Humans ; Hypertension, Pulmonary ; genetics

Adult ; Antibiotics, Antineoplastic ; therapeutic use ; Benzamides ; Blast Crisis ; drug therapy ; Drug Resistance, Neoplasm ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; drug therapy ; Male ; Piperazines ; pharmacology ; Pyrimidines ; pharmacology ; Sirolimus ; therapeutic use

Objective To study the effect of bromocriptine(BRC) on the activation of T lymphocyte stimulated by phytohemagglutinin(PHA).Methods After CD4+ T cell line Jurkat E6-1 cells were stimulated by PHA,prolactin(PRL) and BRC,respectively,the expression of linker for activation of T cells(LAT) and zeta-chain T cell receptor associated protein kinase 70 000(ZAP-70) mRNA of T lymphocytes were checked by RT-PCR.The expression of PRL mRNA of T lymphocytes was detected by Real time PCR.The expression of CD25(cluster of differentiation) as a marker of early activation on the surface of T lymphocytes was detected by flow cytometry,and the activation of nuclear factor-?B(NF-?B) was detected by luciferase reporter system.Results 1.BRC inhibited the expression of ZAP-70 as the common signal molecules both in the T lymphocyte activation pathway and PRL-prolactin-prolactin receptor(PRLR) signal transduction pathway,and decreased the expression of PRL mRNA produced by activation T lymphocytes.2.BRC enhanced the expression of LAT mRNA as another important signal molecular on the T lymphocytes and CD25 on the surface of the T lymphocytes.3.The activation of NF-?B of T lymphocytes was decreased.Conclusions BRC might inhibit the activation of T lymphocytes by inhibiting the expression of ZAP-70,the common signal molecules between T lymphocytes activation and PRL-PRL pathway,and PRL mRNA,the like-T lymphocyte growth factor.

Acid Anhydride Hydrolases ; metabolism ; Apoptosis ; Biomarkers, Tumor ; metabolism ; Caspases ; metabolism ; Cell Adhesion Molecules ; metabolism ; Chromosome Deletion ; Drug Delivery Systems ; GPI-Linked Proteins ; metabolism ; Humans ; Hyaluronoglucosaminidase ; metabolism ; In Situ Hybridization, Fluorescence ; methods ; Lung Neoplasms ; diagnosis ; drug therapy ; genetics ; metabolism ; Neoplasm Proteins ; metabolism ; Neoplasm Staging ; Receptor, Epidermal Growth Factor ; metabolism ; Vascular Endothelial Growth Factor A ; metabolism

Adenocarcinoma ; drug therapy ; genetics ; metabolism ; pathology ; surgery ; Adenocarcinoma, Bronchiolo-Alveolar ; drug therapy ; genetics ; metabolism ; pathology ; surgery ; Adenocarcinoma, Papillary ; metabolism ; pathology ; Cadherins ; metabolism ; Diagnosis, Differential ; Genes, erbB-1 ; genetics ; Humans ; Lung Neoplasms ; drug therapy ; genetics ; metabolism ; pathology ; surgery ; Lymphatic Metastasis ; Mucin-1 ; metabolism ; Mutation ; Neoplasm Invasiveness ; beta Catenin ; metabolism

The author analyzes the basic information in recent years,including overall students scale,students' age,application trends,etc.Some suggestions are made,regarding to recruiting plan,applicant qualification,recruiting mode,etc,in order to further improve the recruiting and graduate management.

Objective To study the effect of astragaloside on proliferation and apoptosis in human keloid fibroblasts.Methods The human keloid fibroblast ceils were treated with different concentration of astragaloside(10、20、40 ng/mL).Cell proliferation was detected by MTT,the gene expreesion levels and protein levels of apoptosis-related proteins,survivin,p53 and Bcl-2.were determined by real-time PCR and Western blot,respectively.Results Comparecl with control group(treated with 0 ng/mL astragaloside),the absorbance values (A490 nm) of each concentration group were significantly reduced,which suggest that the proliferation of all keloid fibroblast were markably inhibited in a dose-dependent way (P＜0.05).The gene expreesion levels and protein levels of apoptosis-related proteins,survivin、Bcl-2 were largely suppressed and P53 werelargely promoted in a dose-dependent.Conclusion The keloid fibroblasts cells proliferation and apoptosis could be regulated by astragaloside.

Carcinoma, Non-Small-Cell Lung ; genetics ; metabolism ; pathology ; DNA Mutational Analysis ; DNA, Neoplasm ; genetics ; isolation & purification ; Genes, erbB-1 ; Humans ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Mutation ; Paraffin Embedding ; methods ; Polymerase Chain Reaction ; methods ; Real-Time Polymerase Chain Reaction ; methods ; Receptor, Epidermal Growth Factor ; genetics

Background and purpose:Pterostilbene is a natural antioxidant, whose role in retinoblastoma remains unclear. The aim of this study is to probe the effects of pterostilbene on the proliferation, apoptosis and autophagy in retinoblastoma WERI-Rb-1 cell lines.Methods:Cell counting kit-8 (CCK-8) assays were used to analyze the effects of pterostilbene on the proliferation of WERI-Rb-1 cells. Apoptosis rate was determined by Annexin V/PI. Autophagic vacuoles were observed by acridine orange staining. LC3 and P62 protein expressions were determined using Western blot.Results:Pterostilbene significantly inhibited the proliferation of WERI-Rb-1 cells (P<0.01). The cell viability were (93.02±0.47)%, (55.10±2.04)% and (30.33±1.45)% after WERI-Rb-1 cells were treated with 25, 50 and 100 μmol/L pterostilbene for 24 h, and the cell viability were (88.38±3.70)%, (53.37±1.17)%, (29.60±1.05)% after WERI-Rb-1 cells were treated with 50 μmol/L pterostilbene for 12, 24 and 48 h. Pterostilbene induced cell apoptosis (P<0.01), the apoptosis rates of control group, 24 h treated group and 48 h treated group were (4.08±0.79)%, (13.44±2.12)% and (23.49±2.01)%. Pterostilbene induced autophagy of WERI-Rb-1 cells, increased LC3 expression, downregulated P62 expression and increased the number of autophagic vacuoles in WERI-Rb-1 cells (P<0.01). 3-MA and Beclin1 were able to rescue pterostilbene-induced cell death (P<0.01). After 3-MA was used to blunt autophagosome formation, the apoptosis rate markedly decreased in 3-MA+pterostilbene-treated cells compared with cells treated with pterostilbene alone [(12.97±2.09)%vs (8.35±1.11)%], and after siRNA was used to knockdown Beclin1, the apoptosis rate had the same change [(13.80±2.19)%vs (9.62±0.52)%].Conclusion:Pterostilbene can inhibit the proliferation of WERI-Rb-1 cells and induce cell apoptosis via autophagy activation.

BACKGROUND:Excessive apoptosis and decreased infiltration of cytotrophoblasts are essential causes for hypertension in pregnancy. Human placenta-derived mesenchymal stem cels contribute to damage repair, which has been shown in many studies, and moreover, human placenta-derived mesenchymal stem cels have a certain endocrine function and can act on the other tissues in an autocrine or paracrine manner. Therefore, we attempt to explore whether the human placenta-derived mesenchymal stem cel can repair damaged cytotrophoblasts, and then to gestational hypertension.
METHODS/DESIGN:This is a randomized controled cytological experiment. Human placenta-derived mesenchymal stem cel culture medium is colected and filtrated as human placenta-derived mesenchymal stem cel conditioned medium. Human cytotrophoblasts, JEG-3 cels, are cultured and randomized into three groups:15% normal pregnant serum is added in control group; 15% serum from severe pre-eclampsia patients is added in gestational hypertension model group; and in condition medium group, 15% serum from severe pre-eclampsia patients is added for 24 hours of culture, and then human placenta-derived mesenchymal stem cel conditioned medium containing 15% serum from severe pre-eclampsia patients is used instead. Flow cytometry is used to detect cel apoptosis rate.
DISCUSSION: This study wil help to find the feasibility of cel transplantation for gestational hypertension by exploring the effect of human placenta-derived mesenchymal stem cels on cytotrophoblasts function in gestational hypertension.
ETHICAL APPROVAL: The protocol is approved by the Ethics Committee of Shenyang Central Hospital of Shenyang Medical University. Informed consent is obtained from normal and pre-eclampsia women in pregnancy.