The Global Initiative for Asthma (GINA) Strategy Report provides a comprehensive, annually updated evidence-based approach to asthma diagnosis, assessment, treatment, and prevention across the lifespan. Its central approach is personalized, iterative care based on the Assess-Adjust-Review cycle for both symptom control and reduction of future risk (including severe exacerbations, persistent airflow limitation, and treatment-related harm). GINA emphasizes objective confirmation of diagnosis wherever possible, and regular assessment of lung function, inhaler technique, adherence, multimorbidity, risk factors (including Type-2 biomarkers), and patient goals and preferences. GINA strongly recommends that all adults, adolescents, children and most preschoolers with asthma should receive inhaled corticosteroid (ICS)-containing treatment. GINA recommends against short-acting beta2-agonist (SABA)-only treatment. For adults/adolescents, GINA Track 1 using low-dose ICS-formoterol, an anti-inflammatory reliever (AIR), either as-needed-only (AIR-only) or as maintenance-and-reliever therapy (MART), is preferred because of its substantial reduction in severe exacerbations compared with SABA-based regimens, and its simplicity. Age-specific treatment pathways in children also emphasize ICS-containing therapy and exacerbation prevention. For difficult-to-treat and severe asthma, GINA provides structured guidance, emphasizing diagnostic verification, optimization of modifiable factors, inflammatory phenotyping, biologic therapy selection, and (as for all patients) systemic corticosteroid stewardship. Acute exacerbation care incorporates long-term preventive treatment, including post-discharge reassessment of management and action plan. Key 2026 updates include expanded AIR options for adults and children, revised guidance on severe asthma and selection of biologic treatment, and substantial updates to acute asthma management. GINA integrates evidence-based management with shared decision-making, self-management education, implementation, and global advocacy to reduce preventable asthma morbidity and mortality.

While short-acting beta-agonists have been a mainstay of therapy during acute asthma exacerbations and for patients with intermittent asthma, there is increasing evidence that the use of combination inhalers, containing both an inhaled corticosteroid and a fast-acting bronchodilator, lead to improvement in symptom control, reduction in severe asthma exacerbations, and increased adherence to medications. These combination inhalers may be used in the form of stand-alone anti-inflammatory reliever therapy or as single maintenance and reliever therapy.

Persistent hypereosinophilia may be overlooked during stroke evaluation when conventional vascular risks coexist. We report the case of a man in his late 50s who had hypertension, type 2 diabetes, continued active smoking, and eight clinically apparent magnetic resonance imaging-confirmed strokes in multiple bilateral territories over 29 months. Before systemic glucocorticoid exposure, absolute eosinophil counts ranged from 1.87 to 3.23 × 10[9]/L on repeated measurements. Bone marrow morphology and flow cytometry revealed eosinophil expansion without aberrancy, and common tested clonal drivers were negative. Transthoracic echocardiography, two 24-h Holter recordings, and a bubble study identified no intracardiac source. Aortic computed tomography angiography in April 2026 demonstrated thoracic aortic atherosclerosis with calcified plaques and focal ulceration; transesophageal echocardiography and prolonged rhythm monitoring were not performed. A new left pontine infarct occurred in April 2026 while he was on oral prednisone (20 mg/day). In August 2026, after systemic glucocorticoid withdrawal despite continued inhaled budesonide/formoterol, a new right temporal infarct occurred, with an absolute eosinophil count of 2.66 × 10[9]/L. Worsening wheeze suggested possible eosinophilic airway inflammation; however, emphysema alone did not explain systemic eosinophilia, and eosinophilic granulomatosis with polyangiitis remained unproven. The available evidence favored a multifactorial interpretation; eosinophilia provides biological plausibility, whereas conventional vascular risks and an incompletely characterized thoracic aortic abnormality remain competing explanations. Persistent eosinophilia should prompt repeated etiological reassessment without inferring causality based on blood count or imaging pattern alone.

The delayed nonmatch to position (DNMTP) task is an instrumental learning paradigm applied to assess higher executive functions including attention and working memory in rats. In this study, the effect of systemic challenge with the acute inflammatory stimulus [lipopolysaccharide (LPS) 0.25 mg/kg, intraperitoneally] was assessed in Wistar rats on performance in the DNMTP task. By means of validation, the effect of treatment with the muscarinic receptor antagonist scopolamine [0.02 mg/kg, subcutaneously (s.c.)], known to disrupt performance in the task, and its reversal by coadministration of the cognitive-enhancing agent and acetylcholinesterase inhibitor donepezil (0.3 mg/kg, s.c.) were confirmed. Sex differences emerged between males' and females' mnemonic response to LPS 24-h postadministration with males showing reduced performance in the DNMTP task at higher working memory loads compared with females. Noradrenaline is an endogenous neurotransmitter with innate anti-inflammatory properties. The impact of targeting the noradrenergic system with the β2-adrenoceptor agonist Formoterol was further assessed on LPS-induced cognitive impairment in the DNMTP task. Coadministration of Formoterol (0.5 mg/kg, s.c.) attenuated LPS-driven mnemonic impairments in males but not females. Overall, the results show the DNMTP task is a paradigm sensitive to acute systemic inflammation and indicate that Formoterol may have useful anti-inflammatory properties in mitigating inflammatory-associated cognitive impairment.