1.Atypical cellular chorangioma: report of a case.
Qian-he LIAO ; Nan WU ; Dan XU
Chinese Journal of Pathology 2012;41(11):769-770
Antigens, CD34
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metabolism
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Choriocarcinoma
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pathology
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Diagnosis, Differential
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Female
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Hemangioma
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metabolism
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pathology
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Humans
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Keratin-18
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metabolism
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Mesenchymoma
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pathology
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Placenta
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pathology
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Placenta Diseases
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metabolism
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pathology
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Platelet Endothelial Cell Adhesion Molecule-1
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metabolism
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Pregnancy
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Pregnancy Complications, Neoplastic
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metabolism
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pathology
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Young Adult
2.Ultrastructural changes and effects of gestational diabetes mellitus on placental tissue.
Chinese Journal of Pathology 2011;40(12):856-859
Chorionic Villi
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metabolism
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pathology
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ultrastructure
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Diabetes, Gestational
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metabolism
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pathology
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Female
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Glucose
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metabolism
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Glycogen
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metabolism
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Humans
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Lipids
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analysis
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Microscopy, Electron, Scanning
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Microscopy, Electron, Transmission
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Placenta
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metabolism
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pathology
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ultrastructure
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Pregnancy
3.Clinicopathological study of intermediate trophoblastic non-tumor lesions: exaggerated placental site and placental site nodule.
Dan-hua SHEN ; Xiao-yun LIAO ; Yan-li LIU ; Hua WANG ; You-zhi YU
Chinese Journal of Pathology 2004;33(5):441-444
OBJECTIVETo investigate the clinicopathological features of intermediate trophoblastic non-tumor lesions, and to evaluate the position of immunohistochemistry in differential diagnoses.
METHODSClinical presentation and morphological study of 15 cases of exaggerated placental site (EPS) and 4 cases of placental site nodule or plaque (PSNP) were reviewed. Immunohistochemical stains for hCG, hPL, inhibin-alpha, PLAP, CK18 and Ki-67 were performed.
RESULTSThe age of patients ranged from 25 to 40 years with an average of 31.5 years for EPS and 26 to 39 years with an average of 34.3 years for PSNP. Microscopically, EPS was characterized by cords and small sheets of implantation site intermediate trophoblasts infiltrating the endometrium, myometrium and arterial walls. The general histological structures of the endometrium and myometrium were preserved. PSNP was characterized by multiple circumscribed nodular lesions consisting of so-called chorionic-type intermediate trophoblasts and hyaline-like matrix present in the endometrium. Immunohistochemical stainings for hPL and CK18 were positive in the 15 EPS cases. Immunoreactivity for CK18, Inhibin-alpha and PLAP was detected in 4 PSNP cases. The Ki-67 labeling index in 15 EPS cases was low (< or = 5%), while Ki-67 index in 4 PSNP cases was close to 0.
CONCLUSIONSThe clinical presentation and pathological features of EPS and PSNP differ from those of trophoblastic tumors (placental site trophoblastic tumor, epithelioid trophoblastic tumor and choriocarcinoma). Immunochemical staining is of great value in their differential diagnoses.
Adult ; Diagnosis, Differential ; Endometrium ; pathology ; Female ; Follow-Up Studies ; Humans ; Hysterectomy ; methods ; Inhibins ; metabolism ; Keratins ; metabolism ; Myometrium ; pathology ; Placenta ; metabolism ; pathology ; Placenta Diseases ; metabolism ; pathology ; surgery ; Placental Lactogen ; metabolism ; Pregnancy ; Trophoblastic Neoplasms ; pathology ; Trophoblastic Tumor, Placental Site ; pathology ; Trophoblasts ; pathology ; Uterine Neoplasms ; pathology
4.Intrahepatic cholestasis of pregnancy and fetal injury.
Lijuan ZHANG ; Fenghua ZHANG ; Lili TANG ; Weihong YANG ; Xue ZHANG
Journal of Central South University(Medical Sciences) 2013;38(6):645-652
Intrahepatic cholestasis of pregnancy (ICP) is an unique complication in pregnancy, which usually manifests in the second or third trimester, and mainly harms the fetus. Its pathogenesis is not yet clear, and placental pathological changes are insufficient to explain the clinical phenomenon.Recent studies had shown that the important cause of perinatal deaths may be the damage to the placental structure and function caused by the high bile acid level. In addition, the change of placental structure and function, umbilical cord factors, and endocrine changes can also cause the fetal development and intrauterine hypoxia. In recent years related researches focus on the toxic effect of bile acid on fetus heart, lungs, brain, liver, and other important organs, the placental vascular pathology, hemodynamic changes, umbilical cord blood vessel factors and the endocrine changes.
Bile Acids and Salts
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metabolism
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Cholestasis, Intrahepatic
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metabolism
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pathology
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Female
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Fetal Diseases
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etiology
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metabolism
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Fetus
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metabolism
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Humans
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Maternal-Fetal Exchange
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Placenta
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pathology
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Pregnancy
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Pregnancy Complications
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metabolism
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pathology
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Umbilical Cord
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metabolism
;
pathology
5.Twin pregnancy and partial hydatidiform mole following in vitro fertilization and embryos transfer: a novel case of placental mosaicism.
Cheng-juan SUN ; You-ping ZHAO ; Song YU ; Ling FAN ; Qing-qing WU ; Guang-hui LI ; Wei-yuan ZHANG
Chinese Medical Journal 2012;125(24):4517-4519
Twin pregnancy with mosaic partial hydatidiform mole (PHM) and survival of two healthy fetuses following in vitro fertilization and embryos transfer (IVF-ET) is a rare situation and is considered a challenge for management. A 32-year-old Chinese woman conceived twin pregnancy following IVF-ET. At 22 weeks' gestation, an additional intrauterine echogenic mass with features of PHM were shown by successive ultrasound examinations. At 35 weeks' gestation, two live male infants and two placentas were delivered by caesarean section (CS). Histologic examination of the abnormal placenta confirmed mosaic PHM. Genetic study showed the abnormal placental mosaicism (expressed in molar-69XXY and normal vili-46XY), co-existing with a hypospadia new-born (46XY) in one amniotic sac. However, the other one was normal. Serial serum β-hCG levels showed a declining trend and serum β-human chorionic gonadotropin (hCG) were undetectable at 6 months after delivery. The case demonstrated that it is possible to prolonged gestation by PHM under close surveillance during the entire pregnancy.
Adult
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Female
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Fertilization in Vitro
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Humans
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Hydatidiform Mole
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genetics
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Infant, Newborn
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Male
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Mosaicism
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Placenta
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metabolism
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pathology
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Pregnancy
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Pregnancy, Twin
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genetics
6.Partial rescue of the Na+-Ca2+ exchanger (NCX1) knock-out mouse by transgenic expression of NCX1.
Chung Hyun CHO ; So Young LEE ; Hee Sup SHIN ; Kenneth D PHILIPSON ; Chin O LEE
Experimental & Molecular Medicine 2003;35(2):125-135
The null mutation of cardiac Na+-Ca2+ exchanger (NCX1) gene in mice caused death of embryo in utero at embryonic day (ED) 9.0-9.5 and this embryonic lethality appears resulted from abnormal heart development. In the present study, we investigated whether transgenic re-expression of NCX1 in mutant cardiac myocytes could rescue these lethal defects. Transgenic mice expressing the canine NCX1 in a cardiac specific manner were bred into the NCX1 knock-out background but did not prevent the fetal lethality associated with the NCX1 null allele. However, the NCX1 knock-out embryos with an NCX1 transgene survived with heart beatings until ED 10.5 which was one day longer than the survival of the NCX1 knock-out embryos (ED 9.5). At ED 10.5, however, the partially rescued NCX1 embryos might have succumbed to the lack of an organized vasculature in the yolk sacs. The placental labyrinth layer was reduced in size and largely avascular. The transgenic re-expression of NCX1 rescued heart beatings and survived longer, but was still insufficient for the mice to be completely rescued. Importantly, NCX1 was observed to express in the yolk sac and the placenta of wild type mice. The results suggest that defects in extra-embryonic compartments are causal to the lethality, and that NCX1 may play an important role in establishing vascularization in extra-embryonic tissues.
Animals
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Embryo/*metabolism/pathology
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Embryo Loss
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Female
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Gene Deletion
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*Gene Expression
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Genetic Complementation Test
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Mice
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Mice, Knockout
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Mice, Transgenic
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Myocytes, Cardiac/metabolism
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Phenotype
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Placenta/metabolism/pathology
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Sodium-Calcium Exchanger/*genetics/*metabolism
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Survival Rate
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Yolk Sac/embryology/metabolism/pathology
7.Expression profiles of IL-10, TNF-a, and SOCS3 in placenta of pregnant women with intrahepatic cholestasis.
Li-qiong CAO ; Guang-di QU ; Dong-mei WANG
Chinese Journal of Hepatology 2012;20(12):935-938
OBJECTIVETo detect the expression profiles of suppressor of cytokine signaling 3 (SOCS3), interleukin (IL)-10, and tumor necrosis factor-alpha (TNF-a) in the placenta of women with intrahepatic cholestasis of pregnancy (ICP) and determine the clinical significance of the differential expressions.
METHODSPlacentas were collected from 37 ICP gravidas who delivered through cesarean section at the First Teaching Hospital of Xingjiang Medical University from October 2010 to May 2011 and from 35 healthy pregnant women (controls). SOCS3, TNF-a, and IL-10 protein levels were detected by immunoblotting and the Envision immunohistochemical method.
RESULTSTNF-a and IL-10 expression was detected in placentas of both groups, and was present mainly in the cytoplasm of trophoeytes. IL-10 expression was obviously lower in the ICP placentas than in the control placentas; meanwhile, TNF-a expression was obviously higher than in the control placentas (Z=-2.63, P less than 0.01). SOCS3 protein was significantly more abundant in the control placentas than in the ICP placentas. Furthermore, SOCS3 and IL-10 placental expressions were positively correlated (r=0.494, P less than 0.01), but there was a negative correlation between SOCS3 and TNF-a placental expressions (r=-0.472, P less than 0.01).
CONCLUSIONIn ICP, an increase of the type 1 cytokine, TNF-a, is associated with decreases of the type 2 cytokine, IL-10, and of SOCS3, which may reduce the secretion of IL-10. Furthermore, SOCS3 may contribute to ICP pathogenesis by modulating the Th1/Th2 cytokine balance.
Adult ; Case-Control Studies ; Cholestasis, Intrahepatic ; metabolism ; pathology ; Female ; Humans ; Interleukin-10 ; metabolism ; Placenta ; metabolism ; Pregnancy ; Pregnancy Complications ; metabolism ; pathology ; Pregnancy Trimester, Third ; Suppressor of Cytokine Signaling 3 Protein ; Suppressor of Cytokine Signaling Proteins ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism ; Young Adult
8.Effects of pregnancy cocaine exposure on the mother and fetus: a murine model.
Jun SONG ; Xiao-Wei GUAN ; Jia-Qian REN ; Wei HE
Acta Physiologica Sinica 2002;54(4):342-348
The aim of the experiments was to develop and characterize a murine model for investigating the effects of prenatal cocaine exposure on the mother and fetus. Pregnant mice were separated into three groups: group 1 was treated with cocaine HCl at 10 mg/kg twice daily (COC); group 2 was treated with saline at 10 ml/kg twice daily (SAL); and group 3 was pair-fed with the COC dams and was injected with saline following the same schedule (SPF) from embryonic day (E) 8 to 17. We utilized high-pressure liquid chromatography (HPLC) with UV detector and electrochemical detector to test the concentrations of cocaine, dopamine and serotonin, as well as HE staining to observe morphological alterations of liver and placenta. Though less food intake and lower weight gain were observed in COC and SPF groups but not in SAL dams, lower fetal body weight and brain weight were only seen in COC offspring. Pharmacological analysis revealed that cocaine was found in fetal plasma at 15 min following intraperitoneal administration on E17, accompanied with elevated concentrations of dopamine (DA) and serotonin (5-HT) in fetal brain. We also observed morphological changes in liver and placenta of cocaine-exposed fetuses. The present study indicates that pregnancy cocaine exposure can lead to maternal undernutrition and developmental abnormality of the fetal brain, liver and placenta. It is suggested that the developmental abnormality of the fetuses induced by cocaine is due to the toxicological effect of cocaine but not to maternal undernutrition.
Animals
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Brain
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metabolism
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pathology
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Cocaine
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adverse effects
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blood
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Disease Models, Animal
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Dopamine
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metabolism
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Female
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Fetus
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drug effects
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pathology
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Liver
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pathology
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Malnutrition
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Maternal Exposure
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adverse effects
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Maternal Nutritional Physiological Phenomena
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Mice
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Mothers
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Placenta
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pathology
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Pregnancy
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Serotonin
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metabolism
9.p16 protein expression in the transplacental induced brain tumor in rat.
Zhong-yuan ZHANG ; Yan-fang ZHANG
Chinese Journal of Surgery 2004;42(6):358-361
OBJECTIVETo study in series the p16 protein expression on the rat brain tumor induced transplacentally by ENU.
METHODSThe p16 protein expression was determined with immuno-histochemistry stain on the offspring's brain at their 60, 90, 120, 150 days after birth.
RESULTS(1) p16 proteins were expressed in all of the brain samples in the 60-day group; occasionally negative in the 90-day group; partly expressed in the 120-day group; significantly less expressed in the 150-day group. (2) The rate of expression in the tissue around tumor was higher than that in the tumor. (3) The p16 protein was mainly orientated in the nuclear of cell and sporadically orientated in the cytoplasm.
CONCLUSION(1) It shows the p16 protein expression decreases with the increase of tumor incidence in the rat brain, which accompanies the start and development of the induced tumor. So we speculate that the dysfunction of p16 gene is one of the factors related to tumor incidence in this animal model. (2) The p16 protein is mainly orientated in the nuclear of cell and sporadically orientated in the cytoplasm.
Animals ; Brain ; metabolism ; pathology ; Brain Neoplasms ; chemically induced ; metabolism ; pathology ; Cyclin-Dependent Kinase Inhibitor p16 ; biosynthesis ; Disease Models, Animal ; Ethylnitrosourea ; Female ; Glioma ; chemically induced ; metabolism ; pathology ; Immunohistochemistry ; Male ; Placenta ; drug effects ; Pregnancy ; Rats ; Rats, Sprague-Dawley
10.Increased expression of placenta growth factor in lung tissue of paraquat-induced rat pulmonary fibrosis model.
Min-hui ZHENG ; Mu-sen DAI ; Li-fang LIN
Chinese Journal of Industrial Hygiene and Occupational Diseases 2007;25(9):527-531
OBJECTIVETo investigate the dynamic expression of placenta growth factor (PLGF) in the lungs with paraquat (PQ)-induced pulmonary fibrosis.
METHODSForty-two adult healthy female Sprague-Dawley (SD) rats were randomly divided into two groups: the control group and the PQ group. Each group was divided into three subgroups, seven animals each. The rats in PQ group were treated intragastrically (ig) with PQ (40 mg/kg) and the rats in control group were treated with the same volume of saline at the beginning of the experiment. The animals of model and control group were sacrificed and lungs were harvested on the 7(th), 14(th) and 28th days respectively. A semiquantitative assay of histological examination and hydroxyproline in lung tissues were used to determine the severity of alveolitis and fibrosis. RT-PCR and immunohistochemistry were used to detect the mRNA and protein expression of PLGF.
RESULTSHydroxyproline contents in lung tissue were significantly increased after PQ administration. Inflammatory cell infiltration and fibrotic scores were more prominent in the model group compared to the control group. Further study showed that PLGF mRNA on day 7, 14 and 28 (1.28 +/- 0.29, 0.80 +/- 0.07, 0.65 +/- 0.13) and positive index of protein expression (2.27 +/- 0.34, 1.78 +/- 0.41, 1.25 +/- 0.69) in the PQ group were all upregulated as compared with those of the control group.
CONCLUSIONThe PLGF expression in the lung tissue in rats with paraquat-induced pulmonary fibrosis is upregulated.
Animals ; Disease Models, Animal ; Female ; Hydroxyproline ; metabolism ; Lung ; metabolism ; pathology ; Paraquat ; poisoning ; Placenta Growth Factor ; Pregnancy Proteins ; genetics ; metabolism ; Pulmonary Fibrosis ; chemically induced ; metabolism ; pathology ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley