RESUMEN
Based on the NOx emission information of 671 coal-fired power units, the NOx emission characteristics of non-ultra-low-emission (non-ULE) and ultra-low-emission (ULE) coal-fired power units during the start-up process were compared and analyzed. The results showed that in the start-up stage of non-ULE units, the exceeding standard rate (ESR) of NOx emission concentration was 81.53%, the average exceeding standard hours (ESHs) was 2.64 h, and the average maximum emission hourly mean concentration (MEHC) was 284.06 mg·m-3. The NOx ESR of ULE units was 79.86%, the average ESHs was 2.52 h, and the average MEHC was 231.61 mg·m-3. There was no significant difference in the ESR and the average ESHs between non-ULE and ULE units, but the difference in the average MEHC was significant. There was no significant difference in the ESR, average ESHs, and average MEHC between different grades of non-ULE units, except that the average MEHC of 300 MW units was significantly lower than that of 200 MW units. There was statistical difference in the ESR, average ESHs, and average MEHC among different grades of ULE units, and 600 MW units performed best in the ESHs control, whereas 1000 MW units performed best in the emission concentration control.
RESUMEN
The present study aimed to investigate the effect of tanshinone II, isolated from Salvia miltiorrhiza Bunge, on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Male Sprague-Dawley rats were divided into three groups: Control, LPS and tanshinone II. Animals in the tanshinone II and LPS groups were administered 10 mg/kg LPS, whereas those in the control group received an equal volume of normal saline. Tanshinone II treatment group were injected with 30 nm/kg tanshinone II at 1 h after LPS administration. The results revealed that LPS administration increased the bronchoalveolar lavage fluid protein concentration significantly compared with the control group. However, tanshinone II treatment significantly inhibited the LPS-induced increase in protein level. Treatment of the LPS-administered rats with tanshinone II prevented the formation of pulmonary edema, which was evidenced by low values for wet to dry lung weight ratio. The activity of myeloperoxidase and expression of malondialdehyde were significantly lower in lung homogenates from the tanshinone II group compared with the LPS group. Furthermore, tanshinone II treatment inhibited the expression of tumor necrosis factor-α and interleukin-6 in the blood plasma. Tissue sections of the tanshinone II group exhibited normal morphology and absence of neutrophil accumulation. However, in the LPS group, neutrophils accumulated and penetrated into the pulmonary tissues. These results suggested that tanshinone II protects the rats from LPS-induced ALI. Therefore tanshinone II may have clinical applications in the treatment of ALI.