Miracle-dz/UniFAR-FTUs huggingface dataset:
Dubhe: A Reliable and Low-Latency Data Dissemination Mechanism for VANETs

Many attractive applications over vehicular ad hoc networks (VANETs) need data to be transmitted to the remote destinations through multihop data forwarding, but some unique characteristics of VANETs (i.e., high node mobility, dynamic topology changes with frequent link breakage, and unstable quality of wireless transmission) incur unstable data delivery performance. In order to reliably and quickly disseminate the data, we present Dubhe which includes a delay model and an improved greedy broadcast algorithm embedded with a coverage elimination rule. The former is used for making decisions for path selection with the aim of minimizing the transmission latency, while the latter focuses on boosting the reliability of one-hop data transmission. We also analyze the necessity and effectiveness of Dubhe and the retransmission overheads theoretically. It is shown from the experiments that Dubhe can achieve high-reliability and low-latency data delivery in comparison with the epidemic-based protocol and the static-node-assisted adaptive data delivery protocol.
Animal models for viral infection and cell exhaustion

Purpose of reviewDespite eliciting an early antiviral T cell response, HIV-specific T cells are unable to prevent disease progression, partly because of their loss of effector functions, known as T cell exhaustion. Restoring this T cell functionality represents a critical step for regaining immunological control of HIV-1 replication, and may be fundamental for the development of a functional cure for HIV. In this context, the use of animal models is invaluable for evaluating the efficacy and mechanisms of novel therapeutics aimed at reinvigorating T cell functions. Recent findingsAlthough nonhuman primates continue to be a mainstay for studying HIV pathogenesis and therapies, recent advances in humanized mouse models have improved their ability to recapitulate the features of cell exhaustion during HIV infection. Targeting coinhibitory receptors in HIV-infected and simian immunodeficiency virus (SIV)-infected animals has resulted in viral load reductions, presumably by reinvigorating the effector functions of T cells. Additionally, studies combining programmed death-1 (PD-1) blockade with suppressive antiretroviral therapy provide further support to the use of coinhibitory receptor blockades in restoring T cell function by delaying viral load rebound upon antiretroviral therapy interruption. Future in-vivo studies should build on recent in-vitro data, supporting the simultaneous targeting of multiple regulators of cell exhaustion. SummaryIn this review, we describe the most recent advances in the use of animal models for the study of cell exhaustion following HIV/SIV infection. These findings suggest that the use of animal models is increasingly critical in translating immunotherapeutics into clinical practice.
Detection of bacterial pathogens including potential new species in human head lice from Mali

In poor African countries, where no medical and biological facilities are available, the identification of potential emerging pathogens of concern at an early stage is challenging. Head lice, Pediculus humanus capitis, have a short life, feed only on human blood and do not transmit pathogens to their progeny. They are, therefore, a perfect tool for the xenodiagnosis of current or recent human infection. This study assessed the occurrence of bacterial pathogens from head lice collected in two rural villages from Mali, where a high frequency of head lice infestation had previously been reported, using molecular methods. Results show that all 600 head lice, collected from 117 individuals, belonged to clade E, specific to West Africa. Bartonella quintana, the causative agent of trench fever, was identified in three of the 600 (0.5%) head lice studied. Our study also shows, for the first time, the presence of the DNA of two pathogenic bacteria, namely Coxiella burnetii (5.1%) and Rickettsia aeschlimannii (0.6%), detected in human head lice, as well as the DNA of potential new species from the Anaplasma and Ehrlichia genera of unknown pathogenicity. The finding of several Malian head lice infected with B. quintana, C. burnetii, R. aeschlimannii, Anaplasma and Ehrlichia is alarming and highlights the need for active survey programs to define the public health consequences of the detection of these emerging bacterial pathogens in human head lice.
The Nonlinear Steepest Descent Method: Asymptotics for Initial-Boundary Value Problems

We consider the rigorous derivation of asymptotic formulas for initial-boundary value problems using the nonlinear steepest descent method. We give detailed derivations of the asymptotics in the similarity and self-similar sectors for the modified Korteweg--de Vries equation in the quarter-plane. Precise and uniform error estimates are presented in detail.
Comparison of ultrasound and CT in the evaluation of pneumonia complicated by parapneumonic effusion in children.

OBJECTIVE The purpose of our study was to compare chest ultrasound and chest CT in children with complicated pneumonia and parapneumonic effusion. MATERIALS AND METHODS We retrospectively compared chest ultrasound and chest CT in 19 children (nine girls and 10 boys; age range, 8 months-17 years) admitted with complicated pneumonia and parapneumonic effusion between December 2006 and January 2009. Images were evaluated for effusion, loculation, fibrin strands, parenchymal consolidation, necrosis, and abscess. In the subset of patients who underwent surgical management, imaging findings were correlated with operative findings. RESULTS Eighteen of 19 patients had an effusion on both chest ultrasound and chest CT. The findings of effusion loculation as well as parenchymal consolidation and necrosis or abscess were similar between the two techniques. Chest ultrasound was better able to visualize fibrin strands within the effusions. Of the 14 patients who underwent video-assisted thoracoscopy, five had surgically proven parenchymal abscess or necrosis. Preoperatively, chest ultrasound was able to show parenchymal abscess or necrosis in four patients, whereas chest CT was able to show parenchymal abscess or necrosis in three. CONCLUSION In our series, chest ultrasound and chest CT were similar in their ability to detect loculated effusion and lung necrosis or abscess resulting from complicated pneumonia. Chest CT did not provide any additional clinically useful information that was not also seen on chest ultrasound. We suggest that the imaging workup of complicated pediatric pneumonia include chest radiography and chest ultrasound, reserving chest CT for cases in which the chest ultrasound is technically limited or discrepant with the clinical findings.
An Optimal Transmission Strategy for Kalman Filtering Over Packet Dropping Links With Imperfect Acknowledgements

This paper presents a novel design methodology for optimal transmission policies at a smart sensor to remotely estimate the state of a stable linear stochastic dynamical system. The sensor makes measurements of the process and forms estimates of the state using a local Kalman filter. The sensor transmits quantized information over a packet dropping link to the remote receiver. The receiver sends packet receipt acknowledgments back to the sensor via an erroneous feedback communication channel which is itself packet dropping. The key novelty of this formulation is that the smart sensor decides, at each discrete time instant, whether to transmit a quantized version of either its local state estimate or its local innovation. The objective is to design optimal transmission policies in order to minimize a long-term average cost function as a convex combination of the receiver's expected estimation error covariance and the energy needed to transmit the packets. Under high-resolution quantization assumptions, the optimal transmission policy is obtained by the use of dynamic programming techniques. Using the concept of submodularity, the optimality of a threshold policy in the case of scalar systems with perfect packet receipt acknowledgments is proved. Suboptimal solutions and their structural results are also discussed. Numerical results are presented, illustrating the performance of the optimal and suboptimal transmission policies.
Sparsity-aware field estimation via ordinary Kriging

In this paper, we consider the problem of estimating a spatially varying field in a wireless sensor network, where resource constraints limit the number of sensors selected in the network that provide their measurements for field estimation. Based on a one-to-one correspondence between the selected sensors and the nonzero elements of Kriging weights, we propose a sparsity-promoting ordinary Kriging approach where we minimize the Kriging error variance while penalizing the number of nonzero Kriging weights. This yields a combinatorial optimization problem, which is intractable in general. To solve the proposed non-convex optimization problem, we employ the alternating direction method of multipliers (ADMM) and the reweighted ℓ1 minimization method, respectively. Numerical results are provided to illustrate the effectiveness of our proposed approaches that provide a balance between the estimation accuracy and the number of selected sensors.
A hybrid complete-graph partial-crossbar routing architecture for multi-FPGA systems

Multi-FPGA systems (MFSs) are used as custom computing machines, logic emulators and rapid prototyping vehicles. A key aspect of these systems is their programmable routing architecture; the manner in which wires, FPGAs and Field-Programmable Interconnect Devices (FPIDs) are connected. Several routing architectures for MFSs have been proposed [Arno92] [Butt92] [Hauc94] [Apti96] [Vuil96] and previous research has shown that the partial crossbar is one of the best existing architectures [Kim96] [Khal97]. In this paper we propose a new routing architecture, called the Hybrid Complete-Graph and Partial-Crossbar (HCGP) which has superior speed and cost compared to a partial crossbar. The new architecture uses both hard-wired and programmable connections between the FPGAs. We compare the performance and cost of the HCGP and partial crossbar architectures experimentally, by mapping a set of 15 large benchmark circuits into each architecture. A customized set of partitioning and inter-chip routing tools were developed, with particular attention paid to architecture-appropriate inter-chip routing algorithms. We show that the cost of the partial crossbar (as measured by the number of pins on all FPGAs and FPIDs required to fit a design), is on average 20% more than the new HCGP architecture and as much as 35% more. Furthermore, the critical path delay for designs implemented on the partial crossbar increased, and were on average 9% more than the HCGP architecture and up to 26% more. Using our experimental approach, we also explore a key architecture parameter associated with the HCGP architecture: the proportion of hard-wired connections versus programmable connections, to determine its best value.
Dominance orders in animal societies: The self-organization hypothesis revisited

In previous papers (Theraulaz et al., 1995; Bonabeau et al., 1996) we suggested, following Hogeweg and Hesper (1983, 1985), that the formation of dominance orders in animal societies could result from a self-organizing process involving a double reinforcement mechanism: winners reinforce their probability of winning and losers reinforce their probability of losing. This assumption, and subsequent models relying on it, were based on empirical data on primitively eusocial wasps (Polistes dominulus). By reanalysing some of the experimental data that was previously thought to be irrelevant, we show that it is impossible to distinguish this assumption from a competing assumption based on preexisting differences among individuals. We propose experiments to help discriminate between the two assumptions and their corresponding models—the self-organization model and the correlational model. We urge other researchers to be cautious when interpreting their dominance data with the ’self-organization mindset’; in particular, ‘winner and loser effects’, which are often considered to give support to the self-organization assumption, are equally consistent with the correlational assumption.
Hotspots of Biased Nucleotide Substitutions in Human Genes

Genes that have experienced accelerated evolutionary rates on the human lineage during recent evolution are candidates for involvement in human-specific adaptations. To determine the forces that cause increased evolutionary rates in certain genes, we analyzed alignments of 10,238 human genes to their orthologues in chimpanzee and macaque. Using a likelihood ratio test, we identified protein-coding sequences with an accelerated rate of base substitutions along the human lineage. Exons evolving at a fast rate in humans have a significant tendency to contain clusters of AT-to-GC (weak-to-strong) biased substitutions. This pattern is also observed in noncoding sequence flanking rapidly evolving exons. Accelerated exons occur in regions with elevated male recombination rates and exhibit an excess of nonsynonymous substitutions relative to the genomic average. We next analyzed genes with significantly elevated ratios of nonsynonymous to synonymous rates of base substitution (d N /d S) along the human lineage, and those with an excess of amino acid replacement substitutions relative to human polymorphism. These genes also show evidence of clusters of weak-to-strong biased substitutions. These findings indicate that a recombination-associated process, such as biased gene conversion (BGC), is driving fixation of GC alleles in the human genome. This process can lead to accelerated evolution in coding sequences and excess amino acid replacement substitutions, thereby generating significant results for tests of positive selection.
FATIGUE CRACK TIP PLASTIC STRAIN IN HIGH‐STRENGTH ALUMINUM ALLOYS

— Plastic zone size and shape and the distribution of strain within the plastic zone are determined for the high-strength aluminium alloys 2024-T4, 6061 T6, and 7075-T6 using the technique of selected area electron channeling. Plastic zone size is found to correlate with the work done in creating a unit of new crack surface and the yield stress, rather than with the stress intensity factor and yield stress. Plastic strain distribution is found to be a logarithmic function of distance from the crack tip, in agreement with the mathematical analysis for a moving crack in plane strain.
Intracellular modifications induced by poliovirus reduce the requirement for structural motifs in the 5' noncoding region of the genome involved in internal initiation of protein synthesis

A series of genetic deletions based partly on two RNA secondary structure models (M. A. Skinner, V. R. Racaniello, G. Dunn, J. Cooper, P. D. Minor, and J. W. Almond, J. Mol. Biol. 207:379-392, 1989; E. V. Pilipenko, V. M. Blinov, L. I. Romanova, A. N. Sinyakov, S. V. Maslova, and V. I. Agol, Virology 168:201-209, 1989) was made in the cDNA encoding the 5' noncoding region (5' NCR) of the poliovirus genome in order to study the sequences that direct the internal entry of ribosomes. The modified cDNAs were placed between two open reading frames in a single transcriptional unit and used to transfect cells in culture. Internal entry of ribosomes was detected by measuring translation from the second open reading frame in the bicistronic mRNA. When assayed alone, a large proportion of the poliovirus 5' NCR superstructure including several well-defined stem-loops was required for ribosome entry and efficient translation. However, in cells cotransfected with a complete infectious poliovirus cDNA, the requirement for the stem-loops in this large superstructure was reduced. The results suggest that virus infection modifies the cellular translational machinery, so that shortened forms of the 5' NCR are sufficient for cap-independent translation, and that the internal entry of ribosomes occurs by two distinct modes during the virus replication cycle.
Differential expression of S100A2 and S100A4 in lung adenocarcinomas: Clinicopathological significance, relationship to p53 and identification of their target genes

Previous studies suggest that some S100 proteins are involved in the progression of certain types of cancer. However, no comprehensive data is currently available on the expression of S100 family genes in lung adenocarcinomas. Oligonucleotide array, quantitative reverse transcription–polymerase chain reaction and western blot analyses of lung adenocarcinoma cell lines and bronchiolar epithelial cells (SAEC and NHBE) revealed that S100A2 and S100A4 were the most strikingly downregulated and upregulated members of the S100 family, respectively. Immunohistochemical analyses of 94 primary lung adenocarcinomas showed that positive S100A2 expression (33/94, 35.1%) was significantly associated with lymphatic invasion (P = 0.0233) and positive S100A4 expression (19/94, 20.2%) with vascular invasion (P = 0.0454). Interestingly, a strong inverse relationship was found between S100A4 and p53 expression (P = 0.0008). Survival analyses showed that S100A4 positivity was associated with poor patient prognosis (P = 0.042). S100A2 positivity was not associated with patient survival when the whole patient group was analyzed; however, S100A2 positivity was a favorable prognostic indicator in patients with p53‐negative tumors (P = 0.0448). Finally, we used oligonucleotide array analyses and identified potential S100A2 and S100A4 target genes involved in cancer progression: S100A2 induced RUNX3 and REPRIMO; S100A4 induced EZRIN, RUNX1 and WISP1; S100A2 repressed EGFR, NFKB2 and RELA2; and S100A4 repressed ANXA10 and IL1RN. Thus, the present study demonstrates involvement of S100A2 and S100A4 in the progression of lung adenocarcinomas and an inverse association between S100A4 and p53 expression, and provides a list of targets regulated by S100A2 and S100A4. (Cancer Sci 2005; 96: 844–857)
Estimation of the cell loss ratio in ATM networks with a fuzzy system and application to measurement-based call admission control

An important parameter in asynchronous transfer model (ATM)-based network design and management is the cell loss ratio (CLR) in ATM multiplexers. It is a key parameter to many vital functions in the network such as call admission control (CAC), bandwidth allocation, etc. However, the CLR depends usually on many unknown and unpredictable traffic parameters such as input traffic correlations. In this paper, we propose a simple and robust fuzzy-based algorithm to predict the CLR in large-sized systems based on both a small amount of information from small-sized systems, and the asymptotic behavior for very large systems. Unlike the model-based approaches, our approximation avoids the problem of assuming any traffic parameters or arrival process. This algorithm is used with real-time traffic measurement to propose an effective measurement-based call admission control framework for ATM networks.
HSPB1 Facilitates the Formation of Non-Centrosomal Microtubules

The remodeling capacity of microtubules (MT) is essential for their proper function. In mammals, MTs are predominantly formed at the centrosome, but can also originate from non-centrosomal sites, a process that is still poorly understood. We here show that the small heat shock protein HSPB1 plays a role in the control of non-centrosomal MT formation. The HSPB1 expression level regulates the balance between centrosomal and non-centrosomal MTs. The HSPB1 protein can be detected specifically at sites of de novo forming non-centrosomal MTs, while it is absent from the centrosomes. In addition, we show that HSPB1 binds preferentially to the lattice of newly formed MTs in vitro, suggesting that its function occurs by stabilizing MT seeds. Our findings open new avenues for the understanding of the role of HSPB1 in the development, maintenance and protection of cells with specialized non-centrosomal MT arrays.
The Neonatal CD4+ T Cell Response to a Single Epitope Varies in Genetically Identical Mice

Neonatal infection is a major cause of morbidity and mortality worldwide. Increased susceptibility to infection in the neonate is attributed in part to defects in T cell–mediated immunity. A peptide:MHC class II tetramer-based cell enrichment method was used to test this hypothesis at the level of a single epitope. We found that naive T cells with TCRs specific for the 2W:I-Ab epitope were present in the thymuses of 1-d-old CD57BL/6 mice but were barely detectable in the spleen, likely because each mouse contained very few total splenic CD4+ T cells. By day 7 of life, however, the total number of splenic CD4+ T cells increased dramatically and the frequency of 2W:I-Ab–specific naive T cells reached that of adult mice. Injection of 2W peptide in CFA into 1-d-old mice generated a 2W:I-Ab–specific effector cell population that peaked later than in adult mice and showed more animal-to-animal variation. Similarly, 2W:I-Ab–specific naive T cells in different neonatal mice varied significantly in generation of Th1, Th2, and follicular Th cells compared with adult mice. These results suggest that delayed effector cell expansion and stochastic variability in effector cell generation due to an initially small naive repertoire contribute to defective peptide:MHC class II–specific immunity in neonates.
Inhibition of Histone Deacetylation Potentiates the Evolution of Acquired Temozolomide Resistance Linked to MGMT Upregulation in Glioblastoma Xenografts

Purpose: The therapeutic benefit of temozolomide in glioblastoma multiforme (GBM) is limited by resistance. The goal of this study was to elucidate mechanisms of temozolomide resistance in GBM. Experimental Design: We developed an in vivo GBM model of temozolomide resistance and used paired parental and temozolomide-resistant tumors to define the mechanisms underlying the development of resistance and the influence of histone deacetylation (HDAC) inhibition. Results: Analysis of paired parental and resistant lines showed upregulation of O6-methylguanine-DNA methyltransferase (MGMT) expression in 3 of the 5 resistant xenografts. While no significant change was detected in MGMT promoter methylation between parental and derivative-resistant samples, chromatin immunoprecipitation showed an association between MGMT upregulation and elevated acetylation of lysine 9 of histone H3 (H3K9-ac) and decreased dimethylation (H3K9-me2) in GBM12 and GBM14. In contrast, temozolomide resistance development in GBM22 was not linked to MGMT expression, and both parental and resistant lines had low H3K9-ac and high H3K9-me2 within the MGMT promoter. In the GBM12TMZ-resistant line, MGMT reexpression was accompanied by increased recruitment of SP1, C-JUN, NF-κB, and p300 within the MGMT promoter. Interestingly, combined treatment of GBM12 flank xenografts with temozolomide and the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) favored the evolution of temozolomide resistance by MGMT overexpression as compared with treatment with temozolomide alone. Conclusion: This study shows, for the first time, a unique mechanism of temozolomide resistance development driven by chromatin-mediated MGMT upregulation and highlights the potential for epigenetically directed therapies to influence the mechanisms of resistance development in GBM. Clin Cancer Res; 18(15); 4070–9. ©2012 AACR.