Objective To discuss the effects of pressure control (PC) and positive end-expiratory pressure (PEEP) incremental method lung recruitment maneuver (RM) on haemodynamics in piglets with acute lung injury (ALI) induced by paraquat (PQ) poisoning. Methods The ALI/acute respiratory distress syndrome (ARDS) model was reproduced by intraperitoneal injection of 20% PQ (20 mL) in 10 healthy female piglets, and they were randomly divided into PC lung RM group (RM1 group) and PEEP incremental method lung RM group (RM2 group), with 5 piglets in each group. Heart rate (HR), mean arterial pressure (MAP), and cardiac index (CI) were monitored by pulse-indicated continuous cardiac output (PiCCO) monitoring before model reproduction (baseline), on the time of successfully set up of model and at 5, 15 and 30 minutes after RM. At the same time the arterial partial pressure of oxygen (PaO2) and arterial partial pressure of carbon dioxide (PaCO2) were recorded, and oxygenation index was calculated. Lung tissues were collected before model reproduction, on the time of successfully set up of model, and at 30 minutes after RM respectively, and pulmonary pathology changes were observed after hematoxylin and eosin (HE) staining under light microscopy. Results The HR, MAP, and PaCO2 on the time of successfully set up of model in both groups were increased obviously while CI, PaO2, and oxygenation index were decreased obviously as compared with those at baseline, all of which conformed to the expression of ALI/ARDS. With RM time extended, the HR in both groups was declined while MAP and CI were increased gradually. The HR and MAP at 5 minutes after RM of RM1 group were significantly lower than those of the RM2 group [HR (bpm): 126.8±5.2 vs. 134.0±3.8, MAP (mmHg, 1 mmHg = 0.133 kPa): 98.4±3.3 vs. 102.8±2.6, both P < 0.05]. The CI at 5 minutes and 15 minutes after RM of RM1 group was significantly higher than that of the RM2 group (mL·s-1·m-2: 56.7±5.0 vs. 46.7±6.7, 65.0±5.0 vs. 56.7±5.0, both P < 0.05). PaO2 and oxygenation index at 5 minutes after RM in both groups were significantly higher than those on the time of sucessfully set up of model. The PaO2 and oxygenation index were gradually decreased, and PaCO2 was increased with RM time extended, but no statistically significant differences at all time points were found between the two groups (all P > 0.05). The lung tissue in both groups showed a variety of pathological changes at 30 minutes after RM. The main performances were the loss of alveolar epithelial cells, the further wideness of alveolar interval and the distension of alveolar, and the part breakage of alveolar interval. The wideness of alveolar interval was more significant in RM2 group than that of RM1 group, and alveolar cleft was more common too. Conclusion Both PC and PEEP incremental method lung RM can improve the oxygenation of the piglets with ALI/ARDS induced by PQ, and the PC lung RM has less impact on haemodynamics.

Objective To explore the effects of estrogen on oxidative stress of the lung tissue induced by acute paraquat (PQ) poisoning. Methods Thirty-two male adult New Zealand rabbits were randomly divided into model group and estrogen intervention group, 16 rabbits in each group. The model of lung injury induced by PQ poisoning was reproduced by feeding 16 mg/kg of 20% PQ through gastric tube. The rabbits in estrogen intervention group received intravenous infusion of 5 mg/kg estrogen after PQ challenge for 7 days, and the rabbits in model group received an equal volume of normal saline. Three rabbits in each group were sacrificed at 1, 2 and 3 days respectively after exposure. The lung tissue was harvested, the levels of reactive oxygen species (ROS) was determined by 2',7'-dichlorofluorescin diacetate (DCFH-DA), malondialdehyde (MDA) was determined by thiobarbituric acid (TBA), the mRNA expression of manganese-containing superoxide dismutase (MnSOD) was determined by reverse transcription-polymerase chain reaction (RT-PCR), and adenosine triphosphatase (ATP) content in mitochondrion was determined by enzyme linked immunosorbent assay (ELISA). The pathological changes in lung were observed under light microscopy using hematoxylin and eosin (HE) staining, and the lung injury was evaluated with lung injury score. Results The contents of ROS and MDA in lung within 3 days after PQ poisoning were gradually increased, and MnSOD mRNA expression and ATP content were gradually decreased. Estrogen intervention could significantly reduce the production of ROS and MDA after PQ poisoning [3-day ROS (fluorescence intensity): 161.05±30.04 vs. 188.30±31.80, 3-day MDA (mmol/L): 98.71±0.92 vs. 122.12±1.24], up-regulate MnSOD mRNA expression (integral A value: 3.05±0.90 vs. 1.22±0.24), and increase ATP content in mitochondrion (ng/L: 3.75±0.92 vs. 2.28±0.29) with statistically significant differences (all P < 0.01). In lung tissue after PQ poisoning, congestion, edema, focal pulmonary consolidation, pulmonary interstitial and alveolar space were infiltrated by a large number of neutrophil, alveolar interval were thickened obviously and the above phenomenon were most serious at 3 days after poisoning as shown under optical microscope. Estrogen intervention could significantly improve lung injury as compared with that of model group, and the lung injury score at 3 days was significantly lower than that of model group (11.8±0.7 vs. 13.5±1.0, P < 0.01). Conclusions The oxidative stress indicators in the lung tissue after PQ poisoning were obviously abnormal, the pathological damage was serious with time dependence. The administration of estrogen can reduce acute lung injury after PQ poisoning by reducing the oxidative stress.

Objective To explore the expression of discoidin domain receptor 1 (DDR1) in rats with pulmonary fibrosis induced by paraquat (PQ) poisoning, and its relationship with the expression of transforming growth factor-β1 (TGF-β1). Methods 120 Sprague-Dawley (SD) rats were divided into control group and 20, 40, and 80 mg/kg PQ poisoning groups (each n = 30). Pulmonary fibrosis induced by PQ poisoning model was reproduced by one time administration of 20, 40, 80 mg/kg of 20% PQ, and the rats in control group were given 4 mL normal saline. Fifteen rats in control and different doses of PQ groups were sacrificed at 7 days and 21 days after intragastric administration, and lung tissues were collected. Pulmonary fibrosis was observed after hematoxylin-eosin (HE) staining. The immune-histochemical method was used to determine the expressions of DDR1 and TGF-β1. The relationship between the expression of TGF-β1 and DDR1 was analyzed by Pearson correlation analysis. Results The rats in control group were active, and no pathological changes in lung tissue were found. The rats in PQ groups became shortness of breath, bristles, and slow reaction etc. 0.5 hours after intragastric administration. After 7 days, the lung tissue was dark red, hard texture, appearance of yellow soil fiber nodules and obsolete hemorrhage, destruction of alveolar structure. The extent of lung injury increased gradually with the time of poisoning and the increase of PQ dose. It was shown by immune-histochemical staining that the control group had only a small amount of DDR1 and TGF-β1 positive expressions; in PQ groups, there were a large number of DDR1 and TGF-β1 positive expression particles in the alveolar wall, pulmonary interstitial and alveolar cavity. It was displayed by quantitative analysis that compared with the control group, DDR1 and TGF-β1 expressions were significantly increased in 20, 40, 80 mg/kg PQ groups with time- and dose-dependent [DDR1 (integral A value): 0.221±0.014, 0.249±0.021, 0.364±0.016 vs. 0.121±0.036 at 7 days; 0.247±0.025, 0.321±0.015, 0.432±0.027 vs. 0.139±0.021 at 21 days; TGF-β1 (integral A value): 0.230±0.016, 0.265±0.015, 0.339±0.016 vs. 0.129±0.032 at 7 days; 0.248±0.011, 0.295±0.016, 0.399±0.026 vs. 0.119±0.026 at 21 days; all P < 0.05]. It was shown by Pearson correlation analysis that DDR1 expression was positively correlated with TGF-β1 expression with the increase of PQ dose and poisoning time (DDR1 with TGF-β1: r = 0.996, P < 0.000; DDR1 with PQ dose: r = 0.985, P < 0.000; DDR1 with poisoning time: r = 0.989, P < 0.000; TGF-β1 with PQ dose: r = 0.992, P < 0.000; TGF-β1 with poisoning time: r = 0.972, P < 0.000). Conclusions The expression of DDR1 in the lung tissue in PQ poisoning rats showed a time- and dose-dependent change, and it was positively correlated with TGF-β1 expression. DDR1 may be involved in the process of pulmonary fibrosis induced by PQ poisoning.

Objective To approach the effects of full Marathon on striated muscle and renal function of Marathon amateurs without complaints. Methods A prospective self-paired design study was conducted. The amateurs without body discomfort, hematuria, brown urine, or persistent muscle pain within 1 week after the 2012 Xiamen International Marathon Race were enrolled voluntarily. The peripheral blood and random urine specimens of all subjects under static status 1 week before the race and after the race instantly (within 10 minutes after finishing the race) were collected to detect markers of renal function and striated muscle injury. Results Sixty-one subjects were included in the final analysis of the study with full Marathon of 42.195 km and mean race time of (297.05± 55.60) minutes. Compared with those under static status before the race, the markers of renal function including the levels of urinary N-acetyl-beta-D-glucusamidase [NAG (U/L): 64.00 (54.50, 85.50) vs. 9.50 (8.10, 11.50)], urinary β2-microspheres protein [β2-MG (μg/L): 261.00 (128.50, 1 608.00) vs. 66.60 (33.75, 123.00)], random urinary creatinine [UCr (μmol/L): 19 066.56±10 938.31 vs. 5 872.52±4 363.20] and serum creatinine [SCr (μmol/L): 129.97±25.84 vs. 97.39±14.51] immediately after the race were significantly increased (all P < 0.01); the markers of muscle injury including the levels of serum creatine kinase [CK (U/L): 864.00 (504.00, 1 644.00) vs. 164.00 (128.00, 256.00)], lactic dehydrogenase [LDH (U/L): 383.26±141.69 vs. 182.23±41.12], myoglobin [Mb (mg/L): 1 880.00 (1 080.00, 3 300.00) vs. 42.00 (36.00, 54.50)], alanine aminotransferase [ALT (U/L): 27.0 (19.5, 38.0) vs. 24.0 (15.0, 29.5)] and aspartate transaminase [AST (U/L): 52.07±25.13 vs. 28.28±11.86] were also significantly increased (all P < 0.01), and the increase in CK, Mb, and LDH were more significant. It was shown by correlation analysis that CK after race was negatively correlated with age (r = -0.352, P = 0.005) and body mass index (r = -0.271, P = 0.035), and it was positively correlated with racing time (r = 0.387, P = 0.002) and urinary β2-MG after the race instantly (r = 0.364, P = 0.004). Mb after race was negatively correlated with body mass index (r = -0.331, P = 0.009), and it was positively correlated with urinary β2-MG after the race instantly (r = 0.315, P = 0.013). LDH after race was negatively correlated with age (r = -0.275, P = 0.032) and body mass index (r = -0.377, P = 0.003), and it was positively correlated with urinary β2-MG after the race instantly (r = 0.424, P = 0.001). Conclusion Full Marathon could significantly impact striated muscle and renal function of Marathon amateurs without complaints.

Objective To investigate the protective effect of autophagy inducer rapamycin on acute kidney injury (AKI) induced by sepsis. Methods Twenty-four Sprague-Dawley (SD) male rats were randomly divided into sham group, caecal ligation and puncture (CLP) model group, and rapamycin treatment group (Rap treatment group), with 8 rats in each group. The septic AKI model was reproduced by CLP in rats, and rats in sham group were given appendix isolation without ligation and puncture. The rats in Rap treatment group were given 1.6 mg rapamycin by intraperitoneal injection immediately after model reproduction, and the rats in CLP model group were injected with an equal amount of normal saline. The rats in all groups were sacrificed after collecting peripheral blood specimen at 24 hours after model reproduction, and the levels of blood urea nitrogen (BUN) and serum creatinine (SCr) were determined. The pathomorphology change in renal tissue was observed under light microscope after periodic acid Schiff (PAS) staining. Real-time polymerase chain reaction (real-time PCR, RT-PCR) was used to determine the mRNA expressions of renal tubular autophagy related molecules Atg-5 and Beclin-1. Western Blot was used to detect the expressions of renal tubular autophagy associated protein microtubule labeled protein 1 light chain 3-Ⅱ (LC3-Ⅱ) and Beclin-1 as well as apoptosis protein cytochrome C (Cyt C), Bax and Bcl-2. TdT-mediated dUTP nick-end labeling (TUNEL) assay was used to determine the renal tubular epithelial cell apoptosis. Results Rapamycin could alleviate pathomorphology changes in rats with septic AKI, and decrease the levels of BUN and SCr. Compared with sham group, the expressions of Atg-5, Beclin-1 and LC3-Ⅱ in CLP model group were significantly increased [Atg-5 mRNA (2-ΔΔCt): 2.34±0.04 vs. 1.00±0.03, Beclin-1 mRNA (2-ΔΔCt): 1.40±0.02 vs. 1.00±0.03, LC3-Ⅱ protein (gray value): 0.82±0.03 vs. 0.45±0.04, Beclin-1 protein (gray value): 0.59±0.06 vs. 0.29±0.03, all P < 0.01]. Rapamycin could further up-regulate the expressions of Atg-5, Beclin-1, and LC3 Ⅱ [Atg-5 mRNA (2-ΔΔCt): 3.28±0.19 vs. 2.34±0.04, Beclin-1 mRNA (2-ΔΔCt): 2.38±0.08 vs. 1.40±0.02, LC3-Ⅱ protein (gray value): 1.11±0.07 vs. 0.82±0.03, Beclin-1 protein (gray value): 0.85±0.05 vs. 0.59±0.06, all P < 0.01]. Compared with sham group, the apoptotic cells in CLP model group were increased significantly [(34.49±10.45)% vs. (2.78±1.40)%, P < 0.01], Cyt C and Bax protein expressions were significantly up-regulated (gray value: 0.87±0.02 vs. 0.46±0.03, 1.20±0.06 vs. 0.46±0.01, both P < 0.01), and Bcl-2 expression was significantly down-regulated (gray value: 0.64±0.02 vs. 1.33±0.09, P < 0.01). Rapamycin could effectively inhibit cell apoptosis [(15.44±5.50)% vs. (34.49±10.45)%, P < 0.01] and the protein expressions of Cyt C and Bax (gray value: 0.72±0.03 vs. 0.87±0.02, 0.84±0.03 vs. 1.20±0.06, both P < 0.01), and up-regulate the protein expression of Bcl-2 (gray value: 0.77±0.04 vs. 0.64±0.02, P < 0.01). Conclusion The protective effect of rapamycin on renal tissue of rat with AKI induced by sepsis was depended on cell apoptosis inhibition through inducing and promoting cell autophagy.

Objective To evaluate the prognostic value of urine paraquat (PQ) concentrations combined with poisoning time and creatinine clearance rate (CCr) on prognosis of patients with acute paraquat poisoning (APP). Methods A retrospective case control study was conducted. Clinical data of 96 patients with APP admitted to Department of Emergency of Shengjing Hospital of China Medical University from March 2014 to May 2016 were analyzed. The gender, age, body weight, urine PQ concentrations (determined by semi-quantitative colorimetric method), poisoning time (time from oral poison to urine detection) and CCr of patients were collected, and poisoning index (poisoning index = urine PQ concentrations × poisoning time/CCr) and simplified poisoning index (simplified poisoning index = urine PQ concentrations × poisoning time) were calculated. The patients were divided into death group and survival group according to 2-month outcome after poisoned with clinical data and telephone follow-up. The urine PQ concentrations, poisoning index, and simplified poisoning index between the two groups were compared. Binary classification logistic regression was used to analyze the risk factors affecting prognosis. Receiver-operating characteristic curve (ROC) and diagnostic test were used to analyze the prognostic value of the parameters. Results Compared with survival group, the urine PQ concentrations [mg/L: 30.00 (10.00, 100.00) vs. 10.00 (3.00, 10.00)], poisoning index [mg·h-1·μmol-1: 12.72 (1.86, 33.75) vs. 0.56 (0.18, 1.12)], and simplified poisoning index [mg·h-1·L-1: 600.00 (150.00, 1 000.00) vs. 60.00 (18.00, 120.00)] in death group were significantly increased (all P < 0.01). It was shown by logistic regression analysis that both urine PQ concentrations [odds ratio (OR) = 1.046, 95% confidence interval (95%CI) = 1.006-1.087, P = 0.022] and poisoning index (OR = 1.353, 95%CI = 0.029-1.815, P = 0.031) were independent risk factors affecting the prognosis of patients with APP. It was shown by ROC curve and diagnostic test that the poisoning index had greater area under ROC curve (AUC was 0.902) for evaluating the prognosis of patients with APP. When the best cut-off value was greater than 1.23 mg·h-1·μmol-1, the sensitivity was 90.91%, and the specificity was 73.08%. The AUC of urine PQ concentrations for evaluating the prognosis was 0.759. When the best cut-off value was greater than 20.00 mg/L, the sensitivity was 63.64%, and the specificity was 76.92%. The AUC of simplified poisoning index for evaluating the prognosis was 0.846. When the best cut-off value was greater than 135.00 mg·h-1·L-1, the sensitivity was 81.82%, and the specificity was 76.92%. Conclusion The poisoning index calculated with urine PQ concentrations combined with poisoning time and CCr has prognostic value for prognosis of APP patients, and the prognostic value of poisoning index is greater than that of the urine PQ concentrations alone.

Objective To study the liver protection of crocetin against paraquat (PQ) poisoning induced acute liver injury in rats. Methods Fifty-four male Wistar rats were randomly divided into control group, exposure group and treatment group, and the rats in each group were subdivided into the 0.5th, 2nd, and 6th day after exposure subgroups (n = 6). The model of acute liver failure induced by PQ poisoning was reproduced by intraperitoneal injection of 20 mg/kg of 20% PQ, and the rats in control group was injected with the same amount of normal saline. The rats in treatment group were given with intraperitoneal injection of 50 mg/kg crocetin after 0.5 day, once a day until they were sacrificed; the other two groups were injected with the same amount of normal saline. The rats in all groups were sacrificed at the corresponding time points, and blood was collected from inferior vena cava and hepatic tissue was harvested. Hematoxylin and eosin (HE) staining was used to observe the pathological changes in liver tissue on the 6th day under light microscope. Enzyme linked immunosorbent assay (ELISA) was used to detect the serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA expressions of inducible nitric oxide synthase (iNOS) and nuclear factor-κB (NF-κB). The activities of apoptosis related factors, including caspase-8, -9, -12, in hepatic tissue were determined on the 6th day with chromogenic substrate method. Results In the liver tissue of exposed group, extensive infiltration of the inflammatory cells and the diffuse fragments necrosis were visible, and the regeneration of the liver cells was not obvious, and severity of the injury in a time dependent way. In the treatment group, the structure of hepatic artery was visible, and the infiltration of necrosis, congestion and inflammatory cells were not obvious. On the 0.5th, 2nd, and 6th day, serum levels of IL-6 and TNF-α, the mRNA expressions of iNOS and NF-κB in liver tissue, and the caspase-8, -9, -12 activities on the 6th day in the exposure group and treatment group were significantly higher than those in the control group. And the parameters in treatment group were significantly lower than those of the exposure group [IL-6 (ng/L): 188.37±64.21 vs. 376.61±82.42 on the 0.5th day, 287.18±58.69 vs. 432.77±96.28 on the 2nd day, 234.24±10.17 vs. 375.41±37.59 on the 6th day; TNF-α (ng/L): 472.36±76.43 vs. 688.33±102.19 on the 0.5th day, 189.32±87.54 vs. 296.21±89.77 on the 2nd day, 99.28±16.13 vs. 168.41±66.78 on the 6th day; iNOS mRNA (gray value): 2.998±0.801 vs. 3.453±0.026 on the 0.5th day, 3.126±0.306 vs. 5.259±0.153 on the 2nd day, 0.841±0.135 vs. 1.225±0.057 on the 6th day; NF-κB mRNA (gray value): 1.569±0.818 vs. 2.361±0.063 on the 0.5th day, 2.345±0.489 vs. 4.668±0.368 on the 2nd day, 2.348±0.316 vs. 3.972±0.449 on the 6th day; caspase-8 (pmol/mg): 126.77±9.97 vs. 199.18±66.48 on the 6th day; caspase-9 (pmol/mg): 213.12±69.06 vs. 321.62±89.39 on the 6th day; caspase-12 (pmol/mg): 183.46±70.52 vs. 219.68±53.93 on the 6th day, all P < 0.05]. Conclusion Crocetin has protective effect on liver in rats with PQ poisoning, which role is related with reducing the blood level of inflammatory factors, inhibiting the hepatic caspase-8, -9, -12 activities and gene expressions of iNOS and NF-κB.

Objective To assess the clinical value of systemic vascular resistance index (SVRI) combined with serum procalcitonin (PCT) and sequential organ failure assessment (SOFA) score in the early diagnosis of sepsis. Methods A retrospective study was conducted. The data of critical patients admitted to Department of Critical Care Medicine of the Third People's Hospital of Hechi from November 2013 to April 2016 were enrolled. The clinical data were recorded as follows: gender, age, infection site, SOFA score, serum PCT level (enzyme linked fluorescence analysis) within 1 hour after intensive care unit (ICU) admission, hemodynamics parameters, including mean arterial pressure (MAP), central venous pressure (CVP), cardiac index (CI), SVRI, global end diastolic volume index (GEDVI), extravascular lung water index (EVLWI), which were monitored by pulse indicator continuous cardiac output (PiCCO) after ICU admission. The patients were divided into sepsis and non-sepsis groups according to the diagnostic criteria of sepsis. Septic patients were divided into low SVRI group, normal SVRI group, and high SVRI group according to SVRI normal value (170-240 kPa·s·L-1·m-2), and the differences in parameters among the three groups were compared. The correlations between SVRI and various parameters were analyzed by using Pearson correlation analysis. The receiver operating characteristic curve (ROC) was plotted to evaluate the diagnostic efficiency of each parameter. Results Totally 103 critical patients were enrolled, 55 in sepsis group, and 48 in non-sepsis group. Compared with non-sepsis group, SVRI in septic group was significantly lowered (kPa·s·L-1·m-2: 146.56±45.17 vs. 188.04±56.27), and serum PCT was significantly increased (μg/L: 10.43±6.17比0.32±0.11) with statistically significant differences (both P < 0.05). In 55 sepsis patients, there were 21 in low SVRI group, 19 in normal SVRI group, and 15 in high SVRI group. There were no statistically significant differences in gender, age and infection site among the three groups, indicating that the baseline data among all groups was balanced with comparability. SOFA score, PCT, and CI in the low SVRI group were significantly higher than those of normal SVRI and high SVRI groups [SOFA: 10.57±2.89 vs. 5.73±2.28, 5.73±2.15, PCT (μg/L): 24.15±12.43 vs. 7.18±5.05, 7.39±4.38, CI (mL·s-1·m-2): 71.01±9.67 vs. 62.01±8.34, 62.51±8.67, all P < 0.05], but no significant difference was found between the normal SVRI group and high SVRI group. There was no statistically significant difference in MAP, CVP, EVLWI, and GEDVI among the three groups. It was shown by Pearson correlation analysis that SVRI was negatively correlated with PCT, SOFA score, and CI (r value was -0.622, -0.598, -0.398, all P = 0.000). It was shown by ROC curve that area under ROC curve (AUC) of PCT combined with SVRI for diagnosis of sepsis was higher than that of PCT or SVRI alone (0.943 vs. 0.911, 0.884). When the cut-off value of PCT was 3.79 μg/L, and cut-off value of SVRI was 156.81 kPa·s·L-1·m-2, the sensitivity and specificity were 94.6% and 92.3% respectively. Conclusions For sepsis patients, SVRI is related to PCT and SOFA score. Combined monitoring of PCT, SVRI, SOFA score can accurately reflect the severity of sepsis patients, guide diagnosis and treatment, and estimate prognosis. The efficacy of PCT combined with SVRI in the early diagnosis of sepsis is better than that of the two alone.

Objective To study the influence of Qingzao Runfei Huazhuo Xingxue decoction on pulmonary tissue and lung function in mouse model of lung injury induced by PM2.5, and to provide an idea of clinical prevention and treatment of respiratory diseases induced by PM2.5. Methods Totally 30 clean level male ICR mice were randomly divided into three groups: normal control group, model group and Qingzao Runfei Huazhuo Xingxue decoction intervention group, with 10 mice in each group. Model of PM2.5-induced respiratory disease in mice was reproduced by instilling nasal cavity drip PM2.5 suspension 40 mg/kg once a day for 6 weeks. In the treatment group, the mice were fed with the Qingzao Runfei Huazhuo Xingxue decoction twice a day from the 4th week of instilling PM2.5 suspension until the end of experiment. In the normal control group, the mice were fed as usual. At the end of the experiment, the total protein content in bronchoalveolar lavage fluid (BALF), and lung wet/dry weight (W/D) ratio was determined. Hematoxylin-eosin (HE) staining was used to observe the histopathological changes in lung tissue under light microscope. The inflammatory mediators levels in lung tissue were determined by antibody-sandwich enzyme linked immunosorbent assay (ELISA). Results Respiratory system damage model was successfully reproduced by dripping of PM2.5 suspension in nasal cavity. Compared with normal control group, inflammatory changes and inflammatory cell infiltration in model group were significant, and lung W/D ratio (4.71±0.33 vs. 3.13±0.12), total protein content in BALF (mg/L: 363.98±18.24 vs. 82.13±12.78), tumor necrosis factor-α [TNF-α (ng/L): 185.72±0.23 vs. 31.03±0.16], interleukin-8 [IL-8 (ng/L): 531.85±37.83 vs. 72.64±16.72], and leukotriene B4 [LTB4 (ng/L): 931.74±48.64 vs. 483.81±41.74] in lung tissue were significantly increased (all P < 0.05). Compared with the model group, the inflammatory changes of lung tissue in Qingzao Runfei Huazhuo Xingxue decoction intervention group were significantly reduced, lung W/D ratio (3.92±0.41 vs. 4.71±0.33), total protein content in BALF (mg/L: 213.21±19.62 vs. 363.98±18.24), TNF-α (ng/L: 124.15±0.27 vs. 185.72±0.23), IL-8 (ng/L: 238.42±35.82 vs. 531.85±37.83) and LTB4 (ng/L: 582.85±31.00 vs. 931.74±48.64) levels in lung tissue in Qingzao Runfei Huazhuo Xingxue decoction intervention group were significantly decreased (all P < 0.05). Conclusion Qingzao Runfei Huazhuo Xingxue decoction can improve PM2.5-induced damage and pathological inflammatory changes in lung tissue, which provided some new ideas for the treatment of PM2.5-induced respiratory diseases.

Objective To explore early prognostic value of quantitative detection of paraquat (PQ) plasma concentration and urine sodium dithionite assay for prognosis in patients with acute PQ poisoning. Methods A prospective study was conducted. The patients with acute PQ poisoning admitted to Department of Emergency of First Hospital of China Medical University from August 2013 to December 2015 were enrolled. At admission, blood samples and urine samples were collected. The PQ plasma concentration was determined by high-performance liquid chromatography (HPLC), and the PQ urine concentration was determined by sodium dithionite, meanwhile the biochemical parameters were determined to carry out sequential organ failure assessment (SOFA) score. According to the prognosis of 90-day follow-up, the patients were divided into survival group and death group. Logistic regression analysis was used to analyze the relationship between the prognosis and the indexes, and the receiver operating characteristic curve (ROC) was drawn to evaluate the prognosis. Results There were 148 patients with acute PQ poisoning, with 43 alive and 105 dead, and the 90-day mortality rate was 70.9%. The ingestion volume (mL: 22.69±18.57 vs. 9.91±4.61), plasma concentration of PQ (mg/L: 2.28±1.52 vs. 0.91±0.38) and positive rate of urine sodium dithionite (87.6% vs. 14.0%) in death group were significantly higher than those of survived group (all P < 0.01), but no significant differences in gender, age, poisoning time, gastric lavage time between the two groups were found. Significant differences in white blood cell count [WBC (×109/L): 13.45±6.12 vs. 23.03±7.67] and blood lactate [Lac (mmol/L): 1.50±0.45 vs. 8.10±4.51] between survival group and death group were found (both P < 0.01), while no significant difference in SOFA score was found (0.98±0.72 vs. 1.34±1.29, P > 0.05). It was shown by logistic regression analysis that the key factors affecting the prognosis of patients with PQ poisoning were urine sodium dithionite assay [odds ratio (OR) = 8.731, 95% confidence interval (95%CI) = 2.828-26.954, P = 0.000], PQ plasma concentration (OR = 2.082, 95%CI = 1.204-3.603, P = 0.009) and ingestion volume (OR = 1.175, 95%CI = 1.048-1.318, P = 0.006) respectively. It was shown by ROC curve that the area under ROC curve (AUC) of plasma PQ concentration, urine sodium dithionite assay, poisoning dose and SOFA score for predicting the prognosis in patients with acute PQ poisoning was 0.866, 0.857, 0.826, and 0.631 respectively (all P < 0.05). The sensitivity of urine sodium dithionite assay for predicting the prognosis was 87.6%, and the specificity was 83.7%. Conclusions Early plasma PQ concentrations can objectively reflect the body absorbed toxicant doses and actual situation after poisoning, and help to judge the early evaluation of prognosis. The accuracy of urine sodium dithionite assay in judging the prognosis of PQ poisoning is high. Because of its simplicity and availability, it was easier to be performed in the primary hospital.