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WIVACE_leaflet The Workshop on Artificial Life and Evolutionary Computation (WIVACE) was first held in 2007 in Sampieri (Ragusa), as the incorporation of two previously separately running workshops (WIVA and GSICE). After the success of the first edition, the workshop was organized in the following years in Venice (2008), Naples (2009), Parma (2012), Milan (2013), Vietri (2014) with the aim to offer a forum where different disciplines could effectively meet. Organizing this workshop means to force the hybridization among single research ‘niches’ often too little populated to allow for creating their own event, and this can lead to surprising “crossover” and “spillover” effects.

Furthermore, events like WIVACE are usually a very nice opportunity for new-generation or soon-to-be scientists to get in touch with new subjects in a more relaxed, informal, and (last but not least) less expensive environment than in large-scale international conferences. Diversity and renovation are key requirements for species to survive and to evolve in nature as well as in science, and we hope that the many young scientists that will attend WIVACE will contribute to make the scientific communities involved in the workshop more and more lively and healthy over the years.

WIVACE 2015 is open to contributions from foreign researchers. International guest speakers will be invited to open each session with a lecture. This year the accepted papers will be published on “Communications in Computer and Information Science” edited by Springer (
WIVACE 2015 has been scheduled with an extended final session (25/8 morning) that overlaps with the initial session of a COST Action CM1304 meeting. The theme of this meeting, Emergence in Compartmentalized Chemical Systems, offers several intriguing topics to WIVACE participants, who are all invited to take part actively to this final special joint session.

Come to Bari and join the workshop for fruitful and provocative scientific discussions!

More info WIVACE_leaflet

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Biochimica et Biophysica Acta (BBA)-Biomembranes Stefano Piotto, Alfonso Trapani, Erminia Bianchino, Maitane Ibarguren, David J López, Simona Concilio

The synthetic fatty acid 2-hydroxyoleic acid (2OHOA) is an antitumor drug that regulates membrane lipid composition and structure. An important effect of this drug is the restoration of sphingomyelin (SM) levels in cancer cell membranes, where the SM concentration is lower than in non-tumor cells. It is well known that free fatty acid concentration in cell membranes is lower than 5%, and that fatty acid excess is rapidly incorporated into phospholipids. In a recent work, we have considered the effect of free 2OHOA in model membranes in liquid ordered (Lo) and liquid disordered (Ld) phases, by using all-atom molecular dynamics. This study concerns membranes that are modified upon incorporation of 2OHOA into different phospholipids. 2OHOA-containing phospholipids have a permanent effect on lipid membranes, making a Ld membrane surface more compact and less hydrated, whereas the opposite effect is observed in Lo domains. Moreover, the hydroxyl group of fatty acid chains increases the propensity of Ld model membranes to form hexagonal or other non-lamellar structures.

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Thin Solid Films, S Concilio, V Bugatti, HC Neitzert, G Landi, A De Sio, J Parisi, S Piotto, ...

A mononuclear Zn(II) complex containing two carbazole/oxadiazole moieties, Zn(OC)2, was synthesized and characterized by means of elemental and thermal analyses and infrared spectroscopy. Current–voltage measurements of Ag/Zn(OC)2/p-Si and Ag/Zn(OC)2/n-Si heterostructures have been performed and compared to that of reference structures with the same metal contacts but without the insertion of the Zn(OC)2 layer. Good rectification behavior has been observed for both hetero-diodes, independent of the silicon substrate doping type, confirming that the metal–organic layer can act both as electron or hole-conductor. Zn(OC)2 complex displayed blue photo-luminescence in solution and in film.

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Annexin I Binding S100/AnnI

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Yadamp2 Preparare script Yadamp/grimd per il folding di corti peptidi Lo script deve incorporare le idee del bias exchange metadynamics
APP Binding energy

Effetto della membrana

SMS1 Folding bias exchange
Valinomycin Best conformation

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PLoS ONE 8(8): e72052. doi:10.1371/journal.pone.0072052

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) are a family of COX1 and COX2 inhibitors used to reduce the synthesis of pro-inflammatory mediators. In addition, inflammation often leads to a harmful generation of nitric oxide. Efforts are being done in discovering safer NSAIDs molecules capable of inhibiting the synthesis of pro-inflammatory lipid mediators and nitric oxide to reduce the side effects associated with long term therapies. Methodology/Principal Findings The analogue of arachidonic acid (AA), 2-hydroxy-arachidonic acid (2OAA), was designed to inhibit the activities of COX1 and COX2 and it was predicted to have similar binding energies as AA for the catalytic sites of COX1 and COX2. The interaction of AA and 2OAA with COX1 and COX2 was investigated calculating the free energy of binding and the Fukui function. Toxicity was determined in mouse microglial BV-2 cells. COX1 and COX2 (PGH2 production) activities were measured in vitro. COX1 and COX2 expression in human macrophage-like U937 cells were carried out by Western blot, immunocytochemistry and RT-PCR analysis. NO production (Griess method) and iNOS (Western blot) were determined in mouse microglial BV-2 cells. The comparative efficacy of 2OAA, ibuprofen and cortisone in lowering TNF-α serum levels was determined in C57BL6/J mice challenged with LPS. We show that the presence of the –OH group reduces the likelihood of 2OAA being subjected to H* abstraction in COX, without altering significantly the free energy of binding. The 2OAA inhibited COX1 and COX2 activities and the expression of COX2 in human U937 derived macrophages challenged with LPS. In addition, 2OAA inhibited iNOS expression and the production of NO in BV-2 microglial cells. Finally, oral administration of 2OAA decreased the plasma TNF-α levels in vivo.