Objective The genetic toxicity of copper was studied in Hemiculter leucisculus erythrocytes to find the sensitive fishes for mutagens. Methods Cu2+ was used as the mutagen and H. leucisculus as the testee. 120 H. leucisculus were randomly divided into 8 groups, treated with Cu2+ at the concentration of 0.01, 0.02, 0.04, 0.08, 0.16, 0.32, 0.64 and 1.28 mg/L respectively. Results Compared with the control, the frequency of micronuclei and nuclear abnormalities of erythrocytes in the Cu2+ treated groups significantly increased (P

Objective To explore the roles of bacterial infection in the pathogenesis and progression of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Methods The clinical data of 604 patients with ALI or ARDS hospitalized from April 1991 to March 2001 were analyzed. Results (1) The cause of direct lung injury was predominantly ascribed to lung infection, whereas indirect lung injury was due to sepsis. (2) The gram positive cocci (50.76%) and gram negative bacilli (40.15%) in the isolated pathogenic bacteria from patients were approximately similar. Furthermore, Staphylococcus aureus and Pseudomonas aeruginosa were the first and second pathogenic bacteria, respectively. (3) The incidences of ALI and ARDS in infected patients significantly increased with the grade elevation of systemic inflammatory response syndrome (SIRS) ( P

Objective To investigate changes in glucocorticoid receptor (GR) expression and activity in lung tissue of acute lung injury induced by lipopolysaccharide (LPS) within 24h in rat. Methods A total of 70 Wistar rats were divided randomly into LPS treatment group and LPS+ Dexamethasone (Dex) treatment group. The GR mRNA and GR protein expressions in the lung tissue of LPS challenged rats were assessed by RT-PCR and Western blot at different time points. Electrophoretic mobility shift assays (EMSA) were used to determine the GR activity in the lung tissue. Results The expression level of GR mRNA was depressed, but it returned to normal level at 24h after LPS challenge. The expression level of GR was also lowered, reaching the lowest level at 8h. GR activity was decreased, reaching the lowest level at 1h, and remaining lower than that of normal control at 24h. Dex treatment showed no obvious effect on GR activity during the late period of treatment. Conclusion The GR protein expression decreases in lung tissue of acute lung injury in rats, and it maybe associated with the decreased expression of mRNA and accelerated degradation of GR protein. The activity of GR is inhibited sharply, resulting in glucocorticoid resistance.

To investigate the interleukin 10 (IL 10) content in plasma in rats with acute lung injury(ALI) induced by oleic acid (OA) and lipopolysaccharide(LPS). OA (0.2ml/kg) and LPS (2mg/kg) was given to Wister rats to produce ALI. The respirtory rate,PaO 2 , wet weight/dry weight (W/D) of the lung, and pathological changes were observed, and IL 10 was determined with enzyme linked immunosorbent assay (ELISA). The results showed that ALI was produced in rats with OA+LPS, and there was a significant increase in IL 10 content in plasma in rats, especially in OA+LPS/4h group. The above results suggested that OA+LPS might produce ALI in rats, and the development of ALI was related to an obvious increase of the IL 10 content in plasma.

To investigate the interleukin 13(IL 13) content in plasma in rats with acute lung injury (ALI) induced by lipopolysaccharide (LPS), Wistar rats were given increasing doses of LPS (2mg/kg,4mg/kg,6mg/kg,8mg/kg) to produce ALI. The respirtory rate,PaO 2 ,wet weight/dry weight (W/D) of the lung, and pathological changes in the lung were observed. ELISA was used to determine plasma IL 13. It was found that: (1)ALI could be produced in rats with LPS, but ARDS occurred only when the dose of LPS reached 6mg/kg. or larger. (2)LPS produced an elevation of the content of IL 13 in plasma in rats, peaking when the dose of LPS reaching 6mg/kg or over. These results suggested that LPS might induce ALI in rats, and ARDS could be produced when the dose of LPS reached ≥6mg/kg. (3)The high increase in plasma IL 13 content might play an important role in producing ARDS induced by LPS.

AIM: To research clinical effect of curing patients with CHF(congestive heart failure) with Metoprolol and Shexiang Baoxing Pills(SBP). METHODS: 156 CHF patients were divided into three groups,including M(Metoprolol),SBP and M-SBP at random.The first dosage of Metoprolol was specified by the heart function,taking SBP 3 times per day and 2 pieces once,totally 8 weeks.Observeing Plasma Cyclic Nucleotide(Cyclic Adenosine monophosphate and Cyclic Guanosine Monophosphate),Norepinephrine(NE),Atrial Natriuretic Peptide(ANP) and Heart Ejection Fraction(EF),Cardiac Output(CO),heart and chest proportion,Before and after the curing. RESULTS: The curing effect of M-HMP group obviously surpasses simply M group and HMP group. CONCLUSION: Curing CFH patients by metoprolol assistant with SBP is better method.

Objective To evaluate the clinical value of spectral CT mode in imaging liver by comparing the radiation dose and image quality between spectral CT and conventional multi-slice spiral CT (MSCT).Methods Thirty patients (group A) underwent three-phasic enhanced CT scans spectral CT mode in the portal phase (PP) and conventional helical mode in other phases (Discovery CT 750 HD,GE Healthcare).Another 30 patients in group B underwent conventional three-phasic enhanced CT on a 64-slice MSCT (VCT,GE Healthcare) with 120 kVp and automatic tube current modulation (ATCM) and noise index of 15.The images in PP from the two imaging modes were retrospectively compared.The contrast-noiseratio (CNR) for the veins was calculated using liver parenchyma as background.For the spectral CT mode,101 sets of monochromatic images were reconstructed from 40 to 140 keV,and the optimal energy level for obtaining the highest CNR was determined using the Gemstone Spectral Imaging (GSI)-viewer software.Image noise (at 70 keV),CNR (at the optimal keV level) for the vein and radiation dose to the patient were obtained for spectral images and statistically compared with those in group B with the conventional MSCT using t test.Results The CTDIw value in PP for spectral CT was 15.64 mGy,30％lower than the (22.44 ± 5.09) mGy for the conventional MSCT (t =29.56,P ＜ 0.01).Image noises on the liver parenchyma were 22.81 ±2.85 and 23.80 ±3.31 for the conventional MDCT and spectral CT images at 70 keV,respectively,with no significant difference (t =0.76,P ＞ 0.05).On the other hand,CNR for the vein at the optimal energy level in spectral CT was 7.17 ± 2.09,which was significantly higher than the 2.76 ± 1.34 for the conventional MSCT (t =7.21,P ＜ 0.01).Conclusion Compared with conventional standard-dose liver MSCT,spectral CT imaging provides improved CNR for vessels,comparable image noise for liver parenchyma with 30％ dose reduction.

AIM: To establish the model of systemic inflammatory response syndrome (SIRS)/acute lung injury (ALI) by LPS administration in rats and to measure the content of interleukin-10 massage RNA(IL-10 mRNA) and activator protein-1 (AP-1) activity in order to investigate the anti-inflammatory mechanism.METHODS: Wistar rats were injured with increased dose of LPS to set up the SIRS/ALI model. Reverse transcriptase-polymerase chain reaction(RT-PCR) and electrophoretic mobility shift assays (EMSAs) were used to measure IL-10 mRNA content and the AP-1 binding activity in rat lung, respectively.RESULTS: ①LPS could be applied to simulate SIRS-ALI in rats.②Acute respiratory distress syndrome (ARDS) could be induced under condition of LPS≥6 mg/kg, which was similar to that of the excessive expression of SIRS. ③ LPS may cause the increase content of IL-10 mRNA and AP-1 activity in lung in rat. ④Content of IL-10 mRNA and AP-1 activity were increased significantly under LPS≥6 mg/kg. CONCLUSIONS: ①LPS≥6 mg/kg might cause the SIRS/acute lung injury in rats.②The rats with excessive SIRS/acute lung injury had an obvious increase of transcription of IL-10 gene and upregulated AP-1. ③ Intensified anti-inflammatory mechanism plays a pathological role in SIRS/acute lung injury.

Objective To study the effect of hypoxia on the expression of interleukin 6 (IL 6) in cocultured pulmonary arterial smooth muscle cells (PASMC) Methods Rat PASMC were cocultured with rat lung microvascular endothelial cells, and randomly divided into 5 groups: normal group (N), 2 h hypoxia (H2), 6 h hypoxia (H6), 12 h hypoxia (H12), and 24 h hypoxia (H24) The expression level of IL 6 mRNA in PASMC was detected with RT PCR, and the activity of IL 6 in the supernatant with radioimmunoassay Results The expression level of IL 6 mRNA increased in PASMC in H2, reached the highest in H6, and decreased in H12, but still higher than that of N The changes of the IL 6 activity in the supernatant as well as IL 6 mRNA expression in the cells were in a time dependent manner Conclusion Hypoxia can enhance the expression of IL 6 in cocultured PASMC And it may activate others genes which regulate the hypoxic response of PASMC and signal transduction

Objective To investigate the changes of plasma interleukin 4 (IL 4) in rats with acute lung injury (ALI) induced by lipopolysaccharide (LPS) and to explore the relationship between IL 4 and ALI. Methods A total of 120 Wistar rats were randomly divided into 2, 4, 6, and 8 mg/kg groups according to different doses of LPS administration at each observing time point. A control group (NS), receiving saline injection, was also employed. The indexes of respiratory rate, PaO 2, wet weight/dry weight (W/D) of lung lobes, and pathological changes were observed at 1, 2, 4, and 6 h after injury. The plasma IL 4 content was detected by enzyme linked immunosorbant assay. Results ① Various degrees of ALI in rats were induced by different doses of LPS. Acute respiratory distress syndrome (ARDS) was induced under the condition of LPS ≥6 mg/kg. ② LPS could induce increased plasma IL 4 in rats. The peak value of plasma IL 4 in rats increased significantly under the condition of LPS ≥6 mg/kg. Conclusion ① ALI model can be duplicated by injection of LPS. ② LPS ≥6 mg/kg is the critical dosage for ARDS in rats. ③ The obvious increase of plasma IL 4 may be associated with the occurrence of ALI/ARDS.