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

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.

Objective To study the clinical value of mammography and ultrasound needle localization biopsy technique in clinical nonpalpable breast disease.Methods 148 patients with negative clinical palpation were operated only because of the mammography or ultrasound findings of lesions.They were undergone localized excision biopsy and derived definite pathological diagnosis.By histopathology diagnosis,benign and malignant lesions,lesion size,complete resection rate were statistically analyzed.Results 21 cases in 148 cases were malignant lesions(14.2％),which were all early breast cancer.The other 127 cases were benign breast disease(85.8％).147 cases were successfully resected at the first time and 1 case was successfully resected at the second time.Conclusion Mammography and Ultrasound fine needle localized biopsy in nonpalpable breast disease diagnosis and treatment has great significance,which can raise early diagnosis rate of breast cancer without mass,and this method is simple and easy for promotion.

Objective:This study aims to investigate the method and clinical outcomes of feeding tube placement and periopera-tive nutritional support for esophageal carcinoma patients. Methods:A total of 513 esophageal carcinoma patients who have undergone radical resection and reconstruction by a single operating group between January 2012 and December 2013 participated this study. Feed-ing tubes were inserted via the nasal path of 497 cases and by jejunostomy in 16 cases. Early enteral nutrition (EN) was administered through the feeding tubes 24 h postoperatively with a stepwise increase, whereas supplementation of parenteral nutrition (PN) was ter-minated until total EN. Results:Feeding tubes were successfully inserted in all patients during operation. No death or nutritional and metabolic disorders were documented during the observation period. No differences in anastomotic fistula, pulmonary complication, and incision infection were identified between the nasointestinal and jejunostomy groups (P>0.05). A higher incidence of intestinal ob-struction was observed in the jejunostomy group than in the nasointestinal group (P<0.05). Conclusion:Effective placement of nasoin-testinal tube and early enteral feeding are safe and effective methods for patients who have undergone esophagectomy for esophageal carcinoma.