Size-specific clonidine-loaded liposomes: Advancing melanoma microenvironment suppression with safety and precision.

The immunosuppressive tumor microenvironment (TME) plays a crucial role in the progression and treatment resistance of melanoma. Modulating the TME is thus a key strategy for enhancing therapeutic outcomes. Previousstudies have identified clonidine (CLD), an α2-adrenergic receptor agonist, as a promising agent that enhances T lymphocyte infiltration and reduces myeloid-derived suppressor cells within the TME, thereby promoting antitumor immune responses.

The Roles of T cells in Immune Checkpoint Inhibitor-Induced Arthritis.

Immune checkpoint inhibitor (ICI) therapy, a novel anti-tumor strategy, can specifically eliminate tumors by activating the immune system and inhibiting tumor immune escape. However, ICI therapy can lead to notable negative outcomes known as immune-related adverse events (irAEs). ICI-induced arthritis, also known as ICI arthritis, stands as the prevailing form of irAEs.

Cavitation-on-a-Chip Enabled Size-Specific Liposomal Drugs for Selective Pharmacokinetics and Pharmacodynamics.

The size of liposomal drugs has been demonstrated to strongly correlate with their pharmacokinetics and pharmacodynamics. While the microfluidic method successfully achieves the production of liposomes with well-controlled sizes across various buffer/lipid flow rate ratio (FRR) settings, any adjustments to the FRR inevitably influence the concentration, encapsulation efficiency (EE), and stability of liposomal drugs. Here we describe a controllable cavitation-on-a-chip (CCC) strategy that facilitates the precise regulation of liposomal drug size at any desired FRR.

Mimicking Tumor Metastasis Using a Transwell-Integrated Organoids-On-a-Chip Platform.

The mortality rate among cancer patients is primarily attributed to tumor metastasis. The evaluation of metastasis potential provides a powerful framework for personalized therapies. However, little work has so far been undertaken to precisely model tumor metastasis in vitro, hindering the development of preventive and therapeutic interventions.

Association of multiple air pollutants with oxygen saturation during sleep in COPD patients: Effect modification by smoking status and airway inflammatory phenotypes.

Air pollution contributes substantially to the development of chronic obstructive pulmonary disease (COPD). To date, the effect of air pollution on oxygen saturation (SpO) during sleep and potential susceptibility factors remain unknown. In this longitudinal panel study, real-time SpO was monitored in 132 COPD patients, with 270 nights (1615 h) of sleep SpO recorded.