1.Determination of Genetic Polymorphism of Properdin Factor B in Patients With Graves Disease
Jian-Hua CHENG ; Xiu-Zhu ZHAO ;
Chinese Journal of Immunology 1985;0(03):-
Genetic polymorphism of properdin factor B (Bf)of alternative complement pathway was investigated in 110 patients with Gravesldisease and in 220 blood donors in Wuhan Blood Transfusion Center using high voltage agarose gel electrophoresis andsubsequent immunofixation. Results show that distributions of Bf phenotype observed in normals are in agreement with those expected from the Hardy-Weivr, erg equilibrium (XZ=5.4337, Pc~0.10),but in patients donlt (XZ=29.689~, Pc.
2.Treatment of Cranialfacial Fibrous Dysplasia
Journal of Shanghai Jiaotong University(Medical Science) 2006;0(07):-
Objective To discuss the treatment of cranialfacial fibrous dysplasia. Methods The treatment of 10 cases of cranialfacial fibrous dysplasia was analyzed. Results The cosmetic deformity was corrected in all the cases.No new symptom of nervous system occurred. Conclusion It is important to carry out the correct surgical plan according to patients' age,location,mono-or poly-ostotic form of fibrous dysplasia,presence or absence of functional limitations,and aesthetic problem.
3.Relationship between Placental Vascular Anastomosis and Physical Development and Morbidity of Disease in Twin Neonates
xiu-yong, CHENG ; lei, XIA ; ling, LIU ; hua-li, HUO
Journal of Applied Clinical Pediatrics 2003;0(10):-
Objective To investigate the relationship of placental vascular anastomosis and physical development and morbidity of the disease in twin neonates.Methods Fourteen pairs of twin neonates deliveried from Sep.2005 to Aug.2009 were enrolled in Newborn Intensive Care Unit,the Third Affiliated Hospital of Zhengzhou University.These twins were divided into 2 groups according the conditions of placental vascular anastomosis:significant placental vascular anastomosis group(group A) and no significant vascula anastomosis group(group B).Birth weight,head circumference,length,the morbidity of disease were all investigated in 2 groups.Clinic follow-up included neonatal behavioral neurological assessment(NBNA) and children′s development center of China(CDCC).The correlation of neonates placental vascular anastomosis between twin neonates were compared.Results There were statistically significant differences between group A and group B in birth weight,head circumference and body length(t=6.070,5.237,5.784,Pa
4.Resection of the cholesteatoma combined brain abscess with the access of back wall of maxillary sinus under nasal endoscopy and navigation.
Hua ZHANG ; Xi-cheng SONG ; Chun-ming XIU
Chinese Journal of Otorhinolaryngology Head and Neck Surgery 2012;47(5):420-421
Adult
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Brain Abscess
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Cholesteatoma
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surgery
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Endoscopy
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Female
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Humans
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Maxillary Sinus
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surgery
5.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.
6.Effects of xuefu zhuyu decoction on antioxidant and drug-metabolizing enzymes in liver of rats.
Xing-hua FAN ; Wei-Zhou SHI ; Yun-xiang CHENG ; Kai-jie ZOU ; Xiu-fen YANG
China Journal of Chinese Materia Medica 2014;39(22):4453-4458
Xuefu Zhuyu decoction (XFZYD) is a famous traditional Chinese medicine (TCM) formula, is widely used in the treatment of cardiovascular and cerebrovascular diseases in China over one hundred years. But its effect on antioxidant and drug-metabolizing enzymes are unknown. This study was to observe the effects of Xuefu Zhuyu decoction (XFZYD) on the activities of antioxidant and drug metabolism enzymes (DMEs) in liver of rats. Male SD rats, treated with XFZYD at the dosage of 3.51, 7.02 and 14.04 g x kg(-1) per day for 15 days, serum were collected, tissue fluid, cytosols and microsomes isolated from liver tissues were prepared by centrifugation according to the standard procedure, the activities of antioxidant enzymes and drug-Metabolizing Enzymes were determined by UV-V is spectrophotometer. In serum, the activities of AST was not significantly affected by the treatment with XFZYD, at the high- est dose, the levels of ALT, Cr and BUN were significantly decreased (P < 0.05). GPX were significantly increased at the dose of 7.02, 14.04 g x kg(-1) (P < 0.05), CAT were significantly increased at the highest dose (P < 0.05). T-SOD was not significantly af- fected by this treatment. In the liver tissue, GPX was significantly increased at the dose of 3.51, 7.02 g x kg(-1) (P < 0.05), GST, CAT and T-SOD were not significantly affected following this treatment. In cytosols, GST was significantly increased at the dose of 3.51 g x kg(-1) (P < 0.05), T-SOD was remarkable induced at the dose of 3.51 and 7.02 g x kg(-1) (P < 0.05). In microsomes, XFZYD had no significant effect on Cytochromeb5, NADPH-Cytochrome P450 reductase, CYP3A, CYP2E1 and UGT, XFZYD significantly in- duced GST at the dose of 3.51 and 7.02 g x kg(-1) (P < 0.05), and the level of GSH were significantly increased by XFZYD at the dose of 3.51, 7.02 and 14.04 g kg(-1) (P < 0.05). These findings suggest XFZYD can induce the activities of GPX, CAT, SOD, GST and increase GSH level in liver of rats, which indicate XFZYD may have detoxification and antioxidant functions.
Animals
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Antioxidants
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metabolism
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Drugs, Chinese Herbal
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pharmacology
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Inactivation, Metabolic
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drug effects
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Liver
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drug effects
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enzymology
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Male
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Rats
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Rats, Sprague-Dawley
9.Effects of sodium butyrate on growth, apoptosis and telomerase activity in Hep-2 cells.
Ling GAO ; Ming-min DONG ; Hua CAO ; Xiu-lian CHENG
Chinese Journal of Otorhinolaryngology Head and Neck Surgery 2007;42(1):58-63
OBJECTIVETo study the effects of sodium butyrate (SB) on growth, apoptosis and telomerase activity in Hep-2 cells.
METHODSGrowth inhibition effect of SB on Hep-2 cells was assessed by methyl thiazolyl tetrazolium (MTT) assay. Morphological alterations were observed by electronic microscope. Cell apoptosis was confirmed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling (TUNEL) method, DNA fragmentation and flow cytometry (FCM). Cell cycle was analyzed by FCM. Telomerase activity was examined by telomeric repeat amplification protocol (TRAP)-silver staining. The expression status of telomerase subunits was analyzed by reverse transcription-polymerase chain reaction (RT-PCR).
RESULTSA time-and dose-dependent inhibition was detected in cells treated with SB. Typical morphological changes of apoptotic cells were observed under electronic microscopy. The characteristic DNA fragmentation of apoptotic cells was detected by agarose gel electrophoresis. Apoptosis and the changes of cell cycle were confirmed by TUNEL method and FCM. The apoptosis indexes of the cells before treatment and at 72 h after SB (2.5 mmol/L) treatment were 2.27 +/- 1.18 and 33.50 +/- 2.75 respectively, the apoptosis rates were 2. 86% and 31. 28% respectively, the proportion of the cells at G0/G1 stage were 50.38% and 70.88% respectively, the proportion of the cells at S stage were 27.40% and 8.20% respectively, and the proliferation indexes of the cells were 49.62% and 29.12% respectively. Telomerase activity and expression level of human telomerase reverse transcriptase (hTERT), the key subunit of telomerase, decreased after SB treatment. No significant changes were observed in the expression of human telomerase RNA (hTR) and human telomerase associated protein (hTP1), the other two subunit of telomerase.
CONCLUSIONSB could inhibit growth of Hep-2 cells and induce apoptosis in the cells, and inhibit telomerase activity by decrease expression level of hTERT.
Apoptosis ; drug effects ; Butyrates ; pharmacology ; Cell Cycle ; drug effects ; Hep G2 Cells ; Humans ; Sodium ; pharmacology ; Telomerase ; metabolism