A Flexible MXene-Black Phosphorus/Zinc Oxide Hybrid Structure with Excellent UVA-Specific Photoelectric Sensing Properties for Human Skin Protection.

Ultraviolet A (UVA) radiation causes various irreversible damages to human skin, so the research about UVA-specific sensing device is urgent. 2D black phosphorus (BP) is used in many photosensors due to its advantages of high carrier mobility and tunable bandgap, but its application for UVA-specific photosensor is not reported. Here, a MXene-BP/Zinc oxide (ZnO) hybrid structure with lamellar-spherical interfaces like finger lime fruit is prepared by the layer-by-layer assembly (LLA) method, and p-n junctions are constructed between BP and ZnO with the Ti3C2Tx electrode, showing excellent photoelectric performance. Density functional theory (DFT) calculations demonstrate that the enhanced performance is attributed to the rapid separation of photogenerated carriers in the presence of a built-in electric field at interface. Furthermore, a flexible MXene-BP/ZnO based UVA-specific photosensor is prepared, which shows a specific response to UVA as high as 7 mA W-1 and excellent mechanical stability, maintaining 98.46% response after 100 bending cycles. In particular, the integrated anti-UVA skin protection device shows excellent UVA-specific identification and wireless transmission capability, which can provide timely UVA exposure information and skin protection warning for the visually impaired. This work demonstrates a new approach for further developments of advanced photoelectric sensing technology toward improving people's skin health protection.

Function of unconventional T cells in oral lichen planus revealed by single-cell RNA sequencing.

OBJECTIVE: We intended to map the single-cell profile of OLP, explore the molecular characteristics of unconventional T cells in OLP tissues. METHODS: Buccal mucosa samples from OLP patients and healthy individuals were used to prepare single-cell suspension. Single-cell RNA sequencing was used to analyze the proportion of all the cells, and the molecular characteristics of unconventional T cells. Immunohistochemical staining was used to detect the expression of unconventional T cells marker genes. RESULTS: The cell clusters from buccal mucosa were categorized into immune cells, fibroblasts, endothelial cells, and epithelial cells. Unconventional T cells with phenotype of CD247+TRDC+NCAM1+ were identified. Immunohistochemical staining revealed higher expression of unconventional T cell marker genes in OLP tissue, predominantly in the lamina propria. In OLP, unconventional T cells are in a unique stress response state, exhibited enhanced NF-κB signaling and apoptosis inhibition, enhanced heat shock protein genes expression, weakened cytotoxic function. A large number of ligand-receptor pairs were found between unconventional T cells and other cells, particularly with fibroblasts and endothelial cells. CONCLUSIONS: This study mapped the single-cell profile of OLP, delineated the molecular characteristics of unconventional T cells in OLP, and uncovered that these unconventional T cells are in a stress response state.

Artemisia argyi extracts overcome lapatinib resistance via enhancing TMPRSS2 activation in HER2-positive breast cancer.

Breast cancer stands as the predominant malignancy and primary cause of cancer-related mortality among females globally. Approximately 25% of breast cancers exhibit HER2 overexpression, imparting a more aggressive tumor phenotype and correlating with poor prognoses. Patients with metastatic breast cancer receiving HER2 tyrosine kinase inhibitors (HER2 TKIs), such as Lapatinib, develop acquired resistance within a year, posing a critical challenge in managing this disease. Here, we explore the potential of Artemisia argyi, a Chinese herbal medicine known for its anti-cancer properties, in mitigating HER2 TKI resistance in breast cancer. Analysis of the Cancer Genome Atlas (TCGA) revealed diminished expression of transmembrane serine protease 2 (TMPRSS2), a subfamily of membrane proteolytic enzymes, in breast cancer patients, correlating with unfavorable outcomes. Intriguingly, lapatinib-responsive patients exhibited higher TMPRSS2 expression. Our study unveiled that the compounds from Artemisia argyi, eriodictyol, and umbelliferone could inhibit the growth of lapatinib-resistant HER2-positive breast cancer cells. Mechanistically, they suppressed HER2 kinase activation by enhancing TMPRSS2 activity. Our findings propose TMPRSS2 as a critical determinant in lapatinib sensitivity, and Artemisia argyi emerges as a potential agent to overcome lapatinib via activating TMPRSS2 in HER2-positive breast cancer. This study not only unravels the molecular mechanisms driving cell death in HER2-positive breast cancer cells induced by Artemisia argyi but also lays the groundwork for developing novel inhibitors to enhance therapy outcomes.

Function of normal oral mucosa revealed by single-cell RNA sequencing.

The functions of oral mucosa include barrier, sensation, and secretion. The barrier protection function is particularly important, which includes physical barrier and immunological barrier. Few studies have revealed the function of oral mucosa by displaying the map of normal oral mucosal cells from the perspective of single cells. Here, single-cell transcriptome sequencing was used to bring a relatively comprehensive map of the normal oral mucosal cells. In total, 26,398 cells from three cases of normal oral mucosa were analyzed by single-cell RNA-sequencing and 14 distinct cell groups were defined, 7 of which were immune cells. We performed subgroup classification and heterogeneity analysis of epithelial cells, T cells, and macrophagocytes, which found a subpopulation of epithelial cells with high expression of major histocompatibility complex class II molecules, a subpopulation CD8+ GZMK+ T cells, and two kinds of active macrophagocytes. Meanwhile, we identified ligand-receptor pairs among the major cell types to explore the interactions and how they maintain the homeostasis of normal oral mucosa. Based on these results, the epithelial barrier function, immunological barrier function, and potential maintenance function of stromal cells in the oral mucosa were described at the single-cell level, which provides basic data resources for further studies of oral mucosal diseases.

Sonochemical regulation of oxygen vacancies for Bi2WO6 nanosheet-based photoanodes to promote photoelectrochemical performance.

Integration of oxygen vacancies (Vo) into nanostructured semiconductor-based photocatalysts has been recognized as a promising strategy for enhancing the performance of photoelectrochemical (PEC) water splitting. However, precisely controlling the Vo concentration in photocatalysts via an effective and tunable approach remains challenging. Herein, a series of optimized bismuth tungstate (Bi2WO6) nanosheet-based photoanodes with varying concentrations of Vo were prepared by a sonochemical method with in situ cavitation detection, which enables accurate manipulation of the acoustic cavitation intensity applied to the surface of Bi2WO6 photoanodes in alkaline solution. Based on the analysis of the Vo concentration and sound field characteristics, the mechanism of sonochemical regulation of Vo in Bi2WO6 nanosheets was interpreted. Specifically, the increase in Vo concentration can be attributed to the enhancement of Bi-O bond dissociation. This enhancement is influenced not only by the intensified impact of shear force and the generation of active radicals by transient cavitation, but also by the accelerated diffusion of the reactant, a result of stable cavitation. By optimizing the transient and stable cavitation intensity, a Vo-rich Bi2WO6 photoanode was obtained without altering the microstructure of Bi2WO6 nanosheets. The presence of high concentration Vo facilitates the interfacial chemical reactivity and the transmission of photogenerated carriers, leading to the drastic promotion of the PEC water splitting performance. The transient photocurrent density of the Vo-rich Bi2WO6 photoanode reaches 69.2 µA cm-2 (1.23 V vs. RHE), 7.86 times that of the untreated Bi2WO6 photoanode. Additionally, the charge injection efficiency increases to 35.4%. This work provides a controllable and effective method for defect engineering of nanostructured semiconductor-based electrodes.

The role of p21 in cellular senescence and aging-related diseases.

During the aging process or disease progression, normal cells and tissues in the body undergo various stresses, leading to cell damage and the need for repair, adaptation, apoptosis, or defense responses. Cellular senescence is a key player in this process, influencing the rate of aging and disease progression. It can be triggered by different stress factors, resulting in irreversible cell cycle arrest and functional decline. Senescent cells often show high expression of cell cycle factors such as p21 and p16, which are involved in cell cycle arrest. p16 has long been recognized as a significant marker of aging. Recent evidence suggests that p21high cells and p16high cells represent distinct cell populations in terms of cell type, tissue location, accumulation kinetics, and physiological functions. This article focuses on recent advancements in understanding p21-dependent cellular senescence. It starts by providing an overview of the role of p21 in 3 primary cellular senescence phenotypes where it plays a crucial role. It then delves into the pathogenesis of diseases closely linked to p21-dependent cellular senescence, particularly metabolic disorders and cardiovascular diseases. The article also discusses progress in p21-related animal models and outlines strategies for utilizing p21 to intervene in cellular senescence by delaying aging, eliminating senescent cells, and rejuvenating senescent cells. This review systematically examines the pathogenesis of p21-dependent cellular senescence, emphasizing its importance in studying aging heterogeneity and developing new senolytic therapies. It aims to stimulate future research on leveraging p21 to enhance the characteristics of senescent cells, allowing more precise methods for eliminating harmful senescent cells at the right time, thereby delaying aging and potentially achieving rejuvenation.

Streptococcus salivarius ameliorates the destructive effect on the epithelial barrier by inhibiting the growth of Prevotella melaninogenica via metabolic acid production.

BACKGROUND: Oral lichen planus (OLP) is one of the most common oral mucosal diseases, exhibiting a higher prevalence in women than men, but its pathogenesis is still unclear. Current research suggests that microbial dysbiosis may play an important role in the pathogenesis of OLP. Our previous research has found that the increase of Prevotella melaninogenica and decrease of Streptococcus salivarius have been identified as a potential pathogenic factor in OLP. Consequently, the objective of this study is to examine whether S. salivarius can counteract the detrimental effects of P. melaninogenica on the integrity of the epithelial barrier function. MATERIALS AND METHODS: Epithelial barrier disruption was induced by P. melaninogenica in human keratinocytes (HaCaT cells). HaCaT cells were pretreated with S. salivarius(MOI = 20) or cell-free supernatant for 3 h, followed by treatment with P. melaninogenica (MOI = 5) for 3 h. The epithelial barrier integrity of HaCaT cells was detected by FD4 permeability. The mRNA level of tight junction protein was detected by quantitative real-time polymerase chain reaction (PCR). Immunofluorescence and Western Blot were used to detect the protein expression of zonula occludin-1 (ZO-1). The serial dilution-spotting assay was applied to monitor the viability of P. melaninogenica at the end of 8 and 24 h incubation. RESULTS: Challenge by P. melaninogenica decreased the levels of tight junction proteins, including occludin, ZO-1, and claudin in HaCaT cells. S. salivarius or its cell-free supernatant inhibited the down-regulation of ZO-1 mRNA and protein expression levels induced by P. melaninogenica and thus improved the epithelial barrier function. The inhibitory effect of the cell-free supernatant of S. salivarius on the growth of P. melaninogenica is associated with metabolic acid production rather than with bacteriocins and hydrogen peroxide. CONCLUSIONS: These results suggest that live S. salivarius or its cell-free supernatant significantly ameliorated the disruption of epithelial tight junctions induced by P. melaninogenica, likely through the inhibition of P. melaninogenica growth mediated by metabolic acid production.