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Cigarette smoke is a complex aerosol containing a large number of compounds with a variety of toxicity and carcinogenicity. Long-term exposure to cigarette smoke significantly increases the risk of a variety of diseases, including chronic obstructive pulmonary disease (COPD) and lung cancer. Epithelial–mesenchymal transition (EMT) is a unique biological process, that refers to epithelial cells losing their polarity and transforming into mobile mesenchymal cells, playing a crucial role in organ development, fibrosis, and cancer progression. Numerous recent studies have shown that EMT is an important pathophysiological process involved in airway fibrosis, airway remodeling, and malignant transformation of COPD. In this review, we summarized the effects of cigarette smoke on the development and progression of COPD and focus on the specific changes and underlying mechanisms of EMT in COPD induced by cigarette smoke. We spotlighted the signaling pathways involved in EMT induced by cigarette smoke and summarize the current research and treatment approaches for EMT in COPD, aiming to provide ideas for potential new treatment and research directions.

Periodontal disease is an inflammatory and destructive disease of tissues supporting the tooth. A large number of studies have confirmed that periodontal pathogens and their metabolites can lead to adverse pregnancy outcomes in direct or indirect ways. Adverse pregnancy outcomes, such as preterm birth, low birth weight, and pre-eclampsia, have a serious impact on human reproductive health. In recent years, although the level of global medical technology has gradually improved, the incidence of adverse pregnancy outcomes has not declined and is still a global public health problem. The purpose of this review is to summarize the current data on periodontal disease in pregnancy and adverse pregnancy outcomes, including the association between periodontal disease and adverse pregnancy outcomes, the pathogenic mechanism related to this association, the efficacy of different nutrition supplements for both periodontal disease and adverse pregnancy outcomes and the effect of providing periodontal treatment on the occurrence of adverse pregnancy outcomes, to provide guidance for the prevention and treatment of adverse pregnancy outcomes in clinical practice.

This narrative review aimed to critically synthesize and evaluate the current evidence on the association between hypothyroidism and periodontitis, with a particular focus on elucidating the underlying pathophysiological mechanisms. A comprehensive literature search was conducted on PubMed, encompassing animal, cellular, and clinical studies. The synthesized findings indicate that hypothyroidism exacerbates periodontitis through multiple interconnected pathways, including dysregulated bone metabolism, induction of systemic osteoporosis, amplification of immune-inflammatory responses, and disruption of oral microbiome homeostasis. Furthermore, evidence suggests a potential bidirectional relationship, wherein periodontal therapy may positively influence thyroid function parameters. A key takeaway from this review is the importance of interdisciplinary collaboration between endocrinologists and dental professionals. Incorporating thyroid function evaluation into periodontal management may enhance treatment outcomes. This review concludes that although existing evidence supports a significant association, further high-quality longitudinal human studies are required to definitively establish causality and elucidate the precise underlying molecular mechanisms.

The aetiology of oral mucosal diseases, such as recurrent aphthous ulcer (RAU), oral lichen planus (OLP) and burning mouth syndrome (BMS), involves many factors, and it remains difficult for clinicians to effectively relieve disease symptoms and formulate coping strategies. With the rapid development of psychology, the role of mental and psychological factors in RAU, OLP and BMS has gradually attracted researchers attention, but the specific mechanism has not been completely determined. This narrative review describes the potential neurobiological mechanism of oral mucosal diseases and detailed psychological factors after introducing relevant research into psychological factors and oral mucosal diseases. Future research strategies and innovations needed to understand and treat oral mucosal diseases and psychological factors, as well as how to prevent oral mucosal diseases by regulation of the neuroendocrine system, are also discussed.

Over the past few years, the correlation between periodontal disease (PD) and polycystic ovary syndrome (PCOS) has attracted widespread attention owing to the increased incidence of these diseases. Several studies have suggested a possible link between the two. In this narrative review, we examined the epidemiology, common risk factors, and pathological mechanisms of PCOS and PD to investigate the potential association between these diseases. Evidence from the literature indicates that PCOS and PD can interact with each other. Common risk factors, such as microbial homeostasis imbalance owing to dysbiosis, along with multiple hormone and inflammatory mediators, as well as inflammatory responses owing to oxidative stress and oxidative responses owing to ferroptosis, are all associated with the pathogenesis of both diseases. Further studies are needed to clarify the specific mechanisms of interaction between PCOS and PD, which could clarify future directions in disease management and combined multidisciplinary treatment.

PurposeTo develop a comprehensive PET radiomics model to predict the pathological response after neoadjuvant toripalimab with chemotherapy in resectable stage III non-small-cell lung cancer (NSCLC) patients.MethodsStage III NSCLC patients who received three cycles of neoadjuvant toripalimab with chemotherapy and underwent 18F-FDG PET/CT were enrolled. Baseline 18F-FDG PET/CT was performed before treatment, and preoperative 18F-FDG PET/CT was performed three weeks after the completion of neoadjuvant treatment. Surgical resection was performed 4–5 weeks after the completion of neoadjuvant treatment. Standardized uptake value (SUV) statistics features and radiomics features were derived from baseline and preoperative PET images. Delta features were derived. The radiologic response and metabolic response were assessed by iRECIST and iPERCIST, respectively. The correlations between PD-L1 expression, driver-gene status, peripheral blood biomarkers, and the pathological responses (complete pathological response [CPR]; major pathological response [MPR]) were assessed. Associations between PET features and pathological responses were evaluated by logistic regression.ResultsThirty patients underwent surgery and 29 of them performed preoperative PET/CT. Twenty patients achieved MPR and 16 of them achieved CPR. In univariate analysis, five SUV statistics features and two radiomics features were significantly associated with pathological responses. In multi-variate analysis, SUVmax, SUVpeak, SULpeak, and End-PET-GLDM-LargeDependenceHighGrayLevelEmphasis (End-GLDM-LDHGLE) were independently associated with CPR. SUVpeak and SULpeak performed better than SUVmax and SULmax for MPR prediction. No significant correlation, neither between the radiologic response and the pathological response, nor among PD-L1, driver gene status, and baseline PET features was found. Inflammatory response biomarkers by peripheral blood showed no difference in different treatment responses.ConclusionThe logistic regression model using comprehensive PET features contributed to predicting the pathological response after neoadjuvant toripalimab with chemotherapy in resectable stage III NSCLC patients.

Background Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD) and lung cancer. Epithelial–mesenchymal transition (EMT) is an essential pathophysiological process in COPD and plays an important role in airway remodeling, fibrosis, and malignant transformation of COPD. Previous studies have indicated FERMT3 is downregulated and plays a tumor-suppressive role in lung cancer. However, the role of FERMT3 in COPD, including EMT, has not yet been investigated. Methods The present study aimed to explore the potential role of FERMT3 in COPD and its underlying molecular mechanisms. Three GEO datasets were utilized to analyse FERMT3 gene expression profiles in COPD. We then established EMT animal models and cell models through cigarette smoke (CS) or cigarette smoke extract (CSE) exposure to detect the expression of FERMT3 and EMT markers. RT-PCR, western blot, immunohistochemical, cell migration, and cell cycle were employed to investigate the potential regulatory effect of FERMT3 in CSE-induced EMT. Results Based on Gene Expression Omnibus (GEO) data set analysis, FERMT3 expression in bronchoalveolar lavage fluid was lower in COPD smokers than in non-smokers or smokers. Moreover, FERMT3 expression was significantly down-regulated in lung tissues of COPD GOLD 4 patients compared with the control group. Cigarette smoke exposure reduced the FERMT3 expression and induces EMT both in vivo and in vitro. The results showed that overexpression of FERMT3 could inhibit EMT induced by CSE in A549 cells. Furthermore, the CSE-induced cell migration and cell cycle progression were reversed by FERMT3 overexpression. Mechanistically, our study showed that overexpression of FERMT3 inhibited CSE-induced EMT through the Wnt/β-catenin signaling. Conclusions In summary, these data suggest FERMT3 regulates cigarette smoke-induced epithelial–mesenchymal transition through Wnt/β-catenin signaling. These findings indicated that FERMT3 was correlated with the development of COPD and may serve as a potential target for both COPD and lung cancer.

SISR is an important research topic in computer vision. Its goal is to reconstruct HR images with rich details from LR inputs. Early methods based on CNNs made some progress, but their performance reached a limit due to limited model capacity and expressiveness. Recently, methods based on Transformers have shown significant improvements in this field. Their ability to capture long-range dependencies makes them well-suited for image reconstruction. However, these models often require high computational resources, which limits their practical use. This paper presents a detailed analysis of SISR and provides one key insight: the reconstruction performance depends on both low-level and high-level features. Then, we propose a novel SR model called HGFormer. This model uses a shallow architecture and introduces a Dynamic Spatial Information Compression (DSIC) module, which reduces computational complexity by converting the spatial information of mid-level features into the channel dimension. This improves both the efficiency and effectiveness of the model. HGFormer is the first method to expand the self-attention window to 32 × 32 while keeping low computational costs. It achieves a performance gain of 0.69 dB on the Urban100 dataset. Extensive experiments on public datasets show that HGFormer outperforms existing methods in both objective metrics and visual quality.

Introduction Chronic periodontitis (CP) is an inflammatory periodontal disease with high incidence and complex pathology. This research is aimed to investigate the function of exosomal miR‐205‐5p (Exo‐miR‐205‐5p) in CP and the underlying molecular mechanisms. Method Exo‐miR‐205‐5p was isolated from miR‐205‐5p mimics‐transfected periodontal ligament stem cells (PDLSCs), and subsequently cocultured with lipopolysaccharide (LPS)‐induced cells or injected into LPS‐treated rats. The mRNA expression of inflammatory factors and Th17/Treg‐related factors were measured by quantitative real‐time PCR. The contents of inflammatory factors and the percentages of Th17/Treg cells were measured by enzyme‐linked immunosorbent assay and flow cytometry, respectively. Besides, the target relation between miR‐205‐5p and X‐box binding protein 1 (XBP1) was explored. Results MiR‐205‐5p was downregulated in LPS‐induced PDLSCs and corresponding exosomes. Exo‐miR‐205‐5p inhibited inflammatory cell infiltration, decreased the production of TNF‐α, IL‐1β, and IL‐6, and decreased the percentage of Th17 cells in LPS‐treated rats. In addition, XBP1 was a target of miR‐205‐5p. Overexpression of XBP1 weakened the effects of Exo‐miR‐205‐5p on inhibiting inflammation and regulating Treg/Th17 balance in LPS‐induced cells. Conclusions Exo‐miR‐205‐5p derived from PDLSCs relieves the inflammation and balances the Th17/Treg cells in CP through targeting XBP1.