1.Peutz-Jeghers syndrome complicated by cervical adenoma malignum and ovarian sex cord tumor with annular tubules: report of a case.
Chinese Journal of Pathology 2006;35(12):761-762
Adenocarcinoma
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complications
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metabolism
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pathology
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Adult
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Carcinoembryonic Antigen
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metabolism
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Diagnosis, Differential
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Female
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Humans
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Immunohistochemistry
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Ki-67 Antigen
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metabolism
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Ovarian Neoplasms
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complications
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metabolism
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pathology
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Peutz-Jeghers Syndrome
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complications
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metabolism
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pathology
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Proliferating Cell Nuclear Antigen
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metabolism
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Sex Cord-Gonadal Stromal Tumors
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complications
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metabolism
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pathology
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Uterine Cervical Neoplasms
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complications
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metabolism
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pathology
5.Inhibitory Effect of Chenodeoxycholic Acid-verticinone Ester on Tumor Growth of H22-bearing Mice
Qing ZHOU ; Jiuliang ZHANG ; Yi WANG
Herald of Medicine 2015;(4):467-470
Objective To evaluate the antitumor effects of chenodeoxycholic acid-verticinone ester ( CDCA-Ver ) on tumor growth and immune system of H22-bearing mice. Methods Antitumor activity against a solid tumor mass was evaluated in Kunming mice. H22 cells were transferred into the abdomen cavity of Kunming mice. H22 cells were inoculated through subcutaneous injection at the right armpit of the mouse to establish a solid tumor model. At 24 h after H22 tumor cells inoculation, 40 tumor-bearing Kunming mice were randomly divided into 4 groups according to random number table ( n=10 each group):model control group, cyclophosphamide ( CTX) group, intraperitoneal CDCA-Ver injection group and intravenous CDCA-Ver injection group. In model control group, sterile 0. 9% sodium chloride solution (10 mL·kg-1 ) was intraperitoneally injected once daily. In CTX group and intraperitoneal CDCA-Ver injection group, CTX (20 mg·kg-1 ) and CDCA-Ver (20 mg·kg-1 ) was intraperitoneally injected once daily, respectively. In intravenous CDCA-Ver injection group, CDCA-Ver ( 20 mg · kg-1 ) was injected through tail vein once daily. CDCA-Ver, CTX and NS were injected into the mice of the experimental groups once daily for 10 days, respectively. The dose volume was 0. 1 mL · ( 10 g )-1 body weight. The positive control drug was cyclophosphamide. Ten mice were treated with 20 mg · kg-1 CDCA-Ver through intravenous injection ( i. v. ) . Ten mice were treated with 20 mg·kg-1 CDCA-Ver through intraperitoneal injection. The thymus and spleen indices and the tumor inhibition rate were assessed, and histopathological examination with haematoxylin and eosin ( H&E) staining was carried out to evaluate the antitumor effects of CDCA-Ver. Results CDCA-Ver ( ivor ip) suppressed the growth of solid tumor in H22-bearing mice. The inhibition rate was 48. 3% at the dose of 20 mg·kg-1 CDCA-Ver (ip). There was no significant difference between CDCA-Ver (ip) and CTX treated group (P<0. 05). Compared with the control, the weight of thymus and spleen of CDCA-Ver (ip) treated group was not obviously changed. But a significant weight loss of thymus and spleen in CTX group was observed, which was attributed to the immune suppression from CTX. The thymus and spleen indices in the CTX-treated mice were significantly lower than those of the control group (P<0. 01). We further conducted histopathological examination to confirm the results. The immune system was not suppressed by CDCA-Ver ( ip ) in tumor-bearing animals. The low toxicity of CDCA-Ver was an outstanding advantage for the development of newly anticancer drug. Conclusion CDCA-Ver treatment can significantly inhibit tumor growth in mice.
6.In vitro study of the treatment of human osteosarcoma by pSilence APE1 combined with neutron-ray
Yi QING ; Dong WANG ; Zhaoyang ZHONG
Medical Journal of Chinese People's Liberation Army 2001;0(07):-
Objective Apuinic/apyrimidic endonuclease/redox effector factor-1(APE1/Ref-1,abbreviated as APE1) is a major member of the base excision repair(BER) pathway involved in oxidative DNA damage repair.To knock down APE1 gene expression in HOS cells with pSilence APE1,and explore its effect in combination with 252Cf neutron ray radiotherapy.Methods The constructed APE1 siRNA expression vector pSilence APE1 was transfected into HOS cells by SuperFect Transfection liposome,and it was used to knock down the expression of APE1.The HOS cells and transfected HOS cells were respectively irradiated by 252Cf neutron ray,then the cell survival(D0),DNA single strand breaks(SSB) and cell apoptosis were determined by clone formation assay,alkaline comet assay and flow cytometer.Results The cell-survival curve was plotted by clone formation assay,the D0 value was 2.80 vs.1.89 and Dq value was 2.66 vs.2.00 for the control and transfected HOS cells,respectively,after being irradiated by 252Cf neutron ray.The tail moments at 2,5 and 10 Gy were 6.664?0.648 vs.7.997?0.542,20.322?1.433 vs.25.238?1.185 and 33.909?1.245 vs.39.191?1.052,respectively,for the control and transfected HOS cells,and the cell apoptosis rate at 2,5 and 10 Gy was 4.00 vs.5.68,5.91 vs.7.55 and 9.63 vs.13.51,respectively,for the control and transfected HOS cells.All these findings showed significant difference between the two groups(P
7.Hospital Infection in Fracture Patients and Corresponding Strategy
Shunfu WANG ; Yanyu ZHONG ; Yi QING
Chinese Journal of Nosocomiology 2006;0(03):-
OBJECTIVE To investigate the prevention from hospital infection and therapy in fracture patients.METHODS We analyzed the situation of hospital infection in the fracture patients ranged from 2000 to 2005 with reviewing and perspective statistical method.RESULTS Totally 43 cases were infected from 1345 fracture patients,taken 3.2%.It was the highest with infection rate under the age of 5(6.0%),then was successively at the 15-44 years old age,5-14 years old age,≥60 and 45-59 years old age.CONCLUSIONS The fracture patients or those experiencing surgical operation are easy to have hospital infection.It is a multifactorial result.For instance,the environment of ward,the disinfection measure in operation,the skilled degree of surgical operators,the length of operation time,rational selection antibiotics and so on,are all the important factors to prevent and cure hospital infection.Pay attention to the quality controlling every link,can reduce the rate of hospital infection among fracture patients.
8.Serum Gastrin Concentrations of Mothers and Neonates via Vaginal Delivery and Cesarean Section
Jingyin WANG ; Qing YANG ; Xiaoru YI
Chinese Journal of Perinatal Medicine 2000;0(04):-
Objective To study the serum gastrin levels of mothers and neonates via vaginal delivery and cesarean section. Methods The serum gastrin concentrations of 60 women underwent vaginal delivery and elective cesarean section, and the umbilical serum gastrin concentrations of neonates delivered via vagina (20 cases) and cesarean section (22 cases) were measured by radioimmuno assay. Results The serum gastrin concentrations of women in labor(108.23?24.39) ng/L were significantly higher than that of women during cesarean section( P
9.Relationship Between p53 Gene Mutation and Apoptosis and Cell Ploidy of Ovarian Carcinoma
Yi, SUN ; Qing, SHI ; Li, WANG
Journal of Shanghai Jiaotong University(Medical Science) 2000;20(5):439-441,449
Objective To study the relationship among p53 gene mutation, apoptosis and cellploidy as well as to explore the role of mutated p53 gene in tumorigenesis. MethodsA total of 85 speci-mens (20 normal ovarian specimens, 20 ovarian benign tumors, 20 non - metastatic carcinomas and 25metastatic carcinomas) were chosen. p53 gene mutations were detected by PCR- SSCP (single strand con-formation polymorphism). Cell ploidy, apoptosis role of carcinoma cells and cell distribution in each cellstage were detected by flow cytometry. Resultsp53 gene mutation and non- mutation of ovarian carci-noma was 60% and 40% respectively ( P >0.05). The rate of apoptosis of carcinoma cells with mutationof p53 gene (20.25%) was much lower than that without p53 mutation (41.68%, P <0.05). Aneuploidcarcinoma cells had been found in 17/23 carcinoma specimens with p53 gene mutation and 8/22 carcinomaspecimens without p53 mutation ( P < 0.05). Aneuploid carcinoma cells metastasize more easily thandiploid carcinoma cells ( P < 0.05). The rate of apoptosis was not different between aneuploid and diploidpatients. ConclusionMutation of p53 gene decreases the apoptosis rate of ovarian carcinoma and maypromote tumorigenesis. Cell ploidy had a linkage with p53 gene mutation, but not with cell apoptosis.