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Abstract We carry out a model study on the interaction of a V -type three-level emitter with two quantized cavity modes which are weakly driven by two classical fields. The emitter may be an atom or a molecule with nondegenerate upper levels in general. The lifetimes of the two upper levels are assumed to be much longer than the lifetime of the cavity photons. We calculate the two-time second order coherence function, namely Hanbury Brown–Twiss function g (2) (τ) where τ is the time delay between the two modes. We analyze the photon–photon correlations between the two cavity modes in terms of g (2) (τ). The variation of g (2) (τ) as a function of τ exhibits collapse and revival type oscillations as well as quantum beats for relatively short τ while in the limit τ → ∞ , g (2) (τ) ≃ 1. We further show that the two cavity field modes are entangled when g (2) (0) > 2. We develop a dressed state picture with single photon in each mode to explain the results and use the negativity of the partial transpose of the reduced field density matrix to show the entanglement between field modes. The model presented in this paper may be useful for generating entangled photon pairs, and also manipulating photon–photon correlations with a cavity QED set up. [ABSTRACT FROM AUTHOR]

MicroRNA-223 is known as a myeloid-enriched anti-inflammatory microRNA that is dysregulated in numerous inflammatory conditions. Here, we report that neutrophilic inflammation (wound response) is augmented in miR-223-deflcient zebraflsh, due primarily to elevated activation of the canonical nuclear factor κB (NF-κB) pathway. NF-κB over-activation is restricted to the basal layer of the surface epithelium, although miR-223 is detected throughout the epithelium and in phagocytes. Not only phagocytes but also epithelial cells are involved in miR-223-mediated regulation of neutrophils' wound response and NF-κB activation. Cul1a/b, Traf6, and Tab1 are identifled as direct targets of miR-223, and their levels rise in injured epithelium lacking miR-223. In addition, miR-223 is expressed in cultured human bronchial epithelial cells, where it also downregulates NF-κB signaling. Together, this direct connection between miR-223 and the canonical NF-κB pathway provides a mechanistic understanding of the multifaceted role of miR-223 and highlights the relevance of epithelial cells in dampening neutrophil activation. [ABSTRACT FROM AUTHOR]

Abstract: We perform a study on extended adiabatic potential energy curves of nearly 38 states of 1,3Σ+, 1,3Π and 1,3Δ symmetries for the (SrNa)+ ion, though only the ground and first two excited states are used for the study of scattering processes. Full interaction configuration (CI) calculations are carried out for this molecule using the pseudopotential approach. In this context, it is considered that two active electrons interact with the ionic cores and all single and double excitations were included in the CI calculations. A correction including the core-core electron interactions is also considered. Using the accurate potential energy data, the ground state scattering wave functions and cross sections are obtained for a wide range of energies. We find that, in order to get convergent results for the total scattering cross sections for energies of the order 1 K, one need to take into account at least 87 partial waves. In the low energy limit ( <1 mK), elastic scattering cross sections exhibit Wigner law threshold law behavior while in the high energy limit the cross sections go as E−1∕3. A qualitative discussion about the possibility of forming the cold molecular ion by photoassociative spectroscopy is presented. Graphical abstract: [ABSTRACT FROM AUTHOR]

The in-cell western (ICW) is an immunocytochemical technique that has been used to screen for effects of siRNAs, drugs, and small molecule inhibitors. The reduced time and number of cells required to follow this protocol illustrates its semi-high-throughput nature. Performing a successful ICW protocol requires fixing and permeabilizing adherent cells directly in the plate that specifically exposes the epitope of interest. After blocking of non-specific proteins, the cells are incubated overnight with a primary antibody of interest, which is detected via a host-specific near-infrared fluorescently labeled LI-COR secondary antibody. In the final step, the plate is scanned using an Odyssey LI-COR Imaging System or similar, and each of the wells is quantified. For the first time, this technique has been demonstrated to be reproducibly utilized for semi-high-throughput selection of knockout or overexpression clones. Graphical abstract., Competing Interests: Competing interests The authors declare no competing financial interests., (Copyright © 2022 The Authors; exclusive licensee Bio-protocol LLC.)

EGFR inhibitors (EGFRi) are standard-of-care treatments administered to patients with non-small cell lung cancer (NSCLC) that harbor EGFR alterations. However, development of resistance posttreatment remains a major challenge. Multiple mechanisms can promote survival of EGFRi-treated NSCLC cells, including secondary mutations in EGFR and activation of bypass tracks that circumvent the requirement for EGFR signaling. Nevertheless, the mechanisms involved in bypass signaling activation are understudied and require further elucidation. In this study, we identify that loss of an epigenetic factor, lysine methyltransferase 5C (KMT5C), drives resistance of NSCLC to multiple EGFRis, including erlotinib, gefitinib, afatinib, and osimertinib. KMT5C catalyzed trimethylation of histone H4 lysine 20 (H4K20), a modification required for gene repression and maintenance of heterochromatin. Loss of KMT5C led to upregulation of an oncogenic long noncoding RNA, LINC01510, that promoted transcription of the oncogene MET, a component of a major bypass mechanism involved in EGFRi resistance. These findings underscore the loss of KMT5C as a critical event in driving EGFRi resistance by promoting a LINC01510/MET axis, providing mechanistic insights that could help improve NSCLC treatment., Significance: Dysregulation of the epigenetic modifier KMT5C can drive MET-mediated EGFRi resistance, implicating KMT5C loss as a putative biomarker of resistance and H4K20 methylation as a potential target in EGFRi-resistant lung cancer., (©2022 American Association for Cancer Research.)

MicroRNA-223 is known as a myeloid-enriched anti-inflammatory microRNA that is dysregulated in numerous inflammatory conditions. Here, we report that neutrophilic inflammation (wound response) is augmented in miR-223-deficient zebrafish, due primarily to elevated activation of the canonical nuclear factor κB (NF-κB) pathway. NF-κB over-activation is restricted to the basal layer of the surface epithelium, although miR-223 is detected throughout the epithelium and in phagocytes. Not only phagocytes but also epithelial cells are involved in miR-223-mediated regulation of neutrophils' wound response and NF-κB activation. Cul1a/b, Traf6, and Tab1 are identified as direct targets of miR-223, and their levels rise in injured epithelium lacking miR-223. In addition, miR-223 is expressed in cultured human bronchial epithelial cells, where it also downregulates NF-κB signaling. Together, this direct connection between miR-223 and the canonical NF-κB pathway provides a mechanistic understanding of the multifaceted role of miR-223 and highlights the relevance of epithelial cells in dampening neutrophil activation., (Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.)