Search Results (3,966)

Background/Objectives: The co-occurrence of asthma and obesity presents a significant clinical challenge, but the underlying mechanisms remain unclear. Reduced adiponectin and vitamin D levels have been associated with both conditions, suggesting that their potential modulatory roles warrant further investigation. This study aimed to evaluate whether vitamin D and adiponectin levels differ among pediatric groups defined by their asthma and obesity status, to better characterize the metabolic and inflammatory profile of the obesityasthma phenotype. Methods: A total of 120 participants aged 6–18 were enrolled and categorized into four groups: Asthma (n = 30), Obesity (n = 30), Asthma + Obesity (n = 30), and Control group (n = 30). All participants underwent lung function testing, anthropometric assessment and measurement of fraction of exhaled nitric oxide (FeNO). Participants were further categorized according to BMI percentiles. Adiponectin levels were measured using ELISA, while vitamin D levels were detected using HPLC. Results: Vitamin D levels and lung function parameters did not differ across groups, although deficiency was most prevalent in the obesity group. FeNO was elevated in asthmatics relative to obese children (p = 0.038) and in obese asthmatics compared with both controls (p = 0.040) and obese children (p = 0.021). Adiponectin levels were lower in obese asthmatic children compared to the controls (p = 0.024). A similar difference was observed between the controls and obese asthmatics among children with low vitamin D levels (p = 0.014). Conclusions: The dominant mechanisms underlying the obesity–asthma phenotype remain unclear; however, our findings indicate a link between adiponectin dysregulation and heightened airway inflammation, as evidenced by increased FeNO levels, though the precise pathways involved are still not well-understood. The role of vitamin D appears less consistent. These results highlight the need for further research to clarify the interplay between metabolic and inflammatory pathways and to support more personalized management strategies in children with obesity-related asthma. Full article

Open-heart surgery with cardiopulmonary bypass (CPB) is a high-risk procedure with significant morbidity and mortality. CPB, tissue injury, blood loss, endotoxemia and ischemia–reperfusion injury induce a pronounced systemic inflammatory response, leading to endothelial glycocalyx (EG) damage and vascular endothelial dysfunction. Consequently, immune cells, reactive oxygen species, and enzymes gain free access to vascular endothelial cells, resulting in their dysfunction and enhancing inflammation, vascular permeability, and microvascular impairment. EG degradation is most commonly assessed by measuring the circulating levels of its degradation products. Additionally, CPB triggers an early inflammatory response that is characterized by the secretion of interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor alpha, and IL-18, which play roles in initiating the process of EG injury. EG damage is further propagated by the sustained release of cytokines, inhibiting the regeneration of the glycocalyx layer. Heparanase and matrix metalloproteinases are enzymatic pathways involved in cytokine-mediated EG degradation after cardiac surgery, and the balance between the pro- and anti-inflammatory cytokines determines the magnitude and duration of the inflammatory response and EG impairment, which correlates with adverse clinical outcomes, including myocardial dysfunction, acute lung and kidney injury, neurological complications, and prolonged need for intensive care. Thus, identifying patients with an exaggerated cytokine response could potentially provide more personalized therapy based on the circulating biomarkers of EG shedding, and cytokine-directed preservation of EG represents a promising therapeutic strategy in vascular dysfunction prevention during and after open-heart surgery. In this review, we summarize the current knowledge on cytokine-mediated EG impairment following open-heart surgery with CPB. Full article

Cancer remains a leading cause of morbidity and mortality globally, with current therapies often limited by toxicity, drug resistance, and reduced efficacy in advanced stages. Medicinal plants represent important sources of bioactive compounds (BACs) with anticancer and chemopreventive potential; however, their successful application is strongly influenced by extraction strategies that determine phytochemical recovery and downstream biological activity. This review evaluates solvent-based extraction techniques used to extract BACs from medicinal plants with reported anticancer properties, synthesizing peer-reviewed articles from PubMed and Google Scholar published between 2020 and 2025. Solvent-based methods, including Soxhlet and maceration, were most widely applied due to their operational simplicity and the preservation of structurally diverse metabolites while percolation, decoction, infusion, and hydro-distillation were sparsely utilized. Extraction strategy and solvent polarity emerged as primary factors shaping phytochemical profiles, with phenolics, flavonoids, alkaloids, and terpenoids identified as dominant classes. Reported half maximal inhibitory concentration (IC₅₀) ranged from highly potent (0.12 µg/mL) to weak (30,000 µg/mL), reflecting variability driven by extraction parameters and plant matrix complexity. Anticancer mechanisms commonly involved apoptosis induction, cell-cycle arrest, reactive oxygen species-mediated cytotoxicity, and inhibition of proliferative signaling pathways across breast, cervical, colon, lung, liver, and prostate cancer models. Although solvent-based extraction approaches remain widely used, their context-dependent nature and lack of standardization limit reproducibility. Overall, anticancer and chemotherapeutic efficacy is primarily governed by BAC composition, while extraction methods act as upstream modulators. Future progress requires phytochemical-informed, standardized workflows supported by hybrid extraction systems, AI-assisted optimization, and advanced bioavailability and delivery systems to enable reproducible and clinically relevant translation of plant-derived chemotherapeutics. Full article

Diagnosis of cancer is one of the hardest problems faced in modern medicine and involves integrating different data sources such as medical images, genomic profiles and clinical records. Traditional machine learning methods have difficulty handling the high-dimensional and complex correlation properties of multimodal medical data. In view of this, we propose a new Quantum-Enhanced Multimodal Fusion Network (QEMFN) framework to break through traditional image–text matching based on quantum computing principles for CT imaging with genomic sequencing data and EHR information. Our approach utilizes variational quantum circuits for feature encoding, quantum kernel methods for crossmodal attention, and hybrid quantum–classical architectures for final classification. We realize the framework using Google Cirq quantum computing library and validate it on publicly available datasets including TCIA (The Cancer Imaging Archive), TCGA (The Cancer Genome Atlas), and MIMIC-III clinical database. The matched multimodal cohort comprises 847 lung cancer patients, 623 colorectal cancer patients, and 401 liver cancer patients with complete imaging, genomic, and clinical records, assembled via de-identified patient ID linkage across the three archives. The experiment takes steps toward the realization of quantum-enhanced diagnostic systems and offers a path for subsequent experimental confirmation. We theoretically analyze the potential quantum advantage, present detailed implementation details using Cirq, and describe a roadmap to clinical translation for quantum-enhanced diagnostic tools. Full article

Introduction and Importance: Colorectal adenocarcinoma typically metastasizes to the liver and lungs, with pleural, breast, or osseous involvement being exceedingly rare. Here, we report an unusual case of rectal adenocarcinoma metastasizing to the chest wall with simultaneous involvement of the lung, pleura, ribs, and subcutaneous breast tissue, forming a dominant giant metastasis (25 × 18 × 16 cm) accompanied by additional satellite lesions between the ribs and pectoral muscles, as well as intrapulmonary nodules. Presentation of case: The patient underwent radical resection including rib excision, followed by hyperthermic intrathoracic chemotherapy (HITHOC) with mitomycin. Chest wall integrity was restored using a synthetic mesh and titanium plating, ensuring both oncologic clearance and structural stability. Multimodal therapy also included neoadjuvant chemotherapy with bevacizumab, which was continued postoperatively. Clinical discussion: This case underscores the critical role of a multidisciplinary strategy in managing rare and aggressive metastatic patterns of colorectal cancer. In selected patients, a combination of systemic therapy, extensive surgical resection, advanced reconstruction, and regional chemotherapy may offer the potential for short-term local disease control. Conclusions: The radical excision of the giant tumour enabled continuation of systemic therapy under the national drug programme, was associated with short-term local control, and improved the patient’s quality of life. Full article

Post-viral pulmonary fibrosis represents a clinically significant and mechanistically complex consequence of severe respiratory infection. The COVID-19 pandemic has highlighted that a subset of survivors, particularly those with severe pneumonia or acute respiratory distress syndrome, develop persistent fibrosis-like lung abnormalities, including reticulation and traction bronchiectasis, often accompanied by impaired gas transfer. Although the clinical course is heterogeneous and many lesions regress over time, longitudinal studies indicate that structural and functional impairment may persist for years in susceptible individuals. Oxidative stress has emerged as a plausible convergent mechanism linking acute epithelial injury, dysregulated inflammatory resolution, and chronic fibrotic remodeling. Reactive oxygen and nitrogen species amplify inflammatory signaling, promote epithelial cell death and senescence, influence macrophage polarization, and activate canonical profibrotic pathways, notably the TGF-β axis. Redox imbalance is embedded within reinforcing circuits involving NOX4-dependent ROS amplification, mitochondrial dysfunction, endoplasmic reticulum stress, inflammasome activation, and senescence-associated secretory programs. Persistent immune activation and organelle stress may sustain redox dysregulation beyond viral clearance, thereby bridging acute lung injury to maladaptive remodeling. This review integrates epidemiological, clinical, and mechanistic evidence to position oxidative stress as a central mediator of post-viral lung fibrosis and discusses therapeutic and translational implications. Full article

Pneumonia, an acute inflammatory condition of the lung tissue, imposes a significant burden on global health and is characterized by a high rate of illness and death. The pathogenesis of the disease extends beyond infection to breakdown of redox hemostasis, where the excessive reactive oxygen species produced during the immune response inflict damage on the alveolar tissues and hence promote varying complications. This dual role of oxygen and oxidative mechanisms makes the management of pneumonia challenging, as the very oxygen that is vital for host defense, when not regulated, imposes severe lung damage. Antioxidant administration and oxygen therapy offer limited efficacy, mostly due to their non-specific action and iatrogenic harm from oxygen oversupply. These limitations are overcome by the use of emerging therapeutic strategies, which primarily focus on precision-targeted approaches. These include inhalable antioxidants, nanoparticle-based systems and biomaterials that are engineered to respond to local ROS concentrations, which aim to deliver the therapeutic agent directly to the inflamed regions of the lung. Calcium peroxide- and manganese dioxide-incorporating materials are being designed to modulate the oxygen levels, either by releasing it in hypoxic zones or scavenging it in hyperoxic microenvironments. This approach simultaneously addresses hypoxia and oxidative stress. Despite showing promising results in experimental and preclinical studies, complications related to product stability, regulatory compliance, and manufacturing scalability need to be addressed. Personalized treatment protocols, guided by biomarkers, involve the future generation of treatments, aiming to achieve a delicate recalibration of the lung’s oxidative environment for improved patient outcomes. Full article

Background: Hepatic ischemia–reperfusion (I/R) injury induces systemic oxidative stress and inflammatory responses that may lead to remote lung injury. This study investigated whether taxifolin attenuates hepatic I/R-induced lung damage and examined the involvement of the nuclear factor-κB (NF-κB) and high-mobility group box-1 (HMGB1) signaling axis. Methods: Twenty-eight male Wistar rats were divided into four groups (n = 7): control, taxifolin, hepatic I/R, and taxifolin+I/R. Serum oxidative stress markers (malondialdehyde [MDA], interleukin [IL]-6, total antioxidant/oxidant status [TAS/TOS]) and wet-to-dry lung weight ratio were measured. Lung tissues were evaluated histopathologically and immunohistochemically for NF-κB and HMGB1 expression. Bioinformatics pathway enrichment and molecular docking analyses were also performed. Results: Hepatic I/R significantly increased serum MDA, IL-6, and TOS levels and decreased TAS (p < 0.05). Severe lung injury was observed in the hepatic I/R group (median score: 11), whereas taxifolin pretreatment significantly reduced the injury score (median score: 5, p < 0.001). NF-κB and HMGB1 expression were markedly elevated following hepatic I/R and significantly decreased with taxifolin treatment (p < 0.05). A strong positive correlation was found between NF-κB and HMGB1 expression (r = 0.82, p < 0.001). Pathway enrichment analysis indicated involvement of Toll-like receptor (TLR)-related inflammatory signaling, and docking analysis demonstrated favorable binding of taxifolin to TLR4 and NF-κB p65. Conclusion: Taxifolin attenuated hepatic I/R-induced lung injury by reducing oxidative stress and suppressing HMGB1–TLR4–NF-κB-mediated inflammatory signaling. Full article

Background and Clinical Significance: Acetazolamide is routinely used post-cataract surgery to prevent intraocular pressure (IOP) spikes. Rare non-cardiogenic pulmonary edema (NCPE) cases highlight its risks in elderly comorbid patients. This report details acetazolamide-induced NCPE and provides a review of current evidence from the literature. Case Presentation: A 74-year-old male with chronic kidney disease, atrial fibrillation, and aortic aneurysm repair received 250 mg oral acetazolamide post-cataract extraction. Clinical, imaging, and lab data were documented during Intensive Care Unit (ICU) stay. PubMed/Google Scholar review identified similar cases. Within 30 min, severe hypoxemia with SpO₂ (peripheral oxygen saturation) of 77%, accompanied by tachypnea and hypertension, necessitated endotracheal intubation. Echocardiography showed preserved left ventricular (LV) function; computed tomography (CT) confirmed bilateral alveolar opacities without cardiomegaly or embolism, indicating permeability-mediated NCPE. Lung-protective mechanical ventilation and vasopressor therapy resulted in hemodynamic and respiratory stabilization. On day 4, ventilator-associated pneumonia (VAP) due to Acinetobacter baumannii resolved with targeted antibiotic therapy. The patient made a full recovery following ICU discharge. To date, nine prior cases have been reported, alongside 31 entries in EudraVigilance reflecting a 19.4% mortality rate. Conclusions: Rapid-onset NCPE from acetazolamide involves endothelial injury, distinct from cardiogenic pulmonary edema. Early recognition, drug cessation, and admission to the intensive care unit (ICU) are vital components of therapeutic intervention. Risk stratification and pharmacovigilance are recommended for perioperative safety. Full article

Cancer is an alarming health concern and economic burden in both developed and developing countries. Recently, there has been a growing demand for new alternative medications with more effectiveness and fewer harmful effects. During the past decades, a set of chemotherapeutic agents has been developed to fight against a large spectrum of cancer types. Unfortunately, their use is associated with a high level of toxicity; they are expensive, also, and their deployment is restricted by the emergence of cellular resistance. Plant-based components are garnering attention due to their low toxicity, selectivity, efficiency, and ease of accessibility. Alkaloids are one of these targeted compounds. Indeed, they are a highly diverse group with basic heterocyclic nitrogen-containing alkaloids that exhibit potent anticancer effects against a large panel of solid and liquid tumors, such as lung, breast, leukemia, liver, and colon cancer. The main molecular mechanisms involved in alkaloids’ anticancer effect are the induction of apoptosis via the extrinsic and intrinsic pathways, DNA damage, and the inhibition of cell cycle progression. Amazingly, these auspicious compounds exhibited strenuous inhibitory effects against a whole range of key enzymes involved in cancer progression and metastasis, such as Cytochrome P450 (CYP450), Cyclooxygenase-2 (Cox-2), Lysine-Specific Demethylase 1 (LSD1), Poly [ADP-ribose] polymerase (PARP), and topoisomerase, mainly through two action modes, namely irreversible and reversible inhibition. Furthermore, several conventional extraction methods have been developed to extract bioactive compounds from natural matrices, such as Soxhlet and hot water extraction. However, these techniques have many drawbacks, as they require a large amount of organic solvents, which not only affect human health but also generate severe environmental issues. To overcome these limitations, multiple eco-extraction techniques have emerged as potential alternatives to traditional extraction methods such as ultrasonic extraction, microwave-assisted extraction, and supercritical fluid extraction. In fact, they are considered eco-friendly and efficient technologies with less time and solvent consumption. Overall, this review aims to provide an updated overview of the most prominent anticancer alkaloids that have not been well reviewed already, as well as the main green extraction techniques relevant to the extraction of antineoplastic alkaloids. Full article

Alpha-1 antitrypsin deficiency (AATD) is a genetic disorder characterized by reduced circulating levels and/or impaired function of alpha-1 antitrypsin (AAT), a key serine protease inhibitor, in which loss of effective antiprotease protection results in unchecked neutrophil elastase activity and progressive lung tissue destruction. Although AATD accounts for approximately 1% of chronic obstructive pulmonary disease (COPD) cases and up to 2% of emphysema, AATD-related COPD remains largely underdiagnosed, despite guideline recommendations for systematic evaluation in patients with COPD, particularly in high-risk clinical settings. Pathologically, AATD-related COPD is not limited to the typical early-onset, lower-lobe-predominant emphysema, also including upper-lobe or mixed emphysema patterns, airway-predominant disease, small airways dysfunction, and bronchiectasis. Clinically, AATD-related COPD is distinguished from smoking-related COPD by its earlier onset, physiological impairment that is often disproportionate to smoking exposure, and its potential presence of certain extrapulmonary manifestations. Diagnosis and monitoring are also challenged by the frequent discordance between airflow limitation and gas transfer impairment, as well as the early involvement of small airways, limiting reliance on spirometry alone. A multimodal assessment incorporating more sensitive functional techniques and CT densitometry may provide a more precise evaluation of disease burden, progression, and prognosis. Management generally follows standard COPD principles, with intravenous AAT augmentation therapy remaining currently the only established disease-modifying therapy for selected patients with severe deficiency. The advent of new pharmacological and gene-based therapies emphasizes the importance of developing personalized management strategies that integrate genotype and longitudinal disease behavior. This narrative review summarizes current evidence on AATD-associated COPD, focusing on its genetic basis and pathophysiological features, clinical and functional heterogeneity, current and emerging diagnostic and monitoring approaches, and disease-specific management considerations. Full article

Background: Diffuse alveolar haemorrhage (DAH) is a rare but potentially life-threatening pulmonary complication of systemic autoimmune diseases. Although interstitial lung disease (ILD) is a hallmark of antisynthetase syndrome (ASyS), DAH has been only exceptionally reported in this setting. Methods: We present two patients with ASyS who developed DAH confirmed by bronchoalveolar lavage. Results: The first case involved a 52-year-old woman initially diagnosed with rheumatoid arthritis, later reclassified as rheumatoid arthritis–ASyS overlap, who developed DAH in the context of progressive ILD. The second case concerned a 37-year-old man with newly diagnosed ASyS who presented with recurrent DAH early in the disease course. Both patients required high-dose corticosteroids, followed by escalation of immunosuppressive therapy with rituximab or mycophenolate mofetil, resulting in clinical and radiological improvement. These cases illustrate the diagnostic challenges posed by DAH in ASyS, particularly due to overlapping features with infection and ILD exacerbation. They also highlight the importance of early bronchoscopy and timely intensification of immunosuppression. Conclusions: Increased awareness of DAH as a rare manifestation of ASyS may facilitate earlier recognition and improve outcomes in patients presenting with acute respiratory deterioration, anaemia, or haemoptysis. Full article

Background: The introduction of targeted therapy in oncology has led to several challenges. These medicines are relatively new in clinical practice and are not well known to specialists with regard to adverse drug reactions (ADRs) and potential drug–drug interactions (pDDIs). In addition, cancer affects multiple body systems, including weight loss, anemia, liver and kidney function, depression, and pain. Patients frequently have comorbidities, leading to polypharmacy and the use of special foods, nutritional supplements, and herbal products for self-medication. Identification of pDDIs is essential, as concomitant use of multiple medicinal products increases the risk of ADRs and may compromise treatment. Objective: This study aims to retrospectively review and analyze data on ADRs and pDDIs in the treatment of non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) inhibitors and to evaluate the relationship between them. Method: EudraVigilance and UpToDate^® Lexidrug™ application were used to screen suspected ADRs and pDDIs, respectively. Descriptive statistical analysis was performed. Results: After reviewing Line Listing Reports (LLRs) from 2021 to 2023 in EudraVigilance, the number of suspected adverse drug reactions (ADRs) reported was higher when drug interactions classified as risk categories D and X were identified, compared with cases involving EGFR inhibitor monotherapy or other drug combinations. Of the 144 cases involving category D and/or X interactions, 63 demonstrated a possible association with the reported ADRs of EGFR inhibitors. The most common pDDIs detected were erlotinib–ranitidine (14 cases, category D) and osimertinib–amiodarone (13 cases, category D). Conclusions: Although EGFR inhibitors improve overall and progression-free survival in NSCLC, screening for pDDIs before treatment is essential to improve safety and quality of life. Full article

Chronic obstructive pulmonary disease (COPD) is increasingly recognized as a systemic disorder with clinically significant extrapulmonary manifestations. Among these, renal dysfunction—manifesting as chronic kidney disease (CKD) and acute kidney injury (AKI)—is highly prevalent, frequently underdiagnosed, and strongly associated with adverse clinical outcomes. Meta-analytic data indicate that COPD is associated with more than a twofold increase in CKD prevalence, independent of shared risk factors such as age, smoking, hypertension, and diabetes. CKD in COPD is associated with increased mortality, exacerbation burden, and healthcare utilization. AKI represents a particularly severe expression of renal involvement, occurring most commonly during acute exacerbations of COPD (AECOPD). Although the reported incidence of AKI during AECOPD varies widely by clinical setting—from approximately 2% in population-based studies to over 20% in hospitalized cohorts—its presence is consistently associated with marked increases in mortality, respiratory failure, need for mechanical ventilation, and hospital length of stay. This review synthesizes current evidence supporting a lung–kidney interorgan crosstalk framework in COPD, whereby chronic and acute pulmonary pathophysiology generates systemic disturbances that progressively impair renal structure and function. The heart is incorporated as a physiological intermediary, modulating hemodynamic transmission and venous congestion, without constituting the primary disease axis. Recognizing the role of kidney complications in COPD is crucial, as it influences how we diagnose, predict outcomes, and treat patients—especially when there are sudden flare-ups. Full article

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease characterized by irreversible fibrosis. Aberrant cell differentiation plays a crucial role in the development of IPF. Although recent studies have suggested that mitochondrial dysfunction may play a role in IPF, its direct impact on fibrosis remains unclear. This study aimed to clarify the role of mitochondria in lung cell differentiation and pulmonary fibrosis development by employing mito-mice ND6^M, in which the activity of respiratory chain complex I is decreased due to a mitochondrial DNA mutation (G13997A). Pulmonary fibrosis was induced by administering bleomycin (BLM) to both wild-type and mito-mice ND6^M. Bone marrow-derived macrophages and primary lung fibroblasts, generated from both types of mice, were analyzed to evaluate M1/M2 polarization and myofibroblast differentiation, respectively. Compared to wild-type mice, mito-mice ND6^M exhibited more severe fibrosis and lower survival rates following BLM inoculation. Lactate production in the lungs after BLM administration was significantly higher in mito-mice ND6^M than in wild-type mice. TGF-β1-treated fibroblasts from mito-mice ND6^M exhibited increased α-smooth muscle actin expression. While type I collagen expression was not different between these mice, TGF-β1-induced expression of phosphoserine phosphatase and serine hydroxymethyltransferase2, two of the enzymes involved in the serine–glycine pathway, was significantly higher in mito-mice ND6^M than in wild-type mice. On the other hand, mitochondrial dysfunction had a small effect on pulmonary inflammation and on M1/M2 macrophage polarization. In conclusion, mitochondrial dysfunction promotes TGF-β1-induced myofibroblast differentiation and BLM-induced pulmonary fibrosis. Mitochondria-dependent metabolic reprogramming may therefore represent a promising therapeutic target in IPF. Full article