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.

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

Antihypertensive Agents ; therapeutic use ; Endothelin Receptor Antagonists ; therapeutic use ; Familial Primary Pulmonary Hypertension ; Humans ; Hypertension ; drug therapy ; Hypertension, Pulmonary ; drug therapy

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

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

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 explore the clinical effect of multidisciplinary cooperation model in the prevention of acquired dysphagia in ICU.Methods:A multidisciplinary team was set up to collect 118 patients in Neurosurgery ICU of our hospital as the research object. The patients were divided into the experimental group and the control group, 59 cases in each group. The control group implemented the routine nursing measures of ICU, and the experimental group implemented the multidisciplinary cooperative nursing mode. The incidence of ICU acquired swallowing disorders (ICU-ASD) and complications of the two groups were compared.Results:There was no significant difference between the two groups in the incidence of swallowing dysfunction 24 hours after tracheal extubation ( P>0.05). The incidence of swallowing dysfunction 48 hours and 72 hours after tracheal extubation in the control group was 11.86% (7/59) and 16.95% (10/59) respectively, while the test group was 1.69% (1/59) and 3.39% (2/59) respectively. The difference was statistically significant ( χ 2values were 4.827 to 7.230, P< 0.05 or 0.01); the incidence of aspiration, aspiration pneumonia and malnutrition in the control group were 11.86% (7/59), 10.17% (6/59) and 8.47% (5/59), respectively, while the test group were 1.69% (1/59), 0 and 0, respectively, with statistically significant difference ( χ 2value was 4.827, P< 0.05). Conclusion:Multidisciplinary cooperation model can effectively prevent the incidence of ICU-ASD, and ultimately reduce the incidence of complications.

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.