Objective To study the effect of Bi-level positive airway pressure (BiPAP) on hemodynamics in patients with the chronic obstructive pulmonary disease (COPD) combined coronary heart disease.Methods One hundred patients with COPD combined coronary heart disease treated by BiPAP ventilation were enrolled.The blood gas analysis and the hemodynamics were monitored and analyzed in patients with the COPD combined coronary heart disease before treatment and after BiPAP ventilation treatment for 2 hours,24 hours,72 hours and 1 week.Results PaCO2 decreased significantly after 2-hour's treatment by BiPAP ventilation( P ＜ 0.05) and the heart rate and systolic blood pressure also decreased significantly after 24-hour's treatment by BiPAP ventilation.The left ventricurlar ejection fraction( [ 65.63 ± 6.86 ] ％ vs.[ 56.21 ±5.26]％,P ＜ 0.05 )was significantly improved after BiPAP reatilation treatment for one week.The mean pulmonary arterial pressure ( [ 3.74 ± 0.96 ] vs [ 5.12 ± 1.12 ] kPa,P ＜ 0.01 ),angina pectoris ( [ 0.20 ± 0.01 ]time/d vs [ 0.69 ± 0.03 ] time/d,P ＜ 0.05 ) were significantly decreased.Conclusion COPD combined coronary heart disease patients may achieve an optimal effect by BiPAP ventilation.BiPAP ventilation has no impact on the hemodynamics in patients with the COPD combined coronary heart disease.

Objective To construct a qseC-deleted mutant strain of E.coli by Red recombination and to study the effect of qseC gene on biofilm formation in the mutants.Methods The chloramphenicolresistant gene flanked by homologues of target genes was amplified by PCR and electro-transformed into E.coli MC1000.When induced by L-arabinose,the plasmid pKD46 could express three recombinant proteins of λ-prophage,which led to the replacement of target gene(qseC) with chloramphenicol-resistant gene.Then the chloramphenicol-resistant gene was eliminated by FLP-promoted recombination events.The biofilm formation of wild-type and mutant strain was detected by crystal violet staining.Results The qseC-deleted mutant of E.coli was confirmed by various PCR and DNA sequencing.Gene qseC was completely deleted.There was no significant difference in growth ability between the qseC mutant strain and the wild-type strain MC1000.The biofilm formation of wild-type and mutant strain was quantified by crystal violet staining.The absorbance determined with a plate reader at 570 nm was 1.00±0.15 and 0.47±0.10 respectively.Conclusion The qseC-deleted mutant of E.coli was constructed successfully.And the qseC gene plays an important role in regulation of biofilm formation in E.coli.

The ptrpose of this study was to investigate the effects of long-term estradiol and progesterone combined therapy on bone mineral density (BMD) in patients with Turner syndrome.Eight patients with Turner syndrome received estradiol and progesterone combined therapy for six years were observed and BMD was measured for each of them before hormone replacement therapy (HRT) and at an interval of one to two years after HRT and compared with that in normal age-sex matched women.BMD was significantly lower in patients with Turner syndrome than that in normal controls before HRT.All the patients with Turner syndrome had breast enlargement and irregular vaginal bleeding after HRT.BMD increased slightly in the patients with Turner syndrome after six-year HRT ,but still much lower than that in normal controls.Their BMD of the 2nd to 4th lumbar vertebra increased to (0.84±0.22) g/cm2 after HRT from (0.75±0.12)g/cm2 before it,with Z-score increased to -2.2±0.6 from -3.2±0.9,respectively; and overall BMD of the hip increased to (0.81±0.08) g/cm2 after HRT from (0.68±0.07) g/cm2 before it,with Z-score increased to-1.2 ± 0.3 from-2.2 ± 0.5,respectively.Long-term HRT can improve their BMD for patients with Turner syndrome but can not restore it to normal.

The mechanism of Tongmai Oral Liquid (TOL) for chronic nephritis rat model with Qi-deficiency and blood-stasis syndrome was studied.The model was established by adding Qi-deficiency and blood-stasis syndrome to the chronic nephritis rats. The experimental rats were randomly allocated to 5 groups: Group A (treated with high dosage of TOL), Group B (treated with low dosage of TOL), Group C (treated with Jinshuibao), Group D (model control group) and Group E (normal control group). After 4 weeks of treatment, general health state, biochemical indexes including T lymphocyte subgroup and blood rheology, and pathological damage of kidney tissue were much improved in Group A than Group B and Group C. It is indicated that TOL can improve the renal function and delay the occurrence of glomerular arteriosclerosis in rats by reinforcing Qi, activating blood flow, regulating immune function, lessening the hypercoagulative state and reducing renal damage.

Objective To study the effect of epinephrine on biofilm formation of the qseC-deleted mutant of Escherichia coli on biomaterial.Methods The strains used in this study are Escherichia coli MC1000 and MC1000AqseC.LB was used for all the experiments.To determine the effect of epinephrine on motility,halos were measured in LB medium at 37℃ in the presence of epinephrine(50 μmol/L).LB with epinephrine and without epinephrine were used,and then the experiment of bacterial biofilm formation on PVC material was taken.The relative amount of biofilm was estimated.The thickness of bacterial community and bacterial community quantity in the unit area on PVC materials were measured by confocal laser scanning microscope( CLSM),and the surface structure of biofilm formation was observed by scanning electron microscope(SEM).Results The mutant strain formed less biofilm than the wild-type strain in LB.The increment in motility of wild-type strain due to epinephrine addition was shown,but mutant strain is unaffected.Similarly,biofilm formation of the wild-type strain was increased by epinephrine,but epinephrine did not affect the biofilm formation of the qseC mutant.The CLSM and SEM showed that epinephrine stimulated biofilm formation of wild-type strain on PVC materials,but had no effect on qseC-deleted mutant strain.Conclusion Epinephrine increases Escherichia coli biofilms on biomaterials through qseC.

Objective To study the effect of endothelial progenitor cells(EPCs) transplantation on chronic deep venous thrombosis.Methods Bone marrow-derived mouonuclear cells (BMMNCs) were isolated from rat bone marrow by ficoll and cultured with EGM-2MV medium.A rat model of chronic deep vein thrombosis was established by partial ligation of the inferior vena cava and intravenous injection of thrombosin.Model rats were randomly divided into three groups:A(n =25),EPCs group,1 ml 10~6 EPCs transplantation;B(n = 25),EGM-2MV medium group,1 ml EGM-2MV medium transplantation;C (n =25),control group,without any treatment.After transplantation,HE staining and immunohistochemical staining was conducted to detect recanalization of the inferior vena cava.Western blotting of inferior vena cava thrombosis was used to detect VEGF,bFGF protein expression changes.SPSS13.0 software was used for analysis.Results Compared with group B and C,VEGF,bFGF protein significantly increased in group A.The recanalization capillary density was significantly higher in group A than that in group B,and C (P ＜0.05).The neovascularization was identified by immunohistochemical staining using vWF antibody,as endothelial cells.Conclusions EPCs were the precursor of endothelial cells,when transplanted into the deep vein thrombos,initiating angiogenesis and accelerating organization and recanalization of vein thrombus.

Objective To investigate the effect of bone marrow derived endothelial progenitor cells (EPC)transplantation on microenvironments in a murine model of chronic vein thrombosis.EPCs transplantation was evaluated whether it can up-regulate thrombus organization and recanalization associated cytokines(VEGF,ANG-1 and MCP-1). Method EPCs from immature Wister rats' bone marrow were isolated using a Ficoll density gradient centrifugation,and cultured in fibronectin-coated plate in EGM-2M Vmedium.EPCs were harvested on the 10th day,then were transplanted into chronic inferior vens cava thrombus of adult Wister rat through the femoral vein.Rats were divided into three groups:blank control group(group A,sham operation),the control group(group B,the medium injected)and the experimental group(group C,EPCs injected).The rats were sacrificed after 28 days.VEGF,ANG-1 and MCP-1 mRNA was measured by real-time quantitative PCR and protein expression change by Western blotting from IVC and thrombus tissue. Results EPCs were identificated successfullv by immunohistochemistry,immunofluorescence and function,then were transplanted into chronic inferior vena cava thrombus of adult rats.After EPCs transplantation,the VEGF,ANG-1 and MCP-1 mRNA expression in group C expression was significantly up-regulated with statistical significance(P＜0.01)compared with group A and group B in IVC and thrombus tissue by real-time PCR.There was no significant difference between group A and group B (P＞0.05).VEGF,ANG-1 and MCP-1 protein expression were similar to mRNA expression.There was significant increase in group C compared to group A and group B(P＜0.01)and no statistical significance between group A and group B(P＞0.05).Conclusion EPCs deriving from bone marrow may change the microenvimnment of chronic vein thrombus through up-regulating thrombus organization and recanalization associated cytokines(VEGF,ANG-1 and MCP-1).

Child ; Contracture ; congenital ; therapy ; Humans ; Male ; Neck Muscles ; pathology ; Torticollis ; congenital

Objective To investigate the role of quorum sensing Escherichia coli regulator C (qseC) in intestinal bacterial translocation in rats subjected to hemorrhagic shock.Methods Thirty Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 5 groups (n =6 each):control group (group C),MC1000-sham shock group (group M-SS),MC1000qseC-sham shock group (group △-SS),MC1000-hemorrhagic shock group (group M-HS),and MC1000△ qseC-hemorrhagic shock group (group △-HS).The rats drank 150 μg/ml of disinfect water containing streptomycin in 3 consecutive days to inhibit the autochthonous flora in the intestinal tract.From 4th day,the rats were fed with Escherichia Coli MC1000 or MC1000△ qseC 1 ml/100 g by gastric perfusion once a day for another 3 consecutive days in the other 4 groups,while the rats were fed with normal saline instead in group C.Hemorrhagic shock was induced by blood-letting.The mesenteric lymph node (MLN),spleen and liver specimens were obtained at 24 h after operation for bacterial culture and the bacteria were identified.Bacterial translocation from gut to MLN,spleen and liver was observed and the number of bacteria in MLN,spleen and liver tissues were counted.Results The rate of bacterial translocation was significantly higher,and the number of bacterial colonies in MLN,spleen and liver tissues and the total number of bacterial colonies were significantly larger in groups M-HS and △-HS than in group C,and in group M-HS than in groups M-SS and △-SS (P ＜ 0.05).The rate of bacterial translocation was significantly lower,and the number of bacterial colonies in MLN,spleen and liver tissues and the total number of bacterial colonies were significantly smaller in group △-HS than in group MHS.Conclusion QseC is involved in the intestinal bacterial translocation following hemorrhagic shock in rats.

Objective:To analyze the effects of espO gene knockout on the biological characteristics of enterhemorrhagic Escherichia coli (EHEC). Methods:Two-step methods mediated by the suicide plasmid pCVD442-Δ espO and plasmid pTrc99a were used to construct the espO gene-deleted strain (Δ espO) and the complemented mutant (CΔ espO), respectively. HeLa cells were infected with different EHEC strains to analyze the biological functions and lethal effects of espO gene during infection. Results:PCR, electrophoresis and gene sequencing showed that the Δ espO and CΔ espO mutants were successfully constructed. Compared with the wild-type strain, neither the Δ espO nor CΔ espO mutant showed significant difference in growth rate, indicating that the espO gene had no influence on the growth and replication of EHEC. Furthermore, EspO could activate the tumor necrosis factor receptor (TNF)-induced NF-κB signaling pathway, while the effector protein NleB could inhibit the process. EspO could not inhibit the death of HeLa cells induced by TNF or TNF-related apoptosis-inducing ligand (TRAIL) after EHEC infection. Conclusions:In this study, we successfully constructed the espO gene-deleted and complemented mutants of EHEC and preliminarily analyzed the interaction between espO gene and host cells and the effects of espO gene on cell apoptosis during infection, which provided reference for further research on the in vitro biochemical activity and in vivo pathogenic roles of EspO.