A matrix solid phase dispersion ( MSPD) method was developed for the simultaneous preparation of samples of 15 mycotoxin biomarkers including deoxynivalenol, aflatoxins and zearalenone from eggs, which were subsequently determined by liquid chromatography-electrospray ionization tandem mass spectrometry ( LC-ESI-MS/MS) under the multiple reaction monitoring ( MRM) mode. For the analysis, the samples were first mixed with C18 particles and loaded into an empty column, then 20 mL of acetonitrile/methanol (1:1, V/V) containing 1 mmol/L ammonium formate was used to elute the sample. The eluent was then dried with nitrogen flow and redissolved into the mobile phase. After filtration, samples were brought into vials and used for analysis. Different from other methods, no extra complicated purification and centrifugation steps were required in the procedure of MSPD. This method had good linearity in the range of 0. 2-100 ng/mL, with the correlation coefficient (r2) greater than 0. 9931. The limits of detection (LODs, S/N=3) and limits of quantification ( LOQs, S/N=3 ) of this method were 0. 05-2 μg/kg and 0. 2-4 μg/kg respectively. Comprehensive extraction recoveries of the 15 compounds ranged from 61% to 90%.

MicroRNAs (miRNAs) are small, non-coding RNAs that function as post-transcriptional regulators of gene expression. The deregulated expression of miRNAs is associated with a variety of diseases, including breast cancer. In the present study, we found that miR-495 was markedly up-regulated in clinical breast cancer samples by quantitative real time-PCR (qRT-PCR). Junctional adhesion molecule A (JAM-A) was predicted to be a potential target of miR-495 by bioinformatics analysis and was subsequently verified by luciferase assay and Western blotting. JAM-A was found to be negatively correlated with the migration of breast cancer cells through loss-of-function and gain-of-function assays, and the inhibition of JAM-A by miR-495 promoted the migration of MCF-7 and MDA-MB-231 cells. Furthermore, overexpression of JAM-A could restore miR-495-induced breast cancer cell migration. Taken together, our findings suggest that miR-495 could facilitate breast cancer progression through the repression of JAM-A, making this miRNA a potential therapeutic target.
3' Untranslated Regions ; genetics ; Adult ; Aged ; Blotting, Western ; Breast Neoplasms ; genetics ; metabolism ; pathology ; Cell Adhesion Molecules ; genetics ; metabolism ; Cell Line, Tumor ; Cell Movement ; genetics ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; MCF-7 Cells ; MicroRNAs ; genetics ; Middle Aged ; RNA Interference ; Receptors, Cell Surface ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo analyze the clinical features of clonal evolution of acquired aplastic anemia (AA) into myelodysplastic syndrome/acute myeloid leukemia (AML) and review of literatures.

METHODSAA developing MDS/AML patients between December 1994 and December 2011 enrolled into this study to analyze their clinical characteristics.

RESULTSDuring the median follow-up of 49(15-97) months, 19 patients evolved to MDS/AML, of whom 10, 8 and 1 were from VSAA, SAA and NSAA subgroups, respectively. The median G-CSF therapy was 270(29-510) days. There were monosomy 7 in 11(57.9%) of 19 patients with AA evolved to MDS/AML. The median AA evolved to MDS/AML was 33(11-88) months. The median MDS/AML transformation in responders (54.2 months) was significantly longer than of non-responders (25.7 months, P<0.01).

CONCLUSIONAA patients could evolved into MDS/AML concomitant with abnormal karotype and worse prognosis.

Anemia, Aplastic ; Chromosome Deletion ; Chromosomes, Human, Pair 7 ; Granulocyte Colony-Stimulating Factor ; Humans ; Leukemia, Myeloid, Acute ; Myelodysplastic Syndromes