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Periodontitis is a global inflammatory oral disease, and plaque-induced host excessive immune response is recognized as a major cause of its pathogenesis. In recent years, the relevance of mitochondrial dysfunction to periodontitis has been increasingly investigated, particularly with respect to macrophages, the key immune cells in the periodontal immune microenvironment. Mitochondrial dysfunction drives macrophage M1 polarization and osteoclast differentiation through mechanisms such as metabolic reprogramming, reactive oxygen species release, abnormal mitophagy, abnormal mitochondrial biogenesis and damaged mitochondrial dynamic. In addition, mitochondrial transfer in the periodontitis setting has been reported in several researches. In this review, we highlight the impact of mitochondrial dysfunction on macrophages in the periodontitis setting and summarize emerging therapeutic strategies for targeting mitochondria in periodontitis, including antioxidants, modulators of metabolic reprogramming, nanomaterials and photodynamic therapy.

Heterojunction constructions are usually used to promote the separation of photocarriers and improve the photocatalytic activities. However, misuse and confusion often occur in current research because there are no unified rules for the classification and naming of heterojunctions. In order to avoid this problem, this review summarizes and standardizes the classification and naming rules of heterojunctions, based on different band structure distribution of the two semiconductors in heterojunctions and transfer paths of photogenerated carriers. Moreover, the distinctions in photogenerated carrier behavior among O–scheme heterojunction, Z–scheme heterojunction, and S–scheme heterojunction within type II heterojunction are clearly elucidated. Additionally, current methodologies for identifying heterojunction types, including metal–ion photo–deposition, in situ X–ray photoelectron spectroscopy, surface photovoltage spectroscopy, transient absorption spectroscopy, and cathodoluminescence spectrometry, are summarized. This review also highlights the applicability of various heterojunction types across different photocatalytic applications and suggests future directions for heterojunction research. Currently, there is no unified standard for the classification and nomenclature of heterojunctions. To address this issue, this article systematically summarizes and standardizes the classification and naming rules for heterojunctions. Furthermore, it provides a clear elucidation of the differences in photogenerated carrier behavior among O–scheme, Z–scheme, and S–scheme heterojunctions within the Type II heterojunction system.

Oral diseases such as dental caries, periodontitis, and oral cancer are prevalent and present significant challenges to global public health. Although these diseases are typically treated through procedures like dental preparation and resin filling, scaling and root planning, or surgical excision, these interventions are often not entirely effective, and postoperative drug therapy is usually required. Traditional drug treatments, however, are limited by factors such as poor drug penetration, significant side effects, and the development of drug resistance. As a result, there is a growing need for novel drug delivery systems that can enhance therapeutic efficacy, reduce side effects, and improve treatment outcomes. In recent years, drug-loaded vesicles, such as liposomes, polymersomes, and extracellular vesicles (EVs), have emerged as promising drug delivery platforms due to their high drug encapsulation efficiency, controlled release properties, and excellent biocompatibility. This review provides an in-depth examination of the characteristics, advantages, and limitations of liposomes, polymersomes, and extracellular vesicles in the context of oral disease treatment. It further explores the reasons for their advantages and limitations and discusses the specific applications, development prospects, and strategies for optimizing these vesicle-based systems for improved clinical outcomes.

Introduction: Sleep disorders are common clinical psychosomatic disorders that can co-exist with a variety of conditions. In humans and animal models, sleep deprivation (SD) is closely related with gastrointestinal diseases. Shu-Xie Decoction (SX) is a traditional Chinese medicine (TCM) with anti-nociceptive, anti-inflammatory, and antidepressant properties. SX is effective in the clinic for treating patients with abnormal sleep and/or gastrointestinal disorders, but the underlying mechanisms are not known. This study investigated the mechanisms by which SX alleviates SD-induced colon injury in vivo . Methods: C57BL/6 mice were placed on an automated sleep deprivation system for 72 h to generate an acute sleep deprivation (ASD) model, and low-dose SX (SXL), high-dose SX (SXH), or S-zopiclone (S-z) as a positive control using the oral gavage were given during the whole ASD-induced period for one time each day. The colon length was measured and the colon morphology was visualized using hematoxylin and eosin (H&E) staining. ROS and the redox biomarkers include reduced glutathione (GSH), malondialdehyde (MDA), and superoxide dismutase (SOD) were detected. Quantitative real-time PCR (qRT-PCR), molecular docking, immunofluorescence and western blotting assays were performed to detect the antioxidant signaling pathways . Results: ASD significantly increased FBG levels, decreased colon length, moderately increased the infiltration of inflammatory cells in the colon mucosa, altered the colon mucosal structure, increased the levels of ROS, GSH, MDA, and SOD activity compared with the controls. These adverse effects were significantly alleviated by SX treatment. ASD induced nuclear translocation of NRF2 in the colon mucosal cells and increased the expression levels of p62, NQO1, and HO1 transcripts and proteins, but these effects were reversed by SX treatment. Conclusion: SX decoction ameliorated ASD-induced oxidative stress and colon injury by suppressing the p62/KEAP1/NRF2/HO1/NQO1 signaling pathway. In conclusion, combined clinical experience, SX may be a promising drug for sleep disorder combined with colitis.

[This corrects the article DOI: 10.3389/fphar.2023.1107507.].

To identify osteoclastogenic macrophage subsets and their regulatory mechanisms in periodontitis. We integrated single-cell RNA sequencing datasets from human and murine periodontitis to construct a comprehensive macrophage and monocyte atlas. Employing functional enrichment, cell-cell communication, pseudotime, transcription factor, and machine learning analyses, we characterized and selected the specific macrophage subset involved in cell interactions. In vitro and in vivo experiments, including enzyme-linked immunosorbent assay, TRAP staining, micro-CT, qPCR, flow cytometry, and immunofluorescence staining, were performed to dissect the osteoclastogenic potential of specific macrophage subsets and to identify the key pathways. We discovered that the IL7R macrophage subset possesses significant osteoclast differentiation potential. Our findings indicate that the IL7/IL7R signaling axis facilitates osteoclast differentiation. Genes highly expressed in IL7R macrophages were identified as strong predictors for periodontitis by machine learning models. In vivo and in vitro experimental validation confirmed an increase in IL7R macrophages, along with their enhanced osteoclastogenic capacity. confirmed an increase in IL7R macrophages, along with their osteoclastogenic capacity. The inhibition of the IL7/IL7R signaling pathway was found to mitigate periodontitis progression by impeding osteoclast differentiation. Furthermore, fibroblasts were found to secret IL7 interacting with IL7 receptors on macrophages. Our study identifies IL7R macrophages as potential osteoclast precursors in periodontitis. We demonstrate that the IL7/IL7R signaling pathway is a critical driver of osteoclast differentiation. Moreover, targeting IL7R is a potential therapeutic strategy to curb periodontitis bone resorption.

Abstract Smoking during pregnancy leads to decreased pulmonary function and increased respiratory illness in offspring. Our laboratory has previously demonstrated that many effects of smoking during pregnancy are mediated by nicotine. We now report that vitamin C supplementation can prevent some of the effects of maternal nicotine exposure on pulmonary function of offspring. Timed-pregnant rhesus monkeys were treated with 2 mg/kg/day nicotine bitartrate from Gestation Days 26 to 160. On Gestation Day 160 (term, 165 days) fetuses were delivered by C-section and subjected to pulmonary function testing the following day. Nicotine exposure significantly reduced forced expiratory flows, but supplementation of mothers with 250 mg vitamin C per day prevented the effects of nicotine on expiratory flows. Vitamin C supplementation also prevented the nicotine-induced increases in surfactant apoprotein-B protein. Neither nicotine nor nicotine plus vitamin C significantly affected levels of cortisol or cytokines, which have been shown to affect lung development and surfactant expression. Prenatal nicotine exposure significantly decreased levels of elastin content in the lungs of offspring, and these effects were slightly attenuated by vitamin C. These findings suggest that vitamin C supplementation may potentially be clinically useful to limit the deleterious effects of maternal smoking during pregnancy on offspring's lung function.

The expression of nicotinic acetylcholine receptors (nAChR) in fetal lung suggests maternal smoking during pregnancy effects newborn lung structure and function by the direct interaction of nicotine with nAChR in the developing lung. The recent identification of the lynx1 nAChR modulator protein in nicotinic neurons in the brain suggests that lynx1 may be similarly expressed in the lung. To study this, cDNAs encoding lynx1 were cloned from rhesus monkey lung. The temporal expression of lynx1 was studied in pre- and postnatal monkey lungs by in situ hybridization, immunohistochemistry, and realtime polymerase chain reaction (PCR). Lynx1 mRNA signal and lynx1 immunohistochemical staining were localized predominantly in airway epithelial cells, submucous glands, and smooth muscle cells, in endothelial and smooth muscle cells in vessel walls, and in alveolar type II cells. The distribution of lynx1 was similar to that of alpha4, beta2, and beta4 nAChR expression as determined by immunohistochemistry. Immunohistochemical staining also co-localized choline acetyltransferase, the enzyme that synthesizes acetylcholine, with lynx1 expression. Lynx1 expression was first observed in 71-day fetal lungs and increased with age. Immunohistochemistry, Western analysis, and realtime PCR analysis showed increased lynx1 expression in lungs following prenatal nicotine exposure. Thus, lynx1 is co-expressed with nAChR in the lung. Alteration of lynx1 levels is a potential new mechanism by which nicotine affects lung development.

Type II Heterojunction In order to avoid the misuse and confusion of the classification and naming of different types of heterojunction in photocatalysis, this review categorizes Type II heterojunctions into O‐scheme, Z‐scheme and S‐scheme heterojunctions according to different transfer paths of photocarriers. More details can be found in article 2500191 by Hongna Zhang, Hai‐Ying Jiang, and co‐workers.

Pulmonary embolism is a rare but serious complication in Mycoplasma pneumoniae pneumonia patients, leading to serious sequelae and even death. We aim to retrospectively analyze the clinical features of Mycoplasma pneumoniae pneumonia with pulmonary consolidation in children and to explore the independent risk factors for progression to pulmonary embolism. Clinical data of 207 children with Mycoplasma pneumoniae pneumonia complicated with pulmonary consolidation were collected, and the patients were divided into the pulmonary embolism group (69 patients) and the control group (138 patients). Multivariate logistic regression was used to analyze the risk factors and the predictive efficacy was evaluated by receiver operating characteristic curve. Multivariate logistic regression analysis showed that fever days, D-dimer, immunoglobulin A, chest pain, extra-respiratory symptoms, plastic bronchitis and cutaneous mucosal system complications were the independent risk factors. Fever days ≥ 7.5, D-dimer ≥ 0.895 mg/L, immunoglobulin A ≥ 1.015 g/L, chest pain, extra-respiratory symptoms, plastic bronchitis and cutaneous mucous system complications significantly increased the risk of pulmonary embolism in children with Mycoplasma pneumoniae pneumonia complicated with pulmonary consolidation.