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In this work, two ionic liquids (ILs) immobilized metal‐organic frameworks (MOFs), Fe‐MIL‐101‐3N(BuBr) and Fe‐MIL‐101‐N(Bnme2)Br, were obtained by modifying amino groups in Fe‐MIL‐101‐NH2 with bromobutane and quaternary ammonium salt. The ionic liquid immobilized MOFs have Lewis acid sites (Fe3+) and nucleophilic sites (Br−), which can synergistically catalyze the cycloaddition reaction of CO2 and epoxides. Various cyclic carbonate derivatives were obtained in excellent yields under the optimal conditions. Additionally, we found that Fe‐MIL‐101‐N(Bnme2)Br exhibited the highest catalytic activity and it can be easily recovered and reused for at least 5 times without loss of catalytic activity. Our method of preparing bifunctional catalysts provides a new approach to design catalysts for the chemical conversion of CO2. [ABSTRACT FROM AUTHOR]

Sulfondiimines, which contain a tetrasubstituted sulfur centre bearing two nitrogens and two carbon substituents, are a class of underexplored scaffolds in organic chemistry. Fascinated by some unique yet intriguing properties, sulfondiimines appear as leads in discovery industry, but the lack of efficient synthetic approaches holds back their further uptake by medicinal chemistry. Herein, a general and practical copper‐catalyzed Chan‐Lam coupling of NH‐diaryl sulfondiimines with arylboronic acids is presented. A simple copper catalyst efficiently facilitated the highly chemoselective construction of C−N bond, allowing the preparation of a variety of N‐arylated diaryl sulfondiimines in good yields under mild and environmentally benign conditions. An array of protecting groups on imine moieties were well tolerated, offering diversified accesses to NH,NAr‐diaryl sulfondiimines, a class of versatile building blocks. Moreover, an aza‐analogue of an EphB4 inhibitor featuring a sulfondiimine‐based pharmacophore was generated employing our Chan‐Lam coupling as the key step. [ABSTRACT FROM AUTHOR]

The immune system plays an indispensable role in maintaining human health against the invasion of foreign materials, microorgainisms and pathogens. The autoimmune diseases and chronic inflammatory disorders are characterized by dysregulated immune responses resulting in excessive and uncontrolled tissue inflammation, as well as tumour, and others. In recent years, flavonoids are widely recognized as potentially natural polyphenol compounds for the treatment of multiple diseases, given their immunomodulatory activity, antioxidant and antineoplastic activities. However, the exact mechanisms of flavonoids on the immune system and inhibiting tumour remains unclear. This review article provides an overview of the impact and mechanism of flavonoids on innate and adaptive immune system through the analysis of various immune cells. Meanwhile, we also explain the probable therapeutic mechanism of flavonoids on tumour and other chronic diseases. Overall, this review may provide a certain theoretical direction and theoretical basis for the application of flavonoids in the treatment of immune‐related disorders and tumour. [ABSTRACT FROM AUTHOR]

A series of ester‐based thermoplastic polyurethane elastomer (TPU) and bismuth sodium titanate polycrystalline oxide (Bi0.5Na0.5TiO3, BNT) co‐blended poly (vinylidene fluoride) (PVDF) composite films were prepared. Mechanical test confirms the optimum BNT blending content (25 wt%) and further reveals a linear growth of tensile elongation by increasing TPU content. Microstructure modifications including strengthened hydrogen bond and valence band edge elevation are evidenced to be highly correlated to the dielectric and piezoelectric properties. Significant enhancement (7–13 times) in face shear piezoelectric coefficient (d36) is achieved by adjusting the blending content of TPU. Cross‐section image presents a featuring multilayer structure with improved dispersity of BNT particle under a transverse tensile force which effectively increases the interfacial contact area between BNT and polymer blends. This work reveals the significance of band structure modification and anisotropic texture construction on influencing the transfer of piezoelectric charge in TPU blended BNT‐PVDF composite film. [ABSTRACT FROM AUTHOR]

Carbonyl sulfide (COS), whose molecular structure is similar to CO2 and CS2, could be used as a better alternative carbonyl reagent due to its high chemical activity. However, the unfriendly by‐product H2S would be generated when COS is used as a carbonyl reagent in the carbonylation reaction. In this report, the odorless and stable disulfide was used to replace the traditional foul smelling and unstable o‐aminobenzenethiol to react with COS for preparing benzothiazolone derivatives in excellent yield, in which coupling reaction of H2S generation and S–S bond cleavage was firstly designed. Notably, the C=O of COS was converted into benzothiazolone derivatives by carbonylation reaction and the sulfur of COS was transformed into sulfur and sulfide after cleaving the S–S bond by a domino reaction of disulfide and COS under mild conditions. This efficient synthetic methodology provided a promising process for the utilization of COS. An efficient method for preparing benzothiazolone derivatives was developed by a domino coupling reaction between the disulfide and COS in the present of NaOH. Notably, the C=O of COS was converted into benzothiazolone by carbonylation reaction and the sulfur of COS was transformed into sulfur and sulfide after cleaving the S–S bond under mild conditions. This efficient synthetic methodology could provide a promising process for the utilization of COS. [ABSTRACT FROM AUTHOR]

Abstract: Silver nanoparticles (AgNPs) are widely used in health and consumer products that routinely contact skin. However, the biological effects and possible mechanisms of AgNPs on skin remain unclear. Gap junctional intercellular communication (GJIC) plays a critical role in multicellular organisms to maintain tissue homeostasis. The aim of this study is to examine if non‐coated AgNPs affect GJIC in human keratinocytes (HaCaT cells), and to identify the possible molecular mechanisms responsible for the effects. GJIC, connexin (Cx)43 protein and mRNA expression, and the effect of siRNA‐mediated knockdown of Cx43 on GJIC were assessed. HaCaT cells exposed to non‐coated AgNPs at different doses after a 24 hour exposure. To explore further the underlying mechanism, reactive oxygen species and mitogen‐activated protein kinase pathway were evaluated after 2, 6, 12 and 24 hours. Our results revealed that non‐coated AgNP exposure at subcytotoxic doses increase GJIC partially via Cx43 upregulation. Reactive oxygen species and extracellular signal‐regulated kinase and activation of c‐Jun N‐terminal kinase were involved in the AgNP‐induced upregulation of Cx43. This study provides new insight into the potential mechanism of AgNP biological activity. [ABSTRACT FROM AUTHOR]

Senescent cells display a senescence-associated secretory phenotype (SASP) which contributes to tumor suppression, aging, and cancer. However, the underlying mechanisms for SASP regulation are not fully elucidated. SIRT1, a nicotinamide adenosine dinucleotide-dependent deacetylase, plays multiple roles in metabolism, inflammatory response, and longevity, etc. However, its posttranscriptional regulation and its roles in cellular senescence and SASP regulation are still elusive. Here, we identify the RNA-binding protein hnRNP A1 as a posttranscriptional regulator of SIRT1, as well as cell senescence and SASP regulator. hnRNP A1 directly interacts with the 3′ untranslated region of SIRT1 mRNA, promotes its stability, and increases SIRT1 expression. hnRNP A1 delays replicative cellular senescence and prevents from Ras OIS via upregulation of SIRT1 expression to deacetylate NF-κB, thus blunting its transcriptional activity and subsequent IL-6/IL-8 induction. hnRNP A1 overexpression promotes cell transformation and tumorigenesis in a SIRT1-dependent manner. Together, our findings unveil a novel posttranscriptional regulation of SIRT1 by hnRNP A1 and uncover a critical role of hnRNP A1-SIRT1-NF-κB pathway in regulating cellular senescence and SASP expression. [ABSTRACT FROM AUTHOR]

The nicotinamide adenine dinucleotide-dependent protein deacetylase silent information regulator 2 (Sir2) regulates cellular lifespan in several organisms. Histone deacetylase 4 (HDAC4) belongs to the class IIa group of HDACs; this class of HDACs is composed of proteins that are important regulators of gene expression that control pleiotropic cellular functions. However, the role of HDAC4 in cellular senescence is still unknown. This study shows that the expression patterns of HDAC4 and Sirtuin 1 (SIRT1; the mammalian homolog of Sir2) are positively correlated during cellular senescence. Moreover, the overexpression of HDAC4 delays senescence, whereas the knockdown of HDAC4 leads to premature senescence in human fibroblasts. Furthermore, it is demonstrated that HDAC4 increases endogenous SIRT1 expression by enhancing its sumoylation modification levels, thereby stabilizing its protein levels. This study, therefore, provides a new molecular mechanism for the regulation of cellular senescence. [ABSTRACT FROM AUTHOR]

Sirtuin ( SIRT) 1 is a key protein in mediating the benefits of calorie restriction ( CR) in mammals. However, the molecular mechanisms underlying CR-induced SIRT1 upregulation in mammals remain unclear. Herein we show that the elevated SIRT1 levels are not due to increased SIRT1 mRNA expression. but rather to enhanced SIRT1 protein stability as a result of reduced ubiquitin-proteasome degradation of SIRT1 under limited nutrient conditions. Our observations have important implications for improving healthy aging in humans. [ABSTRACT FROM AUTHOR]

Mechanisms governing the transcription of p16INK4a, one of the master regulators of cellular senescence, have been extensively studied. However, little is known about chromatin dynamics taking place at its promoter and distal enhancer. Here, we report that Forkhead box A1 protein (FOXA1) is significantly upregulated in both replicative and oncogene-induced senescence, and in turn activates transcription of p16INK4a through multiple mechanisms. In addition to acting as a classic sequence-specific transcriptional activator, FOXA1 binding leads to a decrease in nucleosome density at the p16INK4a promoter in senescent fibroblasts. Moreover, FOXA1, itself a direct target of Polycomb-mediated repression, antagonizes Polycomb function at the p16INK4a locus. Finally, a systematic survey of putative FOXA1 binding sites in the p16INK4a genomic region revealed an ∼150 kb distal element that could loop back to the promoter and potentiate p16INK4a expression. Overall, our findings establish several mechanisms by which FOXA1 controls p16INK4a expression during cellular senescence. [ABSTRACT FROM AUTHOR]

The systematic structures search for neutral and Zintl anionic Ti‐doped silicon clusters TiSin0/−/2− (n = 6‐16) have been carried out using the ABCluster global search technique combined with a double‐hybrid density functional method. Based on the predicted energies, adiabatic electron affinities, vertical detachment energies and the consistency between simulated and experimental photoelectron spectroscopy, the true global minimum structures are confirmed. The results show that structural growth pattern of neutral TiSin clusters is from linked structures (n = 10‐12) to encapsulated configurations (n = 13‐16). In contrast, the evolution pattern of Zintl anionic TiSin−/2− clusters begins with the pentagonal bipyramid structure (n = 6). As the Si atoms increase, these Si atoms attach to the surface adjacent to Ti atom, and gradually surround Ti atom. Eventually, the encapsulated structure is formed when n = 12. Moreover, two extra electrons not only perfect the structure of TiSi12 but also improve its chemical and thermodynamic stability. [ABSTRACT FROM AUTHOR]