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 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.

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 study the effect of transfecting anti-sense expression vector of the first subtype of the monocarboxylate transporter (MCT1) gene into human lung adenocarcinoma cells on intracellular pH (pHi) regulation, lactate transportation and cell growth. Methods　MCT1 antisense gene recombinant vector pLXSN-MCT1 was introduced into human lung cancer cells A549 with electroporation. The cell colonies resistant to G418 were selected. Positive clones were examined by PCR to confirm the integration of genomic A549 DNA and antisene MCT1 gene. The changes of pHi and lactate transportation were detected with spectrophotometry. Cell growth was studied with cell growth curve. Results　pHi and lactate transport were remarkably decreased in the transfected cells, and the cell growth was inhibited compared with the cells without transfection（P<0.001）. Conclusion　MCT1 gene may play an important role in pHi regulation, lactate transport and cell growth in lung tumor cells.

Objective To compare the differences in mucin-histochemistry and etiology of Barrett's esophagus (BE) intestinal metaplasia (IM) , cardiac intestinal metaplasia (CIM) and gastric antrum intestinal metaplasia (GA-IM). Methods Alcian blue /periodic acid-schiff (AB/PAS) and high iron diamine / alcian blue (HID/AB) histochemical methods were used to classify IM in BE, cardia and gastric antrum, and IM were classified into three subtypes: complete small intestinal type (type Ⅰ ) , incomplete small intestinal type (type Ⅱ) and incomplete colonic type (type Ⅲ). Compared the prevalence of different subtypes of IM in above-mentioned sites, and investigated their relationships among the symptoms of gastroesophageal reflux disease (GERD) and Helicobacter pylori (Hp) infection. Results The prevalence of type Ⅲ IM in long-segment BE (LSBE) and short-segment BE (SSBE) is 75. 0% and 63. 3% respectively, it is significantly higher than that in CIM (23. 1% ) and GA-IM ( 17. 7% ) (P

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 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.