Novel link adaptation for TETRA cellular systems

One of the main challenges for future wireless systems is to enhance the effective data throughput by exploiting the allocated bandwidth as much as possible. Among several approaches at different layers, one of the most important is constituted by the so‐called link adaptation (LA) techniques. They are characterized by the adaptation of a set of transmission parameters to the channel state in order to improve performance. In this context, this paper is focused on the analysis of a particular class of LA techniques called adaptive modulation and coding, where the modulation and coding rate of transmission can vary according to the channel behavior. In particular, a novel LA algorithm, namely the timed window (TW) method, suitable for time‐division Duplex systems is proposed here. The performance of the TW algorithm is evaluated by taking actual user mobility conditions, communication channel behavior, as well as the physical layer effects into account. Finally, it is important to stress that, even if the wireless bearer considered in this study is TETRA (TErrestrial Trunked RAdio), the approach is quite general and it can be of interest for other wireless networks and can be optimized for different channel models (e.g. TU50, HT200, etc.). Copyright © 2008 John Wiley & Sons, Ltd.     

Gold nanoparticles induce cytotoxicity in the alveolar type-II cell lines A549 and NCIH441

Background  

During the last years engineered nanoparticles (NPs) have been extensively used in different technologies and consequently many questions have arisen about the risk and the impact on human health following exposure to nanoparticles. Nevertheless, at present knowledge about the cytotoxicity induced by NPs is still largely incomplete. In this context, we have investigated the cytotoxicity induced by gold nanoparticles (AuNPs), which differed in size and purification grade (presence or absence of sodium citrate residues on the particle surface) in vitro, in the human alveolar type-II (ATII)-like cell lines A549 and NCIH441.     

Hydrologic scaling for hydrogeomorphic floodplain mapping: Insights into human‐induced floodplain disconnectivity

Hydrogeomorphic approaches for floodplain modelling are valuable tools for water resource and flood hazard management and mapping, especially as the global availability and accuracy of terrain data increases. Digital terrain models implicitly contain information about floodplain landscape morphology that was produced by hydrologic processes over long time periods, as well as recent anthropogenic modifications to floodplain features and processes. The increased availability of terrain data and distributed hydrologic datasets provide an opportunity to develop hydrogeomorphic floodplain delineation models that can quickly be applied at large spatial scales. This research investigates the performance of a hydrogeomorphic floodplain model in two large urbanized and gauged river basins in the United States, the Susquehanna and the Wabash basins. The models were calibrated by a hydrologic data scaling technique, implemented through regression analyses of USGS peak flow data to estimate floodplain flow levels across multiple spatial scales. Floodplain model performance was assessed through comparison with 100‐year Federal Emergency Management Agency flood hazard maps. Results show that the hydrogeomorphic floodplain maps are generally consistent with standard flood maps, even when significantly and systematically varying scaling parameters within physically feasible ranges, with major differences that are likely due to infrastructure (levees, bridges, etc.) in highly urbanized areas and other locations where the geomorphic signature of fluvial processes has been altered. This study demonstrates the value of geomorphic information for large‐scale floodplain mapping and the potential use of hydrogeomorphic models for evaluating human‐made impacts to floodplain ecosystems and patterns of disconnectivity in urbanized catchments.     

Combined Effects of Parallel and Series Detention Basins for Flood Peak Reduction

A simple analytical method is proposed that allows a preliminary evaluation of the overall efficiency of a detention basin system for flood risk reduction in a specific target section. Solutions are provided both for parallel and series systems, under some simplifying assumptions concerning the linearity of detention basin, river network and watershed responses. Further, for the series configuration a regressive model is proposed for the computation of the overall efficiency, because of the complexity of analytical solution. A case study is also presented, where the overall efficiency of a system of nine detention basins is computed by means of both the analytical and the regressive model. Results are discussed to assess the different influence of detention basins in parallel or in a series system.     

A Web‐based Open‐source Geoinformation Tool for Regional Water Resources Assessment

Water Resources Management - To reduce the impact of droughts and increase the resilience of regional water systems, various competing demands, such as hydropower, supply, irrigation and river...     

A novel error observer-based adaptive output feedback approach for control of uncertain systems

We develop an adaptive output feedback control methodology for nonaffine in control of uncertain systems having full relative degree. Given a smooth reference trajectory, the objective is to design a controller that forces the system measurement to track it with bounded errors. A neural network with linear parameters is introduced as an adaptive signal. A simple linear observer is proposed to generate an error signal for the adaptive laws. Ultimate boundedness is shown through Lyapunov's direct method. Simulations of a nonlinear second-order system illustrate the theoretical results.     

Structure-based design of inhibitors of NS3 serine protease of hepatitis C virus

We have designed small focused combinatorial library of hexapeptide inhibitors of NS3 serine protease of the hepatitis C virus (HCV) by structure-based molecular design complemented by combinatorial optimisation of the individual residues. Rational residue substitutions were guided by the structure and properties of the binding pockets of the enzyme's active site. The inhibitors were derived from peptides known to inhibit the NS3 serine protease by using unusual amino acids and alpha-ketocysteine or difluoroaminobutyric acid, which are known to bind to the S1 pocket of the catalytic site. Inhibition constants (Ki) of the designed library of inhibitors were predicted from a QSAR model that correlated experimental Ki of known peptidic inhibitors of NS3 with the enthalpies of enzyme-inhibitor interaction computed via molecular mechanics and the solvent effect contribution to the binding affinity derived from the continuum model of solvation. The library of the optimised inhibitors contains promising drug candidates-water-soluble anionic hexapeptides with predicted Ki* in the picomolar range.     

Human malignant thyroid tumors displayed reduced levels of transforming growth factor beta receptor type II messenger RNA and protein

Transforming growth factor beta (TGF-beta) is a physiological regulator of thyroid epithelial cell growth and differentiation. This factor signals through a heteromeric complex composed of type I (TGF-beta receptor type I) and type II [TGF-beta receptor type II (TbetaRII)] receptors. Loss of TbetaRII expression has been related to resistance to TGF-beta inhibition of cell proliferation. In the present work, we analyzed the TbetaRII expression in a series of human thyroid tumors, from benign lesions (adenomas) to neoplastic lesions of increasing aggressiveness (papillary and follicular carcinomas) up to the extremely aggressive anaplastic tumors. Results obtained indicated a clear reduced expression of TbetaRII mRNA only in the group of thyroid carcinomas when compared with their relative normal tissues. Immunohistochemical analyses with specific anti-TbetaRII antibodies confirm these observations. These data indicate that loss of expression of TbetaRII can contribute to thyroid cancer progression, inducing cancer cells to escape the growth-inhibitory effect of TGF-beta.     

Adiponectin and Leptin Exert Antagonizing Effects on HUVEC Tube Formation and Migration Modulating the Expression of CXCL1, VEGF,MMP-2 and MMP-9

Adiponectin and leptin are two abundant adipokines with different properties but both described such as potent factors regulating angiogenesis. AdipoRon is a small-molecule that, binding to AdipoRs receptors, acts as an adiponectin agonist. Here, we investigated the effects of AdipoRon and leptin on viability, migration and tube formation on a human in vitro model, the human umbilical vein endothelial cells (HUVEC) focusing on the expression of the main endothelial angiogenic factors: hypoxia-inducible factor 1-alpha (HIF-1α), C-X-C motif chemokine ligand 1 (CXCL1), vascular endothelial growth factor A (VEGF-A), matrix metallopeptidase 2 (MMP-2) and matrix metallopeptidase 9 (MMP-9). Treatments with VEGF-A were used as positive control. Our data revealed that, at 24 h treatment, proliferation of HUVEC endothelial cells was not influenced by AdipoRon or leptin administration; after 48 h longer exposure time, the viability was negatively influenced by AdipoRon while leptin treatment and the combination of AdipoRon+leptin produced no effects. In addition, AdipoRon induced a significant increase in complete tubular structures together with induction of cell migration while, on the contrary, leptin did not induce tube formation and inhibited cell migration; interestingly, the co-treatment with both AdipoRon and leptin determined a significant decrease of the tubular structures and cell migration indicating that leptin antagonizes AdipoRon effects. Finally, we found that the effects induced by AdipoRon administration are accompanied by an increase in the expression of CXCL1, VEGF-A, MMP-2 and MMP-9. In conclusion, our data sustain the active role of adiponectin and leptin in linking adipose tissue with the vascular endothelium encouraging the further deepening of the role of adipokines in new vessel’s formation, to candidate them as therapeutic targets.