2.Changes of Serum Glycocholicacid,Hyaluronic Acid,Procollagen Type Ⅲ in Neonatal Diseases
wei, SHENG ; de-zhi, WANG ; yun-long, CHEN ; yuan-xun, FANG ; shi-zhang, CHENG
Journal of Applied Clinical Pediatrics 1994;0(04):-
Objective To investigate the changes of serum glycocholicacid(CG),hyaluronic acid(HA),procollagen type Ⅲ(PCⅢ) in neonatal diseases.Method The levels of serum CG,HA and PCⅢ were measured by radioimmunoassay in 46 neonates with different diseases and 20 healthy neonates.Results Serum CG and HA in patients group were significant higher than those in healthy control group(P
3.Quality of life of patients after cardiac pacemaker implantation as assessed by the Chinese version SF-36
Xiao-Ming TU ; De-Ling ZU ; Qi-Zhi JIN ; Ke-Yun CHENG ; Yi-Ming JIANG ;
Chinese Journal of Physical Medicine and Rehabilitation 2003;0(05):-
Objective To assesse the quality of life of patients after cardiac pacemaker implantation using the Chinese version of SF-36.Methods Ninety-eight patients with permanent cardiac pacemaker implantation were investigated before and after the operation in terms of quality of life by using the Chinese version SF-36.Results Successful surgery was performed on all the 98 patients.The previous symptoms of the patients were improved to vari- ous extend after the operation.The quality of life of the patients was significantly improved after operation as demon- strated by the significant difference of the scores in 9 domains of SF-36 when compared with those before the operation (P
4.Identification and characterization of marker chromosome in Turner syndrome
Yue-Qiu TAN ; De-Hua CHENG ; Yu-Fen DI ; Lu-Yun LI ; Guang-Xiu LU ;
Chinese Journal of Obstetrics and Gynecology 2000;0(10):-
Objective To analyze the karyotypes of 11 cases of Turner syndrome with marker chromosome,and study the phenotypic effects resulting from the abnormal karyotype.Methods Eleven Turner syndrome patients had a mosaic karyotype and carried a marker chromosome,and 6 marker chromosomes were ring chromosomes.Their karyotypes were showed as mos.45,X/46,X,+mar or mos. 45,X/46,X,+r.Fluorescence in situ hybridization(FISH)technique with X/Y centromere probes was performed to determine the origin of the marker chromosome.Reverse chromosome painting technique was used to identify the breakpoints of two largest markers.Phenotype effects with different chromosome breakpoints were compared.Results All the 11 marker chromosomes were ring X chromosomes.The breakpoints of the r(X)were involved in Xp22,Xq22,Xq24 and Xq26,etc.Conclusions The marker chromosomes in Turner syndrome mainly originate from X chromosome and form ring chromosome X.Each r (X)in our patients was mosaic,indicating it was originated from mitosis error during early embryo development.To analyze the origin of the marker chromosome and the breakpoint of r(X)will provide guidance for the therapy and prognosis of the Turner syndrome patient.
5.Regulation of hepatitis C virus core protein on the activity of signal transducers and activators of transcription 3.
De-yun FENG ; Bo LI ; Hui ZHENG ; Rui-xue CHENG ; Ya CAO
Journal of Central South University(Medical Sciences) 2005;30(6):631-635
OBJECTIVE:
To investigate the regulation of hepatitis C virus (HCV) core protein on the activity of signal transducers and activators of transcription 3 (stat3).
METHODS:
A cell line expressing stable HCV core protein-QSG7701-core was constructed by transfecting the pcDNA3. 1-core (expressing HCV core protein) into the human immortalized hepatocyte line QSG7701. The phosphorylation and DNA binding activity of stat3 were detected by immunocytochemistry, Western blot, and electrophoretic mobility shift assay (EMSA).
RESULTS:
The expression level of phosphorylated stat3 in QSG7701-core cells was significantly lower than that in QSG7701-pcDNA3. 1 cells and untransfected QSG7701 cells, but there were no significant differences in the expression levels of total stat3 among the 3 groups. The positive signal of phosphorylated stat3 in nucleus of QSG7701-core cells was obviously weaker than that in QSG7701-pcDNA3. 1 cells and untransfected QSG7701 cells. EMSA showed that DNA binding activity of stat3 in QSG7701-core cells significantly decreased.
CONCLUSION
The expressionof HCV core protein in human hepatocyte line may suppress the phosphorylation and DNA binding activity of stat3, which may be one of the causes for resistance against interferon.
Cell Line
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DNA-Binding Proteins
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metabolism
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Hepatocytes
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cytology
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metabolism
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Humans
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STAT3 Transcription Factor
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metabolism
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Signal Transduction
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Transfection
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Viral Core Proteins
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biosynthesis
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genetics
6.Establishment of human lung squamous carcinoma cell line CHLH-1
Hong-Cheng LIU ; Sheng-Dong HUANG ; De-Jun GONG ; Xiao-Hong LIU ; Yang YUAN ; Zhi-Yun XU ;
Academic Journal of Second Military Medical University 1999;0(12):-
Objective:To establish a human lung squamous carcinoma cell line and to study its biological characteristics. Methods:Lung squamous carcinoma specimens were freshly resected during operation;the tissues were incubated in vitro and the cell line was named CHLH-1.The biological characteristics of the cells were studied by light microscopy,electron microsco- py,chromosome analysis and transplantation experiment.Results:Cells from the specimens of the primary tumor,the CHLC- 1 cell line and the cells from transplanted tumor possessed the characteristics of malignant squamous epithelium under light and electron microscope.The cell growth curve,doubling time and mitotic index were also observed in vitro.Nuclear chromosome analysis revealed that the tumor was a subtriploid with a mode of 60-68 per cell.Tumor nodes were observed under the skin of nude mice by heterogenic transplantation.Conclusion:The characteristics of the established cell line suggest that it is a newly established human squamous carcinoma cell line.
8.Effect of fractalkine on proliferation of pulmonary artery smooth muscle cells.
Xiao-Ju CHEN ; De-Yun CHENG ; Qiao-Li SU ; Li-Li FAN
Chinese Journal of Applied Physiology 2009;25(4):445-448
AIMTo investigate the effect of fractalkine on cell proliferation of cultured rat pulmonary artery smooth muscle cells (PASMCs) in vitro.
METHODSRat PASMCs were cultured in vitro, and treated with different concentrations (10(-10), 10(-9), 10(-8) mol/L) of fractalkine for 12 h, 24 h and 48 h. The cell proliferation was quantified by MTT assay. The cell cycle of PASMCs was measured by flow cytometric(FCM) analysis.
RESULTSMTT assay showed that fractalkine promoted significantly the proliferation of PASMCs, and the effect was concentration-dependent. FCM analysis indicated that fractalkine increased the percentage of S phase and proliferative index (PI). The percentage of S phase and PI of PASMCs were increased after treated with fractalkine for 12 hours, which reached a maximal level at 24 hours.
CONCLUSIONFractalkine promotes rat PASMCs proliferation in a concentration-dependent manner.
Animals ; Cell Proliferation ; drug effects ; Cells, Cultured ; Chemokine CX3CL1 ; pharmacology ; Male ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Pulmonary Artery ; cytology ; Rats ; Rats, Sprague-Dawley
9.Effect of breviscapine on fractalkine expression in chronic hypoxic rats.
Xiao-ju CHEN ; De-yun CHENG ; Li YANG ; Xiu-qiong XIA ; Jian GUAN
Chinese Medical Journal 2006;119(17):1465-1468
Animals
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Arterioles
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metabolism
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pathology
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Blood Pressure
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drug effects
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Chemokine CX3CL1
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Chemokines, CX3C
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analysis
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genetics
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Chronic Disease
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Flavonoids
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pharmacology
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Hypertension, Pulmonary
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prevention & control
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Hypertrophy, Right Ventricular
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prevention & control
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Hypoxia
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complications
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metabolism
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Lung
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metabolism
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Male
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Membrane Proteins
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analysis
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genetics
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Pulmonary Artery
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metabolism
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pathology
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RNA, Messenger
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analysis
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Rats
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Rats, Sprague-Dawley