0.05). After dividing the patients into early-onset and late-onset subgroups, there were significant differences of DRD4 genotype and allele frequency between early-onset patients and controls (P0.05). Conclusion The results suggested that the polymorphism of DRD4 receptor gene may be associated with early-onset OCD. The 3/4 genetype may be the risk factor of early-onset OCD. Early-onset and late-onset OCD may have different etiology.

Objective To study the mechanisms of Curcumin-induced apoptosis on human gastric cancer cell line SGC-7901.Methods SC,C-7901 cells were treated with various concentrations of Curcumin and the growth inhibition rates of it were accessed by MTT method.Apoptosis of gastric cancer cells were in- spected by flow cytometry.The expression of Fas and survivin in gastric cancer cells were evaluated by west- ern blot.Results Curcumin could effectively inhibit the growth of gastric cancer cells in dose-dependent and time-dependent manners,the sub-peak appeared and the apoptotic rate was increased.The expressions of Fas was higher in Western blot,meanwhile,the expressions of survivin was decreased.Conclusion Curcumin could significantly inhibit the growth and induce apoptosis of gastric cancer cells(SGC-7901),Curcumin could probably through up-regulating Fas and down-regulating surviving to induce apoptosis.

OBJECTIVETo observe the anti-proliferation effect of bevacizumab and SN-38 (active metabolite of irinotecan), and investigate the possible mechanisms of these two agents.

METHODSHuman colon cancer LoVo cells were cultured under hypoxic conditions. Inhibition of cell proliferation was evaluated by MTT assay. The drug modulation on HIF-1alpha, VEGF, ERK and AKT were assessed by the following assays. The mRNA expression of HIF-1alpha and VEGF were measured by RT-PCR. The protein expression of HIF-1alpha, ERK and AKT were evaluated by Western blot analysis, and VEGF by ELISA assay.

RESULTSAmong different combination schedules, Bevacizumab given after SN-38 show most synergistic anti-proliferation effect. Under hypoxic conditions, the expression of HIF-1alpha and VEGF increased as time accumulated, Bevacizumab combined with SN-38 almost completely inhibited the expression of HIF-1alpha and VEGF. Moreover, the MAP kinase pathway was involved in the drug modulation of HIF-1alpha and VEGF.

CONCLUSIONThese findings suggest the anti-proliferation effect of bevacizumab and SN-38 was schedule-dependent, and the synergistic effect of Bevacizumab and SN-38 was related to drug modulation of the HIF-1alpha and MAP kinase pathway.

Antibodies, Monoclonal ; pharmacology ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents, Phytogenic ; pharmacology ; Bevacizumab ; Camptothecin ; analogs & derivatives ; pharmacology ; Cell Hypoxia ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Colonic Neoplasms ; metabolism ; pathology ; Drug Synergism ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; metabolism ; RNA, Messenger ; metabolism ; Signal Transduction ; Time Factors ; Vascular Endothelial Growth Factor A ; genetics ; metabolism

0.05),while hyperlactacidemia existed in 21 patients(4.62%).LA levels increased with the creatinine levels,especially in those with Cr more than 90 ?mol/L.However,LA levels increased with the reduction of GFR,especially in those with GFR less than 80 mL/min.It was revealed by correlation analysis that LA level was positively correlated with Cr,ALT and BMI.The optimal cutoff of Cr inducing the lactic acidemia was 95.35 ?mol/L.Conclusion The baseline LA levels of patients with T2DM are similar to those of healthy adults,and LA levels are mainly influenced by BMI and renal and hepatic function.Hyperlactacidemia may be induced when Cr reaches a level more than 95 ?mol/L.

Filamin A and 14-3-3-σ are closely associated with the development of breast cancer.However,the exact relationship between them is still unknown.The present study aimed to examine the interaction of filamin A with 14-3-3-σ in the invasion and migration of breast cancer.RNA interference technology was employed to silence filamin A in MDA-MB-231 cells.Real-time PCR and Western blotting were used to detect the expression of filamin A and 14-3-3-σ at mRNA and protein levels,respectively.Double immunofluorescence was applied to show their colocalization morphologically.Wound healing assay and Trans-well assay were used to testify the migration and invasion of MDA-MB-231 cells in filamin A-silenced cells.The results showed that silencing filamin A significantly increased the mRNA and protein levels of 14-3-3σ.In addition,double immunofluorescence displayed that filamin A and 14-3-3σ were predominantly colocalized in the cytoplasm of MDA-MB-231 cells.Silencing filamin A led to the enhanced fluorescence of 14-3-3σ.Furthermore,cell functional experiments showed that silencing filamin A inhibited the migration and invasion of MDA-MB-231 cells in vitro.In conclusion,silencing filamin A may inhibit the invasion and migration of breast cancer cells by upregulating 14-3-3σ.

A little is known about the specific marker on the surface of acute leukemia cells, leading to the lack of the specific diagnosis method for acute leukemia. Therefore, in this study, cell-systematic evolution of ligands by exponential enrichment (cSELEX) was performed to screen the aptamers binding to CD33(+)/CD34(+) cells from the patients with acute myeloblastic leukemia (AML) of M(2) subtype (AML-M₂) so as to provide the basis for finding the specific marker on the surface of AML-M(2) CD33(+)/CD34(+) cells. Firstly, AML-M₂ CD33(+)/CD34(+) cells were sorted and used as targeted cells, and normal CD33(+)/CD34(+)cells were used as counter-targeted cells; the aptamers binding to CD33(+)/CD34(+) cells from patients with AML-M₂ were screened from the single strand deoxyribonucleic acid (ssDNA) library by cSELEX. Subsequently, each aptamer structure was analyzed after cloning and sequencing. The results indicated that after 13 round of screenings, the enrichment of aptamers in the ssDNA library was ranged from 0.7% to 52.9%, and reached steady state at 13th round screening. Sequence analysis for 30 aptamers showed that most of the aptamers born one of the three conserved sequences of CCCCT, CTCTC, and CTCAC. Secondary structure analysis indicated that three different secondary structures existed in these aptamers. It is concluded that the aptamers binding to the AML-M(2) CD33(+)/CD34(+) cells are successfully screened, which lay the basis for further looking for the specific marker on the surface of AML-M₂ CD33(+)/CD34(+) cells, and the molecular diagnosis of the AML-M₂ leukemia.
Antigens, CD ; genetics ; immunology ; Antigens, CD34 ; genetics ; immunology ; Antigens, Differentiation, Myelomonocytic ; genetics ; immunology ; Aptamers, Nucleotide ; metabolism ; Biomarkers ; Flow Cytometry ; Humans ; Immunophenotyping ; Leukemia, Myeloid, Acute ; genetics ; immunology ; Nucleic Acid Conformation ; SELEX Aptamer Technique ; Sialic Acid Binding Ig-like Lectin 3

OBJECTIVETo screen and analyze CD34(+) cell specific microRNAs (miRNAs) from the patients with acute myelogenous leukemia (AML) and their expression.

METHODSCD34(+) cells were sorted from AML patients or the mobilized peripheral blood of the donors of hematopoietic stem cell transplantation (normal control subjects) and followed by the extraction of the cell total RNAs. The differentially expressed microRNAs (miRNAs, miR) were selected after hybridizing with miRNA microarray, real time polymerase chain reaction (real-time PCR) was subsequently applied to confirm the expression of the selected miRs, and PCR products were further cloned and sequenced to check their specificity.

RESULTSOf the differentially expressed miRNAs, 191 were found to be at least one-fold change in the CD34(+) cells between the AML patients and the normal control subjects. Of the 191 miRNAs, the expression difference of 94 was significant (P < 0.05). Among these 94 miRNAs, the expression of 44 miRNAs was increased and the other 50 miRNAs was decreased in the CD34(+) cells from the bone marrow of AML patients compared with the CD34(+) cells from the mobilized peripheral blood of the normal control subjects. Real time PCR verified that the expression level of miR-10a and miR-220c in the CD34(+) cells from the bone marrow of AML patients was 19.6% and 19.0% of that of CD34(+) cells from mobilized peripheral blood of the normal control subjects. DNA sequencing and BLAST DNA database searching results indicated that the PCR products were really miR-10a and miR-220c.

CONCLUSIONA variety of differentially expressed-miRNAs are existed between AML and normal control subjects CD34(+) cells, the expression of miR-10a and miR-220c was significantly down-regulated in the CD34(+) cells from the bone marrow of AML patients.

Antigens, CD34 ; metabolism ; Female ; Hematopoietic Stem Cells ; Humans ; Leukemia, Myeloid, Acute ; genetics ; metabolism ; Male ; MicroRNAs ; genetics ; metabolism ; Middle Aged ; Oligonucleotide Array Sequence Analysis

OBJECTIVETo investigate the effect of occupational stress on menses and sex hormones.

METHODS415 female knitting workers were investigated using the generic job stress questionnaire. Their venous blood were collected and the six sex hormones were detected by using radio-immune method. The different rate of abnormal menses and sex hormones level between different stress degree groups were analyzed.

RESULTSThe abnormal rate of menses, menstrual blood volume, menstrual cycle, menstrual period was 36.24%, 19.80%, 14.43%, 11.41% respectively. The prevalence rate of dysmenorrheal and premenstrual syndrome was 1.01% and 29.19% respectively. The more depression, the higher menses disorders in non-intrauterine device (IUD) group. The more job demands, the higher daily stress in IUD group while the longer work time, the more abnormal menstrual period in two groups. More physical symptoms and deeper depression in non-IUD group were related to higher abnormal rate of menstrual blood volume. The level of blood E2 was lower in the group of prolonged work-time than that of in normal work-time group. The increasing FSH level and decreasing T level was associated with higher job demands. Multiple factor analysis showed that physical symptom, control of resource and negative life affairs were the risk factors of menses disorder; The physical symptom was the risk factor of menstrual blood volume; More physical symptoms, less positive feeling and shift were the risk factors of premenstrual syndrome; Less positive feeling was the risk factor of menstrual cycle; Prolonged daily work-time was the risk factor of menstrual period.

CONCLUSIONHigher stress degree can lead to higher FSH and E2 and lower T level,and induce menses disorder.

Adult ; Analysis of Variance ; Burnout, Professional ; physiopathology ; Chi-Square Distribution ; Female ; Gonadal Steroid Hormones ; blood ; Humans ; Logistic Models ; Menstruation ; physiology ; Surveys and Questionnaires ; Textile Industry

OBJECTIVETo investigate the association between single nucleotide polymorphisms (SNPs) in cyclic adenosine monophosphate response element-binding protein(CREB1) gene and major depressive disorder (MDD).

METHODSWe recruited 105 parent-offspring trios of Chinese descent, extracted whole blood genomic DNA, and genotyped the SNPs in rs10932201 and rs6740584 loci. Single-marker transmission disequilibrium test (TDT), pairwise SNP linkage disequilibrium(LD) and haplotype-based TDT were performed.

RESULTSNo significant association with MDD was observed for SNPs rs10932201 and rs6740584 (P=0.1004 and P=0.4986). However, there was strong positive association between the rs10932201-rs6740584 haplotype and MDD (P=0.00003241), and both haplotypes of A-C and A-T were significantly associated with MDD (P=0.020 and P=0.00022).

CONCLUSIONThe rs10932201-rs6740584 haplotype of the CREB1 gene may play an important role in the pathogenesis of MDD.

Cyclic AMP Response Element-Binding Protein ; genetics ; Depressive Disorder, Major ; genetics ; Female ; Genetic Predisposition to Disease ; Haplotypes ; Humans ; Male ; Polymorphism, Single Nucleotide ; genetics