The largest nationwide Polish study on migraine and sleep, involving 5,311 adults, found a strong association between migraine and poorer sleep quality. Nearly two-thirds (64.1%) of people with migraine reported poor sleep, compared with 38.7% of participants without headaches. People with migraine experienced problems across all assessed aspects of sleep, including falling asleep, sleep duration and efficiency, nighttime awakenings, and daytime functioning.

Poorer sleep was also associated with a greater migraine burden, including more frequent attacks, greater disability, higher stress and anxiety, and lower quality of life. The study additionally found that people with migraine were more likely to have a later chronotype, although the relationship between chronotype and migraine severity was weak.

The findings support a bidirectional relationship between migraine and sleep disturbances and suggest that sleep assessment should be routinely included in migraine care. However, because the study was cross-sectional and relied on self-reported data, it cannot establish causality. Further longitudinal studies using objective sleep measurements are needed.

A large prospective real-world study in China has confirmed that first-line osimertinib provides substantial clinical benefit to patients with EGFR-mutated advanced non-small cell lung cancer (NSCLC), including those who would have been excluded from pivotal clinical trials.

Over nearly five decades, biomolecular simulation techniques have become indispensable tools for uncovering fundamental principles governing life at molecular scale. These computational approaches enable quantitative characterization of complex biomolecular events including protein folding, conformational dynamics and protein‑protein interactions, and have greatly advanced both fundamental and applied biological research. In recent years, the integration of machine learning, especially deep‑learning algorithms, has sparked substantial innovation within this field.

 

Glucagon-like peptide-1 (GLP-1) is secreted by intestinal L cells in response to postprandial glucose, yet how glucose triggers this secretion has remained unclear. Here, the authors show that glucose itself acts as a ligand for glucokinase (GK), independent of its metabolism. Glucose-bound GK directly interacts with and inhibits K_ATP channels, leading to membrane depolarization and GLP-1 release without any increase in intracellular ATP. This mechanism is distinct from the classical ATP-dependent model and is validated by GK mutations found in MODY2 patients. The study also reveals that SGLT1 mediates basal GLP-1 secretion at low glucose, while the GK-K_ATP axis drives the postprandial response at high glucose. These findings redefine glucose as a signaling molecule and GK as its receptor, offering new therapeutic avenues for diabetes and obesity.

 

HBsAg loss is the preferred endpoint for functional cure in chronic hepatitis B (CHB), but remains uncommon with finite treatment. Peg‑IFNα‑2b may increase HBsAg decline in selected patients, but small real‑world cohorts have limited HBsAg loss events. Binary endpoints do not capture on‑treatment qHBsAg dynamics, which are measured irregularly. This study characterised qHBsAg trajectories using LOESS in NA‑experienced patients receiving Peg‑IFNα‑2b add‑on therapy versus NAs alone.

HBV genotype C is common in East Asia and linked to cirrhosis and HCC. It features persistent replication, delayed HBeAg seroconversion, active inflammation, and high HCC risk. Key drivers include BCP A1762T/G1764A, preC G1896A, abnormal HBx, and viral integration. This review summarises the molecular features, pathogenic mechanisms, and clinical implications, and discusses genotype‑informed risk stratification.