ABSTRACT
Objective@#To investigate the status of eating disorders among overweight and obese adolescents as well as provide the basis for developing obesity precautionary and eating disorders.@*Methods@#910 adolescents of grade 4 to 6 in primary schools and grade 1 to 3 in junior middle schools were recruited in Bengbu by cluster random sampling to examine the association between obesity and eating disorders.@*Results@#A total of 203 children (22.3%) were overweight and obese, 547 children (60.1%) were normal weight and 160 children (17.6%) were low weight. The prevalence of overweight and obese in boys were significantly higher than those in girls (30.6% vs. 13.0%; χ2=40.55, P<0.01). Compared with normal weight group and low weight group, the scores of drive for thinness (DT), body dissatisfaction (BD), low self-esteem (LSE) and eating disorder risk composite (EDRC) were significantly higher in overweight and obese group (P<0.05). There was a positive association between the scores of DT(r=0.19), BD(r=0.30), LSE(r=0.09), interceptive deficits (ID) (r=0.08) and EDRC (rs=0.11) with body mass index (BMI)(P<0.05).@*Conclusion@#Eating disorders were associated with overweight and obesity of adolescents. A targeted strategies and measures should be conducted.
ABSTRACT
The objective of this study was to explore the effects of microRNA-17-92 on the biological characteristics of K562 cells. The expression of miR-17-92 in K562 cells transfected with miRNA-17-92 mimic was detected by real time PCR. The effect of microRNA-17-92 on K562 cell proliferation was detected by CCK-8 method. Apoptosis of K562 cells was detected by Annexin V-PI labeling. Cell cycle distribution was determined by using flow cytometry. Western blot was performed to determine the protein levels of Crk. The results indicated that the transfection with miR-17-92 mimic increased expression of mature miR-17-92 in K562 cells. Compared with control group, cell proliferation and cell amount in S-phase of miR-17-92 mimic transfected group significantly increased, cell apoptosis decreased. The expression of signal connector protein Crk was greatly up-regulated in miR-17-92-mimic-transfected K562 cells. It is concluded that miR-17-92 can promote proliferation, inhibit apoptosis and regulate the cell cycle of K562 cells.
Subject(s)
Humans , Apoptosis , Cell Cycle , Cell Proliferation , Gene Expression Regulation, Leukemic , HL-60 Cells , K562 Cells , Leukemia, Myelogenous, Chronic, BCR-ABL Positive , Genetics , Metabolism , MicroRNAs , Genetics , TransfectionABSTRACT
<p><b>OBJECTIVE</b>To evaluate the association between the polymorphisms of excision repair cross complementation group 1 (ERCC1), X-ray repair cross complementing 1 (XRCC1), glutathione S-transferase Pi 1 (GSTP1) and the survival of advanced gastric cancer patients treated with oxaliplatin-based combination chemotherapy.</p><p><b>METHODS</b>Eighty five patients with advanced gastric cancer accepted oxaliplatin/5-FU-based chemotherapy as first-line chemotherapy were investigated. Peripheral venous blood was taken before chemotherapy. DNA was extracted from peripheral venous blood. The genetic polymorphisms were detected by real-time PCR assay. The association between time to progression, overall survival and the polymorphisms was analyzed.</p><p><b>RESULTS</b>The median time to progression of the 85 cases was 5.3 months, and the median overall survival was 8.0 months. ERCC1-118 C/C, XRCC1-399 G/G and GSTP1-105 A/G + G/G were favorable genotypes and the number of the favorable genotypes was associated with survival of the patients. The median overall survival was 12.5 months, 10.0 months, 6.5 months and 4.5 months for patients with 3 favorable genotypes, 2 favorable genotypes, 1 favorable genotype and none favorable genotype, respectively, with a significant difference (χ(2) = 35.54, P < 0.01).</p><p><b>CONCLUSION</b>Genetic polymorphisms of ERCC1-118, XRCC1-399 and GSTP1-105 are associated with TTP and OS of advanced gastric cancer patients treated with oxaliplatin/5-Fu-based combination chemotherapy as the first-line chemotherapy.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Adenocarcinoma , Drug Therapy , Genetics , Pathology , Adenocarcinoma, Mucinous , Drug Therapy , Genetics , Pathology , Antineoplastic Combined Chemotherapy Protocols , Therapeutic Uses , DNA-Binding Proteins , Genetics , Disease Progression , Endonucleases , Genetics , Fluorouracil , Follow-Up Studies , Glutathione S-Transferase pi , Genetics , Neoplasm Staging , Organoplatinum Compounds , Polymorphism, Genetic , Stomach Neoplasms , Drug Therapy , Genetics , Pathology , Survival Rate , X-ray Repair Cross Complementing Protein 1ABSTRACT
The aim of this study was to evaluate the predictive value of the polymorphism Glutathione S-transferase P1 (GSTP1) Ile(105)Val on oxaliplatin/5-FU-based chemotherapy in advanced gastric cancer. Patients with advanced gastric cancer accepted oxaliplatin/5-FU-based chemotherapy as first-line chemotherapy were investigated. GSTP1 Ile(105)Val polymorphism was detected by TaqMan-MGB probe allelic discrimination method. Response to treatment was assessed by disease controlled rate. Time to progression, overall survival and toxicities were recorded. Final patient outcomes were as follows: the allele frequencies of GSTP1 were (105)Ile/(105)Ile 52%, (105)Ile/(105)Val 41% and (105)Val/(105)Val 7%. For patients with (105)Ile/(105)Ile and those with at least one (105)Val allele, disease control rate was 39% and 71% (P=0.026), respectively; median time to progression was 4.0 and 7.0 months (P=0.002); median overall survival time was 7.0 and 9.5 months (P=0.002). Neurological toxicity was more frequently occurred in patients with two (105)Ile alleles (P=0.005). In conclusion, patients with at least one (105)Val allele have better prognosis and response to oxaliplatin/5-FU-based regimen as first-line treatment for patients with advanced gastric cancer.
ABSTRACT
Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disease of transformed hematopoietic progenitor cells. In order to investigate the role of sphingosine kinase-1 (SphK-1)/sphingosine 1-phosphate (S1P) signal pathway in the expression of CML cells, and to explore whether P210(bcr/abl) involved is activating SphK-1/S1P signal pathwey, the expressions of SphK-1 and S1P receptor mRNA in bcr/abl positive K562 cells and bcr/abl positive primary CML cells were detected by RT-PCR, the imatinib mesylate, the specific inhibitor of P210(bcr/abl) was employed to inhibit the P210(bcr/abl) tyrosine kinases of K562 cells and CML primary cells, and then the intracellular SphK-1 activity was assayed. The results indicated that after being cultured with 2.5 micromol/L imatinib mesylate for 0.5, 2, 6, 24 and 48 hours, the intensions of inhibiting SphK-1 activity were 0.007%, 38.9%, 34.6%, 28.1% and 76.1% resepectively. SphK-1 activity in CML cells also was reduced by 2.5 micromol/L imatinib mesylate (16.8% - 41.9% decrease). It is concluded that the CML cells express SphK-1 and different S1P receptor, and P210(bcr/abl) fusion protein in CML cells can activate SphK-1.
Subject(s)
Humans , Benzamides , Fusion Proteins, bcr-abl , Genetics , Metabolism , Imatinib Mesylate , Leukemia, Myelogenous, Chronic, BCR-ABL Positive , Genetics , Metabolism , Lysophospholipids , Genetics , Metabolism , Phosphotransferases (Alcohol Group Acceptor) , Genetics , Metabolism , Piperazines , Pharmacology , Pyrimidines , Pharmacology , RNA, Messenger , Genetics , Metabolism , Signal Transduction , Genetics , Sphingosine , Genetics , MetabolismABSTRACT
Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disease of transformed hematopoietic progenitor cells. It is now clear that the chimeric bcr/abl P210(bcr/abl) fusion protein, which is generated by the reciprocal translocation t (9; 22), inhibits apoptosis and increase proliferation. P210(bcr/abl) plays a central role in the pathophysiology of CML. The purpose of this study was to construct a cell line model that bcr/abl expression can be regulated by Tet-off inducing-expression-system. The full-length b3a2 bcr/abl cDNA was subcloned into the pTRE2hyg expression vector to construct the pT2-P210 plasmid. 293 cells were firstly transfected with Tet-off plasmid and the clone that the Tet-off system can work effectively after transfected with pTRE2hyg-LUC was selected by luciferase activity assay. The pT2-P210 plasmid was then transfected into the selected clone and cells were then selected for hygromycin B and G418 resistance. The results showed that individual subclones expressing bcr/abl after withdrawing doxycycline were 293pT2-P210 cell line. In conclusion, selected 293pT2-P210 cells are cells that bcr/abl expression can be regulated by Tet-off inducing-expression-system. They are suitable thoroughly to study the function of bcr/abl fusion gene and its signal regulation mechanism.