NKX2–1, a key molecule in lung development, is highly expressed in non-small cell lung cancer (NSCLC), particularly in lung adenocarcinoma (ADK), where it is a diagnostic marker. Studies of the prognostic role of NKX2–1 in NSCLC have reported contradictory findings. Two microRNAs (miRNAs) have been associated with NKX2–1: miR-365, which targets NKX2–1; and miR-33a, which is downstream of NKX2–1. We have examined the effect of NKX2–1, miR-365 and miR-33a on survival in a cohort of early-stage NSCLC patients and in sub-groups of patients classified according to the mutational status of TP53, KRAS, and EGFR. mRNA and miRNA expression was determined using TaqMan assays in 110 early-stage NSCLC patients. TP53, KRAS, and EGFR mutations were assessed by Sanger sequencing. NKX2–1 expression was upregulated in never-smokers (P = 0.017), ADK (P < 0.0001) and patients with wild-type TP53 (P = 0.001). A negative correlation between NKX2–1 and miR-365 expression was found (ρ = −0.287; P = 0.003) but there was no correlation between NKX2–1 and miR-33a expression. Overall survival (OS) was longer in patients with high expression of NKX2–1 than in those with low expression (80.8 vs 61.2 months (P = 0.035), while a trend towards longer OS was observed in patients with low miR-365 levels (P = 0.07). The impact of NKX2–1 on OS and DFS was higher in patients with neither TP53 nor KRAS mutations. Higher expression of NKX2–1 was related to higher OS (77.6 vs 54 months; P = 0.017) and DFS (74.6 vs 57.7 months; P = 0.006) compared to low expression. The association between NKX2–1 and OS and DFS was strengthened when the analysis was limited to patients with stage I disease (P = 0.005 and P=0.003 respectively). NKX2–1 expression impacts prognosis in early-stage NSCLC patients, particularly in those with neither TP53 nor KRAS mutations.

Obstructive sleep apnoea (OSA) together with insomnia are the most common sleep disorders [1]. OSA is secondary to complete or partial airway obstruction caused by recurrent pharyngeal collapse during sleep [2], producing loud snoring or choking and frequent awakenings. This chronic sleep disturbance results in daytime sleepiness and fatigue that impedes patient’s ability to function, thereby negatively affecting his or her quality of life [3, 4]. In 2015, the American Academy of Sleep Medicine (AASM) task force released quality measures for the care of adult patients with OSA. The first quality measure outcome is to improve detection and categorisation of OSA symptoms and severity [4]. Sleep apnoea is a common disease that for accurate management requires the participation of primary care medicine

The aim of this observational, retrospective study was to describe characteristics, treatment patterns, and adherence among patients with asthma who initiated multiple-inhaler triple therapy (MITT) in Catalonia, Spain. This study used data of patients initiating MITT in 2016 from the SIDIAP (Information System for Research in Primary Care) database, which covers ~80% of the Catalonian population (5.8 million). Of 1,204 patients initiating MITT, 361 (30.0%) stepped down (discontinued ≥ 1 and continued ≥1 MITT component) and 89 (7.4%) stopped all three components of MITT for a period of 60 days during the following 12 months. In the follow-up period, 196 (16.3%) patients were considered adherent to MITT (>0.8 proportion of days covered [PDC]), with a mean (standard deviation) PDC of 0.52 (0.51) days. Given the low adherence and substantial rates of step down/discontinuation among patients initiating MITT, there is an urgent need to implement strategies to improve treatment adherence/persistence.

Background: Severe asthma exacerbations (SAEs) significantly contribute to asthma-related morbidity, mortality, and healthcare burden. Despite therapeutic advances, a subset of patients remains exacerbation-prone. This review aims to summarize current evidence on risk factors, phenotypes, and biomarkers associated with SAEs, and explore personalized strategies for their acute management. Methods: We conducted a comprehensive literature review focusing on clinical, inflammatory, and environmental drivers of SAE. Special attention was given to Type 2 (T2) biomarkers—blood eosinophil count (BEC) and fractional exhaled nitric oxide (FeNO)—as tools for phenotyping and treatment guidance. Emerging evidence on the use of biologics during exacerbations was also analyzed. Results: SAEs are heterogeneous in etiology and inflammatory profile. Respiratory infections, allergen exposure, obesity, and comorbidities increase exacerbation risk. T2-high SAEs respond well to corticosteroids and biologics, whereas T2-low SAEs show limited treatment benefit. BEC and FeNO reliably predict exacerbation risk and corticosteroid responsiveness. Recent case reports suggest potential roles for anti-IL-5 and anti-thymic stromal lymphopoietin (TSLP) biologics in acute care. Conclusions: Biomarker-guided management of SAEs may enhance therapeutic precision and avoid overtreatment. Integrating phenotypic (observable characteristics) and endotypic (biological markers) assessment into acute care could improve patient outcomes and optimize resource use. Prospective trials are needed to confirm these approaches.

Background: Proliferative changes in pulmonary hypertension can contribute to the development of idiopathic pulmonary arterial hypertension (iPAH). Energy needed to support cell proliferation may rely on aerobic glycolysis (Warburg effect). Image assessment of cell proliferation in PAH with FDG PET/CT (18F fluorodeoxyglucose positron emission tomography/computed tomography) have shown increased cellular metabolism in right ventricle (RV), while the results in pulmonary artery (PA) and pulmonary parenchyma (PP) are contradictory. In this study we evaluated the relationship between cellular metabolism in PA, RV and PP assessed with FDG PET/CT and the metabolic profile in plasma in patients with iPAH. Methods: We evaluated 12 patients with iPAH who underwent PET/CT scanning and 18F-FDG uptake (SUV) in predefined regions of interest were correlated with clinical and hemodynamic parameters, as well as with levels of plasma metabolites. as well as with levels of plasma metabolites assessed by quantitative targeted metabolomic studies using liquid chromatography (LC) coupled to mass spectrometry. Results: The RV SUV correlated with pro-BNP, 6MWD and cardiac index. Patients with iPAH had increased levels of isoleucine, 15-Hydroxyeicosatetraenoic acid (15-HETE), Glutamic acid and diacylglycerol 36:3 (DG 36:1) among other metabolites that were correlated with FDG uptake in FDG PET/CT (Table 1) Conclusions: In iPAH, the intensity of FDG uptake in pulmonary arteries, right ventricle, and lung parenchyma is associated with systemic parameters that reflect increased cell metabolism. Overall, our findings support the notion of increased cell proliferation in iPAH.