Comparisons of MIDClass , single gene classifiers and standard classifiers.

<p>We report the average accuracy of all tested classifiers on the selected dataset obtained with standard LOOCV. The performances concerning the compared algorithms have been retrieved from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0069873#pone.0069873-Wang1" target="_blank">[17]</a>. Concerning MIDClass , in brackets we report the discretization algorithm, the MFI threshold and the function (1: 2: ).</p

MIDClass ROC curves.

<p>MIDClass ROC curves.</p

MIDClass classification rules in breast cancer 2 dataset.

<p>MIDClass classification rules in breast cancer 2 dataset.</p

Dataset description.

<p>Dataset description.</p

Runninig time of MIDClass to (a) build and establish its reliability using the LOOCV and (b) to create the model and classify a new instance.

<p>Runninig time of MIDClass to (a) build and establish its reliability using the LOOCV and (b) to create the model and classify a new instance.</p

Number of genes used by classifiers in each tested dataset.

<p>Number of genes used by classifiers in each tested dataset.</p

Northern Blot for expression of miR29a in the miR29ab1 hetero and homozygous mice (1 –spleen; 2 –liver).

<p>Northern Blot for expression of miR29a in the miR29ab1 hetero and homozygous mice (1 –spleen; 2 –liver).</p

Gradual Rarefaction of Hematopoietic Precursors and Atrophy in a Depleted microRNA 29a, b and c Environment

<div><p>Background</p><p>The self-renewing ability of HSCs is fundamental for the maintenance of a pool of bone marrow precursors throughout the life of an individual. The genetic mechanisms underlying such a complex process are still poorly understood.</p><p>Results and Significance</p><p>Here, we show that constitutive in vivo deletion of miR29ab1 leads to reduced number of HSCs and that miR29ab1 deficient bone marrow cannot repopulate the bone marrow of irradiated mice. An Affymetrix analysis of the miR29ab1 knockout mice identifies key proteins that could be responsible for this phenotype, as DNMT3a and b. Moreover, our findings reveal that whereas miR29b2c knockout mice do not exhibit any spontaneous abnormality, the double knock out – miR29ab1b2c – has marked generalized atrophy, raising the possibility that the two bi-cistrons might cooperate in order to maintain the stem cell number in general, not only limited to the bone marrow.</p></div

Colony forming assay on 6 months old miR29ab1 knockout bone marrows (n = 8; 4 ko + 4 wt; p = 0.01).

<p>Colony forming assay on 6 months old miR29ab1 knockout bone marrows (n = 8; 4 ko + 4 wt; p = 0.01).</p

Colony forming assay on 2 months old miR29ab1 knockout bone marrows (n = 4; 2 WT and 2 KO; p = 0.04).

<p>Colony forming assay on 2 months old miR29ab1 knockout bone marrows (n = 4; 2 WT and 2 KO; p = 0.04).</p