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ObjectiveThe genomic characteristics， toxicity， drug resistance and genetic diversity of Listeria monocytogenes （Lm） isolated from food and patients based on whole genome sequencing （WGS） in Liaocheng City from 2019 to 2022 were investigated.MethodsThe Lm strains isolated from food and patients were detected by the drug sensitivity test and WGS. The whole genome sequencing data was spliced and assembled by MGAP to carry out gene prediction and functional annotation on the assembled genome， MLST， production of cg MLST minimum spanning tree. The genetic evolution of 18 domestic and foreign foodborne Lm isolated strains obtained from NCBI were analyzed by wg-SNP method.ResultsThe genome size of 33 Lm isolates was 2.89-3.41 Mb， and the CG content ranged from 37.81% to 37.97%. The strains could be divided into 6 ST types （ST9， ST121， ST8， ST87， ST155， ST101）， corresponding to 6 clonal complex groups （CC9， CC121， CC8， CC87， CC155， CC101）. The strains carried fosX and mprF resistance gene， 18 other virulence genes such as lplA1 and prsA2， with varying degrees of deletion of virulence genes. 2 strains were resistant to tetracycline and 1 strain was resistant to lincomycin. The stains carried virulence islands LIPI-1 and LIPI-2 without virulence islands LIPI-3 and LIPI-4. The genetic evolution analysis of wg-SNPs， cgMLST and phylogenetic tree based on single-copy core protein sequence showed that the molecular typing of 33 Lm strains was with high diversity in molecular typing. Patient derived strains were closely related to food isolates， and food isolates were closely related to foreign outbreak isolates in evolutionary relationships.ConclusionThe strains of Lm isolated from food and patients both carry virulence genes with certain potential pathogenic ability. The drug resistance of the isolated strains is not serious. Molecular types exhibit diversity. The close genetic relationship between strains from food sources and patient isolates suggests that the potential risks of foodborne infections in commercially available food.

Translational medicine provides insight into novel drugs and predicts unwanted effects. In well-characterized pathways (e.g., cytokine-Janus kinase [JAK]-signal transducers and activators of transcription [STAT]), a variety of in vitro assessments were used to estimate selectivity of effects on different potential targets (i.e., JAK1, JAK2, JAK3, and tyrosine kinase 2 [TYK2]). Several approved drugs were characterized as selective for the JAK family. These assessments are challenged by a lack of compounds that only inhibit one JAK family member. Deucravacitinib is a first-in-class, oral, selective, allosteric inhibitor of TYK2, a kinase required for IL-12, IL-23, and Type I interferon signaling. Unlike deucravacitinib, which selectively binds to the TYK2 regulatory domain, JAK1,2,3 inhibitors target the catalytic domain, contributing to nonselective targeting of JAK1,2,3. Cytokines associated with JAK1,2,3 signaling are required for both immune and nonimmune functions. A similar laboratory abnormality profile was observed in clinical trials using JAK1,2,3 inhibitors that has not been observed with deucravacitinib. In vitro testing of JAK1,2,3 inhibitors has relied upon assays of signal transduction, such as those measuring STAT phosphorylation, for estimates of potency and selectivity. These assay systems can be effective in estimating in vivo efficacy; however, they may not provide insight into downstream outcomes of receptor signaling, which may be more relevant for evaluating safety aspects. Assay systems assessing functional outcomes from cells may yield a more useful translational evaluation. Here, deucravacitinib was assessed for potency and selectivity versus three representatives of the JAK inhibitor class (tofacitinib, baricitinib, and upadacitinib) based on functional assays. JAK inhibitors had suppressive activity against JAK2-dependent hematopoietic colony-forming assays modeling thrombopoiesis, erythropoiesis, and myelopoiesis; however, deucravacitinib did not. Deucravacitinib had limited potency against NK cells, cytotoxic T cells, Thelper cells, and regulatory T cells activated by JAK1/JAK3-dependent common gamma chain cytokines. These data are consistent with the biologic role of JAK1,2,3 and pharmacodynamic changes in clinical laboratory abnormalities. Against TYK2-dependent cytokines, deucravacitinib selectively inhibited Type I interferon stimulation of monocytes and dendritic cells and was a more potent inhibitor than JAK inhibitors. IL-12 and IL-23 functional outputs were similarly potently inhibited by deucravacitinib. Results are consistent with deucravacitinib selectively inhibiting TYK2. [ABSTRACT FROM AUTHOR]

Although high‐efficiency host‐sensitizer‐TBRb‐based organic light‐emitting diodes (HST‐OLEDs) are widely reported, the reasons for their high performances are still vague because the important role of hot exciton in TBRb emitter (T2, TBRb) has not been recognized previously. Herein, a maximum external quantum efficiency (EQE) of 24.9% is obtained from a HST‐OLED by co‐doping the Ir(ppy)3 sensitizer and TBRb emitter into the CBP host. Such a remarkable efficiency is mainly attributed to the efficient utilization of the T2, TBRb via the cascade Dexter energy transfer (DET) channels from triplet excitons of host and sensitizer to T2, TBRb (T1, CBP→DET$\mathop \to \limits^{{\mathrm{DET}}} $ T1, Ir(ppy)3→DET$\mathop \to \limits^{{\mathrm{DET}}} $ T2, TBRb) followed by the hot‐exciton reverse intersystem crossing (RISC, T2, TBRb→RISC$\mathop \to \limits^{{\mathrm{RISC}}} $ S1, TBRb) and triplet fusion (TF, T2, TBRb + T2, TBRb→TF$\mathop \to \limits^{{\mathrm{TF}}} $ Sm, TBRb→IC$\mathop \to \limits^{{\mathrm{IC}}} $ S1, TBRb) processes for radiative decays. These cascade DET channels are demonstrated by spectroscopic analyses and magneto‐electroluminescence studies. More importantly, this HST‐OLED presents an extremely low‐efficiency roll‐off, that is, the EQEs separately exhibit 24.34% and 19.73% at 1000 and 10 000 cd m−2 compared to the maximum EQE of 24.9%. Obviously, this work paves a promising pathway for fabricating further high‐efficiency HST‐OLEDs for applications in illumination and flat‐panel display. [ABSTRACT FROM AUTHOR]

Using a solid-state technique under low temperature conditions, Er3+/Yb3+ co-doped Bi2Mo2O9 phosphors with different concentrations were prepared, exhibiting excellent green up-conversion luminescence property. A thorough investigation was conducted on the phase structure, optical transition, up-conversion luminescence, and down-shifting luminescence properties of the prepared samples. Bi2Mo2O9: Er3+/Yb3+ phosphors excited at 381, 980, and 1550 nm showed strong green fluorescence together with very faint red emission. The mechanism of up-conversion luminescence and its capacity for temperature sensing were examined under the excitation of various wavelengths. Under 980 nm excitation, the maximal relative and absolute sensitivities were determined to be 1.107%K− 1 and 0.756%K− 1 at 303 K and 513 K, respectively. Furthermore, the Judd-Ofelt intensity parameters of Er3+ in Bi2Mo2O9: Er3+/Yb3+ phosphors were calculated using the diffuse reflectance spectra and fluorescence lifetime of Er3+. In addition, material was combined with polyacrylic acid to make an anti-counterfeiting pattern. The results indicate that Bi2Mo2O9: Er3+/Yb3+ phosphor is an excellent green phosphor with optical temperature measurement function, and it also has certain applications in the field of anti-counterfeiting. [ABSTRACT FROM AUTHOR]

Recent studies have reported the benefits of food-derived peptides for memory dysfunction. Beyond the physiological effects of peptides, their bioavailability to the brain still remains unclear since the blood-brain barrier (BBB) strictly controls the transportation of compounds to the brain. Here, updated transportation studies on BBB transportable peptides are introduced and evaluated using in vitro BBB models, in situ perfusion, and in vivo mouse experiments. Additionally, the mechanisms of action of brain health peptides in relation to the pathogenesis of neurodegenerative diseases, particularly Alzheimer's disease, are discussed. This discussion follows a summary of bioactive peptides with neuroprotective effects that can improve cognitive decline through various mechanisms, including anti-inflammatory, antioxidative, anti-amyloid β aggregation, and neurotransmitter regulation. [ABSTRACT FROM AUTHOR]