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

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.

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.

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 observe effects of the antisense genes of Toll-like receptor 4 (TLR4 ) and myeloid differentiation protein-2 (MD2) on the activation of NF-?B in alveolar typeⅡepithelial cells (ATⅡcells) induced by lipopolysaccharide (LPS). Methods Cultured ATⅡcells were randomized to normal cells (control) group,LPS group,LPS+empty vector group,LPS+TLR4 antisense gene group,LPS+MD2 antisense gene group,LPS+TLR4-MD2 antisense gene group. The expressions of TLR4 and MD2 mRNA and protein in ATⅡcells were detected by Northern blotting and Western blotting respectively. The activity of NF-?B in ATⅡcells was measured with electrophoretic mobility shift assay (EMSA). The TNF-? and IL-6 concentrations in the supernatant of cultured ATⅡcells were tested with ELISA.Results Compared with control groups,the expressions of TLR4 and MD2 mRNA and protein,the NF-?? activity,the levels of TNF-? and IL-6 were increased remarkably in LPS group and LPS+empty vector group (P

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.

Objective To explore the effects of polyclonal antibody to lipopolysaccharide binding protein (pLBPab) on IL 10 and IL 18 mRNA expressions of alveolar macrophages in lipopolysaccharide LPS induced acute lung injury in rats. Methods A total of 40 male Wistar rats were randomly divided into 5 groups: normal control (A), LPS treated group (B), group of pLBPab preconditioning at 30 min before injection of LPS (C), group of treatment with LPS and pLBPab (D), and group of pLBPab preconditioning at 30 min after injection of LPS (E). mRNA expressions of IL 10 and IL 18 in the alveolar macrophages in each group were measured by semi quantitative reverse transcription polymerase chain reaction (RT PCR). Results The IL 10 and IL 18 mRNA expressions were highly increased respectively in the alveolar macrophage (AM?) stimulated with single LPS, but they were significantly decreased in the AM? after stimulation with LPS + pLBPab, particularly stimulation with pLBPab 30 min before LPS injection. Conclusion pLBPab can decrease the mRNA expressions such as IL 10 and IL 18 by alveolar macrophages in acute lung injury in rats induced by LPS, and LBP antibody could be used to cure some diseases such as SIRS, acute lung injury, ARDS, and septic syndrome.