Investigation of rare chronic lipoid pneumonia associated with occupational exposure to paraffin aerosol.

OBJECTIVES: Occupational exposure to paraffin is an infrequent cause of lipoid pneumonia (LP) and related data are scare. We investigated the possible relationship between three rare cases of chronic LP and occupational exposure to paraffin aerosol in an iron foundry. METHODS: The three cases of LP and their workplaces were investigated using data from field investigations, air monitoring, pulmonary radiological examinations, cell staining, and lung biopsies. RESULTS: The patients had long-term occupational exposure to paraffin. X-ray diffraction testing revealed that the raw material from the workshop was paraffin crystal. The air concentrations of paraffin aerosol in workplaces were significantly higher than outdoor background levels. Small diffuse and miliary shadows with unclear edges were observed throughout the whole lungs via radiography. Computed tomography revealed diffuse punctate nodules and a high density of stripe-like shadows in both lungs (ground-glass opacity in a lower lobe, and a mass-like lesion and high translucent area near the bottom of the lung). Lipid-laden macrophages were found in the sputum and bronchial lavage. A broadened alveolar septum and local focal fibrosis were also discovered via lung biopsy. The inflammatory reaction in the lung tissues appeared to resolve over time. CONCLUSIONS: These three rare cases of chronic LP in workers during molding and repair processes were associated with occupational paraffin aerosol exposure. Therefore, primary prevention is essential for molding or repairing workers in the iron foundry, and a differential diagnosis of occupational chronic LP (vs. pneumoconiosis) should be considered when treating these workers.

Panax notoginseng saponins protect kidney from diabetes by up-regulating silent information regulator 1 and activating antioxidant proteins in rats.

OBJECTIVE: To explore the mechanism of the protective effects of Panax notoginseng saponins (PNS) on kidney in diabetic rats. METHODS: Diabetic rat model was obtained by intravenous injection of alloxan, and the rats were divided into model, PNS-100 mg/(kg day) and PNS-200 mg/(kg day) groups, 10 each. Another 10 rats injected with saline were served as control. Periodic acid-Schiff staining and immunological histological chemistry were used to observe histomorphology and tissue expression of bone morphogenetic protein-7 (BMP-7). Silent information regulator 1 (SIRT1) was silenced in rat mesangial cells by RNA interference. The mRNA expressions of SIRT-1, monocyte chemoattractant protein-1 (MCP-1), transforming growth factor ß1 (TGF-ß1) and plasminogen activator inhibitor-1 (PAI-1) were analyzed by reverse transcription polymerase chain reaction. The protein expressions of SIRT1 and the acetylation of nuclear factor κB (NF-κB) P65 were determined by western blotting. The concentration of MCP-1, TGF-ß1 and malondialdehyde (MDA) in culture supernatant were detected by enzyme-linked immuno sorbent assay. The activity of superoxide dismutase (SOD) was detected by the classical method of nitrogen and blue four. RESULTS: In diabetic model rats, PNS could not only reduce blood glucose and lipid (P<0.01), but also increase protein level of BMP-7 and inhibit PAI-1 expression for suppressing fibrosis of the kidney. In rat mesangial cells, PNS could up-regulate the expression of SIRT1 (P<0.01) and in turn suppress the transcription of TGF-ß1 (P<0.05) and MCP-1 (P<0.05). PNS could also reverse the increased acetylation of NF-κB p65 by high glucose. In addition, redox regulation factor MDA was down-regulated (P<0.05) and SOD was up-regulated (P<0.01), which were both induced by SIRT1 up-regulation. CONCLUSIONS: PNS could protect kidney from diabetes with the possible mechanism of up-regulating SIRT1, therefore inhibiting inflammation through decreasing the induction of inflammatory cytokines and TGF-ß1, as well as activating antioxidant proteins.