Les avancées technologiques de ces dernières années, combinées au succès avéré et toujours croissant des communications sans fil, ont tout naturellement donné naissance à un nouveau type de réseaux sans fil, communément appelés Body Area networks. A terme, ces réseaux corporels sans fil doivent permettre à un ensemble de senseurs bio-médicaux répartis sur le corps humain de communiquer, soit pour échanger des informations en vue d'un traitement en temps réel du patient, soit pour enregistrer des données physiologiques en vue d'une analyse ultérieure. L’objectif de cette Thèse vise la réduction de la consommation énergétique au niveau des senseurs de sorte à leur garantir une autonomie de quelques mois, voire de quelques années. En réponse à cette contrainte énergétique, une association innovante de deux technologies émergentes est proposée, à savoir une combinaison des transmissions à ultra-large bande aux systèmes à multiples antennes. Une nouvelle architecture pour les réseaux corporels sans fil est donc envisagée pour laquelle les performances doivent être évaluées. Notre principale contribution à cet objectif consiste en la proposition d'une modélisation spatio-temporelle complète du canal de transmission dans le cadre de senseurs répartis autour du corps. Cette modélisation fait appel à la définition de nouveaux modèles, l'élaboration d'outils spécifiques d'extraction de paramètres et une compréhension fine des mécanismes de propagation liés à la proximité du corps humain. Ce manuscrit présente les résultats majeurs de nos recherches en cette matière.

Chloride ion channels are macromolecular pores providing for passage of chloride ions (and certain other inorganic and organic anions) through the cell membrane, down their electrochemical gradients. Chloride channels are differentially expressed in various cells, to best suit specific cellular activities. They are present in practically all living cells, and regardless of cell specialization they play an important role in vital housekeeping functions of cell-volume and pH regulation and in membrane potential stabilization. Regulation of cell volume underlies the structural integrity and constancy of the intracellular milieu. A variety of metabolic pathways have been shown to be sensitive to cell volume, and alterations of cell volume and osmoregulation processes can influence various intracellular signaling and organizing factors. Volume-regulated anion channels (VRACs) are believed to play a pivotal role in cell-volume regulating processes. In this report I present data from macroscopic patch-clamp studies of VRACs performed in a fibroblast cell line and from single channel studies of chloride channels (tentatively related to VRACs) in mouse brown adipocytes in primary culture. One of the characteristic features of the VRACs is their dependence on the presence of cytoplasmic ATP. In whole-cell experiments, removal of ATP from the pipette solution almost completely prevented activation of VRACs, whereas substitution of ATP with the nonhydrolyzable analog ATPγS did not alter the activation of VRACs. The inhibitors of protein tyrosine kinases (PTK) tyrphostin A25 and B46 depressed VRAC currents in both cases (ATP and ATPγS), but a PTK ineffective analog (tyrphostin A1) did not affect VRAC currents. We infer that in the cell preparation we used, ATP has a dual role in VRAC regulation: it is required for channel-protein phosphorylation and it can influence channel activity through non-hydrolytic binding in a ligand-receptor manner. It can additionally be suggested that tyrosine-specific protein kinases can be involved in the regulation of VRACs, independently of the effects of ATP. We also studied cell cycle-related changes in activation of VRACs by osmotic swelling of cells chemically arrested at different phases of the cell cycle. We found no significant changes during most of the cell cycle, except short periods before and after mitosis and in the quiescent G0 state. The single Cl- channels of brown adipocytes resemble in their electrophysiological phenotype outwardly rectifying Cl- channels (ORCCs). We investigated the sensitivity of these channels to intracellular Ca2+. It appeared that the commonly used Ca2+-chelators EGTA and BAPTA could influence the ORCCs currents by themselves, independently of their calcium chelating effects. In some channels, these chelators induced classical flickery-type block of activity, whereas in others there was quasi-blockage, i.e. a peculiar combination of flickery blockage and overall channel activation. The chloride channel blocking agents DIDS and SITS mimicked the true/quasi blockage of EGTA and BAPTA. These phenomena add to the structure-function characteristics of the ORCC molecule. Moderate inhibitory effect of Ca2+ within a physiological range of intracellular concentrations (sub-µM) was also detected; however, the biological relevance of this observation, as well as of these Cl- channels in general, remains to be clarified.

Aim: The aim of this study is to investigate how retailer’s customer loyalty program can influence the channel power and what relationship between retailer with manufacturer can be created when channel power changes.   Method: A case study was adopted, and a qualitative research and face-to-face interview were used to collect the fundamental data.   Result & Conclusions: The results exhibit that the customer loyalty program implemented by retailer can increase its channel power (both in basic power and market power) and create a dominant relationship with high channel conflict with its manufacturer. Based on the research of the case company, I found a close relationship with cooperation and trust could be developed based on the customer loyalty program between retailer and manufacturer to create benefit for the both.   Suggestions for future research: Only adopted one case and one interview in the research is the main limitation. Additionally, the limited sample size limited the research in some generalizations. It is difficult to use only one case to represent the whole situation of the market. In the further, a larger sample size adopted in research can increases the reliability of researcher’s generalization.   Contribution of the thesis: The research discloses how retailer’s customer loyalty program can influence the channel power. The drawbacks of the dominant relationship which caused by channel power rising have been researched. How to develop close relationship and what benefit it can bring to retailer have also been investigated in the end.

Globo Foods Co., Ltd. has good opportunity to export five Thai seasoning        paste products to Sweden (Västerås). By setting the price as low initial price, sell firstly at ICA Maxi Hälla and Coop Extra in Västerås, use attractive promotion and advertising for Swedish people. This result is from valid, reliable primary and secondary data in order to be guideline and useful information to Globo Foods Co., Ltd. and also can adapt to fit the result with Thai seasoning pastes from other companies or other kind of products to enter to Västerås,Sweden.

Ion channels are fundamental molecules in the nervous system that catalyze the flux of ions across the cell membrane. There are mounting evidences suggesting that the kinetic properties of ion channels undergo activity-dependent changes in various pathophysiological conditions. Here such activity-dependent changes were studied in case of two different ion channels; the rat brain derived voltage-gated Na+ channel, rNav1.2 and the human background leak K+ channel, hTREK1 using the single channel patch-clamp technique. Our results on the voltage-gated Na+ channel (Chapter III) illustrated that sustained membrane depolarization, as seen in pathophysiological conditions like epilepsy, induced a defined non-linear variation in the unitary conductance, activation, inactivation and recovery kinetic properties of the channel. Signal processing tools attributed a pseudo-oscillatory nature to the non-linearity observed in the channel properties. Prolonged membrane depolarization also induced a “molecular memory” phenomenon, characterized by clustering of dwell time events and strong autocorrelation in the dwell time series. The persistence of such molecular memory was found to be dependent on the duration of depolarization. Similar plastic changes were observed in case of the hTREK1 channel in presence of saturating concentrations of agonist, trichloroethanol (TCE) (Chapter IV). TREK1 channel behaves similar to single enzyme molecules with a single binding site for the substrate K+ ion whereas TCE acts as an allosteric activator of the channel. We observed that with increasing concentration of TCE (10 M to 10 mM) the catalytic turnover rate exhibited progressive departure from monoexponential to multi-exponential distribution suggesting the presence of ‘dynamic disorder’ analogous to single enzyme molecules. In addition, we observed the induction of strong correlation in successive waiting times and flux intensities, exemplified by distinct mode switching between high and low flux activity, which implied the induction of memory in single ion channel. Our observation of such molecular memory in two different ion channels in different experimental conditions highlights the importance and generality of the phenomenon which is normally hidden under the ensemble behaviour of ion channels. In the final part of the work (chapter V) we observed strong negative cooperativity and half-of-sites saturation kinetics in the interaction of local anesthetic, lidocaine with hTREK1 channel. We also mapped the specific anesthetic binding site in the c-terminal domain of the channel. Further, single channel analysis and the heterodimer studies enabled us to propose a model for this interaction and provide a plausible paradigm for the inhibitory action of lidocaine on hTREK1.

Urban centers are major sources of contaminants to the surrounding air, water and soils. Above all, combustion-derived carbonaceous aerosols, especially black carbon (BC) and associated polycyclic aromatic hydrocarbons (PAHs), make significant contributions to the pollution in these systems. Here sedimentary records are used to produce a series of historical reconstructions of such contaminants to the Houston Ship Channel (HSC) system and compare these to point source inputs of hydrophobic organic contaminants (HOC). Analytical data on total organic carbon (TOC), BC, PAHs, dioxins and lignin (likely discarded from a pulp and paper mill along the Channel) were determined. This multi-proxy approach revealed that over the last several decades, HOC inputs to the system have been derived from a complex mixture of combustion processes, industrial point-sources, and oil spills. In particular, widespread dioxin contamination was observed throughout the study region with a particular site of the HSC showing total concentrations over 20,000 pg/g and 5000 pg toxic equivalent (TEQ)/g dry weight of sediment. Using two models based on sorption constants of total OC and BC, porewater concentrations were estimated to be lower than expected, at 20 pg/L and 5 pg TEQ/L. These values, however, are recognized as being extremely high for freely dissolved concentrations in porous media. The pulp and paper waste pit has recently been declared a Superfund site based on dioxin concentrations alone. The relationship between lignin biomarkers and dioxins observed in these sediments confirms that discharges of pulp and paper effluents were responsible for such high dioxin levels. Concentrations of BC, amorphous OC, and TOC were then used to calculate sediment binding of dioxins in sediments of the HSC. Our study found BC to be extremely low in HSC sediments (0.04 to 0.20%) indicating minimal dioxin sorption capacity. This suggests strong potential for fluxes of dioxins from sediments to the water column both through passive diffusion and physical mixing during natural and anthropogenic sediment remobilization events in this shallow system (hurricanes, storms, and dredging). The purposeful addition of BC to these sediments might be promising as a remediation strategy.

Karenia brevis is the major harmful algal bloom-forming species in the Gulf of Mexico, and produces neurotoxins, known as brevetoxins, that cause large fish kills, neurotoxic shellfish poisoning, and human respiratory distress. Brevetoxins are polyethers that bind voltage-sensitive sodium channels, opening them for prolonged periods of time. Clonal cultures of K. brevis exhibit unique brevetoxin profiles, which not only differ from one another, but also change when subjected to different environmental conditions. The brevetoxin structures were elucidated 30 years ago without any breakthroughs for the biosynthetic pathway. These unique ladder-like polyethers have 10 (PbTx-1) or 11 (PbTx-2) rings, indicating that they are synthesized as secondary metabolites by polyketide synthases. The extensive size of the genome and the lack of histones and nucleosomes combined with the additional regulatory step of a trans-splicing spliced leader sequence make normal molecular techniques ineffective in determining the genes involved in toxin synthesis. The goal of this project is to identify a potential link between toxin, gene, and function. One objective is to take the next step towards identifying the genes associated with the synthesis and regulation of brevetoxins and to help elucidate the hypothesized gene clusters of multi-protein enzymatic complexes involved in brevetoxin production, one for each backbone. The second objective is to make an effort to determine the in vivo function of the costly brevetoxins by identifying possible ion channels, which could be osmotically regulated by the toxins. Genes for polyketide synthases (PKS) were identified in K. brevis, obtained from Expressed Sequence Tag (EST) libraries. In this work, reverse transcription polymerase chain reactions (RT-PCR) were used to generate pools of complementary DNA (cDNA), which was used in real-time quantitative polymerase chain reactions (qPCR) to give relative amounts of PKS transcripts. K. brevis clones have shown a significant increase in toxin production after a rapid shift from high salinity to low salinity, indicating a regulation of brevetoxin synthesis. To gain a better understanding of regulation of toxin production during algal blooms, we compared the toxin levels under different conditions to the transcript levels of PKS genes, as determined by quantitative RT-PCR. In a separate line of investigation, an in silico analysis of the EST library was performed to identify ion channel genes expressed by K. brevis, which may be the in vivo binding site of brevetoxin. The information generated from this project will help to elucidate the effects of environmental variations on toxin production and the biological function of toxin production -- valuable information for the shellfish industries and public health.

It is indisputable that the internet has become a necessary component of contemporary multi-channel retail, as more consumers are choosing to purchase goods online each year. As online spending continues to grow, many have called into question the future of brick-and-mortar retail. This thesis seeks to empirically prove that brick-and-mortar retail remains not only relevant, but indispensable in direct-to-consumer business models. The basis of this conjecture is the idea of channel synergism, in which online and brick-and-mortar operations are complementary. This theory is predicated on the emergence of the omni-channel retail, which is characterized by the integration of the various direct-to-consumer (D2C) channels to support cross-channel consumer interaction. To empirically test this hypothesis, key operating metrics were examined over the five year period from 2007 to 2011. By examining profitability trends and several D2C channel relationships, empirical support is developed to substantiate the claim that brick-and-mortar operations are not being driven into obsolescence by the growing prevalence of e-commerce transactions.

Hyperkalemic periodic paralysis, HyperKPP, is an inherited progressive disorder of the muscles caused by mutations in the voltage gated sodium channel (NaV1.4). The objectives of this thesis were to develop a technique for measurement symptoms in vivo using electromyography (EMG) and to determine the mechanism by which Ca2+ alleviates HyperKPP symptoms, since this is unknown. Increasing extracellular [Ca2+] ([Ca2+]e) from 1.3 to 4 mM did not result in any increases in45Ca2+ influx suggesting no increase in intracellular [Ca2+] ([Ca2+]i) acting on an intracellular signaling pathway or on an ion channel such as the Ca2+sensitive K+ channels. HyperKPP muscles have larger TTX-sensitive22Na+ influx than wild type muscles because of the defective NaV1.4 channels. When [Ca2+] was increased from 1.3 to 4 mM, the abnormal 22Na+ influx was completely abolished. Thus, one mechanism by which Ca2+alleviates HyperKPP symptoms is by reducing the abnormal Na+ influx caused by the mutation in the NaV1.4 channel.

Compared to mammals, nematodes appear to exhibit a unique GABAergic nervous system. Haemonchus controtus is a parasitic nematode that infects ruminants worldwide. Hco-UNC-49 is a H. contortus GABA-gated chloride channel and is an orthologue to the UNC-49 channel from the free-living nematode Caenorhabditis elegans. Previous research by our group has shown that while the UNC-49 channels from the two nematodes share similar sequence homology they do not share identical sensitivity to GABA. To further investigate the characteristics of the Hco-UNC-49 channel, this study tested the effects of various modulators, insecticides and anti-parasitic drugs on channel function. Most notably, the molecules penicillin G, propofol and pregnenolone sulfate all had similar effects on Hco-UNC-49 as reported previously for Cel-UNC-49. On the other hand, Hco-UNC-49 appears to be less sensitive to picrotoxin inhibition compared to what has been reported for Cel-UNC-49. Novel effects of a number of anthelmintics were also observed. For example, the anthelmintics ivermectin and moxidectin both enhanced Hco-UNC-49 GABA responses, while piperazine was able to directly activate Hco-UNC-49 at high concentrations. These results suggest that Hco-UNC-49 is likely an in vivo target for these anthelmintics. / UOIT