From Thompson to Baer-Suzuki: a sharp characterization of the solvable radical

We prove that an element $g$ of prime order $>3$ belongs to the solvable radical $R(G)$ of a finite (or, more generally, a linear) group if and only if for every $x\in G$ the subgroup generated by $g, xgx^{-1}$ is solvable. This theorem implies that a finite (or a linear) group $G$ is solvable if and only if in each conjugacy class of $G$ every two elements generate a solvable subgroup.Comment: 28 page

Mutagen-Specific Mutation Signature Determines Global microRNA Binding

Micro-RNAs (miRNAs) are small non-coding RNAs that regulate gene products at the post-transcriptional level. It is thought that loss of cell regulation by miRNAs supports cancer development. Based on whole genome sequencing of a melanoma tumor, we predict, using three different computational algorithms, that the melanoma somatic mutations globally reduce binding of miRNAs to the mutated 3′UTRs. This phenomenon reflects the nature of the characteristic UV-induced mutation, C-to-T. Furthermore, we show that seed regions are enriched with Guanine, thus rendering miRNAs prone to reduced binding to UV-mutated 3′UTRs. Accordingly, mutation patterns in non UV-induced malignancies e.g. lung cancer and leukemia do not yield similar predictions. It is suggested that UV-induced disruption of miRNA-mediated gene regulation plays a carcinogenic role. Remarkably, dark-skinned populations have significantly higher GC content in 3′UTR SNPs than light-skinned populations, which implies on evolutionary pressure to preserve regulation by trans-acting oligonucleotides under conditions with excess UV radiation

Is there any sense in antisense editing?

A number of recent studies have hypothesized that sense-antisense RNA transcript pairs create dsRNA duplexes that undergo extensive A-to-I RNA editing. Here we studied human and mouse genomic antisense regions, and found that the editing level in these areas is negligible. This observation puts in question the scope of sense-antisense duplexes formation in-vivo, which is the basis for a number of proposed regulatory mechanisms

Worldwide spreading of economic crisis

We model the spreading of a crisis by constructing a global economic network and applying the Susceptible-Infected-Recovered (SIR) epidemic model with a variable probability of infection. The probability of infection depends on the strength of economic relations between the pair of countries, and the strength of the target country. It is expected that a crisis which originates in a large country, such as the USA, has the potential to spread globally, like the recent crisis. Surprisingly we show that also countries with much lower GDP, such as Belgium, are able to initiate a global crisis. Using the {\it k}-shell decomposition method to quantify the spreading power (of a node), we obtain a measure of ``centrality'' as a spreader of each country in the economic network. We thus rank the different countries according to the shell they belong to, and find the 12 most central countries. These countries are the most likely to spread a crisis globally. Of these 12 only six are large economies, while the other six are medium/small ones, a result that could not have been otherwise anticipated. Furthermore, we use our model to predict the crisis spreading potential of countries belonging to different shells according to the crisis magnitude.Comment: 13 pages, 4 figures and Supplementary Materia

Targeting the centriolar replication factor STIL synergizes with DNA damaging agents for treatment of ovarian cancer

Advanced ovarian cancer is an incurable disease. Thus, novel therapies are required. We wished to identify new therapeutic targets for ovarian cancer. ShRNA screen performed in 42 ovarian cancer cell lines identified the centriolar replication factor STIL as an essential gene for ovarian cancer cells. This was verified in-vivo in orthotopic human ovarian cancer mouse models. STIL depletion by administration of siRNA in neutral liposomes resulted in robust anti-tumor effect that was further enhanced in combination with cisplatin. Consistent with this finding, STIL depletion enhanced the extent of DNA double strand breaks caused by DNA damaging agents. This was associated with centrosomal depletion, ongoing genomic instability and enhanced formation of micronuclei. Interestingly, the ongoing DNA damage was not associated with reduced DNA repair. Indeed, we observed that depletion of STIL enhanced canonical homologous recombination repair and increased BRCA1 and RAD51 foci in response to DNA double strand breaks. Thus, inhibition of STIL significantly enhances the efficacy of DNA damaging chemotherapeutic drugs in treatment of ovarian cancer.Junta de andalucía P12-BIO-515, P. HuertasEspaña Ministerio de Economía y Competitividad SAF2013-43255-

Coexistence of Coulomb blockade and zero bias anomaly in a strongly coupled quantum dot

The current-voltage characteristics through a metallic quantum dot which is well coupled to a metallic lead are measured. It is shown that the I-V curves are composed of two contributions. One is a suppression of the tunneling conductivity at the Fermi level and the second is an oscillating feature which shifts with gate voltage. The results indicate that Zero-Bias-Anomaly and Coulomb Blockade phenomena coexist in an asymmetric strongly coupled quantum dot.Comment: 4 pages, 4 figure