Flow Allocation for Maximum Throughput and Bounded Delay on Multiple Disjoint Paths for Random Access Wireless Multihop Networks

In this paper, we consider random access, wireless, multi-hop networks, with multi-packet reception capabilities, where multiple flows are forwarded to the gateways through node disjoint paths. We explore the issue of allocating flow on multiple paths, exhibiting both intra- and inter-path interference, in order to maximize average aggregate flow throughput (AAT) and also provide bounded packet delay. A distributed flow allocation scheme is proposed where allocation of flow on paths is formulated as an optimization problem. Through an illustrative topology it is shown that the corresponding problem is non-convex. Furthermore, a simple, but accurate model is employed for the average aggregate throughput achieved by all flows, that captures both intra- and inter-path interference through the SINR model. The proposed scheme is evaluated through Ns2 simulations of several random wireless scenarios. Simulation results reveal that, the model employed, accurately captures the AAT observed in the simulated scenarios, even when the assumption of saturated queues is removed. Simulation results also show that the proposed scheme achieves significantly higher AAT, for the vast majority of the wireless scenarios explored, than the following flow allocation schemes: one that assigns flows on paths on a round-robin fashion, one that optimally utilizes the best path only, and another one that assigns the maximum possible flow on each path. Finally, a variant of the proposed scheme is explored, where interference for each link is approximated by considering its dominant interfering nodes only.Comment: IEEE Transactions on Vehicular Technolog

Throughput Optimal Flow Allocation on Multiple Paths for Random Access Wireless Multi-hop Networks

In this paper we consider random access wireless multi-hop mesh networks with multi-packet reception capabilities where multiple flows are forwarded to the gateways through node disjoint paths. We address the issue of aggregate throughput-optimal flow rate allocation with bounded delay guarantees. We propose a distributed flow rate allocation scheme that formulates flow rate allocation as an optimization problem and derive the conditions for non-convexity for an illustrative topology. We also employ a simple model for the average aggregate throughput achieved by all flows that captures both intra- and inter-path interference. The proposed scheme is evaluated through NS-2 simulations. Our preliminary results are derived from a grid topology and show that the proposed flow allocation scheme slightly underestimates the average aggregate throughput observed in two simulated scenarios with two and three flows respectively. Moreover it achieves significantly higher average aggregate throughput than single path utilization in two different traffic scenarios examined.Comment: Accepted for publication at the 9th IEEE BROADBAND WIRELESS ACCESS WORKSHOP (BWA2013), IEEE Globecom 2013 Workshop

NEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-kappaB-Dependent and -Independent Functions

Intestinal epithelial cells (IECs) regulate gut immune homeostasis, and impaired epithelial responses are implicated in the pathogenesis of inflammatory bowel diseases (IBD). IEC-specific ablation of nuclear factor kappaB (NF-kappaB) essential modulator (NEMO) caused Paneth cell apoptosis and impaired antimicrobial factor expression in the ileum, as well as colonocyte apoptosis and microbiota-driven chronic inflammation in the colon. Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but not colitis, suggesting that NEMO prevents colon inflammation by NF-kappaB-independent functions. Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency. Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD

Percutaneous Extraction of Chronically Implanted Left Ventricular Lead Aided by Telescopic Sheaths Spares Patient Major Cardiac Surgery

A 70-year-old patient sustained a severe pocket infection of a biventricular pacemaker system implanted 4 years ago. Patient opted for a percutaneous approach to lead extraction over open heart surgery. However, use of special locking stylets to facilitate lead traction was hampered by inability to insert the stylets due to mechanical lumen blockage and/or uncoiling and fracture of lead conductors. Hence, the procedure was finally carried out successfully only with use of telescoping sheaths, which facilitated extraction by freeing leads from multiple adhesions along their intravascular and intracardiac course, sparing patient major open cardiac surgery which would have been the only alternative should the percutaneous technique have failed

Adaptive diversity of beech seedlings under climate change scenarios

The ability of beech (Fagus sylvatica L.) populations to adapt to the ongoing climate change is especially important in the southern part of Europe, where environmental change is expected to be more intense. In this study, we tested the existing adaptive potential of eight beech populations from two provenances in N.E. Greece (Evros and Drama) that show differences in their environmental conditions and biogeographical background. Seedling survival, growth and leaf phenological traits were selected as adaptive traits and were measured under simulated controlled climate change conditions in a growth chamber. Seedling survival was also tested under current conditions in the field. In the growth chamber, simulated conditions of temperature and precipitation for the year 2050 were applied for 3 years, under two different irrigation schemes, where the same amount of water was distributed either frequently (once every week) or non-frequently (once in 20 days). The results showed that beech seedlings were generally able to survive under climate change conditions and showed adaptive differences among provenances and populations. Furthermore, changes in the duration of the growing season of seedlings were recorded in the growth chamber, allowing them to avoid environmental stress and high selection pressure. Differences were observed between populations and provenances in terms of temporal distribution patterns of precipitation and temperature, rather than the average annual or monthly values of these measures. Additionally, different adaptive strategies appeared among beech seedlings when the same amount of water was distributed differently within each month. This indicates that the physiological response mechanisms of beech individuals are very complex and depend on several interacting parameters. For this reason, the choice of beech provenances for translocation and use in afforestation or reforestation projects should consider the small scale ecotypic diversity of the species and view multiple environmental and climatic parameters in connection to each other

Improved HSC reconstitution and protection from inflammatory stress and chemotherapy in mice lacking granzyme B.

The serine protease granzyme B (GzmB) is stored in the granules of cytotoxic T and NK cells and facilitates immune-mediated destruction of virus-infected cells. In this study, we use genetic tools to report novel roles for GzmB as an important regulator of hematopoietic stem cell (HSC) function in response to stress. HSCs lacking the GzmB gene show improved bone marrow (BM) reconstitution associated with increased HSC proliferation and mitochondrial activity. In addition, recipients deficient in GzmB support superior engraftment of wild-type HSCs compared with hosts with normal BM niches. Stimulation of mice with lipopolysaccharide strongly induced GzmB protein expression in HSCs, which was mediated by the TLR4-TRIF-p65 NF-κB pathway. This is associated with increased cell death and GzmB secretion into the BM environment, suggesting an extracellular role of GzmB in modulating HSC niches. Moreover, treatment with the chemotherapeutic agent 5-fluorouracil (5-FU) also induces GzmB production in HSCs. In this situation GzmB is not secreted, but instead causes cell-autonomous apoptosis. Accordingly, GzmB-deficient mice are more resistant to serial 5-FU treatments. Collectively, these results identify GzmB as a negative regulator of HSC function that is induced by stress and chemotherapy in both HSCs and their niches. Blockade of GzmB production may help to improve hematopoiesis in various situations of BM stress