Treewidth: Computational Experiments.

Many NP-complete graph problems can be solved in polynomial time for graphs with bounded treewidth. Equivalent results are known for pathwidth and branchwidth. In recent years, several studies have shown that this result is not only of theoretical interest but can successfully be applied to find (almost) optimal solutions or lower bounds for diverse optimization problems. To apply a tree decomposition approach, the treewidth of the graph has to be determined, independently of the application at hand. Although for fixed k, linear time algorithms exist to solve the decision problem ``treewidth at most k, their practical use is very limited. The computational tractability of treewidth has been rarely studied so far. In this paper, we compare four heuristics and two lower bounds for instances from applications such as the frequency assignment problem and the vertex coloring problem. Three of the heuristics are based on well-known algorithms to recognize triangulated graphs. The fourth heuristic recursively improves a tree decomposition by the computation of minimal separating vertex sets in subgraphs. Lower bounds can be computed from maximal cliques and the minimum degree of induced subgraphs. A computational analysis shows that the treewidth of several graphs can be identified by these methods. For other graphs, however, more sophisticated techniques are necessary.operations research and management science;

On the design of an energy-efficient low-latency integrated protocol for distributed mobile sensor networks

Self organizing, wireless sensors networks are an emergent and challenging technology that is attracting large attention in the sensing and monitoring community. Impressive progress has been done in recent years even if we need to assume that an optimal protocol for every kind of sensor network applications can not exist. As a result it is necessary to optimize the protocol for certain scenarios. In many applications for instance latency is a crucial factor in addition to energy consumption. MERLIN performs its best in such WSNs where there is the need to reduce the latency while ensuring that energy consumption is kept to a minimum. By means of that, the low latency characteristic of MERLIN can be used as a trade off to extend node lifetimes. The performance in terms of energy consumption and latency is optimized by acting on the slot length. MERLIN is designed specifically to integrate routing, MAC and localization protocols together. Furthermore it can support data queries which is a typical application for WSNs. The MERLIN protocol eliminates the necessity to have any explicit handshake mechanism among nodes. Furthermore, the reliability is improved using multiple path message propagation in combination with an overhearing mechanism. The protocol divides the network into subsets where nodes are grouped in time zones. As a result MERLIN also shows a good scalability by utilizing an appropriate scheduling mechanism in combination with a contention period

Immunoliposome-mediated targeting of doxorubicin to human ovarian carcinoma in vitro and in vivo.

This paper deals with the utility of immunoliposomes for the delivery of doxorubicin (DXR) to human ovarian carcinoma cells in vitro and in vivo. We aimed to investigate whether immunoliposome-mediated targeting of DXR to ovarian cancer cells translates in an enhanced anti-tumour effect compared with that of non-targeted DXR liposomes (lacking the specific antibody). Target cell binding and anti-tumour activity of DXR immunoliposomes were studied in vitro and in vivo (xenograft model of ovarian carcinoma). In vitro we observed that target cell binding and cell growth inhibition of DXR immunoliposomes is superior to that of non-targeted DXR-liposomes. However, in vivo, despite the efficient target cell binding and good anti-tumour response of DXR-immunoliposomes, no difference in anti-tumour effect, compared with non-targeted DXR-liposomes, could be determined. The results indicate that premature DXR leakage from immunoliposomes occurring before the actual target cell binding and subsequent DXR association with the tumour cells, explains why no significant differences in anti-tumour activity between DXR-immunoliposomes and non-targeted DXR-liposomes were observed in vivo

RNAseq Analyses Identify Tumor Necrosis Factor-Mediated Inflammation as a Major Abnormality in ALS Spinal Cord

ALS is a rapidly progressive, devastating neurodegenerative illness of adults that produces disabling weakness and spasticity arising from death of lower and upper motor neurons. No meaningful therapies exist to slow ALS progression, and molecular insights into pathogenesis and progression are sorely needed. In that context, we used high-depth, next generation RNA sequencing (RNAseq, Illumina) to define gene network abnormalities in RNA samples depleted of rRNA and isolated from cervical spinal cord sections of 7 ALS and 8 CTL samples. We aligned \u3e50 million 2X150 bp paired-end sequences/sample to the hg19 human genome and applied three different algorithms (Cuffdiff2, DEseq2, EdgeR) for identification of differentially expressed genes (DEG’s). Ingenuity Pathways Analysis (IPA) and Weighted Gene Co-expression Network Analysis (WGCNA) identified inflammatory processes as significantly elevated in our ALS samples, with tumor necrosis factor (TNF) found to be a major pathway regulator (IPA) and TNFα-induced protein 2 (TNFAIP2) as a major network “hub” gene (WGCNA). Using the oPOSSUM algorithm, we analyzed transcription factors (TF) controlling expression of the nine DEG/hub genes in the ALS samples and identified TF’s involved in inflammation (NFkB, REL, NFkB1) and macrophage function (NR1H2::RXRA heterodimer). Transient expression in human iPSC-derived motor neurons of TNFAIP2 (also a DEG identified by all three algorithms) reduced cell viability and induced caspase 3/7 activation. Using high-density RNAseq, multiple algorithms for DEG identification, and an unsupervised gene co-expression network approach, we identified significant elevation of inflammatory processes in ALS spinal cord with TNF as a major regulatory molecule. Overexpression of the DEG TNFAIP2 in human motor neurons, the population most vulnerable to die in ALS, increased cell death and caspase 3/7 activation. We propose that therapies targeted to reduce inflammatory TNFα signaling may be helpful in ALS patients