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High Purcell enhancement structures and stable emitters are essential prerequisites for the successful development of novel fast-operating active devices. Furthermore, a uniform enhancement of the spontaneous emission rate is critical for practical applications. Despite considerable efforts being made to meet these requirements, achieving them still remains a challenging task. In this work, we demonstrate that placing stable core−shell perovskite quantum dots (PQDs) in the nanogap region of hole/sphere-based nanogap structures (HSNGs) can enhance the spontaneous emission rate by more than a thousand-fold (up to a factor of ∼1080) compared to PQDs in solution. This enhancement factor is the highest value reported using PQDs, exceeding previously reported values by two orders of magnitude. Notably, the enhancement factor of the emission rate in the HSNG maintains large values across the samples, with values ranging from ∼690 to ∼1080. Furthermore, the structural stabilities of the PQDs are remarkably enhanced with the incorporation of SiO2 shells, which is validated by monitoring the changes in photoluminescence intensities over time during continuous laser exposure. As a result, the HSNG with stable core−shell PQDs offers great potential for fast optical device applications that require high performance and long-term operational stability.

Biliverdin IXβ reductase (BLVRB) has emerged as a promising therapeutic target for thrombocytopenia due to its involvement in reactive oxygen species (ROS) mechanisms. During the pursuit of inhibitors targeting BLVRB, olsalazine (OSA) became apparent as one of the most potent candidates. However, the direct application of OSA as a BLVRB inhibitor faces challenges, as it is prone to degradation into 5-aminosalicylic acid through cleavage of the diazenyl bond by abundant azoreductase (AzoR) enzymes in gut microbiota and eukaryotic cells. To overcome this obstacle, we devised olsalkene (OSK), an inhibitor where the diazenyl bond in OSA has been substituted with an alkene bond. OSK not only matches the efficacy of OSA but also demonstrates improved stability against degradation by AzoR, presenting a promising solution to this limitation. Furthermore, we have found that both OSK and OSA inhibit BLVRB, regardless of the presence of nicotinamide adenine dinucleotide phosphate, unlike other known inhibitors. This discovery opens new avenues for investigating the roles of BLVRB in blood disorders, including thrombocytopenia. [ABSTRACT FROM AUTHOR]

Multiple bacterial genera take advantage of the multifunctional autoprocessing repeats-in-toxin (MARTX) toxin to invade host cells. Secretion of the MARTX toxin by Vibrio vulnificus, a deadly opportunistic pathogen that causes primary septicemia, the precursor of sepsis, is a major driver of infection; however, the molecular mechanism via which the toxin contributes to septicemia remains unclear. Here, we report the crystal and cryo-electron microscopy (EM) structures of a toxin effector duet comprising the domain of unknown function in the first position (DUF1)/Rho inactivation domain (RID) complexed with human targets. These structures reveal how the duet is used by bacteria as a potent weapon. The data show that DUF1 acts as a RID-dependent transforming NADase domain (RDTND) that disrupts NAD+ homeostasis by hijacking calmodulin. The cryo-EM structure of the RDTND-RID duet complexed with calmodulin and Rac1, together with immunological analyses in vitro and in mice, provide mechanistic insight into how V. vulnificus uses the duet to suppress ROS generation by depleting NAD(P)+ and modifying Rac1 in a mutually-reinforcing manner that ultimately paralyzes first line immune responses, promotes dissemination of invaders, and induces sepsis. These data may allow development of tools or strategies to combat MARTX toxin-related human diseases. The MARTX toxins secreted by clinical V. vulnificus strains release the DUF1-RID effector duet in infected host cells. Here, the authors show that the duet hijacks calmodulin and Rac1, respectively, and transforms into a potent weapon to promote sepsis. [ABSTRACT FROM AUTHOR]

Surface-enhanced Raman scattering (SERS) is a promising, sensitive, and label-free molecule detection scheme. However, uniformity and reproducibility of signal enhancement have remained elusive, making quantitative evaluation difficult. In this work, we propose a simple fabrication approach to quantitative SERS sensors that satisfies all the sought-after characteristics: a gold hole-sphere nanogap SERS substrate that is uniform, reproducible, sensitive, large, and cost-effective. Here, we achieve a sensing uniformity of 4.2% averaged over 4 points throughout the entire 6-in. substrate and a SERS enhancement of 4.6 × 108. Our approach provides for gap control in the vertical direction, thus granting very precise control with subnanometer accuracy and the statistical distribution of nanospheres in plane. This combination enables a remarkably uniform and reproducible SERS sensitivity over the entire substrate. The SERS spectra from DNA bases are also measured and their corresponding peaks are well defined down to 10 pM concentration. The proposed approach should be a key to quantitative SERS. [ABSTRACT FROM AUTHOR]

Electrical stimulation has recently received attention as noninvasive treatment in skin wound healing with its outstanding biological property for clinical setting. However, the complexity of equipment for applying appropriate electrical stimulation remains an ongoing challenge. Here, we proposed a strategy for skin scar inhibition by providing electrical stimulation via a multilayer stacked electret (MS‐electret), which can generate direct current (DC) electric field (EF) without any power supply equipment. In addition, the MS‐electret can easily control the intensity of EFs by simply stacking electret layers and maintain stable EF with the surface potential of 3400 V over 5 days owing to the injected charges on the electret surface. We confirmed inhibition of type 1 collagen and α‐SMA expression of human dermal fibroblasts (hDFs) by 90% and 44% in vitro, indicating that the transition of hDFs to myofibroblasts was restricted by applying stable electrical stimulation. We further revealed a 20% significant decrease in the ratio of myofibroblasts caused by the MS‐electret in vivo. These findings present that the MS‐electret is an outstanding candidate for effective skin scar inhibition with a battery‐free, physiological electrical microenvironment, and noninvasive treatment that allows it to prevent external infection. [ABSTRACT FROM AUTHOR]