CALD1 facilitates epithelial-mesenchymal transition progression in gastric cancer cells by modulating the PI3K-Akt pathway.

BACKGROUND: CALD1 has been discovered to be abnormally expressed in a variety of malignant tumors, including gastric cancer (GC), and is associated with tumor progression and immune infiltration; however, the roles and mechanisms of CALD1 in epithelial-mesenchymal transition (EMT) in GC are unknown. AIM: To investigate the role and mechanism of CALD1 in GC progression, invasion, and migration. METHODS: In this study, the relationship between CALD1 and GC, as well as the possible network regulatory mechanisms of CALD1, was investigated by bioinformatics and validated by experiments. CALD1-siRNA was synthesized and used to transfect GC cells. Cell activity was measured using the CCK-8 method, cell migration and invasive ability were measured using wound healing assay and Transwell assay, and the expression levels of relevant genes and proteins in each group of cells were measured using qRT-PCR and Western blot. A GC cell xenograft model was established to verify the results of in vitro experiments. RESULTS: Bioinformatics results showed that CALD1 was highly expressed in GC tissues, and CALD1 was significantly higher in EMT-type GC tissues than in tissues of other types of GC. The prognosis of patients with high expression of CALD1 was worse than that of patients with low expression, and a prognostic model was constructed and evaluated. The experimental results were consistent with the results of the bioinformatics analysis. The expression level of CALD1 in GC cell lines was all higher than that in gastric epithelial cell line GES-1, with the strongest expression found in AGS and MKN45 cells. Cell activity was significantly reduced after CALD1-siRNA transfection of AGS and MKN45 cells. The ability of AGS and MKN45 cells to migrate and invade was reduced after CALD1-siRNA transfection, and the related mRNA and protein expression was altered. According to bioinformatics findings in GC samples, the CALD1 gene was significantly associated with the expression of members of the PI3K-AKT-mTOR signaling pathway as well as the EMT signaling pathway, and was closely related to the PI3K-Akt signaling pathway. Experimental validation revealed that upregulation of CALD1 increased the expression of PI3K, p-AKT, and p-mTOR, members of the PI3K-Akt pathway,while decreasing the expression of PTEN; PI3K-Akt inhibitor treatment decreased the expression of PI3K, p-AKT, and p-mTOR in cells overexpressing CALD1 (still higher than that in the normal group), but increased the expression of PTEN (still lower than that in the normal group). CCK-8 results revealed that the effect of CALD1 on tumor cell activity was decreased by the addition of the inhibitor. Scratch and Transwell experiments showed that the effect of CALD1 on tumor cell migration and invasion was weakened by the addition of the PI3K-Akt inhibitor. The mRNA and protein levels of EMT-related genes in AGS and MKN45 cells were greatly altered by the overexpression of CALD1, whereas the effect of overexpression of CALD1 was significantly weakened by the addition of the PI3K-Akt inhibitor. Animal experiments showed that tumour growth was slow after inhibition of CALD1, and the expression of some PI3K-Akt and EMT pathway proteins was altered. CONCLUSION: Increased expression of CALD1 is a key factor in the progression, invasion, and metastasis of GC, which may be associated with regulating the PI3K-Akt pathway to promote EMT.

Potential of Lycii Radicis Cortex as an Ameliorative Agent for Skeletal Muscle Atrophy.

Lycii Radicis Cortex (LRC) is a traditional medicine in East Asia with various beneficial effects, including antioxidant, anti-inflammatory, anti-tumor, anti-diabetic, and anti-depressant properties. However, its potential effects on skeletal muscle atrophy have not been studied. In this study, the protective effects of LRC extract (LRCE) on dexamethasone (DEX)-induced muscle atrophy were investigated in C2C12 myotubes and mice. We evaluated the effect of LRCE on improving muscle atrophy using a variety of methods, including immunofluorescence staining, quantitative polymerase chain reaction (qPCR), Western blot, measurements of oxidative stress, apoptosis, ATP levels, and muscle tissue analysis. The results showed that LRCE improved myotube diameter, fusion index, superoxide dismutase (SOD) activity, mitochondrial content, ATP levels, expression of myogenin and myosin heavy chain (MHC), and reduced reactive oxygen species (ROS) production in dexamethasone-induced C2C12 myotubes. LRCE also enhanced protein synthesis and reduced protein degradation in the myotubes. In mice treated with DEX, LRCE restored calf thickness, decreased mRNA levels of muscle-specific RING finger protein 1 (MuRF1) and atrogin-1, and increased insulin-like growth factor 1 (IGF-1) mRNA level. Moreover, LRCE also repaired gastrocnemius muscle atrophy caused by DEX. Although human studies are not available, various preclinical studies have identified potential protective effects of LRCE against muscle atrophy, suggesting that it could be utilized in the prevention and treatment of muscle atrophy.

A metal-free strategy to construct fluoroalkyl-olefin linkages using fluoroalkanes.

We present a metal-free strategy to access fluoroalkyl-olefin linkages from fluoroalkane precursors and vinyl-pinacol boronic ester (BPin) reagents. This reaction sequence is templated by the boron reagent, which induces C-C bond formation upon oxidation. We developed this strategy into a one-pot synthetic protocol using RCF2H precursors directly with vinyl-BPin reagents in the presence of a Brønsted base, which tolerated oxygen- and nitrogen-containing heterocycles, and aryl halogens. We also found that HCF3 (HCF-23; a byproduct of the Teflon industry) and CH2F2 (HCF-32; a low-cost refrigerant) are amenable to this protocol, representing distinct strategies to generate RCF2H and RCF3 molecules. Finally, we demonstrate that the vinyldifluoromethylene products can be readily derivatized, representing an avenue for late-stage modification after installing the fluoroalkyl unit.

Inhibition of α-amylase digestion by a Lonicera caerulea berry polyphenol starch complex revealed via multi-spectroscopic and molecular dynamics analyses.

Polyphenol-starch complexes exhibit synergistic and beneficial effects on both polyphenols and resistant starches. This study evaluates the inhibitory effects and mechanisms of α-amylase on a Lonicera caerulea berry polyphenol-wheat starch (LPWS) complex following high hydrostatic pressure treatments of 400 MPa for 30 min and 600 MPa for 30 min. The IC50 values for α-amylase inhibition by the complex were 3.61 ± 0.10 mg/mL and 3.42 ± 0.08 mg/mL at a 10 % (w/w) polyphenol content. This interaction was further supported by Fourier-transform infrared spectroscopy and circular dichroism, which confirmed that the alpha helix component of the secondary structure of α-amylase was reduced due to the complex. Multifluorescence spectroscopy revealed that the complex induces changes in the microenvironment of fluorophores surrounding the α-amylase active site. Molecular dynamics simulations and molecular docking revealed that the active site of amylose within the complex becomes enveloped in polyphenol clusters. This wrapping effect reduced the hydrogen bonds between amylose and α-amylase, decreasing from 16 groups to just one group. In summary, the LPWS complex represents a low-digestible carbohydrate food source, thus laying the groundwork for the research and development of functional foods aimed at postprandial hypoglycemic effects.

Photocontrolled chiroptical switch based on the self-assembly of azobenzene-bridged bis-tryptophan enantiomers.

Chirality dynamic tuning plays fundamental roles in chemistry, material science and biological system. Herein, a pair of azobenzene-bridged bis-tryptophan enantiomers (Azo-di-d/l-Trp) were designed and synthesized via simple reactions. With the fuel of glucono-δ-lactone (GdL), releasing protons during its hydrolysis, the alkaline solution of Azo-di-d/l-Trp gradually self-assembled into contrast chiral helical structures and displayed magnitude and mirror image of circular dichroism (CD) signals. While the chiral helices converted to CD silent nanoparticles when the azobenzene moiety isomerized from trans- to cis-form under UV irradiation. More importantly, this chiroptical switch, displaying reversible interconversion between chiral amplification and silent, can be smartly controlled via photoirradiation at various wavelengths.

Integrin αV mediated activation of myofibroblast via mechanoparacrine of transforming growth factor ß1 in promoting fibrous scar formation after myocardial infarction.

BACKGROUND: Myocardial infarction (MI) dramatically changes the mechanical stress, which is intensified by the fibrotic remodeling. Integrins, especially the αV subunit, mediate mechanical signal and mechanoparacrine of transforming growth factor ß1 (TGF-ß1) in various organ fibrosis by activating CFs into myofibroblasts (MFBs). We investigated a possible role of integrin αV mediated mechanoparacrine of TGF-ß1 in MFBs activation for fibrous reparation in mice with MI. METHODS: Heart samples from MI, sham, or MI plus cilengitide (14 mg/kg, specific integrin αV inhibitor) treated mice, underwent functional and morphological assessments by echocardiography, and histochemistry on 7, 14 and 28 days post-surgery. The mechanical and ultrastructural changes of the fibrous scar were further evaluated by atomic mechanics microscope (AFM), immunofluorescence, second harmonic generation (SHG) imaging, polarized light and scanning electron microscope, respectively. Hydroxyproline assay was used for total collagen content, and western blot for protein expression profile examination. Fibroblast bioactivities, including cell shape, number, Smad2/3 signal and expression of extracellular matrix (ECM) related proteins, were further evaluated by microscopic observation and immunofluorescence in polyacrylamide (PA) hydrogel with adjustable stiffness, which was re-explored in fibroblast cultured on stiff matrix after silencing of integrin αV. The content of total and free TGF-ß1 was tested by enzyme-linked immunosorbent assay (ELISA) in both infarcted tissue and cell samples. RESULT: Increased stiffness with heterogeneity synchronized with integrin αV and alpha smooth muscle actin (α-SMA) positive MFBs accumulation in those less mature fibrous areas. Cilengitide abruptly reduced collagen content and disrupted collagen alignment, which also decreased TGF-ß1 bioavailability, Smad2/3 phosphorylation, and α-SMA expression in the fibrous area. Accordingly, fibroblast on stiff but not soft matrix exhibited obvious MFB phenotype, as evidenced by enlarged cell, hyperproliferation, well-developed α-SMA fibers, and elevated ECM related proteins, while silencing of integrin αV almost abolished this switch via attenuating paracrine of TGF-ß1 and nuclear translocation of Smad2/3. CONCLUSION: This study illustrated that increased tissue stiffness activates CFs into MFBs by integrin αV mediated mechanoparacrine of TGF-ß1, especially in immature scar area, which ultimately promotes fibrous scar maturation.

Sensory nerves directly promote osteoclastogenesis by secreting peptidyl-prolyl cis-trans isomerase D (Cyp40).

Given afferent functions, sensory nerves have recently been found to exert efferent effects and directly alter organ physiology. Additionally, several studies have highlighted the indirect but crucial role of sensory nerves in the regulation of the physiological function of osteoclasts. Nonetheless, evidence regarding the direct sensory nerve efferent influence on osteoclasts is lacking. In the current study, we found that high levels of efferent signals were transported directly from the sensory nerves into osteoclasts. Furthermore, sensory hypersensitivity significantly increased osteoclastic bone resorption, and sensory neurons (SNs) directly promoted osteoclastogenesis in an in vitro coculture system. Moreover, we screened a novel neuropeptide, Cyp40, using an isobaric tag for relative and absolute quantitation (iTRAQ). We observed that Cyp40 is the efferent signal from sensory nerves, and it plays a critical role in osteoclastogenesis via the aryl hydrocarbon receptor (AhR)-Ras/Raf-p-Erk-NFATc1 pathway. These findings revealed a novel mechanism regarding the influence of sensory nerves on bone regulation, i.e., a direct promoting effect on osteoclastogenesis by the secretion of Cyp40. Therefore, inhibiting Cyp40 could serve as a strategy to improve bone quality in osteoporosis and promote bone repair after bone injury.

One-step preparation of Pt/Ag nanoclusters for CO2 transformation.

Structurally precise metal nanoclusters with a facile synthetic process and high catalytic performance have been long pursued. These atomically precise nanocatalysts are regarded as model systems to study structure-performance relationships, surface coordination chemistry, and the reaction mechanism of heterogeneous metal catalysts. Nevertheless, the research on silver-based nanoclusters for driving chemical transformations is sluggish in comparison to gold counterparts. Herein, we report the one-step synthesis of Pt/Ag alloy nanoclusters of [PtAg9(C18H12Br3P)7Cl3](C18H12Br3P), which are highly active in catalysing cycloaddition reactions of CO2 and epoxides. The cluster was obtained in a rather simple way with the reduction of silver and platinum salts in the presence of ligands in one pot. The molecular structure of the titled cluster describes the protection of the Pt-centred Ag9 crown by the shell of phosphine ligands and halides. Its electronic structure, as revealed by density function theoretical calculations, adopts a superatomic geometry with 1S21P6 configuration. Interestingly, the cluster displays high activity in the formation of cyclic carbonates from CO2 under mind conditions.

Ligand recognition and G-protein coupling of trace amine receptor TAAR1.

Trace-amine-associated receptors (TAARs), a group of biogenic amine receptors, have essential roles in neurological and metabolic homeostasis1. They recognize diverse endogenous trace amines and subsequently activate a range of G-protein-subtype signalling pathways2,3. Notably, TAAR1 has emerged as a promising therapeutic target for treating psychiatric disorders4,5. However, the molecular mechanisms underlying its ability to recognize different ligands remain largely unclear. Here we present nine cryo-electron microscopy structures, with eight showing human and mouse TAAR1 in a complex with an array of ligands, including the endogenous 3-iodothyronamine, two antipsychotic agents, the psychoactive drug amphetamine and two identified catecholamine agonists, and one showing 5-HT1AR in a complex with an antipsychotic agent. These structures reveal a rigid consensus binding motif in TAAR1 that binds to endogenous trace amine stimuli and two extended binding pockets that accommodate diverse chemotypes. Combined with mutational analysis, functional assays and molecular dynamic simulations, we elucidate the structural basis of drug polypharmacology and identify the species-specific differences between human and mouse TAAR1. Our study provides insights into the mechanism of ligand recognition and G-protein selectivity by TAAR1, which may help in the discovery of ligands or therapeutic strategies for neurological and metabolic disorders.

PtAg18 superatoms costabilized by phosphines and halides: synthesis, structure, and catalysis.

Reported herein is the facial synthesis, molecular structure, and catalysis of a Pt/Ag nanocluster costabilized by organic ligands of phosphines and inorganic ligands of chlorides. The nanocluster with molecular formula of [PtAg18(dppp)6Cl8](SbF6)2 has been obtained facilely by the one pot method. The structure of the cluster could be anatomized as the stabilizaiton of PtAg12-centered icosahedral core by the metalloligand of dppp-Ag-Cl, in which Cl- not only caps the surface Ag atoms but also binds the core and surface motifs. Featuring eight free electrons in its structure, the cluster exhibits high stability. More interestingly, the exposure of surface metal sites endows the cluster with counterintutively  high catalytic activity in hydrogenation reactions.

DppfCuBH4: new reducing agents for the synthesis of ferrocene-functionalized metal nanoclusters.

A facile synthesis of atomically precise metal nanoclusters, especially those decorated with functional groups, is the prerequisite for finding applications in special fields and studying structure-and-property relationships. The exploration of simple and efficient synthetic prototypes for introducing functional ligands (such as ferrocene) into cluster moieties is thus of high interest. In this work, a type of reducing agent of dppfCuBH4 (dppf is 1,1'-bis(diphenyphosphino)ferrocene) is introduced for the first time to prepare ferrocene-functionalized metal nanoclusters. Two new clusters of [Ag25Cu4(dppf)6(3-F-PhCC)12Cl6]3+ (1) and [Ag4(dppf)5Cl2]2+ (2) have been obtained from the simple synthetic method. The two compounds have been fully characterized by advanced techniques of electrospray ionization mass spectroscopy (ESI-MS), nuclear magnetic resonance (NMR), and ultraviolet-visible spectroscopy (UV-Vis). The total structure of the clusters, as determined by X-ray single-crystal diffraction, describes the Ag13@Ag12Cu4(dppf)6(3-F-PhCC)12Cl6 core-shell structure of 1 and [Ag2Cl(dppf)2]+-dppf-[Ag2Cl(dppf)2]+ polymeric structure of 2. This work opens the door to employing dppfCuBH4 as a functional reducing agent to discover many underlying metal nanoclusters and even other nanomaterials which feature ferrocene-groups.

Clinicopathological characteristics of rectal multiple neuroendocrine neoplasms and literature review.

BACKGROUND: There are only a few epidemiological reports available for reference. The clinicopathological features are not clear, so there is no consensus on treating rectal multiple neuroendocrine neoplasms. This study aims to summarize the clinicopathological characteristics and preliminarily discuss the clinical diagnosis and treatment of rectal multiple neuroendocrine neoplasms. METHODS: This study retrospectively analyzed rectal neuroendocrine neoplasm patients diagnosed and treated at the Fourth Hospital of Hebei Medical University from February 2007 to May 2021. The clinicopathological characteristics of rectal multiple neuroendocrine neoplasms were summarized and analyzed in combination with 14 studies on rectal multiple neuroendocrine neoplasms. RESULTS: The incidence of RM-NENs accounted for 3.8% of all R-NENs in this study. The number of tumors varied to some extent, the size of tumors was basically no more than 10 mm, and there were more G1 grade tumors. In the analysis of 46 cases with known lymph node metastasis, the difference in lymph node metastasis rate between the number of tumors < 8 and ≥ 8 was statistically significant (p = 0.002). CONCLUSIONS: The incidence of rectal multiple neuroendocrine neoplasms accounted for 3.8% of all rectal neuroendocrine neoplasms. For rectal multiple neuroendocrine neoplasms, the lymph node metastasis rate was higher when the number of tumors was ≥ 8. The influence of the number of tumors on lymph node metastasis should be considered in the selection of treatment.

Thermodynamics and Physicochemical Properties of Immobilized Maleic Anhydride-Modified Xylanase and Its Application in the Extraction of Oligosaccharides from Wheat Bran.

Xylanases are the preferred enzymes for the extracting of oligosaccharides from wheat bran. However, free xylanases have poor stability and are difficult to reuse, which limit their industrial application. In the present study, we covalently immobilized free maleic anhydride-modified xylanase (FMA-XY) to improve its reusability and stability. The immobilized maleic anhydride-modified xylanase (IMA-XY) exhibited better stability compared with the free enzyme. After six repeated uses, 52.24% of the activity of the immobilized enzyme remained. The wheat bran oligosaccharides extracted using IMA-XY were mainly xylopentoses, xylohexoses, and xyloheptoses, which were the ß-configurational units and α-configurational units of xylose. The oligosaccharides also exhibited good antioxidant properties. The results indicated that FMA-XY can easily be recycled and can remain stable after immobilization; therefore, it has good prospects for future industrial applications.

Chinese chestnut shell polyphenol extract regulates the JAK2/STAT3 pathway to alleviate high-fat diet-induced, leptin-resistant obesity in mice.

Chinese chestnut shell is a by-product of chestnut food processing and is rich in polyphenols. This study sought to investigate the effect of chestnut shell polyphenol extract (CSP) on weight loss and lipid reduction in a 12-week high-fat diet (HFD)-induced murine obesity model. CSP (300 mg per kg body weight) was administered intragastrically daily. AG490, a JAK2 protein tyrosine kinase inhibitor, was also intraperitoneally injected. The results showed that an HFD induced leptin resistance (LR). Compared to corresponding values in the HFD group, CSP treatment improved blood lipid levels, weight, and leptin levels in obese mice (p < 0.01). Additionally, CSP treatment enhanced enzyme activity by improving total antioxidant capacity, attenuating oxidative stress, and reducing fat droplet accumulation and inflammation in the liver, epididymal, and retroperitoneal adipose tissue. CSP also activated the LEPR-JAK2/STAT3-PTP1B-SOCS-3 signal transduction pathway in hypothalamus tissue and improved LR while regulating the expression of proteins related to lipid metabolism (PPARγ, FAS, and LPL) in white adipose tissue in the retroperitoneal cavity. However, the amelioration of lipid metabolism by CSP was dependent on JAK2. Molecular docking simulation further demonstrated the strong binding affinity of procyanidin C1 (-10.3983297 kcal mol-1) and procyanidin B1 (-9.12686729 kcal mol-1) to the crystal structure of JAK2. These results suggest that CSP may be used to reduce HFD-induced obesity with potential application as a functional food additive.

Simple Approach toward N-Heterocyclic Carbene-Protected Gold Nanoclusters.

Little advance has been made toward developing alternative bottom-up synthetic strategies for N-heterocyclic carbene (NHC)-stabilized gold nanoclusters, although this unique class of nanomaterials has exhibited exciting properties. We report in this work a simple and straightforward approach toward NHC-ligated gold nanoclusters by using imidazolium salts rather than free carbenes or NHC-coordinated gold complexes (NHC-Au-X, X is counterions) as precursors. Illustrated here is a one-pot and one-step preparation of an NHC-stabilized Au13Br4 cluster that features a distinct molecular formula, surface motifs, and assembling modes via chemical reduction of dpaAu, NaOMe, and FNHCBn·HBr by NaBH4 (Hdpa is dipyridylamine; FNHCBn·HBr is 1,3-dibenzyl-5,6-difluoro-1H-benzo[d]imidazole-3-ium bromide). In situ UV-vis and NMR studies have elucidated the base-assisted formation of NHCs from imidazolium salts for the protection of the metal core. This work not only reports a new NHC-ligated superatom that completes the Au13 library, thus facilitating structure-property studies, but also opens the door to explore underlying analogues in a facile and reasonable way.

Salvia plebeia R.Br. and Rosmarinic Acid Attenuate Dexamethasone-Induced Muscle Atrophy in C2C12 Myotubes.

Skeletal muscle atrophy occurs when protein degradation exceeds protein synthesis and is associated with increased circulating glucocorticoid levels. Salvia plebeia R.Br. (SPR) has been used as herbal remedy for a variety of inflammatory diseases and has various biological actions such as antioxidant and anti-inflammatory activities. However, there are no reports on the effects of SPR and its bioactive components on muscle atrophy. Herein, we investigated the anti-atrophic effect of SPR and rosmarinic acid (RosA), a major compound of SPR, on dexamethasone (DEX)-induced skeletal muscle atrophy in C2C12 myotubes. Myotubes were treated with 10 µM DEX in the presence or absence of SPR or RosA at different concentrations for 24 h and subjected to immunocytochemistry, western blot, and measurements of ROS and ATP levels. SPR and RosA increased viability and inhibited protein degradation in DEX-treated C2C12 myotubes. In addition, RosA promoted the Akt/p70S6K/mTOR pathway and reduced ROS production, and apoptosis. Furthermore, the treatment of RosA significantly recovered SOD activity, autophagy activity, mitochondrial contents, and APT levels in DEX-treated myotubes. These findings suggest that SPR and RosA may provide protective effects against DEX-induced muscle atrophy and have promising potential as a nutraceutical remedy for the treatment of muscle weakness and atrophy.

Additional endoscopic treatments for patients with positive lateral margins after endoscopic resection of early esophageal squamous cell carcinoma.

There are currently no well-established treatment strategies for early esophageal squamous cell carcinoma (ESCC) for patients with only positive lateral margin (LM+) following endoscopic resection (ER). The present study aimed to find a treatment strategy for patients with early ESCC with non-curative resection (non-CR) and only LM+ following ER. In total, 511 patients with early ESCC treated at the Fourth Hospital of Hebei Medical University (Shijiazhuang, China) with ER were retrospectively analyzed, 41 of which (8%) were patients with only LM+ after non-CR. Of these, 28 patients received re-ER and 13 received additional surgical treatment. The clinicopathological characteristics of patients were analyzed and those who underwent additional surgery vs. re-ER were compared. Residual cancer cells were found in 27 patients (27/41, 65.9%) following re-ER or additional surgery. A significant increase in residual cancer cells was observed in patients with poorly differentiated cancer and patients with multiple LM+ (P=0.03 and P=0.015, respectively). Older patients and patients with single LM+ tended to choose re-ER (P=0.023 and P=0.038, respectively). In addition, there were three cases (3/13, 23.1%) of lymph node metastasis in the additional surgery group. However, within the limited follow-up time (mean, 36.1±24.1 months), no recurrence or metastasis was found in the remaining patients. The results showed that re-ER may be a more suitable additional therapy compared with surgery for patients with LM+ following non-CR, at least in the medium-term.

Carbon dots as light-responsive oxidase-like nanozyme for colorimetric detection of total antioxidant capacity in fruits.

Evaluation of total antioxidant capacity (TAC) in fruits is essential for dietary guidance and health monitoring. Here, we have exploited light-response carbon dots (CDs) as oxidase-like nanozyme to determine the TAC of fruits. The CDs possess excellent oxidase-like activity with light stimulation due to the accelerated intramolecular charge transfer caused by abundant electron donating/drawing groups in precursors. The scavenger experiment reveals that the catalytic intermediate could be hydroxyl radical, which can oxidize the colorimetric substrate. With the introduction of antioxidants, the oxidization of colorimetric substrate will be alleviated due to the scavenging of this intermediate by antioxidants. Based on this, we have successfully detected three antioxidants and obtained TAC of fruits with desirable results. This work affords a rapid, cost-effective and convenient analysis tool for TAC, as well as building a strong bridge between CDs and the development of photo-responsive oxidase-like nanozymes.

Preparation and Functionalization of Mono- and Polyfluoroepoxides via Fluoroalkylation of Carbonyl Electrophiles.

We outline a new synthetic method to prepare mono- and polyfluoroepoxides from a diverse pool of electrophiles (ketones, acyl chlorides, esters) and fluoroalkyl anion equivalents. The initially formed α-fluoro alkoxides undergo subsequent intramolecular ring closure when heated. We demonstrated the versatility of the method through the isolation of 16 mono- and polyfluoroepoxide products. These compounds provide unique entry points for further diversification via either fluoride migration coupled with ring opening, or defluorinative functionalization reactions, the latter of which can be used as a late-stage method to install select bioactive moieties. The reaction sequences described herein provide a pathway to functionalize the commonly observed products formed from 1,2-addition into carbonyl electrophiles.