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Objective To establish an evaluation method of uncertainty for the determination of lead in ambient air PM2.5 by inductively coupled plasma mass spectrometry (ICP-MS). Methods According to HJ657-2013 “Determination of Lead and Other Metal Elements in Air and Exhaust Particulates by Inductively Coupled Plasma Mass Spectrometry”, the concentration of lead in ambient air PM2.5 was determined. A mathematical model was established to analyze the source of uncertainty and to calculate each component of uncertainty. The components were combined into the standard uncertainty, and the relative expanded uncertainty was finally obtained. Results The expanded uncertainty of lead in ambient air PM2.5 was 0.16 ng/m3, and the measurement result of lead was (1.75±0.16)ng/m3. Conclusion The main source of uncertainty of this method comes from the relative standard uncertainty introduced by sample pretreatment.
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Objective@#To explore the pathways of preeclampsia by investigating different effects of pravastatin (Pra) on and soluble FMS tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF) and vascular endothelial growth factor (VEGF) in different preeclampsia (PE)-like mouse models.@*Methods@#C57BL/6J mice were randomly subcutaneously injected with N-nitro-L-arginine methyl ester (L-NAME) or intraperitoneally injected with lipopolysaccharide (LPS) as PE-like mouse model, saline as normal pregnancy control (Con) respectively, daily at gestational 7-18 days. Pra was given daily at gestational 8-18 days in each model group and the mice were divided into Pra (L-NAME+Pra, LPS+Pra, Con+Pra) and saline (L-NAME+NS, LPS+NS, Con+NS) groups. Liver,placental tissue and blood of pregnant mice were collected on the 18th day of pregnancy. The levels of VEGF, PlGF and sFlt-1 in the liver, placenta and serum of mice in each group were compared by western blot, ELISA and real-time fluorescence quantitative PCR (RT-PCR).@*Results@#(1) ELISA: Serum VEGF (205.70±3.43, 154.60±2.31) and PlGF (131.5±3.75, 101.50±4.31) levels were significantly increased in L-NAME+Pra group compared with L-NAME+NS group (all P<0.05). Serum VEGF (202.30±4.90, 144.50±6.71) and PlGF (121.50±3.86, 95.41±4.08) levels were significantly higher in LPS+Pra group than those in LPS+NS group (all P<0.05). Serum sFlt-1 level in LPS+Pra group was significantly lower than that in LPS+NS group (3.01±0.50, 776.60±80.06), serum sFlt-1 level in L-NAME+Pra group was significantly lower than that in L-NAME+NS group (2.60±0.06, 583.70±9.83; all P<0.05). (2) Western blot: the expression levels of PlGF (1.344±0.118, 0.664±0.143) and VEGF (1.34±0.12, 0.66±0.14) in the liver of mice in the L-NAME+Pra group were significantly higher than those in the L-NAME+NS group (all P<0.05), but the expression levels of PlGF and VEGF in the placenta of L-NAME+Pra group were not significantly different from those of L-NAME+NS group (all P>0.05). The expression levels of PlGF and VEGF in placenta and liver of pregnant mice in LPS+Pra group were not significantly different from those in LPS+N group (all P>0.05). (3) RT-PCR: the mRNA expression of PlGF and VEGF in placenta and liver of L-NAME+Pra group were not significantly different from those in L-NAME+NS group (all P>0.05). The mRNA expression levels of PlGF and VEGF in placenta and liver of LPS+Pra group were not significantly different from those of LPS+NS group (all P>0.05).@*Conclusions@#Pra has different regulatory effects on vascular endothelial function in different PE-like models. It reveals that different pathogenesis and pathways exist in different PE-like changes.
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Objective To explore the pathways of preeclampsia by investigating different effects of pravastatin (Pra) on and soluble FMS tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF) and vascular endothelial growth factor (VEGF) in different preeclampsia (PE)?like mouse models. Methods C57BL/6J mice were randomly subcutaneously injected with N?nitro?L?arginine methyl ester (L?NAME) or intraperitoneally injected with lipopolysaccharide (LPS) as PE?like mouse model, saline as normal pregnancy control (Con) respectively, daily at gestational 7-18 days. Pra was given daily at gestational 8-18 days in each model group and the mice were divided into Pra (L?NAME+Pra, LPS+Pra, Con+Pra) and saline (L?NAME+NS, LPS+NS, Con+NS) groups. Liver,placental tissue and blood of pregnant mice were collected on the 18th day of pregnancy. The levels of VEGF, PlGF and sFlt?1 in the liver, placenta and serum of mice in each group were compared by western blot, ELISA and real?time fluorescence quantitative PCR (RT-PCR). Results (1) ELISA: Serum VEGF (205.70±3.43, 154.60±2.31) and PlGF (131.5±3.75, 101.50± 4.31) levels were significantly increased in L?NAME+Pra group compared with L?NAME+NS group (all P<0.05). Serum VEGF (202.30 ± 4.90, 144.50 ± 6.71) and PlGF (121.50 ± 3.86, 95.41 ± 4.08) levels were significantly higher in LPS+Pra group than those in LPS+NS group (all P<0.05). Serum sFlt?1 level in LPS+Pra group was significantly lower than that in LPS+NS group (3.01±0.50, 776.60±80.06), serum sFlt?1 level in L?NAME+Pra group was significantly lower than that in L?NAME+NS group (2.60±0.06, 583.70±9.83;all P<0.05). (2) Western blot: the expression levels of PlGF (1.344±0.118, 0.664±0.143) and VEGF (1.34±0.12, 0.66 ± 0.14) in the liver of mice in the L?NAME+Pra group were significantly higher than those in the L?NAME+NS group (all P<0.05), but the expression levels of PlGF and VEGF in the placenta of L?NAME+Pra group were not significantly different from those of L?NAME+NS group (all P>0.05). The expression levels of PlGF and VEGF in placenta and liver of pregnant mice in LPS+Pra group were not significantly different from those in LPS+N group (all P>0.05). (3) RT?PCR: the mRNA expression of PlGF and VEGF in placenta and liver of L?NAME+Pra group were not significantly different from those in L?NAME+NS group (all P>0.05). The mRNA expression levels of PlGF and VEGF in placenta and liver of LPS+Pra group were not significantly different from those of LPS+NS group (all P>0.05). Conclusions Pra has different regulatory effects on vascular endothelial function in different PE?like models. It reveals that different pathogenesis and pathways exist in different PE?like changes.
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Objective To investigate the modulation of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD)expression by pravastatin in pre-eclampsia-like mouse model. Methods C57BL/6J mice were randomly injected with N-nitro-L-arginine methyl ester (L-NAME) as pre-eclampsia-like model group (PE) or saline as normal pregnancy control group(Con)respectively,from gestational the 7th to 18th day.For each group,pravastatin(PE+Pra,Con+Pra group)or saline(PE+N,Con+N Group)was given from the 8th to 18th day of gestation,respectively.Liver and placenta of pregnant mice were collected on gestational day 18.The LCHAD protein expression and mRNA levels of liver and placenta were detected through western blot, immunohistochemistry and real-time quantitative PCR. Results (1) The average arterial pressure of pregnant mice increased gradually from the 8th to 18th day in PE+N group,but decreased in PE+Pra group from gestational 10th day, 24 hour urinary protein levels in PE+N group [(1 494 ± 201) μg] were significantly higher than that in Con+N group[(935±128)μg,P<0.01],and also higher than that in PE+Pra group [(981 ± 116) μg, P<0.01].(2) The results of western blot: the expression of LCHAD was significantly lower in PE+N group(liver:0.64±0.11,placenta:0.48±0.06)than that in Con+N group(liver:1.06±0.10, placenta:0.60±0.10),and lower than that in PE+Pra group(liver: 0.99±0.04,placenta:0.60±0.08;all P<0.01).(3)The results of real-time quantitative PCR:the levels of LCHAD mRNA in liver and placenta in PE+N group (liver: 0.621 ± 0.128, placenta: 0.646 ± 0.129) were significantly decreased compared with Con+N group (liver: 1.007 ± 0.130, placenta: 1.004 ± 0.103; all P<0.01), but there was no significant difference between PE+Pra group (liver: 0.693 ± 0.678, placenta: 0.662 ± 0.183;P>0.05). (4) LCHAD protein was expressed widely and evenly in liver.The expression in placental cytotrophoblast and syncytial trophoblast cells located in outer layer of villous in labyrinth layer was the most. The expression of LCHAD was significantly lower in PE+N group(liver: 0.062±0.016,placenta:0.147±0.018)than that in Con+N group (liver: 0.126 ± 0.013, placenta: 0.183 ± 0.024), and lower than that in PE+Pra group (liver: 0.111 ± 0.017, placenta: 0.174 ± 0.027; all P<0.05). Conclusion Pravastatin could upregulate the LCHAD protein expression of liver and placenta in the pre-eclampsia-like mouse,which may be a mechanism to improve the clinical manifestations of pre-eclampsia.