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

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.

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

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 establish a glucocorticoid receptor knockdown model of human macrophage cell line U937 with RNA interference technique. Methods Two RNAi recombinant plasmids (named pSilencer 3.1-GR 1 and pSilencer 3.1-GR 2) targeting to GR gene were constructed. After RNAi recombinant plasmids were transfected into human macrophage cell line U937, the expressions of GR mRNA and GR protein were evaluated with RT-PCR and Western blotting respectively. The transcriptional activation function of GR was evaluated through the detection of relative luciferase activity after dexamethasone treatment. Results Two RNAi recombinant expression plamids were constructed and identified by sequencing. pSilencer 3.1-GR 2 transfection could inhibit not only GR mRNA and protein expressions, but also transcriptional activation function of GR specially; pSilencer 3.1-GR 1 transfection had no significant changes as compared to normal control. Conclusion A glucocorticoid receptor knockdown model has been established successfully, which offers a new method for the further research of GR biological functions.

Objective To investigate the effects of nitric oxide donor (SNP) on glucocorticoid receptor function in condition of cell inflammation. Methods After fluorescence expression plasmid pGFP-GR transfected rat alveolar macrophges (AMs), nuclear translocation of GFP-GR following to lipopolysaccharide (LPS) and SNP treatment was observed through fluorescence microscope. The transcriptional activation activity of GR was evaluated by the method of relative activity of luciferase. Electrophoretic mobility shift assays (EMSA) were used to measure the activity of NF-?B. Results GFP-GR showed nuclear translocation in 2 h after nitric oxide donor (500 ?mol/L SNP) treatment, and the transcriptional activation activity of GR increased and the activity of NF-?B decreased remarkedly. The phenomena of depressed activity of NF-?B disappeared after the addition of GR special antagonism RU486. Conclusion Nitric oxide donor (500 ?mol/L SNP) exerts anti-inflammatory effect through GR activation in condition of cell inflammation.

Objective To study the genetics pattern of bronchial hyperresponsiveness and serum total IgE in asthma pedigree. Methods Twenty-eight asthma families were collected, including 124 individuals, 72 with asthma and 52 without. Forty-five normal subjects of three generations without consanguinity among one another, 22 male and 23 female, were chosen as controls, excluding those with family history of asthma and hypersensitivity. Serum total IgE by ELISA and bronchial hyperresponsiveness (BHR) were detected in asthma pedigree members. Genetics pattern of BHR and serum total IgE was analysed. Results The frequency distribution of BHR was bimodal. Individuals with higher level of total IgE occupied 40 of BHR-affected. Conclusion BHR may be controlled by a single major gene. BHR and total IgE may be under separate genetic control.

Objective To investigate changes of glucocorticoid receptor (GR) expression and activity in rat alveolar macrophages (AMs) induced by lipopolysaccharide (LPS) within 24 h. Methods Primary cultured AMs were divided randomly into LPS treatment group and LPS+Dex treatment group. The expressions of GR mRNA and GR protein in AMs at different time points were detected by RT-PCR and Western blot. Electrophoretic mobility shift assay (EMSA) was used to measure the GR activity in AMs. Results The expression level of GR mRNA decreased after LPS treatment, but returned to the normal level at 24 h after LPS treatment. The expression level of GR also decreased and reached the lowest level at 4 h after LPS treatment. GR activity also decreased, reached the lowest level at 1 h after LPS treatment, but was still lower than that in the normal control group at 24 h after treatment. Dexamethasone treatment had no obvious effect on GR activity during the late period of treatment. Conclusion LPS treatment (100 ng/ml) down-regulates the protein expression of GR, which maybe associated with the decreased expression of mRNA and accelerate degradation of GR protein. The activity of GR is inhibited sharply, resulting in glucocorticoid resistance.