Optimal throughput-delay scaling in wireless networks - part I: the fluid model

Gupta and Kumar (2000) introduced a random model to study throughput scaling in a wireless network with static nodes, and showed that the throughput per source-destination pair is /spl Theta/(1//spl radic/(nlogn)). Grossglauser and Tse (2001) showed that when nodes are mobile it is possible to have a constant throughput scaling per source-destination pair. In most applications, delay is also a key metric of network performance. It is expected that high throughput is achieved at the cost of high delay and that one can be improved at the cost of the other. The focus of this paper is on studying this tradeoff for wireless networks in a general framework. Optimal throughput-delay scaling laws for static and mobile wireless networks are established. For static networks, it is shown that the optimal throughput-delay tradeoff is given by D(n)=/spl Theta/(nT(n)), where T(n) and D(n) are the throughput and delay scaling, respectively. For mobile networks, a simple proof of the throughput scaling of /spl Theta/(1) for the Grossglauser-Tse scheme is given and the associated delay scaling is shown to be /spl Theta/(nlogn). The optimal throughput-delay tradeoff for mobile networks is also established. To capture physical movement in the real world, a random-walk (RW) model for node mobility is assumed. It is shown that for throughput of /spl Oscr/(1//spl radic/(nlogn)), which can also be achieved in static networks, the throughput-delay tradeoff is the same as in static networks, i.e., D(n)=/spl Theta/(nT(n)). Surprisingly, for almost any throughput of a higher order, the delay is shown to be /spl Theta/(nlogn), which is the delay for throughput of /spl Theta/(1). Our result, thus, suggests that the use of mobility to increase throughput, even slightly, in real-world networks would necessitate an abrupt and very large increase in delay.     

Universal smoothing factor selection in density estimation: theory and practice

In earlier work with Gabor Lugosi, we introduced a method to select a smoothing factor for kernel density estimation such that, forall densities in all dimensions, theL ₁ error of the corresponding kernel estimate is not larger than 3+∈ times the error of the estimate with the optimal smoothing factor plus a constant times $\sqrt {\log n/n}$ , wheren is the sample size, and the constant only depends on the complexity of the kernel used in the estimate. The result is nonasymptotic, that is, the bound is valid for eachn. The estimate uses ideas from the minimum distance estimation work of Yatracos. We present a practical implementation of this estimate, report on some comparative results, and highlight some key properties of the new method.     

Fat embolism prophylaxis: a study of four treatment modalities

Significant coagulation and blood gas changes may occur with uncomplicated extremity fractures. To more accurately define the effect of therapy on these changes, a prospective study of 58 patients with uncomplicated fractures was undertaken. An initial group of 10 selected patients was studied to determine the changes with "standard therapy." The remaining 48 patients were then randomized into five groups: control, increased fluid intake, increased glucose intake, aspirin, and massive steroids. The patients were studied on 5 consecutive days. Treatment of patients in the latter four groups with aspirin or steroids resulted in significant normalization of blood gases, coagulation proteins, and platelet numbers when compared to controls. These measurements in patients treated with fluid loading or increased glucose intake were not significantly different from controls.     

Biomimetic acellular detoxified glutaraldehyde cross-linked bovine pericardium for tissue engineering

Glutaraldehyde (GLUT) processing, cellular antigens, calcium ions in circulation, and phospholipids present in the native tissue are predominantly responsible for calcification, degeneration, and lack of natural microenvironment for host progenitor cell migration in tissue implants. The study presents an improved methodology for adhesion and proliferation of endothelial progenitor cells (EPCs) without significant changes in biomechanical and biodegradation properties of the processed acellular bovine pericardium. The anti-calcification potential of the processed tissue was enhanced by detoxification of GLUT-cross-linked bovine pericardium by decellularization, pretreating it with ethanol or removing the free aldehydes by citric acid treatment and lyophilization. The treated tissues were assessed for biomechanical properties, GLUT ligand quantification, adhesion, proliferation of EPCs, and biodegradability. The results indicate that there was no significant change in biomechanical properties and biodegradability when enzymatic hydrolysis (p > 0.05) is employed in detoxified acellular GLUT cross-linked tissue (DBP–G–CA–ET), compared with the native detoxified GLUT cross-linked bovine pericardium (NBP–G–CA–ET). DBP–G–CA–ET exhibited a significant (p > 0.05) increase in the viability of EPCs and cell adhesion as compared to acellular GLUT cross-linked bovine pericardium (p < 0.05). Lyophilized acellular detoxified GLUT cross-linked bovine pericardium, employed in our study as an alternative to conventional GLUT cross-linked bovine pericardium, might provide longer durability and better biocompatibility, and reduce calcification. The developed bovine pericardium patches could be used in cardiac reconstruction and repair, arteriotomy, soft tissue repair, and general surgical procedures with tissue regeneration dimensions.     

DNA-PK-independent rejoining of DNA double-strand breaks in human cell extracts in vitro

PURPOSE: To investigate the role of DNA-dependent protein kinase (DNA-PK) in the rejoining of ionizing radiation-induced DNA double-strand breaks (dsb). MATERIALS AND METHODS: This study employed previously described in vitro assays that utilize nuclei or 'naked' DNA prepared from agarose-embedded cells as a substrate and S-HeLa cell extracts as a source of enzymes. Rejoining of dsb in these assays is absolutely dependent on cell extract and it proceeds, under optimal reaction conditions, to an extent similar to that observed in intact cells. Results were confirmed in a plasmid-based assay for in vitro rejoining of dsb. RESULTS: It is shown that concentrations of wortmannin completely inhibiting DNA-PK activity profoundly affect the rejoining of dsb in vivo, but have no effect on dsb rejoining in vitro. Furthermore, fractionation of cell extracts using ammonium sulphate precipitation, generates protein fractions that are able to support dsb rejoining, despite the fact that they do not contain detectable amounts of either DNA-PKcs or Ku80. Efficient rejoining of dsb in vitro is also observed with extracts of MO59J cells that lack DNA-PK activity. Finally, rejoining of dsb remains unaffected by wortmannin in a plasmid-based assay, and is also detectable with extracts of MO59J cells. CONCLUSIONS: These findings are in contrast with genetic studies demonstrating a requirement for DNA-PK activity for efficient rejoining of dsb in vivo. The difference between in vitro and in vivo results may not be attributed to chromatin structure since wortmannin was without an effect when using nuclei as a substrate. It is speculated that the differences between in vivo and in vitro results can be explained either by assuming the operation of multiple pathways in dsb rejoining, some of which do not require DNA-PK, or by postulating a purely regulatory/damage-sensing role for DNA-PK in intact cells but no direct involvement in dsb rejoining.     

Thresholding algorithms, maxisets and well-concentrated bases

The aim of this paper is to synthetically analyse the performances of thresholding and wavelet estimation methods. In this connection, it is useful to describe the maximal sets where these methods attain a special rate of convergence. We relate these “maxisets” to other problems naturally arising in the context of non parametric estimation, as approximation theory or information reduction. A second part of the paper is devoted to isolate two very special properties especially shared by wavelet bases, which allow them to behave almost as in an Hilbertian context even for L _p risks.     

Vector quantization for compression of multichannel ECG

We propose a scheme based on vector quantization (VQ) for the data-compression of multichannel ECG waveforms. N-channel ECG is first coded using m-AZTEC, a new, multichannel extension of the AZTEC algorithm. As in AZTEC, the waveform is approximated using only lines and slopes; however, in m-AZTEC, the N-channels are coded simultaneously into a sequence of N + 1 dimensional vectors, thus exploiting the correlation that exists across channels in the AZTEC duration-parameter. Classified vector quantization (CVQ) of the m-AZTEC output is next performed to exploit the correlation in the other AZTEC parameter, namely, the value-parameter. CVQ preserves the waveform morphology by treating the lines and slopes as two perceptually-distinct classes. Both m-AZTEC and CVQ provide data-compression and their performance improves as the number of channels increases. Moreover, the final output differs little from the AZTEC output and hence ought to enjoy the same acceptability.     

Absolute and comparative subcutaneous bioavailability of ardeparin sodium, a low molecular weight heparin

Ardeparin sodium (Normiflo, Wyeth-Ayerst) is a low molecular weight heparin undergoing clinical evaluation as an antithrombotic agent. The objective of this study was to evaluate the absolute and comparative bioavailability of ardeparin following subcutaneous administration of three different formulations [two formulations of ardeparin at 10,000 anti-factor Xa (aXa) U/ml, but with different preservatives, and a 20,000 aXa U/ml formulation]. The study was conducted using a randomized 4-period crossover design (three subcutaneous treatments and one intravenous treatment) in 24 healthy subjects, and the pharmacokinetics of ardeparin were characterized by plasma anti-factor IIa (aIIa) and anti-factor Xa (aXa) activities. The mean absolute bioavailability of ardeparin based on aIIa activity ranged from 62% to 64% and the mean absolute bioavailability based on aXa activity ranged from 88% to 97%. Based on bioequivalence testing criteria, the three ardeparin formulations were bioequivalent.