Objective To explore the relationship between human papilloma virus(HPV)andUreaplasma urealyticum (UU)in-fection in women.Methods A total of 412 outpatient women were checked for 23 HPV DNA types by PCR-RDB.The patients were divided into observation group with HPV infection and control group(random selection 50 cases without HPV infection).UU was detected by real-time quantitative PCR in two groups.Results The HPV positive rate was 12.86%(53/412).16 of 23 HPV types were detected.HPV52 was the most common type.The positive rates of UU for observation group(60.38%,32/53)was sig-nificantly higher than control group(30.00%,15/50),P <0.05.Conclusion The reproductive tract HPV infection in women is re-lated to UU infection.It should be paid attention to in the clinical treatment.

Objective To investigate changes in serum sclerostin (SO) in postmenopausal women before and after treatment with recombinant human parathyroid hormone (1-34) [rhPTH (1-34)],and to explore the relationship of serum SO with estradiol (E2),and bone mineral density (BMD).Methods Ninety-five postmenopausal women were divided into normal BMD group (n =41) and osteoporosis group (n =54).Body mass index,alkaline phosphatase (ALP),serum E2,calcium,phosphate,and SO were determined in both groups.The patients in osteoporosis group were treated with rhPTH (1-34) 20 μg/d by subcutaneous injection and oral calcium 500 mg/d for 12 months.Serum calcium,serum phosphate,BMD,serum ALP,serum E2,and sclerostin were determined in osteoporosis group by 6 months and 12 months of treatment.Results (1) Serum level of SO in osteoporosis group was raised significantly as compared with normal BMD group (P ＜ 0.05) ; E2 and BMD were negatively correlated with SO; age and postmenopausal years were positively correlated with SO (P ＜ 0.05).(2) Serum SO was reduced gradually with treatment of rhPTH (1-34) by 6 months and 12 months (P ＜ 0.05).Conclusions Serum SO was increased in postmenopausal women,which was related to E2 and BMD,and was reduced gradually with treatment of rhPTH (1-34).SO may participate in the development of postmenopausal osteoporosis.

Patient,competition and change are characteristics of the modern hospital manage environment,clinical laboratory management must be more scientific and more religious.This article lists the main items of clinical laboratory management using ISO15189,and raised some idea on clinical laboratory management using ISO15189 and points out the difficulties of popularization using ISO15189 in clinical laboratory management.

Objective To investigate the impact of 1,25(OH)2D3 on histological changes and activation of STAT3 in BLM?induced pulmonary fibrosis mice. Methods 30 male C57BL/6 mice were randomly divided into control group ,BLM group and BLM+VD group. Mice in BLM group and BLM+VD group received intratracheal injection of BLM(3 U/kg). Control group were intratracheally injected equal volume of sterile saline. From the first day after the surgery,mice in BLM+VD group received intraperitoneal injection of VD (5μg/kg·d). After 21 days, H&E and Masson′s trichrome staining were carried out. Aschroft score were used to evaluate histological changes in lungs. IL?6,IL?4 and INF?γin BALF were assessed by Elisa. p?STAT3,α?SMA and Collagen I were detected by western blot (WB) and immunohistochemistry. Results Fibrosis score and level of α?SMA,Collagen I in BLM group were significantly higher than that in control group (P < 0.05). However ,treatment with VD effectively at?tenuated fibrosis (P<0.05). IL?6 and IL?4 increased while INF?γwas decreased in BALF of BLM group (P<0.05). VD could ameliorate these changes. Upregulation and neuclear translocation of p?STAT3 were observed in BLM group,while VD intervention could inhibit phosphorylation of STAT3. Conclusions VD attenuate BLM?induced pulmonary fibrosis and regulate inflammatory cytokines probably by blocking STAT3 activation.

OBJECTIVETo establish a chronic obstructive pulmonary disease (COPD) model by passive cigarette smoking and (or) intratracheal instillation of lipopolysaccharide (LPS) in spontaneously hypertensive (SH) rats.

METHODSFifteen male SH rats were randomly divided into control group, cigarette smoking exposure (CS) group and CS+LPS (cigarette smoking exposure plus intratracheal instillation of LPS) group. After 8 weeks' treatment, the COPD model was validated by inspecting the general condition and examining lung function and pulmonary pathological changes. The expressions of surfactant-associated protein A (SP-A), NF-κB, histone, p-Iκ-Kα/β, Iκ-Kα/β, and IκB-α were determined with Western blotting, and the expression of TNF-α and IL-6 mRNA were measured using qRT-PCR.

RESULTSThe rats in both CS and CS+LPS groups were marantic with intermittent cough and tachypnea. Lung function test showed increased RI and lowered peak expiratory flow in CS group, which were more prominent in CS+LPS group (P<0.05). HE staining demonstrated typical chronic bronchitic inflammation and emphysema in the lungs of the two model groups with significantly decreased mean alveolar number and significantly increased mean lining intermittent and destruction index. The emphysema level was more serious in CS+LPS group than in CS group. Western blotting showed markedly decreased expressions of SP-A and IκB-α in CS group and CS+LPS , especially the latter group. The protein levels of NF-κB, Iκ-K phosphorylation and mRNA expressions of TNF-α and IL-6 increased obviously in the two model groups.

CONCLUSIONCOPD model can be established by passive smoking and (or) intratracheal instillation of LPS in SH rats, and the model induced by combined exposures is optimal.

Animals ; Disease Models, Animal ; Lipopolysaccharides ; adverse effects ; Male ; Pulmonary Disease, Chronic Obstructive ; etiology ; Rats ; Rats, Inbred SHR ; Tobacco Smoke Pollution ; adverse effects

Objective To establish a chronic obstructive pulmonary disease (COPD) model by passive cigarette smoking and (or) intratracheal instillation of lipopolysaccharide (LPS) in spontaneously hypertensive (SH) rats. Methods Fifteen male SH rats were randomly divided into control group, cigarette smoking exposure (CS) group and CS+LPS (cigarette smoking exposure plus intratracheal instillation of LPS) group. After 8 weeks' treatment, the COPD model was validated by inspecting the general condition and examining lung function and pulmonary pathological changes. The expressions of surfactant-associated protein A (SP-A), NF-κB, histone, p-Iκ-Kα/β, Iκ-Kα/β, and IκB-αwere determined with Western blotting, and the expression of TNF-αand IL-6 mRNA were measured using qRT-PCR. Results The rats in both CS and CS+LPS groups were marantic with intermittent cough and tachypnea. Lung function test showed increased RI and lowered peak expiratory flow in CS group, which were more prominent in CS+LPS group (P<0.05). HE staining demonstrated typical chronic bronchitic inflammation and emphysema in the lungs of the two model groups with significantly decreased mean alveolar number and significantly increased mean lining intermiment and destrction index. The emphysema level was more serious in CS+LPS group than in CS group. Western blotting showed markedly decreased expressions of SP-A and IκB-αin CS group and CS+LPS , especially the latter group. The protein levels of NF-κB, Iκ-K phosphorylation and mRNA expressions of TNF-α and IL-6 increased obviously in the two model groups. Conclusion COPD model can be established by passive smoking and (or) intratracheal instillation of LPS in SH rats, and the model induced by combined exposures is optimal.

Objective To establish a chronic obstructive pulmonary disease (COPD) model by passive cigarette smoking and (or) intratracheal instillation of lipopolysaccharide (LPS) in spontaneously hypertensive (SH) rats. Methods Fifteen male SH rats were randomly divided into control group, cigarette smoking exposure (CS) group and CS+LPS (cigarette smoking exposure plus intratracheal instillation of LPS) group. After 8 weeks' treatment, the COPD model was validated by inspecting the general condition and examining lung function and pulmonary pathological changes. The expressions of surfactant-associated protein A (SP-A), NF-κB, histone, p-Iκ-Kα/β, Iκ-Kα/β, and IκB-αwere determined with Western blotting, and the expression of TNF-αand IL-6 mRNA were measured using qRT-PCR. Results The rats in both CS and CS+LPS groups were marantic with intermittent cough and tachypnea. Lung function test showed increased RI and lowered peak expiratory flow in CS group, which were more prominent in CS+LPS group (P<0.05). HE staining demonstrated typical chronic bronchitic inflammation and emphysema in the lungs of the two model groups with significantly decreased mean alveolar number and significantly increased mean lining intermiment and destrction index. The emphysema level was more serious in CS+LPS group than in CS group. Western blotting showed markedly decreased expressions of SP-A and IκB-αin CS group and CS+LPS , especially the latter group. The protein levels of NF-κB, Iκ-K phosphorylation and mRNA expressions of TNF-α and IL-6 increased obviously in the two model groups. Conclusion COPD model can be established by passive smoking and (or) intratracheal instillation of LPS in SH rats, and the model induced by combined exposures is optimal.

Objective To assess the effect of platycodin D(PD)for alleviating pulmonary fibrosis in mice and explore the underlying mechanism.Methods C57BL/6J mouse models of pulmonary fibrosis induced by bleomycin injection into the airway were treated with daily intragastric administration of 10 mg/kg PD for 28 days.The changes of pulmonary fibrosis and the expression and distribution of transient receptor potential cation channel subfamily C member 6(TRPC6)were evaluated with immunohistochemistry,HE staining and Sirius Red staining.Western blotting was used to detect α-SMA expression in the lung tissues of the mice.Primary cultures of mouse lung fibroblasts were pretreated with PD(2.5,5.0,and 10 μmol/L)or larixyl acetate(LA;10 μmol/L)before exposure to 10 ng/mL transforming growth factor-β1(TGF-β1),and the changes in cell survival rate,expressions of collagen I,α-SMA and TRPC6,reactive oxygen species(ROS)production,mitochondrial membrane potential,and cell proliferation capacity were assessed.Network pharmacology analysis was performed to explore the mechanism by which PD alleviated pulmonary fibrosis.Results PD treatment significantly alleviated pulmonary fibrosis and reduced α-SMA expression in BLM-induced mouse models(P<0.05).In TGF-β1-induced primary mouse lung fibroblasts,PD effectively inhibited the cell proliferation,reduced ROS production(P<0.0001),rescued the reduction of mitochondrial membrane potential(P<0.001),and inhibited the expressions of α-SMA and collagenⅠ(P<0.05).Network pharmacology analysis suggested that TRPC6 mediated the effect of PD for alleviating pulmonary fibrosis.Immunohistochemistry showed that PD significantly reduced TRPC6 expression in the lung tissues of BLM-induced mice.In primary mouse lung fibroblasts,PD significantly inhibited TGF-β1-induced TRPC6 expression(P<0.05),and LA treatment obviously lowered the expression levels of TRPC6,α-SMA and collagenⅠ(P<0.05).Conclusion PD alleviated pulmonary fibrosis in mice possibly by down-regulating TRPC6 and reducing ROS production.

Objective To assess the effect of platycodin D(PD)for alleviating pulmonary fibrosis in mice and explore the underlying mechanism.Methods C57BL/6J mouse models of pulmonary fibrosis induced by bleomycin injection into the airway were treated with daily intragastric administration of 10 mg/kg PD for 28 days.The changes of pulmonary fibrosis and the expression and distribution of transient receptor potential cation channel subfamily C member 6(TRPC6)were evaluated with immunohistochemistry,HE staining and Sirius Red staining.Western blotting was used to detect α-SMA expression in the lung tissues of the mice.Primary cultures of mouse lung fibroblasts were pretreated with PD(2.5,5.0,and 10 μmol/L)or larixyl acetate(LA;10 μmol/L)before exposure to 10 ng/mL transforming growth factor-β1(TGF-β1),and the changes in cell survival rate,expressions of collagen I,α-SMA and TRPC6,reactive oxygen species(ROS)production,mitochondrial membrane potential,and cell proliferation capacity were assessed.Network pharmacology analysis was performed to explore the mechanism by which PD alleviated pulmonary fibrosis.Results PD treatment significantly alleviated pulmonary fibrosis and reduced α-SMA expression in BLM-induced mouse models(P<0.05).In TGF-β1-induced primary mouse lung fibroblasts,PD effectively inhibited the cell proliferation,reduced ROS production(P<0.0001),rescued the reduction of mitochondrial membrane potential(P<0.001),and inhibited the expressions of α-SMA and collagenⅠ(P<0.05).Network pharmacology analysis suggested that TRPC6 mediated the effect of PD for alleviating pulmonary fibrosis.Immunohistochemistry showed that PD significantly reduced TRPC6 expression in the lung tissues of BLM-induced mice.In primary mouse lung fibroblasts,PD significantly inhibited TGF-β1-induced TRPC6 expression(P<0.05),and LA treatment obviously lowered the expression levels of TRPC6,α-SMA and collagenⅠ(P<0.05).Conclusion PD alleviated pulmonary fibrosis in mice possibly by down-regulating TRPC6 and reducing ROS production.

Animals ; Humans ; Thymic Stromal Lymphopoietin ; Pyroglyphidae/metabolism* ; Cytokines/metabolism* ; Asthma/metabolism* ; Respiratory System ; Epithelial Cells/metabolism*