Estudio de modelos de propagación en bandas milimétricas para su futura utilización en redes de comunicaciones móviles 5G

La generalización del uso de dispositivos móviles, con su consiguiente aumento del tráfico de datos, está generando una demanda cada vez mayor de bandas de frecuencia para el despliegue de sistemas de comunicación inalámbrica, así como una creciente congestión en las bandas bajas del espectro (hasta 3 GHz). Entre las posibles soluciones a este problema, se ha propuesto que la próxima generación de sistemas celulares, 5G, hagan uso de la banda milimétrica, entre 30 GHz y 300 GHz, donde hay anchos de banda contiguos disponibles con tamaños muy difíciles de encontrar en las frecuencias en uso en la generación actual. Este Proyecto de Fin de Grado tiene como finalidad estudiar la viabilidad del despliegue de sistemas celulares en dicha banda, basándose en los estudios tanto empíricos como teóricos ya publicados, así como en las recomendaciones de la UIT donde se estudian las características de propagación en estas bandas. En un siguiente apartado, se han analizado los documentos disponibles de los distintos proyectos y grupos, como pueden ser METIS-2020, impulsado por la Comisión Europea o IMT-2020 promovido por la UIT, dedicados a definir los futuros estándares de comunicación y sus características, así como la evolución de los actuales. Aparte del trabajo de documentación, se han realizado una serie de simulaciones. En primer lugar, se ha utilizado MATLAB para estudiar el comportamiento y la atenuación de la onda electromagnética a las frecuencias de interés en diferentes ubicaciones y climas, tanto en ubicaciones habituales como extremas, estudiándose los efectos de los gases atmosféricos y los hidrometeoros. También se ha utilizado software de planificación radioeléctrica profesional para hacer estudios de cobertura en entornos tanto urbanos, entre ellos Madrid o Barcelona, suburbanos, como Tres Cantos (Madrid) y O Barco de Valdeorras (Orense), y rurales como Valdefuentes (Cáceres) y Quiruelas de Vidriales (Zamora). Por último se han recogido todos los resultados, tanto los provenientes de los estudios como los obtenidos de nuestras propias simulaciones, y se ha realizado un breve comentario, comparando estos y analizando su impacto para posibles despliegues futuros de redes 5G. ABSTRACT. The generalization of mobile device use, with its associated data traffic growth, is generating a growing demand of spectrum for its use in the deployment of wireless telecommunication systems, and a growing congestion in the lower end of the spectrum (until 3 GHz). Among the possible solutions for this problem, it has been proposed that the next generation of cellular systems, 5G, makes use of the millimeter band, between 30 GHz and 300 GHz, where there are contiguous bandwidths with sizes hardly available in the bands used in the present. This Project aims to study the feasibility of cellular system deployments in said band, based on published empirical and theoretical studies and papers, and the ITU recommendations, where the propagation characteristics in those bands are studied. In the next section, available documentation coming from the different study groups and projects like METIS 2020 promoted by the European Commission, or IMT-2020, promoted by the ITU has been studied. In the documentation, future telecommunication standards and its characteristics and the evolution of the current ones are defined. Besides the documentation work, a series of simulations have been carried out. First, MATLAB has been used to study the behavior and attenuation of the electromagnetic wave at the frequencies of interest in different locations and climates, studying the effects of atmospheric gasses and hydrometeors in conventional and extreme locations. Industry standard radioelectric planning software has been used to study the coverage in different environments, such as urban locations like Madrid and Barcelona, both in Spain, suburban locations like Tres Cantos (Madrid, Spain) and O Barco de Valdeorras (Orense, Spain) and rural locations such as Valdefuentes (Cáreces, Spain) and Quiruelas de Vidriales (Zamora, Spain). Finally, all the results, both from the documentation and our own simulations, have been collected, and a brief commentary has been made, comparing those results and their possible impact in the future deployment of 5G networks.

Application of Agent Technology for Fault Diagnosis of Telecommunication Networks

La presente tesis doctoral contribuye al problema del diagnóstico autonómico de fallos en redes de telecomunicación. En las redes de telecomunicación actuales, las operadoras realizan tareas de diagnóstico de forma manual. Dichas operaciones deben ser llevadas a cabo por ingenieros altamente cualificados que cada vez tienen más dificultades a la hora de gestionar debidamente el crecimiento exponencial de la red tanto en tamaño, complejidad y heterogeneidad. Además, el advenimiento del Internet del Futuro hace que la demanda de sistemas que simplifiquen y automaticen la gestión de las redes de telecomunicación se haya incrementado en los últimos años. Para extraer el conocimiento necesario para desarrollar las soluciones propuestas y facilitar su adopción por los operadores de red, se propone una metodología de pruebas de aceptación para sistemas multi-agente enfocada en simplificar la comunicación entre los diferentes grupos de trabajo involucrados en todo proyecto de desarrollo software: clientes y desarrolladores. Para contribuir a la solución del problema del diagnóstico autonómico de fallos, se propone una arquitectura de agente capaz de diagnosticar fallos en redes de telecomunicación de manera autónoma. Dicha arquitectura extiende el modelo de agente Belief-Desire- Intention (BDI) con diferentes modelos de diagnóstico que gestionan las diferentes sub-tareas del proceso. La arquitectura propuesta combina diferentes técnicas de razonamiento para alcanzar su propósito gracias a un modelo estructural de la red, que usa razonamiento basado en ontologías, y un modelo causal de fallos, que usa razonamiento Bayesiano para gestionar debidamente la incertidumbre del proceso de diagnóstico. Para asegurar la adecuación de la arquitectura propuesta en situaciones de gran complejidad y heterogeneidad, se propone un marco de argumentación que permite diagnosticar a agentes que estén ejecutando en dominios federados. Para la aplicación de este marco en un sistema multi-agente, se propone un protocolo de coordinación en el que los agentes dialogan hasta alcanzar una conclusión para un caso de diagnóstico concreto. Como trabajos futuros, se consideran la extensión de la arquitectura para abordar otros problemas de gestión como el auto-descubrimiento o la auto-optimización, el uso de técnicas de reputación dentro del marco de argumentación para mejorar la extensibilidad del sistema de diagnóstico en entornos federados y la aplicación de las arquitecturas propuestas en las arquitecturas de red emergentes, como SDN, que ofrecen mayor capacidad de interacción con la red. ABSTRACT This PhD thesis contributes to the problem of autonomic fault diagnosis of telecommunication networks. Nowadays, in telecommunication networks, operators perform manual diagnosis tasks. Those operations must be carried out by high skilled network engineers which have increasing difficulties to properly manage the growing of those networks, both in size, complexity and heterogeneity. Moreover, the advent of the Future Internet makes the demand of solutions which simplifies and automates the telecommunication network management has been increased in recent years. To collect the domain knowledge required to developed the proposed solutions and to simplify its adoption by the operators, an agile testing methodology is defined for multiagent systems. This methodology is focused on the communication gap between the different work groups involved in any software development project, stakeholders and developers. To contribute to overcoming the problem of autonomic fault diagnosis, an agent architecture for fault diagnosis of telecommunication networks is defined. That architecture extends the Belief-Desire-Intention (BDI) agent model with different diagnostic models which handle the different subtasks of the process. The proposed architecture combines different reasoning techniques to achieve its objective using a structural model of the network, which uses ontology-based reasoning, and a causal model, which uses Bayesian reasoning to properly handle the uncertainty of the diagnosis process. To ensure the suitability of the proposed architecture in complex and heterogeneous environments, an argumentation framework is defined. This framework allows agents to perform fault diagnosis in federated domains. To apply this framework in a multi-agent system, a coordination protocol is defined. This protocol is used by agents to dialogue until a reliable conclusion for a specific diagnosis case is reached. Future work comprises the further extension of the agent architecture to approach other managements problems, such as self-discovery or self-optimisation; the application of reputation techniques in the argumentation framework to improve the extensibility of the diagnostic system in federated domains; and the application of the proposed agent architecture in emergent networking architectures, such as SDN, which offers new capabilities of control for the network.

Aeroelastic effects in a traffic sign panel induced by a passing vehicle

Here, a simple theoretical model of the vehicle induced flow and its effects on traffic sign panels is presented. The model is a continuation of a previous one by Sanz-Andrés and coworkers, now including the flexibility of the panel (and, therefore, the flow effects associated to the motion of the panel). Through the paper an aeroelastic one-degree-of-freedom model is developed and the flow effects are computed from unsteady potential theory. The influence of panel's mechanical properties (mass, damping ratio, and stiffness) in the motion induced forces are numerically analyzed.

Vehicle-induced loads on traffic sign panels

The determination of the loads on traffic sign panels in the current standards does not, in general, take into account the vehicle-induced loads, as explained by Quinn, Baker and Wright (QBW in what follows) (J. Wind Eng. Ind. Aerodyn. 89 (2001) 831). On the other hand, a report from Cali and Covert (CC) (J. Wind Eng. Ind. Aerodyn. 84 (2000) 87) indicates that in highway sign support structures, vehicle-induced loads have led to premature failures in some cases. The aim of this paper is to present a mathematical model for the vehicle-induced load on a flat sign panel, simple enough to give analytical results, but able to explain the main characteristics of the phenomenon. The results of the theoretical model help to explain the behaviour observed in the experiments performed in previous studies.

Actin Filaments and Microtubules are Involved in Different Membrane Traffic Pathways That Transport Sphingolipids to the Apical Surface of Polarized HepG2 Cells

In polarized HepG2 hepatoma cells, sphingolipids are transported to the apical, bile canalicular membrane by two different transport routes, as revealed with fluorescently tagged sphingolipid analogs. One route involves direct, transcytosis-independent transport of Golgi-derived glucosylceramide and sphingomyelin, whereas the other involves basolateral to apical transcytosis of both sphingolipids. We show that these distinct routes display a different sensitivity toward nocodazole and cytochalasin D, implying a specific transport dependence on either microtubules or actin filaments, respectively. Thus, nocodazole strongly inhibited the direct route, whereas sphingolipid transport by transcytosis was hardly affected. Moreover, nocodazole blocked “hyperpolarization,” i.e., the enlargement of the apical membrane surface, which is induced by treating cells with dibutyryl-cAMP. By contrast, the transcytotic route but not the direct route was inhibited by cytochalasin D. The actin-dependent step during transcytotic lipid transport probably occurs at an early endocytic event at the basolateral plasma membrane, because total lipid uptake and fluid phase endocytosis of horseradish peroxidase from this membrane were inhibited by cytochalasin D as well. In summary, the results show that the two sphingolipid transport pathways to the apical membrane must have a different requirement for cytoskeletal elements.

Clathrin Assembly Lymphoid Myeloid Leukemia (CALM) Protein: Localization in Endocytic-coated Pits, Interactions with Clathrin, and the Impact of Overexpression on Clathrin-mediated Traffic

The clathrin assembly lymphoid myeloid leukemia (CALM) gene encodes a putative homologue of the clathrin assembly synaptic protein AP180. Hence the biochemical properties, the subcellular localization, and the role in endocytosis of a CALM protein were studied. In vitro binding and coimmunoprecipitation demonstrated that the clathrin heavy chain is the major binding partner of CALM. The bulk of cellular CALM was associated with the membrane fractions of the cell and localized to clathrin-coated areas of the plasma membrane. In the membrane fraction, CALM was present at near stoichiometric amounts relative to clathrin. To perform structure–function analysis of CALM, we engineered chimeric fusion proteins of CALM and its fragments with the green fluorescent protein (GFP). GFP–CALM was targeted to the plasma membrane–coated pits and also found colocalized with clathrin in the Golgi area. High levels of expression of GFP–CALM or its fragments with clathrin-binding activity inhibited the endocytosis of transferrin and epidermal growth factor receptors and altered the steady-state distribution of the mannose-6-phosphate receptor in the cell. In addition, GFP–CALM overexpression caused the loss of clathrin accumulation in the trans-Golgi network area, whereas the localization of the clathrin adaptor protein complex 1 in the trans-Golgi network remained unaffected. The ability of the GFP-tagged fragments of CALM to affect clathrin-mediated processes correlated with the targeting of the fragments to clathrin-coated areas and their clathrin-binding capacities. Clathrin–CALM interaction seems to be regulated by multiple contact interfaces. The C-terminal part of CALM binds clathrin heavy chain, although the full-length protein exhibited maximal ability for interaction. Altogether, the data suggest that CALM is an important component of coated pit internalization machinery, possibly involved in the regulation of clathrin recruitment to the membrane and/or the formation of the coated pit.

Selective Perturbation of Apical Membrane Traffic by Expression of Influenza M2, an Acid-activated Ion Channel, in Polarized Madin–Darby Canine Kidney Cells

The function of acidification along the endocytic pathway is not well understood, in part because the perturbants used to modify compartmental pH have global effects and in some cases alter cytoplasmic pH. We have used a new approach to study the effect of pH perturbation on postendocytic traffic in polarized Madin–Darby canine kidney (MDCK) cells. Influenza M2 is a small membrane protein that functions as an acid-activated ion channel and can elevate the pH of the trans-Golgi network and endosomes. We used recombinant adenoviruses to express the M2 protein of influenza virus in polarized MDCK cells stably transfected with the polymeric immunoglobulin (Ig) receptor. Using indirect immunofluorescence and immunoelectron microscopy, M2 was found to be concentrated at the apical plasma membrane and in subapical vesicles; intracellular M2 colocalized partly with internalized IgA in apical recycling endosomes as well as with the trans-Golgi network marker TGN-38. Expression of M2 slowed the rate of IgA transcytosis across polarized MDCK monolayers. The delay in transport occurred after IgA reached the apical recycling endosome, consistent with the localization of intracellular M2. Apical recycling of IgA was also slowed in the presence of M2, whereas basolateral recycling of transferrin and degradation of IgA were unaffected. By contrast, ammonium chloride affected both apical IgA and basolateral transferrin release. Together, our data suggest that M2 expression selectively perturbs acidification in compartments involved in apical delivery without disrupting other postendocytic transport steps.

The Dynamics of Golgi Protein Traffic Visualized in Living Yeast Cells

We describe for the first time the visualization of Golgi membranes in living yeast cells, using green fluorescent protein (GFP) chimeras. Late and early Golgi markers are present in distinct sets of scattered, moving cisternae. The immediate effects of temperature-sensitive mutations on the distribution of these markers give clues to the transport processes occurring. We show that the late Golgi marker GFP-Sft2p and the glycosyltransferases, Anp1p and Mnn1p, disperse into vesicle-like structures within minutes of a temperature shift in sec18, sft1, and sed5 cells, but not in sec14 cells. This is consistent with retrograde vesicular traffic, mediated by the vesicle SNARE Sft1p, to early cisternae containing the target SNARE Sed5p. Strikingly, Sed5p itself moves rapidly to the endoplasmic reticulum (ER) in sec12 cells, implying that it cycles through the ER. Electron microscopy shows that Golgi membranes vesiculate in sec18 cells within 10 min of a temperature shift. These results emphasize the dynamic nature of Golgi cisternae and satisfy the kinetic requirements of a cisternal maturation model in which all resident proteins must undergo retrograde vesicular transport, either within the Golgi complex or from there to the ER, as anterograde cargo advances.

Characterization of a Novel Yeast SNARE Protein Implicated in Golgi Retrograde Traffic

The protein trafficking machinery of eukaryotic cells is employed for protein secretion and for the localization of resident proteins of the exocytic and endocytic pathways. Protein transit between organelles is mediated by transport vesicles that bear integral membrane proteins (v-SNAREs) which selectively interact with similar proteins on the target membrane (t-SNAREs), resulting in a docked vesicle. A novel Saccharomyces cerevisiae SNARE protein, which has been termed Vti1p, was identified by its sequence similarity to known SNAREs. Vti1p is a predominantly Golgi-localized 25-kDa type II integral membrane protein that is essential for yeast viability. Vti1p can bind Sec17p (yeast SNAP) and enter into a Sec18p (NSF)-sensitive complex with the cis-Golgi t-SNARE Sed5p. This Sed5p/Vti1p complex is distinct from the previously described Sed5p/Sec22p anterograde vesicle docking complex. Depletion of Vti1p in vivo causes a defect in the transport of the vacuolar protein carboxypeptidase Y through the Golgi. Temperature-sensitive mutants of Vti1p show a similar carboxypeptidase Y trafficking defect, but the secretion of invertase and gp400/hsp150 is not significantly affected. The temperature-sensitive vti1 growth defect can be rescued by the overexpression of the v-SNARE, Ykt6p, which physically interacts with Vti1p. We propose that Vti1p, along with Ykt6p and perhaps Sft1p, acts as a retrograde v-SNARE capable of interacting with the cis-Golgi t-SNARE Sed5p.

Role of Dynactin in Endocytic Traffic: Effects of Dynamitin Overexpression and Colocalization with CLIP-170

The flow of material from peripheral, early endosomes to late endosomes requires microtubules and is thought to be facilitated by the minus end-directed motor cytoplasmic dynein and its activator dynactin. The microtubule-binding protein CLIP-170 may also play a role by providing an early link to endosomes. Here, we show that perturbation of dynactin function in vivo affects endosome dynamics and trafficking. Endosome movement, which is normally bidirectional, is completely inhibited. Receptor-mediated uptake and recycling occur normally, but cells are less susceptible to infection by enveloped viruses that require delivery to late endosomes, and they show reduced accumulation of lysosomally targeted probes. Dynactin colocalizes at microtubule plus ends with CLIP-170 in a way that depends on CLIP-170’s putative cargo-binding domain. Overexpression studies using p150Glued, the microtubule-binding subunit of dynactin, and mutant and wild-type forms of CLIP-170 indicate that CLIP-170 recruits dynactin to microtubule ends. These data suggest a new model for the formation of motile complexes of endosomes and microtubules early in the endocytic pathway.

Modulation of Endocytic Traffic in Polarized Madin-Darby Canine Kidney Cells by the Small GTPase RhoA

Efficient postendocytic membrane traffic in polarized epithelial cells is thought to be regulated in part by the actin cytoskeleton. RhoA modulates assemblies of actin in the cell, and it has been shown to regulate pinocytosis and phagocytosis; however, its effects on postendocytic traffic are largely unexplored. To this end, we expressed wild-type RhoA (RhoAWT), dominant active RhoA (RhoAV14), and dominant inactive RhoA (RhoAN19) in Madin-Darby canine kidney (MDCK) cells expressing the polymeric immunoglobulin receptor. RhoAV14 expression stimulated the rate of apical and basolateral endocytosis, whereas RhoAN19 expression decreased the rate from both membrane domains. Polarized basolateral recycling of transferrin was disrupted in RhoAV14-expressing cells as a result of increased ligand release at the apical pole of the cell. Degradation of basolaterally internalized epidermal growth factor was slowed in RhoAV14-expressing cells. Although apical recycling of immunoglobulin A (IgA) was largely unaffected in cells expressing RhoAV14, transcytosis of basolaterally internalized IgA was severely impaired. Morphological and biochemical analyses demonstrated that a large proportion of IgA internalized from the basolateral pole of RhoAV14-expressing cells remained within basolateral early endosomes and was slow to exit these compartments. RhoAN19 and RhoAWT expression had little effect on these postendocytic pathways. These results indicate that in polarized MDCK cells activated RhoA may modulate endocytosis from both membrane domains and postendocytic traffic at the basolateral pole of the cell.

Phloem sap proteins from Cucurbita maxima and Ricinus communis have the capacity to traffic cell to cell through plasmodesmata

In angiosperms, the functional enucleate sieve tube system of the phloem appears to be maintained by the surrounding companion cells. In this study, we tested the hypothesis that polypeptides present within the phloem sap traffic cell to cell from the companion cells, where they are synthesized, into the sieve tube via plasmodesmata. Coinjection of fluorescently labeled dextrans along with size-fractionated Cucurbita maxima phloem proteins, ranging in size from 10 to 200 kDa, as well as injection of individual fluorescently labeled phloem proteins, provided unambiguous evidence that these proteins have the capacity to interact with mesophyll plasmodesmata in cucurbit cotyledons to induce an increase in size exclusion limit and traffic cell to cell. Plasmodesmal size exclusion limit increased to greater than 20 kDa, but less than 40 kDa, irrespective of the size of the injected protein, indicating that partial protein unfolding may be a requirement for transport. A threshold concentration in the 20–100 nM range was required for cell-to-cell transport indicating that phloem proteins have a high affinity for the mesophyll plasmodesmal binding site(s). Parallel experiments with glutaredoxin and cystatin, phloem sap proteins from Ricinus communis, established that these proteins can also traffic through cucurbit mesophyll plasmodesmata. These results are discussed in terms of the requirements for regulated protein trafficking between companion cells and the sieve tube system. As the threshold value for plasmodesmal transport of phloem sap proteins falls within the same range as many plant hormones, the possibility is discussed that some of these proteins may act as long-distance signaling molecules.

A FYVE-finger-containing protein, Rabip4, is a Rab4 effector involved in early endosomal traffic

The small GTPase Rab4 is implicated in endocytosis in all cell types, but also plays a specific role in some regulated processes. To better understand the role of Rab4 in regulation of vesicular trafficking, we searched for an effector(s) that specifically recognizes its GTP-bound form. We cloned a ubiquitous 69-kDa protein, Rabip4, that behaves as a Rab4 effector in the yeast two-hybrid system and in the mammalian cell. Rabip4 contains two coiled-coil domains and a FYVE-finger domain. When expressed in CHO cells, Rabip4 is present in early endosomes, because it is colocated with endogenous Early Endosome Antigen 1, although it is absent from Rab11-positive recycling endosomes and Rab-7 positive late endosomes. The coexpression of Rabip4 with active Rab4, but not with inactive Rab4, leads to an enlargement of early endosomes. It strongly increases the degree of colocalization of markers of sorting (Rab5) and recycling (Rab11) endosomes with Rab4. Furthermore, the expression of Rabip4 leads to the intracellular retention of a recycling molecule, the glucose transporter Glut 1. We propose that Rabip4, an effector of Rab4, controls early endosomal traffic possibly by activating a backward transport step from recycling to sorting endosomes.