As many sensor network applications require deployment in remote and hard-to-reach areas, it is critical to ensure that such networks are capable of operating unattended for long durations. Consequently, the concept of using nodes with energy replenishment capabilities has been gaining popularity. However, new techniques and protocols must be developed to maximize the performance of sensor networks with energy replenishment. Here, we analyze limits of the performance of sensor nodes with limited energy, being replenished at a variable rate. We provide a simple localized energy management scheme that achieves a performance close to that with an unlimited energy source, and at the same time keeps the probability of complete battery discharge low. Based on the insights developed, we address the problem of energy management for energyreplenishing nodes with finite battery and finite data buffer capacities. To this end, we give an energy management scheme that achieves the optimal utility asymptotically while keeping both the battery discharge and data loss probabilities low.Rahul Srivastava is with the Wireless The following notations will be used to compare rates of convergence: an = O(bn) if an goes to zero at least as fast as bn; an = o(bn) if an goes to zero strictly faster than bn; an = Θ(bn) if an and bn go to zero at the same rate; an = Ω(bn) if an goes to zero no faster than bn.

We report the observation of large (approximately 40%) laser-induced above-band-gap transparency in GaAs at room temperature. The induced transparency is present only during the pulse width of the driving midinfrared laser pulses and its spectral shape is consistent with a laser-induced blueshift of the band edge. Our simulations based on the dynamic Franz-Keldysh effect reproduce the salient features of the experimental results, demonstrating, in particular, that the amount of the band edge shift is approximately given by the ponderomotive potential.

One of the main issues in the design of sensor networks is energy efficient communication of timecritical data. Energy wastage can be caused by failed packet transmission attempts at each node due to channel dynamics and interference. Therefore transmission control techniques that are unaware of the channel dynamics can lead to suboptimal channel use patterns. In this paper we propose a transmission controller that utilizes different "grades" of channel side information to schedule packet transmissions in an optimal way, while meeting a deadline constraint for all packets waiting in the transmission queue.The wireless channel is modeled as a finite-state Markov channel. We are specifically interested in the case where the transmitter has low-grade channel side information that can be obtained based solely on the ACK/NAK sequence for the previous transmissions. Our scheduler is readily implementable and it is based on the dynamic programming solution to the finite-horizon transmission control problem.We also calculate the information theoretic capacity of the finite state Markov channel with feedback containing different grades of channel side information including that, obtained through the ACK/NAK sequence. We illustrate that our scheduler achieves a given throughput at a power level that is fairly close to the fundamental limit achievable over the channel.

BCL-2 family proteins regulate the mitochondrial apoptotic pathway. BOK, a multidomain BCL-2 family protein, is generally believed to be an adaptor protein similar to BAK and BAX, regulating the mitochondrial permeability transition during apoptosis. Here we report that BOK is a positive regulator of a key enzyme involved in uridine biosynthesis; namely, uridine monophosphate synthetase (UMPS). Our data suggest that BOK expression enhances UMPS activity, cell proliferation, and chemosensitivity. Genetic deletion of Bok results in chemoresistance to 5-fluorouracil (5-FU) in different cell lines and in mice. Conversely, cancer cells and primary tissues that acquire resistance to 5-FU down-regulate BOK expression. Furthermore, we also provide evidence for a role for BOK in nucleotide metabolism and cell cycle regulation. Our results have implications in developing BOK as a biomarker for 5-FU resistance and have the potential for the development of BOK-mimetics for sensitizing 5-FU-resistant cancers.

Objectives: Eosinophilic esophagitis (EoE) is a clinicopathologic diagnosis characterized by inflammation and infiltration of eosinophils at the esophageal mucosa. The underlying etiology of EoE remains elusive. Inflammatory diseases, such as asthma, are associated with structural remodeling of the airways, which includes angiogenesis. The aims of this study were to determine the angiogenic profile of esophageal mucosa in children presenting with EoE and to evaluate the putative mechanism(s) underlying the early inflammatory angiogenic response observed in EoE. Methods: Endoscopically obtained biopsy samples from 18 EoE and 18 control pediatric patients were analyzed for angiogenic markers (CD31, von Willebrand factor, vascular cell adhesion molecule-1) and tissue levels of angiogenic factors (vascular endothelial growth factor [VEGF]-A, VEGF-R2, angiogenin and interleukin [IL]-8). Expression levels of angiogenic factors and markers in EoE and control samples were characterized by immunofluorescence analysis and quantitative reverse transcriptase-polymerase chain reaction. Vascular density of biopsy samples was evaluated by immunofluorescence analysis. Results: Samples from patients with EoE exhibited higher levels of von Willebrand factor, CD31, and vascular cell adhesion molecule-1, which is suggestive of neovascularization and an activated endothelium. Moreover, EoE biopsies showed greater levels of the angiogenesis promoters VEGFA, angiogenin, and IL-8. Interestingly, there were greater cellular levels of tumor necrosis factor-a in EoE samples compared with controls. Furthermore, there were higher nuclear levels of p50 and p65 subunits of NFkB and lower cellular levels of the inhibitor of NFkB, IkB-a, in EoE samples compared with controls. Conclusions: We demonstrate increased angiogenesis in the esophageal mucosa of pediatric patients with EoE. The data also provided evidence that the angiogenic factors VEGF-A, angiogenin, and IL-8 were prominently involved in promoting angiogenic remodeling.

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Transposable elements (TEs) have been active in the mammalian genome for millions of years and the silencing of these elements in the germline is important for the survival of the host. Mice carrying reporter transgenes can be used to model transcriptional silencing. A mutagenesis screen for modifiers of epigenetic gene silencing produced a line with a mutation in Trim33; the mutants displayed increased expression of the reporter transgene. ChIP-seq of Trim33 in testis revealed 9,109 peaks, mostly at promoters. This is the first report of ChIP-seq for Trim33 in any tissue. Comparison with ENCODE datasets showed that regions of high read density for Trim33 had high read density for histone marks associated with transcriptional activity and mapping to TE consensus sequences revealed Trim33 enrichment at RLTR10B, the LTR of one of the youngest retrotransposons in the mouse genome, MMERVK10C. We identified consensus sequences from the 266 regions at which Trim33 ChIP-seq peaks overlapped RLTR10B elements and found a match to the A-Myb DNA-binding site. We found that TRIM33 has E3 ubiquitin ligase activity for A-MYB and regulates its abundance. RNA-seq revealed that mice haploinsufficient for Trim33 had altered expression of a small group of genes in the testis and the gene with the most significant increase was found to be transcribed from an upstream RLTR10B. These studies provide the first evidence that A-Myb has a role in the actions of Trim33 and suggest a role for both A-Myb and Trim33 in the arms race between the transposon and the host. This the first report of any factor specifically regulating RLTR10B and adds to the current literature on the silencing of MMERVK10C retrotransposons. This is also the first report that A-Myb has a role in the transcription of any retrotransposon.