Heat map showing newly identified miRNA expression patterns in 10 tissues (liver, gill, head kidney, spleen, heart, brain, muscle, stomach, intestines and skin) measured by stem-loop RT-PCR.

<p>Relative expression levels of the 45 novel miRNAs were measured in terms of threshold cycle value (Ct) and were normalized to 5S rRNA. The expression data were analyzed by hierarchical clustering for both tissues and genes.</p

Details of ipu-miR-462 isomiRs including sequence counts.

<p>A portion of the miRNA precursor, multiple isomiRs (each with more than 99 counts) with their sequence counts and the pre-miRNA secondary structure with dominant cleavage sites are presented. Single nucleotide substitutions and additional 5′ or 3′ non-template nucleotides are highlighted by capital letters. The reference miRNA sequence from miRBase is shown in red. Inferred dominant cleavage sites are indicated by arrows. Large arrows represent cleavage sites for the most abundant isomiR, whereas small arrows indicate cleavage sites for secondary abundance isomiRs. The most abundant mature miRNAs are indicated by the sequence in green.</p

Length distribution and annotation of small RNAs derived from Solexa sequencing of channel catfish small RNAs.

<p>A: Length distribution of sequenced small RNAs; B: Clean reads were BLAST searched against the RFam 10.1 database to annotate rRNAs, tRNAs, snoRNAs and other snRNAs.</p

Number and distribution of unique reads mapped to the genome sequence of zebrafish.

<p>Number and distribution of unique reads mapped to the genome sequence of zebrafish.</p

Novel miRNAs identified in channel catfish with the genome of zebrafish.

<p>Novel miRNAs identified in channel catfish with the genome of zebrafish.</p

Conservation analysis of miRNA*s identified in channel catfish.

<p>MiR-1388 and miR-144 are compared among several vertebrates. Let-7a is compared across vertebrates, protochordates and invertebrates. Alignments were performed using ClustalX. Mature miRNA sequences and their star sequences are single line underlined. Seed regions are double underlined. ipu: <i>I. punctatus</i>; has: <i>H. sapiens</i>; mmu: <i>M. musculus</i>; dre: <i>D. rerio</i>; tgu: <i>T. guttata</i>; aca: <i>Anolis carolinensis</i>; oan: <i>Ornithorhynchus anatinus</i>; bta: <i>Bos taurus</i>; ola: <i>O. latipes</i>; rno: <i>Rattus norvegicus</i>; pma: <i>Petromyzon marinus</i>; bfl: <i>B. floridae</i>; sme: <i>S. mediterranea</i>; cin: <i>C. intestinalis.</i></p

Novel miRNAs identified in channel catfish with the EST and GSS database.

<p>Novel miRNAs identified in channel catfish with the EST and GSS database.</p

Data_Sheet_1_Plasma metabolomic analysis reveals the therapeutic effects of Jiashen tablets on heart failure.pdf

BackgroundHeart failure is a chronic progressive condition that significantly affects the quality of life of patients with high hospitalization and mortality rates. Jiashen tablets (JST), a Chinese herbal formula, have been reported to be an effective treatment against heart failure, however the underlying mechanisms remain obscure. This study was designed to determine the effect of JST on the treatment of heart failure and delineate the underlying mechanisms by an untargeted metabolomics approach.Materials and methodsThe chronic heart failure model was established by the permanent ligation of the left anterior descending coronary artery in rats. The cardiac functions of rats, including left ventricular ejection fraction (LVEF) and fractional shortening (LVFS), left ventricular internal diameter end diastole (LVIDd) and end systole (LVIDs), and interventricular septum thickness in diastole (IVSd) and in systole (IVSs), were measured by echocardiography. Biochemical analysis and histopathological examination were also performed to evaluate therapeutic effects of JST for treating heart failure. UHPLC-QTOF-MS/MS coupled with multivariate statistical analyses were applied for plasma metabolic profiling to identify biomarkers and potential mechanisms of JST in the treatment of heart failure.ResultsJiashen tablets could improve the cardiac function of heart failure rats and thus ameliorate heart failure via enhancing rat LVEF and LVFS and decreasing LVIDd, LVIDs, IVSd, and IVSs. Results of biochemical analysis and histopathological examination revealed that JST could reduce the serum lactate dehydrogenase (LDH) activity and the level of NT-pro BNP, markers of heart failure and myocardial damage, and inhibit myocardial fibrosis. Furthermore, in metabolomics analysis, a total of 210 metabolites with significant differences were identified between heart failure rats and normal rats, among which 29 metabolites were significantly restored after JST treatment. These metabolites were primarily involved in tryptophan metabolism, branched-chain amino acid metabolism, fatty acids β-oxidation, and glycerophospholipid metabolism.ConclusionThe present study illustrated the therapeutic effect of JST for the treatment of heart failure and delineated the underlying mechanisms mainly relating to the regulation of amino acid metabolism and lipid metabolism in heart failure rats.</p

Genotype distributions of 1p11.2 and their associations with breast cancer risk.

a<p>Adjusted by age, age at menarche, menopausal status.</p>b<p>Two-sided χ2 test for difference in frequency distribution of genotypes between cases and controls.</p

Overview of the LD block and the new finding marker SNP (rs2580520) in our study for breast cancer susceptibility.

<p>The upper panel shows a view of the genomic region of rs2580520 (in a predicted H3K4Me1 enhancer region) (120,813,325-120,813,825) from the UCSC browser Build 36 assembly (hg18). The following one shows the analyzed linkage disequilibrium (LD) block, its flanking region, related genes and predicted enhancers, marking with the seven SNPs. The lower panel shows the LD plot (120,791,177 - 121,068,797) of European descent and Chinese descent [the block was defined by the confidence intervals (Gabriel et al., 2002)]. The lower left thumbnail shows the r² vaule between seven SNPs in Chinese descent.Several limitations were inherent in this study. First, the power was relatively low due to the limited sample size and low MAF of the rs11249433 SNP. Second, the biological function of the significant SNP rs2580520 is unclear in the development of breast cancer. Therefore, additional large scale population-based studies will be needed to validate the findings in our study and functional characterization to explore the underline mechanisms will be also required.</p