OBJECTIVE To explore the risk factors of lung infection in eldly paitents with hip fracture(≥80 years).METHODS A total of 119 cases of hip fracture treating with surgery from Jan 2004 to Jan 2007 were analyzed retrospectively.RESULTS There were 36 cases of hospital lung infection(infection rate of 30.25%) and 7 death cases(19.44%).It was found that senior age,invasive operation,abuse of antibiotics and previous history involved were the main factors causing hospital lung infection.CONCLUSIONS The effective measures to reduce hospital lung infection among elderly patients with hip fracture include environment management and infection monitoring,strictly hand-washing,cross-infection prevention,rational antibiotics usage and active treatment of underlying diseases.

Silicosis is a leading cause of occupational disease-related morbidity and mortality worldwide, but the molecular basis underlying its development remains unclear. An accumulating body of evidence supports gasdermin D (GSDMD)-mediated pyroptosis as a key component in the development of various pulmonary diseases. However, there is little experimental evidence connecting silicosis and GSDMD-driven pyroptosis. In this work, we investigated the role of GSDMD-mediated pyroptosis in silicosis. Single-cell RNA sequencing of healthy and silicosis human and murine lung tissues indicated that GSDMD-induced pyroptosis in macrophages was relevant to silicosis progression. Through microscopy we then observed morphological alterations of pyroptosis in macrophages treated with silica. Measurement of interleukin-1β release, lactic dehydrogenase activity, and real-time propidium iodide staining further revealed that silica induced pyroptosis of macrophages. Additionally, we verified that both canonical (caspase-1-mediated) and non-canonical (caspase-4/5/11-mediated) signaling pathways mediated silica-induced pyroptosis activation, in vivo and in vitro. Notably, Gsdmd knockout mice exhibited dramatically alleviated silicosis phenotypes, which highlighted the pivotal role of pyroptosis in this disease. Taken together, our results demonstrated that macrophages underwent GSDMD-dependent pyroptosis in silicosis and inhibition of this process could serve as a viable clinical strategy for mitigating silicosis.