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Objective To investigate the value of the maximun standardized uptake value (SUVmax) in 18F-FDG PET-CT before treatment in predicting the survival outcomes of patients with indolent B-cell lymphoma (B-iNHL). Methods The clinical data were collected from 98 patients with B-iNHL diagnosed and treated in our hospital from January, 2012 to December, 2017. All the patients, including 43 with follicular lymphoma and 55 with nonfollicular lymphoma, underwent 18F-FDG PET-CT before treatment, and the correlation of SUVmax with the survival outcomes of the patients were analyzed. Results The median SUVmax was 6.8 (range 1.8-25.4) in the overall 98 patients with B-iNHL. The median SUVmax was significantly higher in patients with follicular lymphoma than those with nonfollicular lymphoma [7.8 (3.6-20.3) vs 5.3 (1.8-25.4)], P=0.001). According to the level of SUVmax, the 98 patients were divided into high SUVmax (> 7.25; n=39) group and low SUVmax (≤7.25; n=59) group, and univariate and multivariate analyses showed that a SUVmax > 7.25 was an independent risk factor that affected progression-free survival (PFS) and overall survival (OS) of the patients (P < 0.05). Compared with those with low SUVmax before treatment, the patients with high SUVmax had a significantly lower 3-year estimated PFS rate (43.8% vs 85.9%, P < 0.05) and 3-year estimated OS rate (79.0% vs 98.3%, P < 0.05). Nine patients in high SUVmax group and 1 in low SUVmax group died, showing a significant difference in the mortality rate between the two groups (9/39 vs 1/59, 23.1% vs 1.7%, P=0.001). Conclusion SUVmax in 18F-FDG PET-CT is an independent risk factor affecting PFS and OS of the patients with B-iNHL and can be used as a predictor of the survival outcomes of the patients. indolent lymphoma B cells

Sepsis is one of the most common pathogenetic causes of acute lung injury (ALI), and at present there is still a lack of effective targeted techniques and methods for its prevention and treatment. Autophagy is a homeostatic mecha- nism common to all eukaryotic cells, including adaption to environment, defense against invasion of pathogens, and maintenance of cellular homeostasis. Autophagy is also involved in a variety of lung-related diseases. In septic lung injury, autophagy not only serves to dissipate dysfunctional organelles, but also inhibits the release of inflammatory cytokines. This review aims at eliciting the role of autophagy in sepsis-induced ALI and further exploring the potential targets of autophagy in inhibiting inflammation, in an effort to provide a new perspective for clinical treatment of sepsis-induced ALI.