Non-small cell lung cancer (NSCLC) is characterized by high morbidity and lethality, causing a great physical and psychological burden on patients. Therefore, effective treatment of NSCLC patients is very important. This study analyzes the impact of a nursing intervention of case management combined with cognitive-behavioral therapy on anxiety and depression and quality of life in postoperative NSCLC patients. A single-center, non-randomized controlled study in which 80 NSCLC patients from the Hospital were enrolled from May 2023 to January 2024, and were categorized into case management (CM) and cognitive-behavioral therapy (CBT) groups depending on treatment modalities, with case management care in both groups, and cognitive-behavioral therapy care added to the CM combined with CBT (CC) group. The Hamilton anxiety scale (HAMA), Hamilton depression scale (HAMD), self-perception burden scale (SPBS), life qualities (QLQ-C30), neurotransmitter levels, and clinical effectiveness were primarily assessed in both groups post-treatment. Secondary outcomes included pain level (VAS score), nursing satisfaction, adverse events, and complications. After treatment, the indicators of both groups were significantly different from those of the pre-treatment. Post-treatment, the CC group demonstrated significantly lower scores than the CM group in HAMA (10.18 ± 2.10 vs. 16.04 ± 3.89), HAMD (11.94 ± 2.91 vs. 16.81 ± 3.19), and SPBS (25.52 ± 3.17 vs. 33.50 ± 5.61) (all P < 0.05). Conversely, the CC group showed significantly higher QLQ-C30 scores and levels of 5-hydroxytryptamine (5-HT) and brain-derived neurotrophic factor (BDNF). The nursing intervention of case management combined with cognitive behavioral therapy has a good improvement effect on the anxiety and depression status of NSCLC patients. It can improve the quality of life, which is worth promoting and using in the clinic.

The number of older patients with cancer is increasing dramatically. Recently , new anti-tumour therapies have led to significant advances in both curative and metastatic situations, with the arrival of immunotherapies as monotherapy or in combination with chemotherapy or targeted therapies, including antibody-drug conjugates. However, these new treatments have been little evaluated in elderly cancer patients, who are rarely included in therapeutic trials and require numerous adjustments to their intensity due to the increasing underlying frailty associated with age.

Increasing evidence suggests that Graves' disease (GD) may increase the risk of thyroid cancer (THCA), but diagnostic biomarkers associated with it remain underexplored. To address this issue, we analyzed the Gene Expression Omnibus (GEO) and TCGA (The Cancer Genome Atlas) databases, identified 21 shared immune-related genes via differential expression analysis and weighted gene coexpression network analysis (WGCNA). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses emphasized immune pathways, and LASSO regression was used to select five core genes (TREM1/S100A11/MRPS16/MET/ACTN1) to construct robust diagnostic models. The CIBERSORT algorithm revealed a significant correlation between the models and immune infiltration of the THCA. Machine learning and protein‒protein interaction (PPI) networks revealed TREM1 as a central gene for predicting the response to immunotherapy. Xenograft tumor models confirmed that TREM1 knockdown suppressed the proliferative capacity of thyroid cancer cells in vivo. Drug sensitivity studies identified VER-155008 as a potential therapeutic compound. Bioinformatics and experimental validation (qRT‒PCR) revealed that the HOTTIP/hsa-miR-204-3p/TREM1 axis serves as a ceRNA to regulate TREM1. Our study identified five core genes, with TREM1 as a central regulator, that demonstrate strong diagnostic potential for both Graves' disease (GD) and thyroid carcinoma (THCA). These findings provide valuable diagnostic biomarkers and therapeutic targets for THCA patients with GD.

Mesothelioma has characteristic genetic changes including inactivation of neurofibromatosis type 2 (NF2) and deletion of the INK4A/ARF region. Cells deficient of NF2 protein (MERLIN) depend on focal adhesion kinase (FAK) for cell adhesion and FAK inhibitors suppress the cell growth. The INK4A/ARF deletion activates MDM2 functions which ubiquitinate and degrade p53, and consequently the cellular p53 levels decrease. The deletion therefore induces loss of p53 functions although a majority of mesothelioma has wild-type TP53 genotype. An MDM2 inhibitor which blocked the ubiquitination increased p53 levels, restored p53 functions and facilitated cell growth arrest. Moreover, FAK and p53 expressions were reciprocally regulated. We examined growth suppressive effects of a FAK inhibitor, defactinib, and MDM2 inhibitors, nutlin-3a and reactivation of p53 and induction of tumor cell apoptosis (RITA), with representative wild-type and mutated TP53 mesothelioma and investigated molecular changes induced by the agents. We analyzed possible combinatory effects of the inhibitors and molecular changes caused by the combination. Our study showed that defactinib inhibited cell growth and induced FAK dephosphorylation irrespective of the TP53 genotype, and that the inhibited FAK phosphorylation was not associated with MERLIN levels or with p53 up-regulation, but linked with AKT dephosphorylation. Nutlin-3a preferentially suppressed growth of wild-type TP53 cells and augment p53 expression without DNA damage, whereas RITA-mediated p53 up-regulation was linked with the damage. A combination of defactinib and the MDM2 inhibitors showed that nutlin-3a showed synergistic/additive effects in wild-type and antagonistic effects in mutated TP53 cells, whereas RITA retained synergistic activity in mutated TP53 cells. These results suggest that the therapeutic success of combined FAK and MDM2 inhibition in mesothelioma depends on the precise matching of MDM2 inhibitors with the TP53 genotypes, and highlight the need for genotype-based selection of MDM2 inhibitors.

In endometrial cancer, research on ferroptosis is still in its nascent stages, yet its potential therapeutic value is becoming increasingly evident. We explore the impact of COX7A1 on mitochondrial dysfunction and ferroptosis in endometrial cancer. In this study, through comprehensive bioinformatics analysis, differentially expressed genes related to ferroptosis in endometrial cancer were identified. In vitro experiments were conducted using cytochrome c oxidase subunit 7A1 (COX7A1) overexpression and knockdown cell lines, followed by ferroptosis-related phenotypic assays to validate the effect of COX7A1 on the inhibition of endometrial cancer cell growth. Mechanistically, mitochondrial function-related parameters were assessed to explore the potential mechanisms by which COX7A1 induces ferroptosis. Online data analysis revealed that COX7A1 acts as a ferroptosis driver and is significantly downregulated in endometrial cancer tissues. In vitro experiments have demonstrated that overexpression of COX7A1 inhibits the proliferation of endometrial cancer cells and induces ferroptosis by regulating intracellular iron metabolism and mitochondrial function. The specific mechanisms include increasing intracellular Fe2+ and malondialdehyde (MDA) levels, decreasing the GSH/GSSG ratio, and disrupting mitochondrial membrane potential, thereby leading to mitochondrial dysfunction. Furthermore, COX7A1 overexpression significantly reduces the expression of glutathione peroxidase 4 (GPX4) and SLC7A11, while upregulating acyl-coenzyme A synthetase long-chain family member 4 (ACSL4). In contrast, knockdown of COX7A1 promotes the proliferation of endometrial cancer cells and inhibits ferroptosis, exhibiting the opposite effects. These findings provide new insights into the molecular mechanisms of endometrial cancer.

Oral cancer has high morbidity rates in the Asian region, specifically Pakistan. However, little insight is available regarding the molecular pathogenesis and inflammatory biomarkers of this preventable cancer. This study determined the association of EGFR, NFκB, COX-2, and miRNAs expression with the chewing habits and high-risk human papillomavirus (HR-HPV) infection in oral cancer patients. Formalin-fixed paraffin-embedded blocks (FFPE) (n = 50) were analyzed for transcriptional expression of EGFR, NFκB, and COX-2 by qPCR and COX-2 protein expression was checked by immunohistochemistry (IHC). Array profiling of ~2500 miRNAs was performed on nine samples, and five miRNAs were selected for validation from this profiling data. Appropriate statistical tests were applied to check the association of EGFR., NFκB, COX-2, and miRNAs with chewing and HR-HPV status, (p < 0.05 and 95% CI). Of the 50 samples, transcriptional expression of EGFR was observed in 13 (26%), NFκB in 11 (22%), and COX-2 in 17 (34%) samples, and the majority were chewers. EGFR and COX-2 expression was significantly associated with chewing gutka (the most carcinogenic form of chewing substance). A total of 281 miRNAs were dysregulated in miRNA profiling, and in validation, miR-222-3p was significantly downregulated in chewers expressing EGFR, NFκB, and COX-2 compared to non-chewers (p < 0.05). HR-HPV positivity was not correlated with miRNAs. This study suggests a significant association of chewing habits with EGFR and COX-2 expression. In addition, the molecular pathogenesis of OSCC suggests the substantial interplay of NFκB, COX-2, EGFR and miRNAs in chronic chewers, irrespective of HR-HPV involvement.

Colorectal cancer (CRC) and Coronavirus Disease 2019 (COVID-19) are distinct diseases that may share overlapping molecular mechanisms, particularly in immune dysregulation. However, the specific regulatory pathways driving this shared pathophysiology have remained elusive, as prior studies have been limited by single-level data. To dissect this common pathobiology, we implemented a synergistic computational framework, integrating bulk transcriptomics with single-cell data. Through a multi-tiered analysis pipeline employing differential expression, weighted gene co-expression networks, and machine learning-based feature selection, we pinpointed a core molecular signature of 31 shared hub genes. Among these, four core candidates-GPR15, PTGDR2, FCER1A, and MAL-were significantly downregulated, a finding robustly associated with impaired CD8+ T cell infiltration. Delving deeper into the regulatory architecture using a modified weighted out-degree centrality algorithm, we constructed an integrated transcription factor-microRNA-target network. Network analysis revealed upregulation of p53 and downregulation of miR-3619-5p as possible drivers of immune dysfunction. Finally, E-4031 was identified through molecular simulation as a potential therapeutic agent targeting all four core genes. These findings uncover a shared regulatory axis involving immune suppression and transcriptional disruption, and provide promising diagnostic and therapeutic targets for CRC and COVID-19.

To explore the application and research progress of tissue-engineered scaffolds in the treatment of long-segment laryngotracheal stenosis (LTS).

A comprehensive review of relevant domestic and international literature was conducted to summarize and analyze the application of different tissue-engineered scaffolds in the treatment of long-segment LTS, including the use of natural materials, synthetic polymers, their composite materials, and biodegradable metals.

Conventional treatment methods for long-segment LTS are often limited in efficacy and associated with a high risk of complications. Tissue-engineered scaffolds can simulate the extracellular matrix and provide a suitable microenvironment for cellular growth, effectively supporting and promoting the repair and regeneration of laryngotracheal tissues. However, different scaffold materials exhibit distinct characteristics in terms of performance and clinical application. Natural materials offer good biocompatibility but insufficient mechanical strength and overly rapid degradation; synthetic polymers provide tunable mechanics but weak bioactivity and a tendency to induce inflammation; composite materials integrate the advantages of both, combining bioactivity with structural strength; biodegradable metal stents possess high mechanical strength and favorable degradability, but optimization of corrosion rate and the safety of degradation products is still required.

Tissue-engineered scaffolds offer a novel therapeutic approach for long-segment LTS. However, further research and optimization of scaffold materials and design are required to enhance treatment efficacy and clinical outcomes.

ObjectiveThis study documented a thunderstorm asthma outbreak that occurred on 9-11 September 2022 in Yulin, Northwest China, and conducted a retrospective analysis of epidemiological patterns from 2018 to 2024.MethodsA retrospective observational design was employed. Patient data were obtained from Yulin Hospital, The First Affiliated Hospital of Xi'an Jiaotong University. Case numbers were retrieved from the Hospital Information System, and detailed clinical records of hospitalized patients were sourced from the medical records database.ResultsFrom 2018 to 2024, the annual incidence of allergic respiratory diseases increased substantially, from 4778 to 26,459 cases. During the thunderstorm period in September 2022, emergency visits surged to 2185 cases, significantly exceeding baseline levels of previous years. Monthly data for 2022 showed a distinct peak in September, with 5647 visits. Pollen monitoring revealed a bimodal distribution, with concentrations sharply rising to 1488 grains/1000 mm² on 8 September. Among 93 hospitalized patients, 58.0% had no prior asthma diagnosis, 70.9% had allergic rhinitis, and 59.1% were sensitized to mugwort pollen.ConclusionThese findings confirmed thunderstorm asthma as a significant public health threat in Northwest China, driven by the convergence of mugwort pollen exposure and thunderstorm conditions, highlighting the urgent need for integrated early-warning systems in susceptible regions.

Congenital lung malformations (CLMs) in pediatric patients encompass various structural abnormalities arising during fetal development, which can range from benign to life-threatening. The most common types include congenital pulmonary airway malformation (CPAM) and bronchopulmonary sequestration (BPS).

This study aimed to retrospectively analyze patients treated surgically for CLMs, focusing on indications for surgery, surgical techniques, and outcomes.

Data were collected from the medical records of patients who underwent thoracoscopy (n = 140) or thoracotomy (n = 52) between 2000 and 2024. Among these, 50 patients were diagnosed with CLMs, who were taken for further analysis. Study group inclusion criteria were performing a CT/X-ray imaging examination indicating the presence of a defect, surgery, and available pathology results. Exclusion criteria were incomplete data or lack of surgical procedure. Final study group included 37 patients who met inclusion criteria for further analysis. Detailed analysis encompassed demographics, clinical presentation, diagnostic methods, treatment, and follow-up.

The cohort included patients diagnosed with CPAM type I (n = 12), CPAM type II (n = 7), pulmonary sequestration (n = 10), and other congenital malformations such as bronchogenic cyst (n = 2), congenital cystic pulmonary disease (n = 2), CPAM type IV-pleuropulmonary blastoma type I (PPB) (n = 1), juvenile emphysema (n = 2), and mediastinal cyst (n = 1). The average age at diagnosis was 37.61 months. The cohort consisted of 17 females and 20 males. The right lung was involved in 41.18% of cases, and the left lung in 58.82%. Symptoms at presentation included pneumonia (n = 9), respiratory failure (n = 8), emphysema (n = 3), and pneumothorax (n = 2). Fifteen patients were asymptomatic, and the diagnosis was incidental. Seven patients had other congenital diseases, such as heart defects. None of the patients other than the child with PPB were offered genetic diagnostics, albeit for DICER1 or KRAS mutations.

The study underscores the heterogeneity in age and clinical presentation at the time of CLM diagnosis, highlighting the importance of an individualized and tailored approach to management.