Objective To investigate the expression of insulin-like growth factor-binding protein-5( IGFBP-5) in full-term rats with hyperoxia-induced chronic lung diseases(CLD) and its mechanism.Methods Ninety-six full-term rats were randomly exposed to hyperoxia (hyperoxia group)and room air(room air group).CLD was induced by hyperoxia exposure.RT-PCR and immunohistochemical metho -ds were used to detect the expression of IGFBP-5 at 1,3,7,10 ,14 and 21 days after exposure.Results The expression of IGFBP -5 was dynamic, the expression of IGFBP-5 increased significantly in hyperoxia group compared with room air group at 3 d to 10 d after hyperoxia exposure (P

Animals ; Diet ; Enterocolitis, Necrotizing ; etiology ; metabolism ; Humans ; Infant, Newborn ; NF-kappa B ; physiology ; Platelet Activating Factor ; chemistry ; metabolism ; Risk Factors ; Tumor Necrosis Factor-alpha ; physiology

Objective To explore the change of occludin mRNA in the lung tissue under hyperoxia induced lung injury condition and their regulation of platelet-derived growth factor B(PDGFB).Methods Three hundred and twenty newborn rats were divided into 4 groups accor-ding to different oxygen concentrations(FiO2):experimental group 1(FiO2=800 mL/L),experimental group 2 (FiO2=600 mL/L),experimental group 3(FiO2=400 mL/L) and room-air control group(FiO2=210 mL/L).Rats were killed at 1st,3rd,5th,7th and 14th day respectively during the experiment,the expression of occludin was examined by reverse transcription polymerase chain reaction(RT-PCR) method.The expression of PDGFB in the lung tissue was also observed by immunohistochemistry.SPSS 11.5 software was used to analyze the data.Results The expressions of PDGFB in the lung tissue in experimental group 1 and experimental group 2 were lower than those of the control group at 1th day(Pa

Objective To investigate the protective effects of recombinant human erythropoietin(rhEPO)treatment on histopathologic changes seen in hyperoxia induced lung injury.Methods Rat pups were randomly divided into four groups:Ⅰ:air-exposed control group,Ⅱ: air-exposed+rhEPO-treated group,Ⅲ:hyperoxia-exposed control group,Ⅳ:hyperoxia-exposed+rhEPO-treated group.GroupⅢ and Ⅳ rats were exposed to 85% oxygen.GroupⅡand Ⅳ rats were received rhEPO (1 200 U/kg) subcutaneously on postnatal 0 day and 2 day.On postnatal 14 day,survival curve,measurement of body weight and lung weight,radical alveolar counts(RAC),microvessel count were compared,CD_ 31 and vascular endothelial growth factor(VEGF) were performed by immunostaining to assess hyperoxia-induced changes in lung morphology.Results Treatment of hyperoxia-exposed rats with rhEPO prolonged the survival and resulted in a significant increase in the weight gain of body and lung[(25.88?2.59) vs(18.8?3.93) P

Animals ; Chronic Disease ; Disease Models, Animal ; Female ; Gene Expression Regulation, Developmental ; Hyperoxia ; Immunohistochemistry ; Lung ; growth & development ; metabolism ; Lung Diseases ; metabolism ; Oxygen ; Pregnancy ; RNA, Messenger ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Transforming Growth Factor beta1 ; genetics ; metabolism

Apoptosis ; physiology ; Bronchopulmonary Dysplasia ; physiopathology ; Chronic Disease ; Humans ; Infant, Newborn ; Infant, Premature ; Lung ; pathology ; physiopathology ; Receptors, Transforming Growth Factor beta ; physiology ; Transforming Growth Factor beta ; classification ; physiology

Objective To investigate the dynamic change of expression of cyclin dependent kinase-4(CDK4)and cyclin dependent kinase inhibitor(p21)in premature rats with hyperoxia-induced chronic lung disease(CLD)and its role.Methods Eighty premature rats were randomly and equally divided into model group(hyperoxia group)and control group(room air group).CLD was induced by hypemxia exposure.The expression of CDK4 and p21 were observed with immunohistochemical method,and the levels of type I collagen were detected by enzyme-linked immunosorbent assay on days 1,3,7,14 and 21.Results Compared with control group,in model group,the expression of CDK4 protein and level of type I collagen statistically increased,but expression of p21 protein decreased significantly on days 14 and 21.The expression of CDK4 was positive correlated with the degree of fibrosis,and expression of p21 was negative correlated with the degree of fibrosis in model group.Conclusion The expression of CDK4 increases and expression of p21 decreases in premature rats exposed to hyperoxia,which may play an important role in the lung fibrosis.

Objective To observe temporal expression of matrix metalloproteinases(MMP-13) and tissue inhibitor of metalloproteina-ses-1 (TIMP-1) in lung of newborn rats with hyperoxia induced chronic lung disease (CLD),and to explore the relationship of CLD with MMPs.Methods The neonatal rats within 24 hours after birth were randomly divided into hyperoxia-exposed group(n=40) and control group(n=40).On postnatal 1,3,7,14 and 21 days,lung tissue of rats in 2 groups were collected.Lung histological changes were evaluated by hematoxylin and eosin and Masson stain;Collagen Ⅰ was detected by enzyme linked immunoadsorbent assay;MMP-13 and TIMP-1 were identifide by immunohistochemistry.Results Exposured to hyperoxia enviroment for 21 days,the number of alveolar decreased,terminal air space enlarged,inter-alveolar septa thickened,and deposition of interstitial collagen fibers.On 14 and 21 days,collagen Ⅰ in the lung of hyperoxia-exposed group increased significantly compared with that of control group(P0.05),obviously decreased on 21 day(P

Objective To investigate the case of left-semicolon cancer with intestinal obstruction for the methods of one-stage resection and anastomosis.Methods The clinical data of ten patients with left-semicolon can- cer with intestinal obstruction treated by transanus ilues tube,were restrospectively analyzed from October 2004 to December 2006.Results No postoperative anastormotic leakage was found and the patients were clinically cured. Conclusion The technical problem that left-semicolon cancer with obstruction for one-stage resection and anastomo- sis was resolved by the application of transanus ilues tube.

ObjectiveTo investigate glutathione S-transferase GSTO 1 Glu155△Glu genetic polymorphism and risks of arsenic poisoning caused by coal-burning in Guizhou.Methods GSTO1 Glu155 △Glu gene polymorphism was analyzed by polymerase chain reaction-with confronting two-pair primers among one hundred and thirty arsenic poisoning patients and one hundred and thirty healthy controls.The results were verified by DNA sequencing.The association between different genotypes and arsenic poisoning was analyzed by unconditional Logistic regression model.ResultsThe results of Glu/Glu and Glu/△Glu genotype detected by this method were consistent with those of DNA sequencing.The frequencies of GSTO1 Glu/Glu genotype and Glu/△Glu genotype were 94.85％(92/97) and 5.15％(5/97) in the patients,99.15％(117/118) and 0.85％(1/118) in the controls,respectively.The difference was statistically significant(x2 =3.896,P ＜ 0.05).△Glu/△Glu genotype was not found in both patients and controls.After age and sex adjusting,GSTO1 Glu155 △Glu polymorphism was found to be a risk factor of arsenic poisoning [odds ratio (OR) =1.85,95％ confidence interval (CI):1.39 - 17.48].ConclusionsThe study finds that GSTO1 Glu 155 △ Glu polymorphism is associated with risk of arsenic poisoning.The relationship between them should be further studied through increasing sample size.