the shell thickness, and the compositions of the double-shelled spheres were systematically characterized by scanning electron microscopy (SEM), transmission electron microscopy (TEM), and Fourier transform infrared (FTIR) spectroscopy. On the basis of our interpretation of experimental results, a mechanism for the formation of the double-shelled PS/POT composite hollow spheres is proposed

Highly Stereoselective Cyclopropanation of Olefins Catalyzed by a Novel <i>C</i>₃-Symmetric Arsine

<div><p></p><p>A novel <i>C</i>₃-symmetric arsine was employed in the one-pot cyclopropanation of olefins with carbonyl-stabilized arsonium ylides formed in situ from phenacyl bromide in the presence of NaHCO₃. This new arsine demonstrates good stereoselectivity and activity in the one-pot cyclopropanation of arylidenemalononitrile.</p> <p>[Supplementary materials are available for this article. Go to the publisher's online edition of <i>Synthetic Communications</i>® for the following free supplemental resource(s): Full experimental and spectral details.]</p> </div

Image_2_Neutrophil autophagy induced by monosodium urate crystals facilitates neutrophil extracellular traps formation and inflammation remission in gouty arthritis.tif

Neutrophil extracellular traps (NETs) are composed of chromatin filaments coated with granular and cytosolic proteins, which contribute to the pathogenesis and progression of immune-related diseases. NETs are frequently observed in gouty arthritis, but the related mechanisms remain poorly understood. The aim of our study was to systematically elucidate the molecular mechanisms of self-remitting effects in gouty arthritis, and the causative relationship between neutrophil autophagy and NETs. The air pouch and paw edema model were used to simulate gouty arthritis in mice. Neutrophil infiltration and the formation of NETs were found in gouty arthritis. Interestingly, monosodium urate (MSU) crystals could induce the formation of NETs, degrade inflammatory factors, and alleviate the inflammatory response in gouty arthritis. In addition, MSU crystals resulted in profound molecular alterations in neutrophils using RNA-seq analysis, including autophagy activation. MSU crystals could activate neutrophil autophagy in vitro, and autophagy activators and inhibitors could regulate the formation of NETs. Furthermore, we explored the mechanism of autophagy-induced NETs. Autophagy related protein 7 (ATG7) produced by neutrophils stimulated with MSU crystals worked synergistically with p53 to enter the nucleus, promoting peptidyl arginine deiminase 4 (PAD4) expression, and inducing the formation of NETs. Finally, we substantiated that neutrophil autophagy regulates the severity of gouty arthritis via the formation of NETs in PAD4 -/- mice. Our results indicated that the autophagy of neutrophils regulates the formation of NETs and degrades inflammatory factors. Regulating autophagy and interfering with the formation of NETs represents a potential therapeutic approach against gouty arthritis during clinical practice.</p

DataSheet_1_Neutrophil autophagy induced by monosodium urate crystals facilitates neutrophil extracellular traps formation and inflammation remission in gouty arthritis.docx

Neutrophil extracellular traps (NETs) are composed of chromatin filaments coated with granular and cytosolic proteins, which contribute to the pathogenesis and progression of immune-related diseases. NETs are frequently observed in gouty arthritis, but the related mechanisms remain poorly understood. The aim of our study was to systematically elucidate the molecular mechanisms of self-remitting effects in gouty arthritis, and the causative relationship between neutrophil autophagy and NETs. The air pouch and paw edema model were used to simulate gouty arthritis in mice. Neutrophil infiltration and the formation of NETs were found in gouty arthritis. Interestingly, monosodium urate (MSU) crystals could induce the formation of NETs, degrade inflammatory factors, and alleviate the inflammatory response in gouty arthritis. In addition, MSU crystals resulted in profound molecular alterations in neutrophils using RNA-seq analysis, including autophagy activation. MSU crystals could activate neutrophil autophagy in vitro, and autophagy activators and inhibitors could regulate the formation of NETs. Furthermore, we explored the mechanism of autophagy-induced NETs. Autophagy related protein 7 (ATG7) produced by neutrophils stimulated with MSU crystals worked synergistically with p53 to enter the nucleus, promoting peptidyl arginine deiminase 4 (PAD4) expression, and inducing the formation of NETs. Finally, we substantiated that neutrophil autophagy regulates the severity of gouty arthritis via the formation of NETs in PAD4 -/- mice. Our results indicated that the autophagy of neutrophils regulates the formation of NETs and degrades inflammatory factors. Regulating autophagy and interfering with the formation of NETs represents a potential therapeutic approach against gouty arthritis during clinical practice.</p

Image_1_Neutrophil autophagy induced by monosodium urate crystals facilitates neutrophil extracellular traps formation and inflammation remission in gouty arthritis.tif

Neutrophil extracellular traps (NETs) are composed of chromatin filaments coated with granular and cytosolic proteins, which contribute to the pathogenesis and progression of immune-related diseases. NETs are frequently observed in gouty arthritis, but the related mechanisms remain poorly understood. The aim of our study was to systematically elucidate the molecular mechanisms of self-remitting effects in gouty arthritis, and the causative relationship between neutrophil autophagy and NETs. The air pouch and paw edema model were used to simulate gouty arthritis in mice. Neutrophil infiltration and the formation of NETs were found in gouty arthritis. Interestingly, monosodium urate (MSU) crystals could induce the formation of NETs, degrade inflammatory factors, and alleviate the inflammatory response in gouty arthritis. In addition, MSU crystals resulted in profound molecular alterations in neutrophils using RNA-seq analysis, including autophagy activation. MSU crystals could activate neutrophil autophagy in vitro, and autophagy activators and inhibitors could regulate the formation of NETs. Furthermore, we explored the mechanism of autophagy-induced NETs. Autophagy related protein 7 (ATG7) produced by neutrophils stimulated with MSU crystals worked synergistically with p53 to enter the nucleus, promoting peptidyl arginine deiminase 4 (PAD4) expression, and inducing the formation of NETs. Finally, we substantiated that neutrophil autophagy regulates the severity of gouty arthritis via the formation of NETs in PAD4 -/- mice. Our results indicated that the autophagy of neutrophils regulates the formation of NETs and degrades inflammatory factors. Regulating autophagy and interfering with the formation of NETs represents a potential therapeutic approach against gouty arthritis during clinical practice.</p

Correlation between serum IGF-1 levels and others predictors.

<p>(a) Correlation between the serum IGF-1 levels and the National Institutes of Health Stroke Scale (NIHSS) score; (b) Correlation between serum IGF-1 levels and Hs-CRP;(c) Correlation between serum IGF-1 levels and infract volume;(d) Correlation between serum IGF-1 levels and HCY.</p