One of the parameters potentially affecting the in vitro growth of preimplantation embryos is the oxygen concentration in the culture environment. An increased oxygen concentration causes the generation of ROS which in turn can cause damage to the cells and seriously disrupt the embryonic development. Previous studies have assessed oxygen concentrations in the fallopian tubes of several mammals of between 5 and 8%, while the oxygen levels in the uterus were found to be even lower; similar measurements have been confirmed in humans. In addition, studies in mammalian embryos showed that low oxygen concentrations improve embryo development. Multiple studies on the effect of the oxygen concentration on human embryos have been conducted so far with diverse methodologies and objectives. Data from these have been included in three meta-analyses. All meta-analyses indicate the potential benefit in favor of a low oxygen concentration, though data are considered to be of a low methodological quality and further studies are considered necessary. However, based on the existing evidence, it is suggested that a low oxygen concentration should be adopted in the routine of the IVF laboratory, especially in the case of blastocyst culture.

Sarcoidosis is a multisystem granulomatous disorder of uncertain origin which still presents major therapeutic dilemmas. Longstanding dependence on corticosteroids, while effective for acute inflammation, carries considerable adverse effects over time. Advances in deciphering sarcoidosis pathobiology—including aberrant Janus kinase (JAK)- signal transducer and activator of transcription (STAT) signaling, mechanistic target of rapamycin (mTOR)-driven metabolic shifts, Th1/Th17.1 immune skewing, effector T-cell exhaustion, and granuloma-centered cytokine circuits—have revealed several targets for intervention. The treatment options are rapidly changing: the SARCORT trial showed that low-dose prednisolone is non-inferior to higher prednisolone doses; the pivotal PREDMETH trial validated methotrexate as a feasible first-line steroid-sparing option; efzofitimod, a novel immunomodulator targeting neuropilin-2, produced steroid-reducing effects in Phase IIbut not in Phase III trials; and JAK inhibitors are accumulating evidence across cutaneous and systemic presentations. The 2025 World Association for Sarcoidosis and Other Granulomatoses (WASOG) statement supports a move toward earlier steroid-sparing approaches. This review methodically connects sarcoidosis molecular and pathophysiological mechanisms to new targeted treatments, examines clinical trial evidence, and proposes future directions toward biomarker-driven individualized care.

Obstructive sleep apnea (OSA) is a common disorder caused by recurrent upper airway obstruction during sleep, affecting individuals across the lifespan. In children, OSA commonly results from adenotonsillar hypertrophy and may resolve spontaneously or following surgical intervention. Among adolescents and adults, OSA is more frequently associated with modifiable lifestyle factors, particularly obesity. The natural history of OSA may evolve from intermittent snoring and mild disease to moderate or severe forms if left untreated, leading to reduced health-related quality of life and overall health deterioration. Early identification of OSA, especially in mild and moderate cases, allows timely interventions to improve OSA-associated indices and may prevent progression to severe disease. Continuous positive airway pressure therapy remains the treatment of choice for adults, providing effective symptom control and reducing long-term complications, although adherence rates vary. In obese patients, sustained weight reduction represents the most effective disease-modifying strategy: a ≥5% weight loss is associated with an approximately 80% reduction in progression risk, while bariatric surgery achieves remission in up to 60–65% of cases at one year. Emerging anti-obesity pharmacotherapies have also demonstrated clinically meaningful reductions in the apnea–hypopnea index. Comorbid conditions such as hypertension, type 2 diabetes, and depression exacerbate OSA severity, impair treatment response, and complicate overall disease management. This review uniquely integrates pediatric and adult longitudinal data, treatment-modified trajectories, and emerging therapeutic approaches to provide a life-course perspective on OSA natural history, highlighting opportunities for early, phenotype-directed intervention to possibly alter disease course and long-term outcomes.

The dipeptidyl peptidase (DPP) family comprises enzymes with important metabolic and immunomodulatory properties. This narrative review summarizes recent clinical and experimental evidence on the role of DPP-1, DPP-4, DPP-9, and DPP-10 in pulmonary diseases. The strongest translational evidence currently supports DPP-1 inhibition in non-cystic fibrosis bronchiectasis, where brensocatib reduces exacerbations and prolongs time to first exacerbation, with additional DPP-1 inhibitors in development. By contrast, the roles of DPP-4, DPP-9, and DPP-10 are supported mainly by preclinical studies in pulmonary hypertension, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), pulmonary fibrosis, asthma, non-small cell lung cancer (NSCLC), and nonsteroidal anti-inflammatory drugs (NSAIDs)/aspirin-exacerbated respiratory disease. Across these models, DPP inhibition modulates inflammation, protease activation, epithelial- or endothelial-to- mesenchymal transition (EMT/ EndMT), extracellular matrix (ECM) remodeling, and related signaling pathways. Overall, DPP-targeted interventions are promising in pulmonary medicine, but broader clinical translation will require well-designed prospective trials.