Objective To assess the expression of thioredoxin reductase(TR)and thioredoxin (Trx)mRNA,TR activity in human placenta in women with preeclampsia,and to discuss the relationship between Trx system and the pathogenesis of preeclampsia.Methods Twenty-sixwomen with preeclampsia(10 mild and 16 severe)and 28 healthy gravidas (control) were included in this study.Semi-quantitative reverse transcription polymerase chain reaction(RT-PCR)were employed to demonstrate the expression of TR and Trx in placentas.TR activity was measured spectrophotometrically.Results The expression of TR mRNA(mild:0.865±0.018;severe:0.800±0.025,P＜0.05)and Trx mRNA(mild:0.873±0.008;severe:0.818±0.025,P＜0.05)were lower in placenta of preeclampsia than in the control group(TR mRNA:0.893±0.023;Trx mRNA:0.918±0.023.P＜0.05),and those levels in the severe preeclampsia group were lower than in the mild ones.Both the mild and severe preeclampsia groups showed lower TR activity than the control(mild:17.732±1.653;severe:15.626±1.543 vs 19.770±2.432,P＜0.05),and that of the severe preeclampsia group was lower than that of the mild ones.Positive correlation was found between the TR activity and TR mRNA expression in both groups(r=0.612,P＜0.001).Conclusions Abnormal decreased expression of TR mRNA and Trx mRNA and TR activity in human placenta of preeclampsia might participate and play an important role in the pathogenesis of preeclampsia.

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.

Objective To evaluate the value of transabdominal sonography(TAS),transvaginal sonography(TVS),sonohysterography(SHG),and hysteroscopy(HS) in the detection of endometrial pathology in the patients with uterine cavity lesions. Methods Uterine abnormality and disease were routinely examined by TAS, TVS, SHG.Results TAS was performed in 88 cases,TVS in 45 cases,SHG in 39 cases,and HS in 23 cases.Comparison was made between different means,showing SHG and HS with the highest sensitivity,accuracy and positive evaluation,respectively as 94.29%, 90.24%, 94.29%,and 95.65%, 91.67%, 95.65%.Conclusions Transvaginal sonohysterography is an easy, accurate,econimical,painless and no-injury technique for detecting endomatrial pathology and endoluminal masses.

Objective: To investigate the changes of the cell cycle regulators ATM, Chk2 and p53 and cell cycle arrest in HeLa cells after cisplatin therapy. Methods: The proliferation-inhibiting rates of HeLa cells induced by cisplatin of different concentrations were measured by MTT assays. The mRNA and protein expressions of ATM, Chk2 and p53 of HeLa cells with and without cisplatin were detected by RT-PCR and Western blot, respectively. The cell cycle analysis was conducted by flow cytometric analysis. Results: Cisplatin inhibited the proliferation of HeLa cells in a dose- and time-dependent manner. The mRNA and protein expressions of ATM, Chk2 and p53 were increased in HeLa cells treated with cisplatin. The cell cycle was arrested in G2/M phase in HeLa cells treated with cisplatin. Conclusion: Activation of ATM, Chk2 and p53 might be critical in determining whether cells survive or undergo apoptosis. Targeting ATM, Chk2 and p53 pathway might be a promising strategy for reversing chemoresistance to cisplatin in cervical cancer.

Objective: To investigate the changes of the cell cycle regulators ATM, Chk2 and p53 and cell cycle arrest in HeLa cells after cisplatin therapy. Methods: The proliferation-inhibiting rates of HeLa cells induced by cisplatin of different concentrations were measured by MTT assays. The mRNA and protein expressions of ATM, Chk2 and p53 of HeLa cells with and without cisplatin were detected by RT-PCR and Western blot, respectively. The cell cycle analysis was conducted by flow cytometric analysis. Results: Cisplatin inhibited the proliferation of HeLa cells in a dose- and time-dependent manner. The mRNA and protein expressions of ATM, Chk2 and p53 were increased in HeLa cells treated with cisplatin. The cell cycle was arrested in G2/M phase in HeLa cells treated with cisplatin. Conclusion: Activation of ATM, Chk2 and p53 might be critical in determining whether cells survive or undergo apoptosis. Targeting ATM, Chk2 and p53 pathway might be a promising strategy for reversing chemoresistance to cisplatin in cervical cancer.

Objective： This study was designed to investigate the relationship between p16 protein expression and gastric carcinogenesis,depth of invasion, lymph node metastasis, and evaluate the role of deletion and mutation of p16 gene in exon 2 in gastric carcinoma. Methods： p16 protein expression in gastric carcinoma and precancerous lesion was examined by streptavidin-peroxidase conjugated(S-P) method; The deletion and mutation of p16 gene were examined respectively by polymerase chain reaction(PCR) and polymerase chain reaction single-strand conformation polymorphism analysis(PCR-SSCP) in gastric carcinoma. Results： ① The positive rates of p16 protein expression were 96.25％ (77/80) in normal gastric mucosa, 92.00％ (45/50) in dysplastic gastric mucosa, and 47.54％ (58/122) in gastric carcinoma. The positive rate of p16 protein expression in gastric carcinoma was significantly lower than that in normal gastric mucosa and in dysplastic gastric mucosa (P<0.05). ② The positive rate of p16 protein expression in mucoid carcinoma (10.00％ ,1/10) was significantly lower than that of poorly differentiated carcinoma (51.22％ ,21/41), undifferentiated carcinoma (57.69％ ,15/26), and signet ring cell carcinoma (62.50％ ,10/16) (P< 0.05). ③ The positive rates of p16 protein in 30 cases paired primary and lymph node metastatic gastric carcinoma were 46.67 ％ (14/30) in primary gastric carcinoma,16.67％ (5/30) in lymph node metastatic gastric carcinoma. The positive rate of lymph node metastatic carcinoma was significantly lower than that of primary carcinoma(P<0.05). ④ Evaluation of mutation and deletion of p16 gene： There was no mutation of p16 gene in exon 2, but there were 5 cases displayed deletion of p16 gene in exon 2 in the 25 primary gastric carcinoma. Conclusions： ① The expression loss of p16 protein is related to carcinogenesis, histopathological subtypes,and lymph metastasis of gastric carcinoma. ② The mutation of p16 gene in exon 2 may not be involved in gastric carcinogenesis. But the deletion of p16 gene in exon 2 might be involved in gastric carcinogenesis.

Aleutian mink disease parvovirus (AMDV) causes a persistent infection associated with immune complex disease, hypergammaglobulinemia, and high levels of antiviral antibodies. Despite the presence of an antibody, the virus is not cleared in vivo. Pre-existing antibodies may enhance viral infections, by Fc-receptor-mediated antibody-dependent enhancement (ADE), but the mechanism that underlies ADE has not been fully defined. Three models have been proposed, including: (1) interactions between antibody and FcR, complement C3 fragment and CR, or between C1q and C1qR, which promotes viral attachment to cells; (2) suppression of IFN-gamma-mediated host-cell antiviral gene expression by the upregulation of negative regulators of pathogen pattern recognition; and (3) the promotion of early IL-10 secretion. In addition, the role of cytokine IL-6 in ADE mediated disease development is discussed, to facilitate a better understanding of the pathogenesis of AMDV infection, as well as give insights into rational vaccine design approaches.
Aleutian Mink Disease ; immunology ; virology ; Aleutian Mink Disease Virus ; genetics ; immunology ; Animals ; Antibodies, Viral ; immunology ; Antibody-Dependent Enhancement ; Mink ; immunology ; virology

ObjectiveTo investigate the effects of vascular endothelial growth factor (VEGF) and dexamethasone on mRNA expressions of surfactant protein B (SP-B) and transforming growth factor-β1 (TGF-β1) of type Ⅱ alveolar epithelial cell (AECⅡ). MethodsAECⅡ were isolated and purified from fetal rat lung tissues,then cultured with different dose of VEGF (25,50 and 100 ng/ml) and dexamethasone (25,50,100 and 200 nmol/ml).The mRNA levels of SP-B and TGF-β1 were detected by real-time quantitative polymerase chain reaction (RT-PCR) and expression of TGF-β1 protein was detected by immunocytochemistry.ANOVAor q-test wasappliedtocompare the difference among groups.ResultsCompared with control group,SP-B mRNA levels in 25 ng/ml VEGF group and 25,50,100 and 200 nmol/ml dexamethasone groups were higher (13.500±3.172,3.547±0.690,5.219±0.782,3.493±0.335,and 3.981 ± 1.133 vs 1.001 ± 0.059,q=-5.286,-4.943,- 7.228,- 9.906 and - 3.525 respectively,P＜0.05) ; TGF-β1 mRNA expression of 25 ng/ml VEGF group,50,100 and 200 nmol/ml dexamethasone group was lower (0.451 ± 0.078,0.579±0.019,0.422 ± 0.020 and 0.769 ± 0.025 vs 1.019±0.226,q=4.110,3.356,4.551 and 1.901 respectively,P＜0.05) ; other groups had no significant differences compared with control group (P＞0.05).Immunocytochemistry showed that the positive rate of TGF-β1 expression in 25 ng/ml VEGF,50,100 and 200 nmol/ml dexamethasone group was 23％,26％,22％ and 29％,respectively,while in the control group,the expression of TGF-β1 was positive in most of the AECⅡ (80％).ConclusionsBoth VEGF and dexamethasone could increase the expression of SP-B at mRNA level at appropriate concentrations.At the same time,the expression of TGF-β1 is inhibited.It is suggested that both VEGF and dexamethasone might increase the mRNA expression of SP-B by inhibiting the expression of TGF-β1.

The normal structure of axonal terminals in lamina V of cervical spinal cordof the adult rat was examined with EM.Among 4039 various types of terminals inlamina V,the terminals with clear round synaptic vesicles(R)and the terminalswith clear flat synaptic vesicles(F)constitute about 40% each,the terminals withlarge granular vesicles(LG)about 16% and the central terminals of syntapticglomeruli about 3%.In addition,about 3.2% of the various types of terminalscontain neurofilaments,about 0.9% exhibit low electron dense axoplasm and thevesicles are partly lost or clumping.The synapses of the terminals in lamina V aremainly axodendritic,a small number of them are axoaxonal.There are more F,fewer R and LG in lamina V than those in lamina Ⅱ;thesynapses between the terminals and proximal dendrites,and axosomatic synapses aremore commonly seen in lamina V than in Ⅱ.

Objective To analyze the incidence rate and mortality of perinatal asphyxia and effects of new resuscitation technique on asphyxia as well as the risk factors of asphyxia in latest 10 years.Methods A retrospective evaluation was done for all the newborns who were born in the provincial women and children′s health care hospital from 1995 to 2004.The morbidity,mortality and fatality rate were calculated for each observed year and different seasons.The influence of gender,body weight,gestational age as well as polyembryony and mode of delivery on the asphyxia was analyzed.Results The morbidity of mild birth asphyxia was decreased dramatically and maintained at about 1.5% after using new resuscitation technique,however,there were no obvious effects on the sever asphyxia.In the same time,no big influence on fatality rate of birth asphyxia was observed.The incidence rate was highest in April,but the mortality and fatality of asphyxia was highest in July.The incidence of asphyxia was also related with gender,polyembryony,birth weight,prematurity babies and aids to delivery from voginal.Conclusions The incidence of perinatal asphyxia is related with the gender,polyembryony,birth weight and gestation age as well as seasons.New resuscitation technique can reduce the morbidity of mild birth asphyxia,and no effect on the severe asphyxia as well as fatality rate.