Consistency and identifiability of football teams: a network science perspective.

We investigated the ability of football teams to develop a particular playing style by looking at their passing patterns. Using the information contained in the pass sequences during matches, we constructed the pitch passing networks of teams, whose nodes are the divisions of the pitch for a given spatial scale and links account for the number of passes from region to region. We translated football passings networks into their corresponding adjacency matrices. We calculated the correlations between matrices of the same team to quantify how consistent the passing patterns of a given team are. Next, we quantified the differences with other teams' matrices and obtained an identifiability parameter that indicates how unique are the passing patterns of a given team. Consistency and identifiability rankings were calculated during a whole season, allowing to detect those teams of a league whose passing patterns are different from the rest. Furthermore, we found differences between teams playing at home or away. Finally, we used the identifiability parameter to investigate what teams imposed their passing patterns over the rivals during a given match.

Leptin gene therapy attenuates neuronal damages evoked by amyloid-ß and rescues memory deficits in APP/PS1 mice.

There is growing evidence that leptin is able to ameliorate Alzheimer's disease (AD)-like pathologies, including brain amyloid-ß (Aß) burden. In order to improve the therapeutic potential for AD, we generated a lentivirus vector expressing leptin protein in a self-inactivating HIV-1 vector (HIV-leptin), and delivered this by intra-cerebroventricular administration to APP/PS1 transgenic model of AD. Three months after intra-cerebroventricular administration of HIV-leptin, brain Aß accumulation was reduced. By electron microscopy, we found that APP/PS1 mice exhibited deficits in synaptic density, which were partially rescued by HIV-leptin treatment. Synaptic deficits in APP/PS1 mice correlated with an enhancement of caspase-3 expression, and a reduction in synaptophysin levels in synaptosome preparations. Notably, HIV-leptin therapy reverted these dysfunctions. Moreover, leptin modulated neurite outgrowth in primary neuronal cultures, and rescued them from Aß42-induced toxicity. All the above changes suggest that leptin may affect multiple aspects of the synaptic status, and correlate with behavioral improvements. Our data suggest that leptin gene delivery has a therapeutic potential for Aß-targeted treatment of mouse model of AD.