Scutellarin Alleviates Diabetic Retinopathy via the Suppression of Nucleotide-Binding Oligomerization Domain (NOD)-Like Receptor Pyrin Domain Containing Protein 3 Inflammasome Activation

Diabetic retinopathy, a prevalent complication of diabetes, represents the leading cause of vision loss and blindness among middle-aged and elderly populations. Recent research has demonstrated the ameliorating effects of scutellarin on diabetes-associated complications such as diabetic retinopathy and type 2 diabetic cardiomyopathy. However, investigations into its protective impact and underlying mechanisms on diabetic retinopathy are scant. This study aims to explore the therapeutic potential of scutellarin in diabetic retinopathy treatment. Diabetic retinopathy was induced in rats through intraperitoneal injections of streptozotocin (STZ, 60 mg/kg) administered daily for three consecutive days. Following this, diabetic retinopathy rats received daily intragastric administration of scutellarin (40 mg/kg) for 42 days. Our findings suggest that scutellarin alleviates histological damage in the retinal tissues of streptozotocin-challenged rats. Furthermore, scutellarin effectively enhances total retinal thickness and increases the number of ganglion cell layer (GCL) cells in the retinal tissues of streptozotocin-treated rats. Scutellarin also demonstrated anti-inflammatory and antioxidant effects in the retinal tissues of STZ-induced rats, as indicated by reduced levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6, and elevated levels of glutathione peroxidase, superoxide dismutase, and catalase. Additionally, scutellarin effectively inhibited the expression of NOD-like receptor pyrin domain containing protein 3 inflammasome-related markers in the retinal tissues of streptozotocin-administered rats. Collectively, our results indicate that scutellarin significantly reduces streptozotocin-induced retinal inflammation, an effect that may be partially attributed to the suppression of NLRP3 inflammasome activation.</p

A Route to the C,D,E Ring System of the <i>Aspidosperma</i> Alkaloids

A short synthetic sequence leading to the formation of the C,D,E-ring subunit of the <i>Aspidosperma</i> alkaloids is reported. This route is based on a ring fragmentation/intramolecular azomethine ylide 1,3-dipolar cycloaddition reaction sequence that gives the desired tricyclic product as a single diastereomer. A γ-amino-β-hydroxy-α-diazo carbonyl compound is shown to fragment in the presence of a Lewis acid to give an iminium product that can be directly reduced to the corresponding amine

Theoretical Investigation of Lactide Ring-Opening Polymerization Induced by a Dinuclear Indium Catalyst

A DFT study of the ring-opening polymerization of lactide (LA) induced by a dinuclear indium catalyst supported by a chiral diamino phenoxy ligand, [(NN_HO)­InCl]₂(μ-Cl)­(μ-OEt) (<b>1</b>), is reported. The nature of the active catalyst, mononuclear vs dinuclear, was investigated and was shown to be dinuclear because of the high energetic cost of its dissociation. The selectivity of the system was investigated for the polymerization of LA with the dinuclear (<i>R,R</i>/<i>R,R</i>)-<b>1</b> catalyst. In complete agreement with experimental results we observed that (1) selectivity is controlled by the nucleophilic addition of LA to the alcoholate, resulting in the chain-end control of polymerization, (2) a slight kinetic preference for the polymerization of l-LA over d-LA is found that translates to a <i>k</i>_rel value of ∼14, which is identical with the experimental value, and (3) when <i>rac</i>-LA is used, no clear preference for d- vs l-LA insertion is found, leading to isotactic PLA

New Mechanism for the Ring-Opening Polymerization of Lactones? Uranyl Aryloxide-Induced Intermolecular Catalysis

The uranyl aryloxide [UO₂(OAr)₂(THF)₂] (Ar = 2,6-^<i>t</i>Bu₂-C₆H₂) is an active catalyst for the ring-opening <i>cyclo</i>-oligomerization of ε-caprolactone and δ-valerolactone but not for β-butyrolactone, γ-butyrolactone, and <i>rac</i>-lactide. ¹H EXSY measurements give the thermodynamic parameters for exchange of monomer and coordinated THF, and rates of polymerization have been determined. A comprehensive theoretical examination of the mechanism is discussed. From both experiment and theory, the initiation step is intramolecular and in keeping with the accepted mechanism, while computational studies indicate that propagation can go via an intermolecular pathway, which is the first time this has been observed. The lack of polymerization for the inactive monomers has been investigated theoretically and C–H···π interactions stabilize the coordination of the less rigid monomers

Thermodynamic Study of Mixed Surfactants of Polyoxyethylene <i>tert</i>-Octyl Phenyl Ether and Dodecyltrimethylammonium Bromide

Mixtures of polyoxyethylene <i>tert</i>-octyl phenyl ether (TX100) and dodecyltrimethylammonium bromide (DTAB) were investigated using isothermal titration calorimetry. On the base of the pseudophase separation model and using the two-parameter Margules equation, the compositions of mixed micelles and activity coefficient of each surfactant in mixed micelles were obtained and further used to calculate the thermodynamic parameters of micellization and excess properties of mixed surfactants in the micelles. Through three titration methods, the tendency of surfactants to form mixed micelles and the interactions between TX100 and DTAB in the micelles were investigated

Robust, Superamphiphobic Fabric with Multiple Self-Healing Ability against Both Physical and Chemical Damages

Superamphiphobic coatings with excellent repellency to low surface tension liquids and multiple self-healing abilities are very useful for practical applications, but remain challenging to realize. Previous papers on self-healing superamphiphobic coatings have demonstrated limited liquid repellency with single self-healing ability against either physical or chemical damage. Herein, we describe a superamphiphobic fabric that has remarkable multi-self-healing ability against both physical and chemical damages. The superamphiphobicity was prepared by a two-step surface coating technique. Fabric after coating treatment showed exceptional liquid-repellency to low surface tension liquids including ethanol. The fabric coating was also durable to withstand 200 cycles of laundries and 5000 cycles of Martindale abrasion without apparently changing the superamphiphobicity. This highly robust, superamphiphobic fabric may find applications for the development of “smart” functional textiles for various applications

Model diagram for bird-human disease transmission model.

<p>Model diagram for bird-human disease transmission model.</p

Chronological timeline of the human avian influenza H7N9 outbreak in China, February 19-May 10, 2013.

<p>April 9 is the turning point for bird-to-human infections as elucidated via the Richards model. April 16 is the turning point for bird epidemic concluded from the bird-human model.</p

Model fit for cumulative human H7N9 case number in China, February 19-May 10, 2013 using the Richards model (2).

<p>Model fit for cumulative human H7N9 case number in China, February 19-May 10, 2013 using the Richards model (2).</p

Estimated model parameter values with 95% CIs (in brackets) via the bird-human epidemic model (Equations (4) and (21)) and the Richards model using H7N9 human case data by onset date in China, February 19––May 30, 2013.

<p>Turning point for human outbreak on the 49^th day (48.94 days after February 19) implies occurring on April 9, while turning point for bird outbreak on the 56^th day (55.96 days after) pinpoints April 16.</p><p>*Estimated from human case data fitting with the Richards model growth function.</p><p>Estimated model parameter values with 95% CIs (in brackets) via the bird-human epidemic model (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0111834#pone.0111834.e013" target="_blank">Equations (4)</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0111834#pone.0111834.e052" target="_blank">(21)</a>) and the Richards model using H7N9 human case data by onset date in China, February 19––May 30, 2013.</p