Benefits and challenges of cervical cancer screening since the implementation of the 'two cancer' screening programme in China: findings from Shangyu, Zhejiang in 2019-23.

Background: Cervical cancer is the fourth most common cancer in women worldwide. The World Health Organization has long targeted its elimination and stressed the need for enhanced screening coverage and improved treatment rates. The Chinese government initiated the 'two cancer' screening programme for cervical and breast cancer in 2009 for women aged 35-64 years, which Shangyu fully implemented in 2017.

Inhibition of cathepsin L ameliorates inflammation through the A20/NF-κB pathway in endotoxin-induced acute lung injury.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe inflammatory condition that remains refractory; however, its molecular mechanisms are largely unknown. Previous studies have shown numerous compounds containing 4-indolyl-2-aminopyrimidine that display strong anti-inflammatory properties. In our research, we identified that a 4-Indole-2-Arylaminopyrimidine derivative named "IAAP" suppressed lipopolysaccharide (LPS)-induced inflammation.

TGF-β signaling promotes eosinophil activation in inflammatory responses.

Eosinophils, traditionally associated with allergic phenomena, play a pivotal role in inflammatory responses. Despite accumulating evidence suggesting their pro-inflammatory function upon activation, the underlying mechanisms governing eosinophil activation remain incompletely characterized. In this study, we investigate the local activation of pulmonary and colon eosinophils within the inflammatory microenvironment.

Macrophage Extracellular Traps Suppress Particulate Matter-Induced Airway Inflammation.

Accumulating evidence has substantiated the potential of ambient particulate matter (PM) to elicit detrimental health consequences in the respiratory system, notably airway inflammation. Macrophages, a pivotal component of the innate immune system, assume a crucial function in responding to exogenous agents. However, the roles and detailed mechanisms in regulating PM-induced airway inflammation remain unclear.