Una «historia» para después del código.

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Il silenzio come esperienza trasformativa. L’importanza del silenzio nella meditazione e in ambito professionale

The article is motivated by the lack of studies which address silence as a context- dependent phenomenon; that is, as a phenomenon whose meaning arises within specific contexts, situations and physical spaces. Accordingly, I address the ways in which the phenomenon of silence plays an essential role in particular professional and vocational domains. The analysis leads through some thoughts and considerations of people who work or are active in specialized fields that have a significant connection with the practice and the experience of silence. I especially examine areas such as meditation, teaching, health professions, and other professional and even – to some extent – artistic practices

Life-or-Death Decisions upon Axonal Damage

In this issue of Neuron, Hu et al. (2012) report that upon axonal damage, CHOP and XBP1 unfolded protein response pathways are not recruited equally and have opposite effects on neuronal survival. XBP1 pathway boosting may represent a valuable neuroprotective strategy

Different causes of closure of Small Business Enterprises: alternative models for competing risks survival analysis

We examine the time until closure of Small Business Enterprises in Umbria, Italy between 2008 and 2013, and the factors that influence it. Earlier analysis, using Cox regression, considered failure (closure) from any cause. However, there are different reasons for inactivity: voluntary winding-up (1808 of15184 firms in our data, 59.3% of the 3049 failures); bankruptcy (236, 7.7%); and closure without action by creditors or courts (1005, 33.0%). While the earlier analysis provides a valuable overall picture, it is also interesting to ex-amine the separate causes, their rates of occurrence and which factors influence them separately. We do this using competing risks analyses, employing both of the regression methods that are prominent in the literature, basedon cause-specific and sub-distribution hazard functions (Fine-Gray model). Furthermore, a proportional odds model was used to estimate cumulative incidences of failure by cause. Data included the firm's year of foundation, location, legal form and sector of activity. Financial indexes were constructedfrom annual balance sheets. The date and reason for closure were recorded if the firrm ceased activity. Findings included major differences between types of firm; for example, cooperatives had greatly increased hazards for winding-up(HR of 2.44 and 2.61 in the two approaches) but greatly reduced hazards for closure (0.48 and 0.45) compared to publicly traded companies. All-causes analysis averaged these strong effects into an insignicant one (1.05). Coefficients from the proportional odds model were similar to those from theFine-Gray model, but have the advantage of interpretability

PI(4,5)P2-dependent microdomain assemblies capture microtubules to promote and control leading edge motility

The lipid second messenger PI(4,5)P2 modulates actin dynamics, and its local accumulation at plasmalemmal microdomains (rafts) might mediate regulation of protrusive motility. However, how PI(4,5)P2-rich rafts regulate surface motility is not well understood. Here, we show that upon signals promoting cell surface motility, PI(4,5)P2 directs the assembly of dynamic raft-rich plasmalemmal patches, which promote and sustain protrusive motility. The accumulation of PI(4,5)P2 at rafts, together with Cdc42, promotes patch assembly through N-WASP. The patches exhibit locally regulated PI(4,5)P2 turnover and reduced diffusion-mediated exchange with their environment. Patches capture microtubules (MTs) through patch IQGAP1, to stabilize MTs at the leading edge. Captured MTs in turn deliver PKA to patches to promote patch clustering through further PI(4,5)P2 accumulation in response to cAMP. Patch clustering restricts, spatially confines, and polarizes protrusive motility. Thus, PI(4,5)P2-dependent raft-rich patches enhance local signaling for motility, and their assembly into clusters is regulated through captured MTs and PKA, coupling local regulation of motility to cell polarity, and organization