Outage thresholds of LDPC codes over nonergodic block-fading channels

This paper derives approximations allowing the estimation of outage probability for standard irregular LDPC codes and full-diversity Root-LDPC codes used over nonergodic block-fading channels. Two separate approaches are discussed: a numerical approximation, obtained by curve fitting, for both code ensembles, and an analytical approximation for Root-LDPC codes, obtained under the assumption that the slope of the iterative threshold curve of a given code ensemble matches the slope of the outage capacity curve in the high-SNR regime.

Optimum pilot overhead in wireless communication: a unified treatment of continuous and block-fading channels

The optimization of the pilot overhead in wireless fading channels is investigated, and the dependence of this overhead on various system parameters of interest (e.g., fading rate, signal-to-noise ratio) is quantified. The achievable pilot-based spectral efficiency is expanded with respect to the fading rate about the no-fading point, which leads to an accurate order expansion for the pilot overhead. This expansion identifies that the pilot overhead, as well as the spectral efficiency penalty with respect to a reference system with genie-aided CSI (channel state information) at the receiver, depend on the square root of the normalized Doppler frequency. It is also shown that the widely-usedblock fading model is a special case of more accurate continuous fading models in terms of the achievable pilot-based spectral efficiency. Furthermore, it is established that the overhead optimization for multiantenna systems is effectively the same as for single-antenna systems with thenormalized Doppler frequency multiplied by the number of transmit antennas.

On iterative performance of LDPC and Root-LDPC codes over block-fading channels

This paper presents our investigation on iterativedecoding performances of some sparse-graph codes on block-fading Rayleigh channels. The considered code ensembles are standard LDPC codes and Root-LDPC codes, first proposed in and shown to be able to attain the full transmission diversity. We study the iterative threshold performance of those codes as a function of fading gains of the transmission channel and propose a numerical approximation of the iterative threshold versus fading gains, both both LDPC and Root-LDPC codes.Also, we show analytically that, in the case of 2 fading blocks,the iterative threshold root of Root-LDPC codes is proportional to (α1 α2)1, where α1 and α2 are corresponding fading gains.From this result, the full diversity property of Root-LDPC codes immediately follows.

Seeking theta's desperately: Estimating the distribution of consumers under increasing block rates

This paper shows that the distribution of observed consumption is not a good proxy for the distribution of heterogeneous consumers when the current tariff is an increasing block tariff. We use a two step method to recover the "true" distribution of consumers. First, we estimate the demand function induced by the current tariff. Second, using the demand system, we specify the distribution of consumers as a function of observed consumption to recover the true distribution. Finally, we design a new two-part tariff which allows us to evaluate the equity of the existence of an increasing block tariff.

Report on the Community Development Block Grant Program administered by the Southern Iowa Council of Governments (Council) for the period October 1, 2003 through September 30, 2007

Report on the Community Development Block Grant Program administered by the Southern Iowa Council of Governments (Council) for the period October 1, 2003 through September 30, 2007

Report on the Community Development Block Grant and Home Investment Partnerships Programs administered by the Region XII Council of Governments for the period July 1, 2005 through November 21, 2008

Report on the Community Development Block Grant and Home Investment Partnerships Programs administered by the Region XII Council of Governments for the period July 1, 2005 through November 21, 2008

A new electrocardiographic criteria for discriminating between Brugada types 2 and 3 patterns and incomplete right bundle branch block

Le syndrome de Brugada, une affection rythmique du sujet jeune potentiellement fatale, se manifeste sur l'ECG par un bloc de branche droit (BBD) complet, avec sus-décalage majeur du segment ST et inversion des ondes Τ de V1 à V3 appelé pattern de type 1. Cette présentation peut être intermittente. Les manifestations incomplètes du syndrome de Brugada sont appelées patterns de types 2 ou 3, et sont caractérisées par un BBD incomplet et un sus-décalage ST plus ou moins prononcé dans les dérivations V-, et V2 de l'ECG. Cette description, cependant, est aussi celle du BBD incomplet fréquemment rencontré chez les sujets jeunes, de moins de 40 ans, et présent dans 3% de la population. Bo nombre de ces sujets sont donc référés pour une recherche de syndrome de Brugada. Le but de cette thèse est donc d'évaluer de nouveaux critères permettant de discriminer les BBD incomplets, banals, des sujets porteurs d'un syndrome de Brugada de types 2 ou 3. Trente-huit patients avec un pattern de Brugada de types 2 et 3, référés pour un test médicamenteux utilisant un antiarythmique révélant un pattern de type 1 chez les sujets porteurs, ont été inclus dans l'étude. Avant le test médicamenteux, deux angles ont été mesurés sur les dérivations Vi et/ou V2 : a, l'angle entre une ligne verticale et la descente de l'onde r', et β, l'angle entre la montée de l'onde S et la descente de l'onde r'. Les mesure à l'état basai des deux angles, seules ou combinées avec la durée du QRS, on été comparées entre les patients avec une épreuve pharmacologique positive et ceux dont l'épreuve s'est révélée négative (i.e. servant de groupe contrôle car porteur d'un véritable BBD incomplet). Des courbes ROC ont été établies afin de déterminer les valeurs d'angles les plus discriminantes. La moyenne des angles β était significativement plus petite chez les 14 patients avec un test pharmacologique négatif comparé aux 24 patients avec un test positif. La valeur optimale pour l'angle β était de 58°, ce qui donnait une valeur prédictive positive de 73% et une valeur prédictive négative de 97% pour une conversion en pattern de type 1 lors du test pharmacologique. L'angle α était un peu moins sensible et spécifique que β. Quand les angles étaient combinés à la durée du QRS, on observait une discrète amélioration de la discrimination entre les deux populations. Notre travail permet donc, chez des patients suspects d'un syndrome de Brugada, de discriminer entre un BBD incomplet et les patterns de Brugada types 2 et 3 en utilisant un critère simple basé sur l'ECG de surface potentiellement applicable au lit du patient

A selective nociceptive block is not sufficient to prevent central changes after peripheral nerve injury

Background: Providing analgesia without suppressing motor or sensory function is a challenge for regional anesthesia and postoperative pain management. Resiniferatoxin (RTX), an ultrapotent agonist for transient receptor potential subtype-1 (TRPV1) can produce this selective blockade, as TRPV1 is selectively expressed on nociceptors. Futhermore, after peripheral nerve injury, spontaneous ectopic activity arises from all types of nerve fibers that can affect spinal neurons and glial cells. The goal of the present experiment is to determine whether spontaneous activity generated in C-fibers or in both A&C-fibers is required for microglia activation. Method: We applied RTX (0.01%) or bupivacaine microspheres to the sciatic nerve of rats to block the conduction of C-fibers or A&C-fibers, respectively, before spared nerve injury (SNI). Behavior was tested and all the rats were sacrificed 2 days later; immunohistochemistry was performed on their spinal cord for mitogen-activated protein kinase (MAPK) p38, bromodeoxyuridine (BrdU, marker of proliferation) and Iba1 (microglial marker). Result: At day 2 after SNI robust mechanical allodynia and p38 activation in spinal microglia were documented. There was also a substantial cell proliferation in the spinal cord, all proliferating cells (BrdU+) being microglia (Iba1+). RTX blocked heat sensitivity and produced heat hypoalgesia without affecting mechanical allodynia and motor function. Microglial proliferation and p38 activation in the spinal cord were not affected by RTX (p >0.05). In contrast, a complete sensory and motor blockade was seen with bupivacaine which also significantly inhibited p38 activation and microglial proliferation in the spinal cord (p <0.05). Conclusion: We conclude that (1) RTX can provide a selective nociceptive blockade but that (2) blocking only nociceptive fibers does not impair the development of mechanical allodynia and microglia activation. Therefore (3) if microglia activation is important for chronic pain development then specific nociceptive blockade won't be sufficient to prevent it.

Identification of amino acid residues in the alpha, beta, and gamma subunits of the epithelial sodium channel (ENaC) involved in amiloride block and ion permeation.

The amiloride-sensitive epithelial Na channel (ENaC) is a heteromultimeric channel made of three alpha beta gamma subunits. The structures involved in the ion permeation pathway have only been partially identified, and the respective contributions of each subunit in the formation of the conduction pore has not yet been established. Using a site-directed mutagenesis approach, we have identified in a short segment preceding the second membrane-spanning domain (the pre-M2 segment) amino acid residues involved in ion permeation and critical for channel block by amiloride. Cys substitutions of Gly residues in beta and gamma subunits at position beta G525 and gamma G537 increased the apparent inhibitory constant (Ki) for amiloride by > 1,000-fold and decreased channel unitary current without affecting ion selectivity. The corresponding mutation S583 to C in the alpha subunit increased amiloride Ki by 20-fold, without changing channel conducting properties. Coexpression of these mutated alpha beta gamma subunits resulted in a non-conducting channel expressed at the cell surface. Finally, these Cys substitutions increased channel affinity for block by external Zn2+ ions, in particular the alpha S583C mutant showing a Ki for Zn2+ of 29 microM. Mutations of residues alpha W582L, or beta G522D also increased amiloride Ki, the later mutation generating a Ca2+ blocking site located 15% within the membrane electric field. These experiments provide strong evidence that alpha beta gamma ENaCs are pore-forming subunits involved in ion permeation through the channel. The pre-M2 segment of alpha beta gamma subunits may form a pore loop structure at the extracellular face of the channel, where amiloride binds within the channel lumen. We propose that amiloride interacts with Na+ ions at an external Na+ binding site preventing ion permeation through the channel pore.

Report on the Iowa Early Intervention Block Grant Program administered by the Department of Education for the period July 1, 2005 through June 30, 2010

Report on the Iowa Early Intervention Block Grant Program administered by the Department of Education for the period July 1, 2005 through June 30, 2010

Mutations in the epithelial Na+ channel ENaC outer pore disrupt amiloride block by increasing its dissociation rate.

The epithelial Na+ channel ENaC mediates transepithelial Na+ transport in the distal kidney, the colon, and the lung and is a key element for the maintenance of Na+ balance and the regulation of blood pressure. Mutagenesis studies have identified residues alphaS583 and the homologous betaG525 and gammaG537 in the outer pore entrance that are critical for ENaC block by the K+-sparing diuretic amiloride. The aim of the present study was to determine first, whether these residues are part of the amiloride binding site, and second, whether they are general determinants of ENaC block by amiloride and its derivatives. Kinetic analysis of the association and dissociation rates of amiloride and benzamil to ENaC showed that mutation of residue alphaS583C and the homologous betaG525C increased the dissociation rate of the drugs from the binding site, with little changes in their association rate. Thus, these mutations destabilize the binding interaction between the blockers and the receptor on the channel, favoring the unbinding of the ligand. This strongly suggests that they are part of the binding site. Because mutations of alphaS583, betaG525, and gammaG537 have similar effects on amiloride, benzamil, and triamterene block, we conclude that these three ENaC blockers share a common receptor within the ion channel pore.