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A molecularly imprinted hypercrosslinked polymer (HCP) was synthesized from the polymerization of mesitylene monomer, terephthaloyl chloride crosslinker, and tannic acid (TA) template through FeCl3-catalyzed Friedel–Crafts acylation. The TA-imprinted HCP (TAHCP) was capable of IUPAC Type I mesoporosity, with specific surface area of 1258 m2 g−1, monolayer adsorption capacity of 289 cm2 g−1, pore sizes ranging from 4.4 to 12.6 Å, amorphous morphology, and characteristic absorption and emission bands. The extended π-conjugation framework of TAHCP was endowed with 385-nm fluorescent emission at 310-nm excitation. The fluorescence intensity of TAHCP could be dynamically quenched by TA and was linearly correlated with 20–1000 nM TA concentrations on the Stern–Volmer plot in the optimized conditions of pH 5.5 buffer, 100 μg mL−1 TAHCP, and 3.5 min equilibrium. The relative standard deviation (RSD) for 50 nM TA was 3.4% (n = 5), and the limit of detection was 6.2 nM based on the 3σ of the TA blanks). For 50nM TA, the imprinted factor was calculated to be 7.8, and the selectivity for 250 nM interferents, including ions, organic acids, saccharides, amino acids, and caffeine, which are commonly found in beverages, was 7.5–9.5, except for gallic acid (1.2). The recoveries of TA spiked in tea and juice beverages at three levels (10–150 nM) were 93.6–101.9% (RSD = 3.6–4.3%). [ABSTRACT FROM AUTHOR]

Background: The endosperm serves as the primary source of nutrients for maize (Zea mays L.) kernel embryo development and germination. Positioned at the base of the endosperm, the transfer cells (TCs) of the basal endosperm transfer layer (BETL) generate cell wall ingrowths, which enhance the connectivity between the maternal plant and the developing kernels. These TCs play a crucial role in nutrient transport and defense against pathogens. The molecular mechanism underlying BETL development in maize remains unraveled. Results: This study demonstrated that the MYB-related transcription factor ZmMYBR29, exhibited specific expression in the basal cellularized endosperm, as evidenced by in situ hybridization analysis. Utilizing the CRISPR/Cas9 system, we successfully generated a loss-of-function homozygous zmmybr29 mutant, which presented with smaller kernel size. Observation of histological sections revealed abnormal development and disrupted morphology of the cell wall ingrowths in the BETL. The average grain filling rate decreased significantly by 26.7% in zmmybr29 mutant in comparison to the wild type, which impacted the dry matter accumulation within the kernels and ultimately led to a decrease in grain weight. Analysis of RNA-seq data revealed downregulated expression of genes associated with starch synthesis and carbohydrate metabolism in the mutant. Furthermore, transcriptomic profiling identified 23 genes that expressed specifically in BETL, and the majority of these genes exhibited altered expression patterns in zmmybr29 mutant. Conclusions: In summary, ZmMYBR29 encodes a MYB-related transcription factor that is expressed specifically in BETL, resulting in the downregulation of genes associated with kernel development. Furthermore, ZmMYBR29 influences kernels weight by affecting the grain filling rate, providing a new perspective for the complementation of the molecular regulatory network in maize endosperm development. [ABSTRACT FROM AUTHOR]

Intestinal stem cells (ISCs) are the reservoir source of various types of intestinal cells, and the decline of stem cell function in the gut may be a potential factor for aging-related disease. The present study aimed to explore the regulatory mechanisms of Panax ginseng C.A.Meyer (Araliaceae , Panax genus) that could restore gut aging by enhancing intestinal function and regulating ISCs in aging mice based on the Wnt/β-catenin signaling pathway. A total of 60 ICR male mice were randomly divided into control, model, metformin, and ginseng water decoction (GWD) 3.6, 1.8, and 0.9 g/kg groups. The aging model was induced by 1 % D-galactose (s.c. 0.1 mL/10 g) for 28 days. Moreover, GWD was given to aging mice intragastrically (i.g.) once a day for 28 successive days. The learning memory ability, pathological status, and function in the ileum tissue, the activity of digestive enzymes, and short-chain fatty acid (SCFA) content in the colon were evaluated, and the related mechanism was investigated. Ginseng can decrease the escape latency time and increase the swimming speed and the number of crossing platforms in aging mice. Moreover, the pathology of ileum tissue improved, the length of the intestinal villi increased, and the width of the villi and the depth of the crypts decreased. The activities of trypsin, α-amylase, and lipase increased in duodenal content and intestinal mucosa. In the colon, the content of SCFA, such as acetic acid, propionic acid and butyric acid, increased, indicating that ginseng significantly improves intestinal function impairment. The mRNA expressions and protein levels of β-catenin, C-myc, GSK-3β, Lgr5, and Olfm4 were upregulated in the ginseng group. Ginseng improves intestinal function and regulates the function of ISCs in order to protect intestinal health by activating the Wnt/β-catenin signaling pathway in aging mice. • Decreased function of intestinal stem cells (ISCs) is one of the marks of intestinal aging. • Ginseng adjusts the digestive enzymes activity, SCFAs production and intestinal microecological structure in aging mice. • Ginseng improves the function of ISCs by enhancing the wnt/ β- catenin signaling pathway in aging mice. [ABSTRACT FROM AUTHOR]

In the present work, the optical properties of GaAs/AlGaAs semiparabolic quantum wells (QWs) are studied under the effect of applied electric field and magnetic field by using the compact-density-matrix method. The energy eigenvalues and their corresponding eigenfunctions of the system are calculated by using the differential method. Simultaneously, the nonlinear optical rectification (OR) and optical absorption coefficients (OACs) are investigated, which are modulated by the applied electric field and magnetic field. It is found that the position and the magnitude of the resonant peaks of the nonlinear OR and OACs can depend strongly on the applied electric field, magnetic field and confined potential frequencies. This gives a new way to control the device applications based on the intersubband transitions of electrons in this system. [ABSTRACT FROM AUTHOR]

Schematic of the preparation of π-conjugated molecularly imprinted hypercrosslinked polymers (MIHCPs) and the fluorescent determination of α-amylase activity by MIHCPs. [Display omitted] • Hypercrosslinked polymer (HCP) was molecularly imprinted for the first time. • The 3,5-dinitrosalicylic acid (DNS) imprinted HCP was a fluorescent probe for DNS. • α-amylase activity was fluorescently determined using the DNS-imprinted HCP. • Microbial, salivary, and pancreatic α-amylase activities were determined. The discovery of a series of coupling reactions between various building blocks has driven the development of porous organic polymers, but the common usage of expensive and air-sensitive organometallic catalysts and complex procedures in harsh syntheses has limited their expansion. A microporous hypercrosslinked polymer (HCP) was synthesized by polymerizing a naphthalene monomer and a 1,4-dimethoxybenzene crosslinker using Friedel–Crafts alkylation over an FeCl 3 catalyst and imprinted with 3,5-dinitrosalicylic acid (DNS). The DNS-molecularly-imprinted HCPs (MIHCPs) were characterized as having IUPAC Type I mesoporosity, a specific surface area of 1134 m2 g−1, a monolayer adsorption capacity of 116 cm2 g−1, pore sizes ranging from 5 to 8.5 Å, amorphous frameworks, and distinctive absorption and emission bands by N 2 adsorption/desorption analyses, scanning and transmission electron microscopies, and FTIR, UV–Vis, and fluorescence spectrometries. The π-conjugated imprinted framework endowed the MIHCPs with 405-nm fluorescent emission at a 330-nm excitation and dynamic quenching, which was confirmed by changes in fluorescence lifetime and followed a linear Stern-Volmer plot against 1.0–200 μM DNS template molecules under optimized conditions of a pH 7.0 buffer, an MIHCP concentration of 125 μg mL−1, and a 3.0-min equilibration time. The MIHCPs exhibited a high imprinted factor of 8.7 against nonimprinted HCP and a selectivity of 8.63 against reduced DNS, which enabled fluorometric detection of DNS molecules produced by the hydrolysis of starch with microbial, salivary, and pancreatic α-amylases and the subsequent redox incubation with the DNS oxidant. The fluorometric measurement of α-amylase activity was higher in accuracy and precision (RSD: 2.6–2.8% vs. 3.9–4.0%) than conventional UV–Vis spectrometry because the excellent fluorescent sensitivity and imprinting selectivity of the MIHCP probes enabled the use of higher dilution factors with weaker matrix effects. [ABSTRACT FROM AUTHOR]

Diltiazem, which is a calcium channel blocker, is involved in the formation of covalent organic frameworks (COFs) through the Schiff base reaction of tetrakis (4-aminophenyl)-porphine (TAPP) and dihydroxynaphthalene-dicarbaldehyde (DHNDC) and the next enol-to-keto tautomerization. The diltiazem-imprinted COFs (DICOFs) were optimally formed using Sc(OTf) 3 as the catalyst, TAPP/DHNDC/diltiazem in a molar ratio of 2/3/4, N -methylpyrrolidone/mesitylene (v/v = 3/5) as the porogen, and a 1-h reaction with a high imprinting factor of 10.5 compared to the nonimprinted counterparts (NICOFs). The optimized DICOF exhibited a more amorphous XRD pattern, a larger surface area (1650 vs. 930 m2/g), a larger pore volume (1.33 vs. 0.75 cm3/g), and a finer porous SEM feature than NICOF. The selectivity of NICOF toward diltiazem and diazepam at 250 nM (α = 1.03, RSD = 1.3%) was smaller than the selectivity of DICOF (α = 2.94, RSD = 1.6%). The diltiazem samples (5.0–300 ng mL−1) dynamically quenched the fluorescence of 15 μg/mL DICOF in 50 mM phosphate buffer at pH 6.5 at 8.0 min equilibrium; thus, Stern−Volmer plots were linearly constructed for sensing diltiazem with an LOD of 3.4 ng mL−1 and an LOQ of 10.2 ng mL−1. According to the plots, 30 ng mL−1 diltiazem solutions that were diluted from 30 mg-specified tablets had an average measured concentration of 29.5 ng mL−1 (σ = 1.3% and n = 5). In addition to application as fluorescent sensors, DICOFs (30 mg) could be used as dispersive extractants to recover 95.2% of 0.6 ng mL−1 diltiazem from 25 mL phosphate buffer with quadruplicate uses of 0.5 mL methanol/acetic acid (v/v = 9/1) as the eluent. Langmuir and pseudo-second-order models were fitted to the isothermal and kinetic sorption mechanisms, respectively. The maximum sorption capacity of DICOF was ten times larger than that of NICOF (156 vs. 15.2 mg/g). The interday recoveries of 0.6 ng mL−1 spiked in 20-fold diluted human urine, and 60-fold diluted human serum were 93.2% and 90.6%, respectively. Preparation of covalent organic framework (COF) and diltiazem-imprinted COF, the interaction between diltiazem and COF, and the fluorescence measurements. [Display omitted] • Fluorescent covalent organic frameworks (COFs) were imprinted with diltiazem. • Diltiazem-imprinted COFs were used as dispersive sorbents and fluorescent sensors. • Analysis of diltiazem at 0.6 ng mL−1 were conducted in human urine and serum. [ABSTRACT FROM AUTHOR]

The mitochondrion is a semi-autonomous organelle that provides energy for cell activities through oxidative phosphorylation. In this study, we identified a defective kernel 66 (dek66)-mutant maize with defective kernels. We characterized a candidate gene, DEK66 , encoding a ribosomal assembly factor located in mitochondria and possessing GTPase activity (which belongs to the ribosome biogenesis GTPase A family). In the dek66 mutant, impairment of mitochondrial structure and function led to the accumulation of reactive oxygen species and promoted programmed cell death in endosperm cells. Furthermore, the transcript levels of most of the key genes associated with nutrient storage, mitochondrial respiratory chain complex, and mitochondrial ribosomes in the dek66 mutant were significantly altered. Collectively, the results suggest that DEK66 is essential for the development of maize kernels by affecting mitochondrial function. This study provides a reference for understanding the impact of a mitochondrial ribosomal assembly factor in maize kernel development. [ABSTRACT FROM AUTHOR]

Type 2 diabetes (T2DM) is a well known risk factor for Alzheimer's disease. Mitochondria are the center of intracellular energy metabolism and the main source of reactive oxygen species. Mitochondrial dysfunction has been identified as a key factor in diabetes-associated brain alterations contributing to neurodegenerative events. Defective insulin signaling may act in concert with neurodegenerative mechanisms leading to abnormalities in mitochondrial structure and function. Mitochondrial dysfunction triggers neuronal energy exhaustion and oxidative stress, leading to brain neuronal damage and cognitive impairment. The normality of mitochondrial function is basically maintained by mitochondrial quality control mechanisms. In T2DM, defects in the mitochondrial quality control pathway in the brain have been found to lead to mitochondrial dysfunction and cognitive impairment. Here, we discuss the association of mitochondrial dysfunction with T2DM and cognitive impairment. We also review the molecular mechanisms of mitochondrial quality control and impacts of mitochondrial quality control on the progression of cognitive impairment in T2DM. [ABSTRACT FROM AUTHOR]

N'²,N'6-bis(m-nilrobenzylidene)pyridine-2,6-dicarbohydrazid (a), N'²,N'6-bis(p-nitro benzylidene)pyridine-2,6-dicarbohydrazid (b), and N'²,N'6-bis(p-chlorobenzylidene) pyridine-2,6-dicarbohydrazid (c) were synthesized and characterized by ¹H NMR, Mass Spectroscopy, and Infrared Spectroscopy. The single crystals of compound C27 H29N9O11 (1), C27H29Ni)O11 (2), and C21H15CI2N5O4 (3) were characterized by X-ray singlecrystal diffraction analysis. The crystal structure analysis revealed that compound 1 crystallizes in a monoclinic system, space group C2/c, a = 24.6504(10) Å, b = 10.4624(6) Å, c = 14.4850(6) Å. The compound 2 crystallizes in monoclinic system, space group C2/c, a = 24.6505(9) Å, b = 10.4618(4) Å, c = 14.4946(5) Å. The compound 3 crystallizes in a monoclinic system, space group P2 (l)/n, a = 8.6377(9) A, b = 14.4815(15) Å, c= 17.6598(19) Å. [ABSTRACT FROM AUTHOR]

Tubular epithelial-to-mesenchymal transition (EMT) plays a crucial role in the progression of renal tubular interstitial fibrosis (TIF), which subsequently leads to chronic kidney disease (CKD) and eventually, end-stage renal disease (ESRD). We propose that augmenter of liver regeneration (ALR), a member of the newly discovered ALR/Erv1 protein family shown to ameliorate hepatic fibrosis, plays a similar protective role in renal tubular cells and has potential as a new treatment option for CKD. Here, we showed that recombinant human ALR (rhALR) inhibits EMT in renal tubular cells by antagonizing activation of the transforming growth factor-β1 (TGF-β1) signaling pathway. Further investigation revealed that rhALR suppresses the expression of TGF-β receptor type II (TβR II) and significantly alleviates TGF-β1-induced phosphorylation of Smad2 and nuclear factor-κB (NF-κB). No apparent adverse effects were observed upon the addition of rhALR alone to cells. These findings collectively suggest that ALR plays a role in inhibiting progression of renal tubular EMT, supporting its potential utility as an effective antifibrotic strategy to reverse TIF in CKD. [ABSTRACT FROM AUTHOR]