Fluid limits for networks with bandwidth sharing and general document size distributions

We consider a stochastic model of Internet congestion control, introduced by Massouli\'{e} and Roberts [Telecommunication Systems 15 (2000) 185--201], that represents the randomly varying number of flows in a network where bandwidth is shared among document transfers. In contrast to an earlier work by Kelly and Williams [Ann. Appl. Probab. 14 (2004) 1055--1083], the present paper allows interarrival times and document sizes to be generally distributed, rather than exponentially distributed. Furthermore, we allow a fairly general class of bandwidth sharing policies that includes the weighted $\alpha$-fair policies of Mo and Walrand [IEEE/ACM Transactions on Networking 8 (2000) 556--567], as well as certain other utility based scheduling policies. To describe the evolution of the system, measure valued processes are used to keep track of the residual document sizes of all flows through the network. We propose a fluid model (or formal functional law of large numbers approximation) associated with the stochastic flow level model. Under mild conditions, we show that the appropriately rescaled measure valued processes corresponding to a sequence of such models (with fixed network structure) are tight, and that any weak limit point of the sequence is almost surely a fluid model solution. For the special case of weighted $\alpha$-fair policies, we also characterize the invariant states of the fluid model.Comment: Published in at http://dx.doi.org/10.1214/08-AAP541 the Annals of Applied Probability (http://www.imstat.org/aap/) by the Institute of Mathematical Statistics (http://www.imstat.org

Bipartite graph structures for efficient balancing of heterogeneous loads

International audienceThis paper considers large scale distributed content service platforms, such as peer-to-peer video-on-demand systems. Such systems feature two basic resources, namely storage and bandwidth. Their efficiency critically depends on two factors: (i) content replication within servers, and (ii) how incoming service requests are matched to servers holding requested content. To inform the corresponding design choices, we make the following contributions. We first show that, for underloaded systems, so-called proportional content placement with a simple greedy strategy for matching requests to servers ensures full system efficiency provided storage size grows logarithmically with the system size. However, for constant storage size, this strategy undergoes a phase transition with severe loss of efficiency as system load approaches criticality. To better understand the role of the matching strategy in this performance degradation, we characterize the asymptotic system efficiency under an optimal matching policy. Our analysis shows that -in contrast to greedy matching- optimal matching incurs an inefficiency that is exponentially small in the server storage size, even at critical system loads. It further allows a characterization of content replication policies that minimize the inefficiency. These optimal policies, which differ markedly from proportional placement, have a simple structure which makes them implementable in practice. On the methodological side, our analysis of matching performance uses the theory of local weak limits of random graphs, and highlights a novel characterization of matching numbers in bipartite graphs, which may both be of independent interest

Transplantation of Quail Collagen-tailed Acetylcholinesterase Molecules Onto the Frog Neuromuscular Synapse

The highly organized pattern of acetylcholinesterase (AChE) molecules attached to the basal lamina of the neuromuscular junction (NMJ) suggests the existence of specific binding sites for their precise localization. To test this hypothesis we immunoaffinity purified quail globular and collagen-tailed AChE forms and determined their ability to attach to frog NMJs which had been pretreated with high-salt detergent buffers. The NMJs were visualized by labeling acetylcholine receptors (AChRs) with TRITC-α-bungarotoxin and AChE by indirect immunofluorescence; there was excellent correspondence (>97%) between the distribution of frog AChRs and AChE. Binding of the exogenous quail AChE was determined using a speciesspecific monoclonal antibody. When frog neuromuscular junctions were incubated with the globular G4/G2 quail AChE forms, there was no detectable binding above background levels, whereas when similar preparations were incubated with the collagen-tailed A12 AChE form >80% of the frog synaptic sites were also immunolabeled for quail AChE attached. Binding of the A12 quail AChE was blocked by heparin, yet could not be removed with high salt buffer containing detergent once attached. Similar results were obtained using empty myofiber basal lamina sheaths produced by mechanical or freeze-thaw damage. These experiments show that specific binding sites exist for collagen-tailed AChE molecules on the synaptic basal lamina of the vertebrate NMJ and suggest that these binding sites comprise a “molecular parking lot” in which the AChE molecules can be released, retained, and turned over

Gibbsian Method for the Self-Optimization of Cellular Networks

In this work, we propose and analyze a class of distributed algorithms performing the joint optimization of radio resources in heterogeneous cellular networks made of a juxtaposition of macro and small cells. Within this context, it is essential to use algorithms able to simultaneously solve the problems of channel selection, user association and power control. In such networks, the unpredictability of the cell and user patterns also requires distributed optimization schemes. The proposed method is inspired from statistical physics and based on the Gibbs sampler. It does not require the concavity/convexity, monotonicity or duality properties common to classical optimization problems. Besides, it supports discrete optimization which is especially useful to practical systems. We show that it can be implemented in a fully distributed way and nevertheless achieves system-wide optimality. We use simulation to compare this solution to today's default operational methods in terms of both throughput and energy consumption. Finally, we address concrete issues for the implementation of this solution and analyze the overhead traffic required within the framework of 3GPP and femtocell standards.Comment: 25 pages, 9 figures, to appear in EURASIP Journal on Wireless Communications and Networking 201

Upregulation of α7 Nicotinic Receptors by Acetylcholinesterase C-Terminal Peptides

BACKGROUND: The alpha-7 nicotinic acetylcholine receptor (alpha7-nAChR) is well known as a potent calcium ionophore that, in the brain, has been implicated in excitotoxicity and hence in the underlying mechanisms of neurodegenerative disorders such as Alzheimer's disease. Previous research implied that the activity of this receptor may be modified by exposure to a peptide fragment derived from the C-terminal region of the enzyme acetylcholinesterase. This investigation was undertaken to determine if the functional changes observed could be attributed to peptide binding interaction with the alpha7-nAChR, or peptide modulation of receptor expression. METHODOLOGY/PRINCIPAL FINDINGS: This study provides evidence that two peptides derived from the C-terminus of acetylcholinesterase, not only selectively displace specific bungarotoxin binding at the alpha7-nAChR, but also alter receptor binding properties for its familiar ligands, including the alternative endogenous agonist choline. Of more long-term significance, these peptides also induce upregulation of alpha7-nAChR mRNA and protein expression, as well as enhancing receptor trafficking to the plasma membrane. CONCLUSIONS/SIGNIFICANCE: The results reported here demonstrate a hitherto unknown relationship between the alpha7-nAChR and the non-enzymatic functions of acetylcholinesterase, mediated independently by its C-terminal domain. Such an interaction may prove valuable as a pharmacological tool, prompting new approaches for understanding, and combating, the process of neurodegeneration

Upregulation of α7 Nicotinic Receptors by Acetylcholinesterase C-Terminal Peptides

BACKGROUND: The alpha-7 nicotinic acetylcholine receptor (alpha7-nAChR) is well known as a potent calcium ionophore that, in the brain, has been implicated in excitotoxicity and hence in the underlying mechanisms of neurodegenerative disorders such as Alzheimer's disease. Previous research implied that the activity of this receptor may be modified by exposure to a peptide fragment derived from the C-terminal region of the enzyme acetylcholinesterase. This investigation was undertaken to determine if the functional changes observed could be attributed to peptide binding interaction with the alpha7-nAChR, or peptide modulation of receptor expression. METHODOLOGY/PRINCIPAL FINDINGS: This study provides evidence that two peptides derived from the C-terminus of acetylcholinesterase, not only selectively displace specific bungarotoxin binding at the alpha7-nAChR, but also alter receptor binding properties for its familiar ligands, including the alternative endogenous agonist choline. Of more long-term significance, these peptides also induce upregulation of alpha7-nAChR mRNA and protein expression, as well as enhancing receptor trafficking to the plasma membrane. CONCLUSIONS/SIGNIFICANCE: The results reported here demonstrate a hitherto unknown relationship between the alpha7-nAChR and the non-enzymatic functions of acetylcholinesterase, mediated independently by its C-terminal domain. Such an interaction may prove valuable as a pharmacological tool, prompting new approaches for understanding, and combating, the process of neurodegeneration

Evidence of Introgression of the ace-1R Mutation and of the ace-1 Duplication in West African Anopheles gambiae s. s

Background: The role of inter-specific hybridisation is of particular importance in mosquito disease vectors for predicting the evolution of insecticide resistance. Two molecular forms of Anopheles gambiae s.s., currently recognized as S and M taxa, are considered to be incipient sibling species. Hybrid scarcity in the field was suggested that differentiation of M and S taxa is maintained by limited or absent gene flow. However, recent studies have revealed shared polymorphisms within the M and S forms, and a better understanding of the occurrence of gene flow is needed. One such shared polymorphism is the G119S mutation in the ace-1 gene (which is responsible for insecticide resistance); this mutation has been described in both the M and S forms of A. gambiae s.s. Methods and Results: To establish whether the G119S mutation has arisen independently in each form or by genetic introgression, we analysed coding and non-coding sequences of ace-1 alleles in M and S mosquitoes from representative field populations. Our data revealed many polymorphic sites shared by S and M forms, but no diversity was associated with the G119S mutation. These results indicate that the G119S mutation was a unique event and that genetic introgression explains the observed distribution of the G119S mutation within the two forms. However, it was impossible to determine from our data whether the mutation occurred first in the S form or in the M form. Unexpectedly, sequence analysis of some resistant individuals revealed a duplication of the ace-1 gene that was observed in both A. gambiae s.s. M and S forms. Again, the distribution of this duplication in the two forms most likely occurred through introgression. Conclusions: These results highlight the need for more research to understand the forces driving the evolution of insecticide resistance in malaria vectors and to regularly monitor resistance in mosquito populations of Africa