Search Results (31,136)

Magnolia officinalis Rehder & E.H.Wilson. bark is famous as a traditional herbal medicine used in prescriptions for treating gastrointestinal discomfort, respiratory and inflammatory disorders. Magnolol, one of its principal bioactive constituents, exhibits potent anti-inflammatory and immunomodulatory properties. However, its therapeutic mechanisms in allergic rhinitis (AR) remain to be elucidated. In this study, the anti-allergic effects and molecular mechanisms of M. officinalis bark aqueous extract (MOAE) and magnolol were investigated using an ovalbumin (OVA)-induced AR mouse model. Nasal symptoms, histopathological alterations, and serum inflammatory mediators, including histamine and immunoglobulins (IgE, IgG1, IgG2a), were evaluated to assess efficacy. Both MOAE and magnolol significantly alleviated nasal rubbing and sneezing, reduced eosinophil infiltration and mucus hypersecretion, and improved tissue morphology in nasal and lung sections. Moreover, treatment markedly decreased serum levels of histamine and OVA-specific antibodies. Integrative network pharmacology, RNA sequencing, and molecular docking analyses revealed 33 co-regulated target genes mainly involved in the NF-κB and MAPK signaling pathways, suggesting that modulation of these pathways underlies the observed anti-inflammatory effects. These findings demonstrate that MOAE and magnolol exert protective effects against AR through the regulation of key inflammatory signaling cascades. This study provides modern pharmacological evidence supporting the traditional use of M.officinalis bark and highlights its potential as a natural therapeutic candidate for AR. Full article

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease characterized by the pathological accumulation of collagen-rich extracellular matrix, resulting in irreversible lung remodeling and respiratory failure. The incomplete understanding of IPF pathogenesis has hindered the development of effective therapeutics. Here, we investigate the mechanism by which the actin-related protein 2/3 complex subunit 2 (ARPC2) contributes to the fibrotic response in lung fibroblasts. Modulating of ARPC2 expression levels altered the expression of profibrotic genes, including α-smooth muscle actin (ACTA2), in TGF-β1-treated MRC-5 cells at the transcriptional level. We further show that ARPC2 regulates the TGF-β1-mediated nuclear translocation of myocardin-related transcription factor-A (MRTFA), a central driver of fibrotic gene induction. Our data indicate that ARPC2 plays a distinct role in profibrotic gene expression and MRTFA nuclear localization, distinguishing its function from other components of the actin-related protein 2/3 (ARP2/3) complex. Furthermore, ARPC2 appears to modulate the TGF-β1-dependent formation of MRTFA/G-actin complexes. Finally, transcriptomic analysis of cells depleted of ARPC2, ACTR2, or MRTFA revealed that ARPC2 and MRTFA co-regulate a specific repertoire of fibrotic genes. These observations support a profibrotic function for ARPC2 during fibroblast-to-myofibroblast transition (FMT), highlighting it as a potential therapeutic target for IPF. Full article

Background: Contrast-enhanced ultrasound (CEUS) recently emerged as a valuable imaging modality for evaluating pleuropulmonary diseases. By combining morphological information from conventional B-mode ultrasound with real-time assessment of microvascular perfusion, CEUS can provide functional insights that improve diagnostic accuracy, guide interventions, and support patient surveillance. Methods: This review summarizes the current evidence on the use of CEUS in major pleuropulmonary disorders, including pneumonia, pleural effusion, pulmonary embolism, neoplasms, and COVID-19-related lung injury. The most relevant clinical studies and meta-analyses were analyzed, focusing on CEUS parameters, diagnostic performance, and integration with other imaging techniques. Results: CEUS enables the differentiation between inflammatory, ischemic, and malignant lesions through qualitative and quantitative analyses of enhancement patterns. Early and homogeneous enhancement is typical of inflammatory or infectious processes, whereas heterogeneous or delayed enhancement with early washout strongly suggests malignancy or ischemia. In pneumonia and pleural infections, CEUS identifies non-perfused or necrotic areas, guiding drainage and evaluating therapeutic responses. In pulmonary embolism, it reveals avascular consolidations corresponding to infarction, even when CT angiography is inconclusive. For peripheral lung tumors, CEUS assesses angiogenesis and vascular supply, correlating perfusion parameters with histopathology, and improving biopsy targeting. Furthermore, in COVID-19 pneumonia, CEUS can detect microvascular alterations related to thrombosis and fibrosis. Conclusions: CEUS is a safe, noninvasive, and radiation-free technique that provides unique real-time information on pulmonary perfusion. Its integration with conventional ultrasound enhances diagnostic precision, optimizes interventional guidance, and allows for dynamic monitoring of treatment response. Future developments in quantitative analysis, artificial intelligence, and targeted contrast agents are expected to further expand CEUS clinical applications in pleuropulmonary imaging. Full article

Objective: This study examined the frequency of entosis in solid tumors of various origins (colorectal cancer, breast cancer, and lung cancer) and its association with clinical and pathological characteristics. It also examined survival and copy number alterations (CNAs) in genes associated with stem cells. The aim was to assess the potential prognostic value of entotic events in tumors. Methods: A total of 238 patients were included: 96 with colorectal cancer (CRC), 45 with lung cancer (LC), and 97 with breast cancer (BC). Entotic cell-in-cell (CIC) structures were evaluated on hematoxylin–eosin–stained slides using Mackay’s criteria. A CIC frequency >0.1 per 20 high-power fields was considered positive. Clinicopathological parameters, overall survival (CRC), metastasis-free survival (LC and BC), and CNA profiles of stemness-related genes were analyzed. Amplifications of MAP1LC3A and other chromosomal loci were assessed. Results: CRC demonstrated the highest entosis rate, more than two-fold higher compared with BC and LC (p < 0.05). Entosis correlated with high tumor grade (G3) in CRC (p = 0.03). In LC, CIC-positive tumors were more frequent in patients with lymph-node metastases (p = 0.02), whereas in BC, the opposite trend was observed (p = 0.02). It was noted that in patients with stage III–IV LC, the frequency of entosis was significantly higher than in patients with stage I–II cancer (p = 0.03). CIC-positive status was associated with poorer overall survival in CRC (p = 0.03) and reduced metastasis-free survival in LC (p = 0.011). In breast cancer, no statistically significant survival differences were observed. Tumors harboring two or more stemness-gene amplifications showed significantly higher entosis frequency regardless of tumor site. A strong association was identified between entosis and MAP1LC3A amplification. Conclusions: Enosis is not a random morphological phenomenon but a process associated with unfavorable tumor characteristics, high malignancy, reduced survival, and amplification of stem cell-related genes. The results of this study confirm the working hypothesis that entosis may contribute to the emergence of aneuploid clones of tumor cells, including those containing amplifications of stem cell-associated genes. This positions entosis as a potential factor in tumor genetic heterogeneity, which is particularly important in the context of therapeutic selection pressure. The observed association between high entosis frequency and the presence of ≥2 stem cell gene amplifications, as well as its association with poor prognosis in colorectal and lung cancer, highlights its potential value as a prognostic indicator. Furthermore, MAP1LC3A amplification data may serve as a molecular marker of entotic activity and a potential therapeutic target. Full article

Background/Objectives: Cancer cells are subjected to various stress conditions and have stress adaptability strategies to survive. Various types of stresses lead to the aggregation of cytoplasmic RNA granules known as stress granules (SGs), seen in normal and tumor cells, and aid in cell survival by avoiding cell apoptosis. G3BP stress granule assembly factor 2 (G3BP2) encodes a multifunctional protein with known roles as a critical component of SGs and is also associated with chemoresistance in cancer, but its known roles in non-small cell cancer (NSCLC) are limited. Methods: We evaluated the expression of G3BP2 via qPCR and immunohistochemistry on a retrospective cohort of NSCLC isolated at surgery in St James’s Hospital, Dublin, Ireland. Expression levels were correlated with clinicopathological parameters. Survival analyses, including Kaplan–Meier analyses, were used to determine the prognostic value. Additional correlations with other available NSCLC datasets were explored. Results: In contrast to other studies, we did not observe upregulated expression of G3BP2. Furthermore, Kaplan–Meier analyses did not identify any prognostic value associated with G3BP2 expression in patient tissues in contrast to other published data. Bioinformatic analyses on these other datasets found strong correlations between G3BP2 and core stress granule genes in NSCLC. Additional analyses also identified correlations between G3BP2 expression and immune cell infiltration, immune cell exhaustion, and DNA Damage Response pathways. An examination of the available datasets did not find any overall prognostic value for altered DNA methylation and survival. However, two individual CpG residues were identified for which higher methylation was associated with worse overall survival. Finally, the effects of a G3BP2 inhibitor on cellular proliferation were assessed. Conclusions: In our analysis, G3BP2 was not associated with survival benefit. However, clear associations were observed between altered expression of this gene and a number of important pathways linked to cancer pathogenesis, and further studies are warranted to assess this gene (and/or) stress granules in cancer. Full article

Background/Objectives: The COVID-19 pandemic emerged in early 2020, disrupting global cancer services. We aimed to assess the pandemic’s impact on lung cancer diagnosis and treatment, including clinical characteristics, diagnostic methods, treatment patterns, and survival outcomes. Methods: A retrospective analysis of 1832 patients visiting Maharaj Nakorn Chiang Mai Hospital from January 2019 to December 2021 with suspected lung cancer was conducted. We evaluated demographic characteristics, diagnostic methods, treatment modalities, and survival results across this period. Results: Among the 698 eligible patients, the pandemic led to a 13% to 17% decline in newly diagnosed lung cancer cases. However, demographic and lung cancer characteristics, including age, gender, and smoking status, remained unchanged. The pandemic also saw an increase in asymptomatic cases and a 1.3 to 2.2 times higher occurrence of early-stage non-small cell lung cancer cases. The rapid implementation of healthcare policies prioritized the diagnosis of suspected cancer patients and maintained cancer care throughout the pandemic, resulting in similar diagnostic methods and waiting times compared to the pre-pandemic era. Treatment patterns displayed continuity, with a notable rise in 2 to 3 times higher surgical interventions and an 8% to 11% decrease in the initial delivery of palliative care. The delivery of systemic therapy for patients with advanced-stage disease was also maintained. One-year survival rates remained consistent across various lung cancer stages during the pandemic. Conclusions: The COVID-19 pandemic led to a modest decrease in new diagnoses, with limited effects on the demographic and clinical profiles of lung cancer cases. Survival rates among patients diagnosed during the pandemic remained stable compared to those diagnosed before the pandemic. These findings underscore the adaptability of the healthcare system, alongside the capabilities of multidisciplinary teams, in providing timely and effective diagnosis and ensuring uninterrupted essential treatment of lung cancer during challenging circumstances. Full article

Background/Objectives: Pulmonary neuroendocrine neoplasms comprise a heterogeneous group of epithelial lung tumors characterized by varying degrees of differentiation and biological aggressiveness. Among high-grade types, large cell neuroendocrine carcinoma (LCNEC) is an uncommon but clinically significant entity, representing approximately 3% of lung cancers, with the optimal first-line therapeutic approach remaining uncertain. Our aim was to evaluate the available prospective therapeutic evidence in patients with advanced or metastatic pulmonary LCNEC, defining the current evidence and identifying key gaps to inform future research. Methods: A systematic literature search was conducted using PubMed, Scopus, and Web of Science (last update: 9 August 2025). Endpoints included the evaluation of clinical outcomes from interventional trials and safety. Results: Overall, 2139 records were identified through the database search and handsearching. After removal of duplicates and non-eligible records, only 4 prospective, non-randomized studies were eligible for the systematic review. Due to the risk of bias and substantial methodological variability, a meta-analysis could not be reliably performed. Three trials investigated first-line platinum-based chemotherapy regimens, while only one study evaluated immunotherapy in lung LCNEC. Overall clinical outcomes were modest, with benefits appearing limited in duration, with median PFS consistently <6 months and median OS rarely exceeding one year. Conclusions: The findings of this review underscore a persistent and substantial evidence gap in the management of advanced pulmonary LCNEC. Closing this gap will require coordinated international collaborations and innovative trial designs, including molecular analysis as a driver for patient management. Without such efforts, the prospect of personalized medicine for lung LCNEC will remain far from reality. Full article

Objectives: To evaluate the short-term safety (30-day and in-hospital morbidity and mortality) and technical feasibility of uniportal video-assisted thoracic surgery (U-VATS) for anatomical lung resection in octogenarians (≥80 years) compared with younger patients (<80 years) at a single center. Methods: Ninety consecutive patients undergoing U-VATS anatomical lung resections between January 2020 and January 2024 were retrospectively analyzed. Patients were stratified by age: 60 patients < 80 years and 30 octogenarians ≥ 80 years. Propensity score matching (nearest-neighbor, 1:2 ratio, caliper 0.2 SD) yielded a matched cohort of 60 patients (40 younger, 20 octogenarians) for comparative analysis. Results: After matching, standardized mean differences (SMD) were <0.25 for most covariates, indicating good balance. Octogenarians demonstrated lower FEV1 (75.2 ± 15.3% vs. 87.5 ± 18.2%, p = 0.012) and DLCO (68.4 ± 12.1% vs. 78.5 ± 14.3%, p = 0.009), consistent with age-related pulmonary changes. Charlson Comorbidity Index was higher (5.3 ± 1.2 vs. 3.8 ± 1.4, p = 0.001). Surgical parameters were comparable: operative time (143.80 ± 42.3 vs. 136.55 ± 38.7 min, p = 0.524), blood loss (median 80 [IQR 50–120] vs. 95 [IQR 60–130] mL, p = 0.742). Zero conversions occurred. Major complications (Clavien–Dindo ≥ 3) occurred in 10% vs. 0% (absolute risk difference 10%, 95% CI: −3.2% to 23.2%). No 30-day mortality. 90-day mortality: 5% vs. 0% (p = 0.333); one-year: 15% vs. 0% (p = 0.035). Conclusions: U-VATS is technically feasible in carefully selected octogenarians with comparable intraoperative parameters to younger patients. Postoperative recovery differed meaningfully, with higher delirium rates, longer hospitalization, and greater rehabilitation needs. One-year mortality was higher in octogenarians, reflecting competing comorbid risk rather than surgical harm. Residual imbalance in comorbidity burden and pulmonary reserve after matching limits causal inference. These hypothesis-generating findings support U-VATS in selected octogenarians when comprehensive geriatric assessment and structured delirium prevention guide perioperative management; validation in larger multicenter prospective studies is required. Full article

Background/Objectives: Lung cancer remains a major global health burden, largely driven by cigarette use. Although electronic cigarettes (e-cigarettes) are viewed as safer alternatives due to their reduced chemical load, growing evidence shows their vapor can disrupt cellular transcriptomes, including long noncoding RNAs (lncRNAs). In this study, we examined the regulation and function of vape-associated lncRNA transcript 1 (VALT1), a novel transcript upregulated in the oral transcriptomes of e-cigarette users and similarly elevated in non-small-cell lung cancer (NSCLC) tumors. Methods: Publicly available RNA-seq datasets were analyzed, and VALT1 was identified as an e-cigarette-responsive lncRNA. Its dose-dependent induction by e-cigarette smoke extract (eCSE) and cytoplasmic localization were confirmed via RT-qPCR. Its effects on cancer-associated phenotypes including proliferation, ROS detoxification, resistance to apoptosis, migration, cytoskeletal disorganization, and nuclear remodeling were assessed through overexpression and siRNA-mediated knockdown in A549 and BEAS-2B cells. Results: Acute eCSE exposure induced a biphasic, dose-dependent increase in VALT1 expression, accompanied by enhanced proliferation, ROS detoxification, apoptosis resistance, migration, cytoskeletal disorganization, and nuclear remodeling in A549 cells. VALT1 overexpression reproduced these phenotypes in both cell lines without eCSE treatment, whereas knockdown attenuated them. VALT1 promoted survival under cytotoxic stress in A549 but not BEAS-2B cells. Conclusions: These findings support an active role for VALT1 as an e-cigarette vapor-upregulated transcript that contributes to its phenotypic readout and enhances cellular survival under extracellular chemical stress—thereby aggravating tumorigenic phenotypes even in the absence of mutations that contribute to malignant transformation. Full article

A 75-year-old man with newly diagnosed high-risk prostate cancer (cT3bN0M0) underwent ¹⁸F-PSMA PET/CT, which demonstrated intense tracer uptake in a left tracheal mass causing near-complete luminal obstruction, raising suspicion of a primary lung malignancy or metastatic disease. Endoscopic debulking was performed due to progressive respiratory symptoms with dyspnea. Histopathology and immunohistochemistry (p63, SMA, CK5/6 positive; PSA, NKX3.1, and AR negative, with downregulated PSMA-expression) established the diagnosis of low-grade epithelial–myoepithelial carcinoma of the trachea. Following debulking, the patient’s symptoms resolved, and a watchful-waiting strategy was adopted for the tracheal tumor, while curative-intent therapy for prostate cancer continued. This case highlights that ¹⁸F-PSMA PET/CT may reveal rare, intensely PSMA-avid non-prostatic neoplasms and underscores the importance of recognizing atypical uptake patterns to avoid misinterpretation during prostate cancer staging. Full article

Sports performance in aquatic environments is governed by biomechanical, physiological, neuromuscular and perceptual–mental constraints that differ fundamentally from those encountered on land. As a result, athletes with comparable general physiological or motor capacities may achieve markedly different performance outcomes in aquatic sports. Within functional kinesiology and sport science, aquatic performance is still frequently interpreted through isolated physiological, biomechanical, or technical variables, which limits both explanatory depth and applied relevance. This Perspective article introduces aquaticity as an integrated latent construct representing a multidimensional determinant of sports performance specific to the aquatic environment. Aquaticity is conceptualized as a functional framework that modulates how general physiological and motor capacities are expressed under aquatic constraints, integrating key domains of exercise physiology, sport biomechanics, neuromuscular control, energetic regulation, and perceptual–mental stability. The relative contribution of these domains is considered discipline-specific and dependent on task and environmental demands. Breath-hold diving is presented as a particularly suitable model for examining aquaticity, as apnea and hypoxic–hypercapnic stress amplify interactions between physiological regulation, neuromuscular control, and biomechanical efficiency. Training and diagnostic tasks performed in real aquatic settings are interpreted as manifest indicators of aquaticity, enabling ecologically valid athlete monitoring and performance assessment. Within this framework, energetic aquaticity is highlighted as a central functional sub-construct linking metabolic regulation, movement efficiency, and neural control during performance under respiratory constraints. The proposed conceptual framework has important implications for functional kinesiology, sport biomechanics, exercise physiology, and applied athlete monitoring in aquatic sports. Aquaticity is advanced not merely as a descriptive concept, but as a unifying framework that can guide future experimental research, discipline-specific diagnostics, individualized training design, and safety-oriented performance assessment in aquatic environments. Full article

Lung cancer progression is regulated by multiple factors, including ferroptosis and gut microbiota-mediated butyrate metabolism. This study investigates the anti-tumor effects of ginsenoside Rh4 on lung cancer cells via ferroptosis mechanisms in vitro and in vivo. In vitro, ginsenoside Rh4 inhibited the proliferation of Lewis lung carcinoma (LLC) and A549 cells and triggered ferroptosis, effects that were suppressed by the ferroptosis inhibitor Ferrostatin-1 (Fer-1). In vivo, tumor-bearing mouse models were established and treated with 100 mg/kg ginsenoside Rh4 for 21 days. Tumor growth, ferroptosis markers, gut microbiota, and butyrate were analyzed, with in vitro validation of butyrate’s pathway effects. Ginsenoside Rh4 induced ferroptosis in LLC cells both in vitro and in vivo, inhibiting tumor growth. It promoted ferroptosis by disrupting iron homeostasis through elevated Fe²⁺ and transferrin receptor (TFRC), and impaired antioxidant defense via depletion of glutathione (GSH) and reduction in ferritin heavy chain 1 (FTH1), solute carrier family 40 member 1 (SLC40A1), solute carrier family 7 member 11 (SLC7A11), and glutathione peroxidase 4 (GPX4). Additionally, ginsenoside Rh4 enhanced lipid peroxidation, indicated by increased lipid peroxides (LPO) and malondialdehyde (MDA). In vivo, it suppressed the KEAP1/NRF2/HO-1 pathway, reducing antioxidant enzyme activity. Gut microbiota modulation and butyrate production further amplified ferroptosis by activating transcription factor 3 (ATF3)-mediated GPX4 suppression. Ginsenoside Rh4 induces ferroptosis by inhibiting the KEAP1/NRF2/HO-1 pathway and remodeling the gut microbiota to increase butyrate levels, which synergistically enhance tumor cell ferroptosis sensitivity through ATF3 activation and suppression of GPX4. Full article

Non-small cell lung cancer (NSCLC) is the leading cause of lung cancer deaths, with resistance to targeted therapies posing a major clinical challenge. Drug-tolerant persister (DTP) cells are key contributors to resistance, and targeting them offers new strategies to enhance existing treatments. MicroRNAs (miRNAs), particularly the tumour-suppressive miR-15/107 family, offer promise due to their ability to target multiple oncogenic pathways. This study evaluated a synthetic consensus miRNA mimic, conmiR-15/107, in NSCLC cell line models. Dose–response assays showed robust, dose-dependent growth inhibition in both EGFR-mutant (PC9) and KRAS-mutant (H358 and A549) lung adenocarcinoma cells, but not in the human bronchial epithelial cell line BEAS-2B. When combined with EGFR inhibitors (osimertinib and gefitinib) in PC9 cells, the mimics showed a higher rate of growth inhibition compared with the controls and reduced IC₅₀ values. Similarly, conmiR-15/107 enhanced growth inhibition by the KRAS inhibitors sotorasib and adagrasib in H358 cells. RT-qPCR confirmed downregulation of conmiR-15/107 targets, including MEK1, BCL2 and BRCA1, suggesting a multi-target mechanism of action. Long-term assays showed that the mimics reduced the survival and delayed the proliferation of DTPs in osimertinib-treated PC9 cells as well as sotorasib-treated H358 cells. These findings support conmiR-15/107 as a potential adjunct to targeted therapy, capable of enhancing treatment efficacy and delaying resistance in lung adenocarcinoma. Full article

The growing popularity of electronic cigarettes (e-cigarettes) necessitates a better understanding of their biological effects. In this study, we aimed to evaluate the effects of e-cigarette aerosol condensates generated from either e-cigarette carrier liquid alone or with e-cigarette liquid with nicotine and flavor on bronchial epithelial cells. BEAS-2B cells were exposed to e-cigarettes for 24 h, and transcriptional and proteomic profiling, including assessment of protein modifications, was performed. Additionally, cell-based assays were used to evaluate mitochondrial function, rate of protein synthesis, lysosomal signal, lipid droplet quantity and actin formation. Our findings reveal that short-term exposure to both types of aerosol condensates altered transcriptome and proteome profiles, disrupting cellular homeostasis in BEAS-2B cells through impaired proteostasis and mitochondrial function in response to both types of condensates. Changes in lipid and lysosome content, as well as a reduction in polymerized actin, were observed with nicotine- and flavor-containing condensate. E-cigarette exposure also induced irreversible protein modifications, including different chemical derivatives (25 out of 49 in nicotine/flavor condensate; 20 out of 48 in nicotine/flavor-free condensate; 4 out of 35 in control), suggesting their particularly harmful effect. Together, these findings point to early-onset cellular stress and impaired lung epithelial fitness caused by acute e-cigarette exposure. Full article

As product aesthetics increasingly drive consumer preference, quantitative evaluation remains hindered by subjective evaluation biases and the black-box nature of modern artificial intelligence. This study proposes an advanced machine learning framework incorporating sensitivity-aware morphological features for the aesthetic evaluation of industrial products, with automotive design as a representative case. An aesthetic index system and its quantitative formulations are first developed to capture the morphological characteristics of product form. Subjective weights are determined via grey relational analysis (GRA), while objective weights are calculated using the coefficient of variation method (CVM) integrated with the technique for order preference by similarity to an ideal solution (TOPSIS). A game-theoretic weighting approach is then employed to fuse subjective and objective weights, thereby establishing a multi-scale aesthetic evaluation system. Sensitivity analysis is applied to identify six key indicators, forming a high-quality dataset. To enhance prediction performance, a novel model—improved lung performance-based optimization with backpropagation neural network (ILPOBP)—is proposed, where the optimization process leverages a maximin latin hypercube design (MLHD) to enhance exploration efficiency. The ILPOBP model effectively predicts aesthetic ratings based on limited morphological input data. Experimental results demonstrate that the ILPOBP model outperforms baseline models in terms of accuracy and robustness when handling complex aesthetic information, achieving a significantly lower test set mean absolute relative error (MARE = 4.106%). To further enhance model interpretability, Shapley additive explanations (SHAP) are employed to elucidate the internal decision-making mechanisms, offering reverse design insights for product optimization. The proposed framework offers a novel and effective approach for integrating machine learning into the aesthetic assessment of industrial product design. Full article