Dinosaur Tracks as Paleogeographic Constraints: New Scenarios for the Cretaceous Geography of the Periadriatic Region

A really unexpected finding of sauropod and theropod footprints in southern Latium raises to four the number of the trampled levels recognized in central and southern Italy. After the recent findings in Latest Jurassic and Early, mid and Late Cretaceous carbonate platform deposits of the Periadriatic region, dinosaur footprints seem to provide very important paleogeographic constraints for reconstructing the geodynamic history of the Mediterranean area. The presence of a varied ichnoassociation makes acceptance of the current paleogeographic models concerning the relative and absolute position of the Laziale-Abruzzese-Campano and of Apulian-Dinaric domains during the Late Cretaceous more and more problematic. Dinosaur footprints, combined with other paleontological data, demonstrate that these areas were never completely pulled apart by deep seaways, while frequent or continuous links between them, and to southern and northern mainlands, probably persisted. These data also allowed us to improve our understanding of the timing of the Mesozoic plate motion in this segment of the Western Tethys.     

Sometimes They Come Back: Recovery and Reinterpretation of a Trackway Slab from the Permian Coconino Sandstone of the Southwestern United States

When a fossil vanishes to a private collection, it must be considered lost to science because, frequently, it is no longer available for study. Fortunately some fossils occasionally are regained. We had the opportunity to recoup an interesting footprint-bearing slab that was part of a private collection in Italy. The specimen, found in 1992 near Seligman, Arizona (USA) was described, before disappearing, as one of the best fossil examples of vertebrate (Chelichnus [Laoporus])-on-invertebrate (Octopodichnus) predation. After a careful re-examination of the slab, the primary conclusions of the former describers are demonstrably groundless. The reanalysis of the tracks, as well as peculiar sedimentary structures associated with the tracks, allowed obtaining new information about the depositional environment and the complex interactions between the type of substrate and trackmaker behavior. The re-examination of the specimen also revealed interesting aspects about trackmaker biomechanics.     

Emergence of Multiplex Communities in Collaboration Networks

Community structures in collaboration networks reflect the natural tendency of individuals to organize their work in groups in order to better achieve common goals. In most of the cases, individuals exploit their connections to introduce themselves to new areas of interests, giving rise to multifaceted collaborations which span different fields. In this paper, we analyse collaborations in science and among movie actors as multiplex networks, where the layers represent respectively research topics and movie genres, and we show that communities indeed coexist and overlap at the different layers of such systems. We then propose a model to grow multiplex networks based on two mechanisms of intra and inter-layer triadic closure which mimic the real processes by which collaborations evolve. We show that our model is able to explain the multiplex community structure observed empirically, and we infer the strength of the two underlying social mechanisms from real-world systems. Being also able to correctly reproduce the values of intra-layer and inter-layer assortativity correlations, the model contributes to a better understanding of the principles driving the evolution of social networks.     

Monoclonal antibodies with broad specificity for hepatitis C virus hypervariable region 1 variants can recognize viral particles

The hypervariable region 1 (HVR1) of the E2 protein of hepatitis C virus (HCV) is a highly heterogeneous sequence that is promiscuously recognized by human sera via binding to amino acid residues with conserved physicochemical properties. We generated a panel of mAbs from mice immunized with HVR1 surrogate peptides (mimotopes) affinity-selected with sera from HCV-infected patients from a phage display library. A high number of specific clones was obtained after immunization with a pool of nine mimotopes, and the resulting mAbs were shown to recognize several 16- and 27-mer peptides derived from natural HVR1 sequences isolated from patients with acute and chronic HCV infection, suggesting that HVR1 mimotopes were efficient antigenic and immunogenic mimics of naturally occurring HCV variants. Moreover, most mAbs were shown to bind HVR1 in the context of a complete soluble form of the E2 glycoprotein, indicating recognition of correctly folded HVR1. In addition, a highly promiscuous mAb was able to specifically capture bona fide viral particles (circulating HCV RNA) as well as rHCV-like particles assembled in insect cells expressing structural viral polypeptides derived from an HCV 1a isolate. These findings demonstrate that it is possible to induce a broadly cross-reactive clonal Ab response to multiple HCV variants. In consideration of the potentially important role of HVR1 in virus binding to cellular receptor(s), such a mechanism could be exploited for induction of neutralizing Abs specific for a large repertoire of viral variants.     

Inhibition of JNK by cellular stress- and tumor necrosis factor alpha-induced AKT2 through activation of the NF kappa B pathway in human epithelial Cells

Previous studies have demonstrated that AKT1 and AKT3 are activated by heat shock and oxidative stress via both phosphatidylinositol 3-kinase-dependent and -independent pathways. However, the activation and role of AKT2 in the stress response have not been fully elucidated. In this study, we show that AKT2 in epithelial cells is activated by UV-C irradiation, heat shock, and hyperosmolarity as well as by tumor necrosis factor alpha (TNFalpha) through a phosphatidylinositol 3-kinase-dependent pathway. The activation of AKT2 inhibits UV- and TNF alpha-induced c-Jun N-terminal kinase (JNK) and p38 activities that have been shown to be required for stress- and TNF alpha-induced programmed cell death. Moreover, AKT2 interacts with and phosphorylates I kappa B kinase alpha. The phosphorylation of I kappa B kinase alpha and activation of NF kappa B mediates AKT2 inhibition of JNK but not p38. Furthermore, phosphatidylinositol 3-kinase inhibitor or dominant negative AKT2 significantly enhances UV- and TNF alpha-induced apoptosis, whereas expression of constitutively active AKT2 inhibits programmed cell death in response to UV and TNFalpha -induced apoptosis by inhibition of stress kinases and provide the first evidence that AKT inhibits stress kinase JNK through activation of the NF kappa B pathway.     

Multi-Target Analysis and Design of Mitochondrial Metabolism

Analyzing and optimizing biological models is often identified as a research priority in biomedical engineering. An important feature of a model should be the ability to find the best condition in which an organism has to be grown in order to reach specific optimal output values chosen by the researcher. In this work, we take into account a mitochondrial model analyzed with flux-balance analysis. The optimal design and assessment of these models is achieved through single- and/or multi-objective optimization techniques driven by epsilon-dominance and identifiability analysis. Our optimization algorithm searches for the values of the flux rates that optimize multiple cellular functions simultaneously. The optimization of the fluxes of the metabolic network includes not only input fluxes, but also internal fluxes. A faster convergence process with robust candidate solutions is permitted by a relaxed Pareto dominance, regulating the granularity of the approximation of the desired Pareto front. We find that the maximum ATP production is linked to a total consumption of NADH, and reaching the maximum amount of NADH leads to an increasing request of NADH from the external environment. Furthermore, the identifiability analysis characterizes the type and the stage of three monogenic diseases. Finally, we propose a new methodology to extend any constraint-based model using protein abundances.