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Sepsis is associated with the highest risk of progression to acute lung injury or acute respiratory distress syndrome. Shen-Fu has been advocated to treat many severely ill patients. Our study was designed to investigate the effect of Shen-Fu on endotoxin-induced acute lung injury in vivo. Adult male Wistar rats were randomly divided into 6 groups: controls; those challenged with endotoxin (5 mg/kg) and treated with saline; those challenged with endotoxin (5 mg/kg) and treated with Shen-Fu (1 mg/kg); those challenged with endotoxin (5 mg/kg) and treated with Shen-Fu (10 mg/kg); increase challenged with endotoxin (5 mg/kg) and treated with Shen-Fu (100 mg/kg); saline injected and treated with Shen-Fu (100 mg/kg). TNF-α, IL-6, and NF-kappa B were investigated in the lung two hours later. Myeloperoxidase (MPO) activity and wet/dry weight ratio were investigated six hours later. Intravenous administration of endotoxin provoked significant lung injury, which was characterized by increment increase of MPO activity and wet/dry lung weight ratio, and TNF-α and IL-6 expression and NF-kappa B activation. Shen-Fu (10,100 mg/kg) decreased MPO activity and wet/dry weight ratio and inhibited TNF-α and IL-6 production, endotoxin-induced NF-kappa B activation. Our results indicated that Shen-Fu at a dose of higher than 10 mg/kg inhibited endotoxin-induced pulmonary inflammation in vivo.

Accurate and automated lung segmentation in high-resolution computed tomography (HRCT) is highly challenged by the presence of pathologies affecting lung parenchyma appearance and borders.

The algorithm presented employs an anatomical model-driven approach and systematic incremental knowledge acquisition to produce coarse lung delineation, used as initialization for the graph-cut algorithm. The proposed method is evaluated on a 49 HRCT cases dataset including various lung disease patterns. The accuracy of the method is assessed using dice similarity coefficient (DSC) and shape differentiation metrics (d_mean, d_rms), by comparing the outputs of automatic lung segmentations and manual ones.

The proposed automatic method demonstrates high segmentation accuracy (DSC = 96.64%, d_mean = 1.75 mm, d_rms = 3.27 mm) with low variation that depends on the lung disease pattern. It also presents good improvement over the initial lung segmentation (ΔDSC = 4.74%, Δd_mean = -3.67 mm, Δd_rms = -6.25 mm), including impressive amelioration (maximum values of ΔDSC = 58.22% and Δd_mean = -78.66 mm) when the anatomy-driven algorithm reaches its limit.

Segmentation evaluation shows that the method can accurately segment lungs even in the presence of disease patterns, with some limitations in the apices and bases of lungs. Therefore, the developed automatic segmentation method is a good candidate for the first stage of a computer-aided diagnosis system for diffuse lung diseases.

Many ultrafine particles comprised classically of low-toxicity, low-solubility materials such as carbon black and titanium dioxide have been found to have greater toxicity than larger, respirable particles made of the same material. The basis of the increased toxicity of the ultrafine form is not well understood and a programme of research has been carried out in Edinburgh on the toxicology of ultrafines aimed at understanding the mechanism. We used fine and ultrafine carbon black, TiO₂ and latex and showed that there was an approximately 10-fold increase in inflammation with the same mass of ultrafine compared with fine particles. Using latex particles in three sizes—64, 202 and 535 nm—revealed that the smallest particles (64 nm) were profoundly inflammogenic but that the 202 and 535 nm particles had much less activity, suggesting that the cut-off for ultrafine toxicity lies somewhere between 64 and 202 nm. Increased oxidative activity of the ultrafine particle surface was shown using the fluorescent molecule dichlorofluorescein confirming that oxidative stress is a likely process by which the ultrafines have their effects. However, studies with transition-metal chelators and soluble extracts showed that the oxidative stress of ultrafine carbon black is not necessarily due to transition metals. Changes in intracellular Ca²⁺ levels in macrophage-like cells after ultrafine particle exposure suggested one way by which ultrafines might have their pro-inflammogenic effects.