1.° Jacobi Alexandri le Taneur disputatio physico-mathematica de aequabili motus acceleratione, et de motu telluris : in qua Galilaei decreta de motu gravium perpendiculariter cadentium confirmantur ; et ostenditur vulgarem seu Ptolemaïcam de motu solis opinionem non minùs esse contrariam sacris litteris, quam Copernicanam de motu terrae : ac proinde nihil certi ex iis, quoad illam quaestionem, posse deduci : ad Petrum Cazraeum, societatis Jesu. — 2.° Ejusdem epistolae duae ad eundem, de descensu gravium. — 3.° Petri Cazraei, societatis Jesu, ad Alexandrum le Taneur epistola, qua sententiam Galilaei de descensu gravium impugnat. — 4.° Lettre de monsieur le Taneur au Pere Mersenne, Minime, sur la chûte des corps. — 5.° Ejusdem ad eundem epistola contra Fabrianam de incremento motus accelerati opinionem.

Melchisedechi Thevenotii

Natural Leishmania sp. reservoirs and phlebotomine sandfly food source identification in Ibitipoca State Park, Minas Gerais, Brazil

Leishmania spp are distributed throughout the world and different species are associated with varying degrees of disease severity. However, leishmaniasis is thought to be confined to areas of the world where its insect vectors, sandflies, are present. Phlebotomine sandflies obtain blood meals from a variety of wild and domestic animals and sometimes from humans. These vectors transmit Leishmania spp, the aetiological agent of leishmaniasis. Identification of sandfly blood meals has generally been performed using serological methods, although a few studies have used molecular procedures in artificially fed insects. In this study, cytochrome b gene (cytB) polymerase chain reaction (PCR) was performed in DNA samples isolated from 38 engorged Psychodopygus lloydi and the expected 359 bp fragment was identified from all of the samples. The amplified product was digested using restriction enzymes and analysed for restriction fragment length polymorphisms (RFLPs). We identified food sources for 23 females; 34.8% yielded a primate-specific banding profile and 26.1% and 39.1% showed banding patterns specific to birds or mixed restriction profiles (rodent/marsupial, human/bird, rodent/marsupial/human), respectively. The food sources of 15 flies could not be identified. Two female P. lloydi were determined to be infected by Leishmania using internal transcribed spacer 1 and heat shock protein 70 kDa PCR-RFLP. The two female sandflies, both of which fed on rodents/marsupials, were further characterised as infected with Leishmania (Viannia) braziliensis. These results constitute an important step towards applying methodologies based on cytB amplification as a tool for identifying the food sources of female sandflies.

1.° Tractatus de laude et utilitate musicae, editus à Magistro Aegidio Carlerii, sacrae theologiae Professore et Decano Cameracensi : praemittitur folium in quo epistola dedicatoria ad Clementem, Papam V. olim praefixa cuidam libro de recuperatione Terrae sanctae. — 2.° Liber statutorum Facultatum juris canonici et juris civilis, ac collegii Doctorum earumdem Facultatum.

Colbertinus

OpenNebula y Hadoop : Cloud Computing con herramientas Open Source

El presente proyecto consiste en una introducción al "cloud computing" y un estudio en profundidad de las herramientas OpenNebula, dentro del modelo IaaS (Infraestructure as a Service), y Hadoop, dentro del modelo PaaS (Platform as a Service). El trabajo también incluye la instalación, integración, configuración y puesta en marcha de una plataforma "cloud computing" utilizando OpenNebula y Hadoop con el objetivo de aplicar los conceptos teóricos en una solución real dentro de un entorno de laboratorio que puede ser extrapolable a una instalación real.

Regulation of the cardiac voltage-gated sodium channel Nav1.5 : regulation of Nav1.5 by ubiquitin-protein ligases of the Nedd4/Nedd4-like family and characterisation of two novel mutations in the gene encoding Nav1.5 (SCN5A) implicated in the Brugada syndrome triggered by fever

Abstract: The genesis of the cardiac action potential, which accounts for the cardiac contraction, is due to the sodium current INa mediated by the voltage-gated sodium channel Nav1.5. Several cardiac arrhythmias such as the Brugada syndrome are known te be caused by mutations in SCN5A, the gene encoding Nav1.5. Studies of these mutations allowed a better understanding of biophysical and functional properties of Nav1.5. However, only few investigations have been performed in order to understand the regulation of Nav1.5. During my thesis, I investigated different mechanisms of regulation of Nav1.5 using a heterologous expression system, HEK293 cells, coupled with a technique of sodium current recording: the patch clamp in whole cell configuration. In previous studies it has been shown that an enzyme of the Nedd4 family (Nedd4-2) regulates an epithelial sodium channel via the interaction with PY-motifs present in the latter. Interestingly, Nav1.5 contains a similar PY-motif, which motivated us to study the role of Nedd4-2 expressed in heart for the regulation of Nav1.5. In a second study, we investigated the implication of two Nav1.5 mutants, which were either less functional or net functional (Nav1.5 R535X and Nav1.5 L325R respectively) implied in the genesis of the Brugada syndrome by fever. Our results established two mechanisms implied in Nav1.5 regulation. The first one implies that following the interaction between the PY-motif of Nav1.5 and Nedd4- 2 Nav1.5 is ubiquitinated by Nedd4-2. This ubiquitination leads to the internalization of Nav1 .5. The second mechanism is a phenomenon called the "dominant negative" effect of Nav1.5 L325R on Nay1.5 where the decrease of 'Na is potentially due to the retention of Nav1.5 by Nav1.5 L325R in an undefined intracellular compartment. These studies defined two mechanisms of Nav1.5 regulation, which could play an important role for the genesis of cardiac arrhythmias where molecular processes are still poorly understood. Résumé La genèse du potentiel d'action cardiaque, permettant la contraction cardiaque, est due au courant sodique INa issu des canaux sodiques cardiaques dépendants du voltage Nav1.5. Nombreuses arythmies cardiaques telles que le syndrome de Brugada sont connues pour être liées à des mutations du gène SCN5A, codant pour Nav1.5. L'étude de ces mutations a permis une meilleure compréhension des propriétés structurelles et fonctionnelles de Nav1.5 et leurs implications dans la genèse de ces pathologies. Néanmoins peu d'études ont été menées afin de comprendre les mécanismes de régulation de Nav1.5. Mon travail de thèse a consisté à étudier des mécanismes de régulation de Nav1.5 en utilisant un système d'expression hétérologue, les cellules HEK293, couplé à une technique d'enregistrement des courants sodiques, le "patch clamp" en configuration cellule entière. La présence sur Nav1.5 d'un motif-PY similaire à ceux nécessaires pour la régulation d'un canal épithélial sodique par une enzyme de la famille de Nedd4, nous a amenée à étudier le rôle de ces ubiquitine-ligases, en particulier Nedd4-2, dans la régulation de Nav1.5. La seconde étude s'est intéressée aux conséquences de deux mutations de SCN5A codant pour deux mutants peu ou pas fonctionnels (Nav1.5 L325R et Nav1.5 R535X respectivement) retrouvées chez des patients présentant un syndrome de Brugada exacerbé par un état fébrile. Nos résultats ont permis d'établir deux mécanismes de régulation de Nav1.5 L'un par Nedd4-2 qui implique rubiquitination de Nav1.5 par cette ligase suite à l'interaction entre le motif-PY de Nav1.5 et Nedd4-2. Cette modification déclenche l'internalisation du canal impliquée dans la diminution d'INa. Le second mécanisme quant à lui est un effet "dominant négatif" de Nav1.5 L325R sur Nav1.5 aboutissant à une diminution d'INa suite à la séquestration intracellulaire potentielle de Nav1.5 par Nav1.5 L325R. Ces études ont mis en évidence deux mécanismes de régulation de Nav1.5 pouvant jouer un rôle majeur dans la genèse et/ou l'accentuation des arythmies cardiaques dont les processus moléculaires au sein des cardiomyocytes, impliquant des modifications du courant sodiques, sont encore mal compris. Résumé destiné à un large public La dépolarisation électrique de la membrane des cellules cardiaques permet la contraction du coeur. La génèse de cette activité électrique est due au courant sodique issu d'un type de canal à sodium situé dans la membrane des cellules cardiaques. De nombreuses pathologies provoquant des troubles du rythme cardiaque sont issues de mutations du gène qui code pour ce canal à sodium. Ces canaux mutants, entrainant diverses pathologies cardiaques telles que le syndrome de Brugada, ont été largement étudiées. Néanmoins, peu de travaux ont été réalisés sur les mécanismes de régulation de ce canal à sodium non muté. Mon travail de thèse a consisté à étudier certains des mécanismes de régulation de ce canal à sodium en utilisant une technique permettant l'enregistrement des courants sodiques issus de l'expression de ces canaux à sodium à la membrane de cellules mammifères. La présence sur ce canal à sodium d'une structure spécifique, similaire à celle nécessaire pour la régulation d'un canal épithélial à sodium par une enzyme appelée Nedd4-2, nous a amenée à étudier le rôle de cette enzyme dans la régulation de ce canal à sodium. La seconde étude s'est intéressée aux rôles de deux mutations du gène codant pour ce canal à sodium retrouvées chez des patients présentant un syndrome de Brugada exacerbé par la fièvre. Nos résultats nous ont permis d'établir deux mécanismes de régulation de ce canal à sodium diminuant le courant sodique l'un par l'action de l'enzyme Nedd4-2, suite à son interaction avec ce canal, qui modifie ce canal à sodium (ubiquitination) diminuant de ce fait la densité membranaire du canal. L'autre par un mécanisme suggérant un effet négatif de l'un des canaux mutants sur l'expression à la membrane du canal à sodium non muté. Ces études ont mis en évidence deux mécanismes de régulation de ce canal à sodium pouvant jouer un rôle majeur dans la genèse et/ou l'accentuation des troubles du rythme cardiaques dont les mécanismes cellulaires sont encore incompris.

Open source software expectations in retail businesses of Igualada : an exploratory study

The emergence of open source software in the last years has become a common topic of study in different fields, from the most technical characteristics to the economical aspects. This paper examines the current status about the literature dealing with economics of open source and explores the uses, infrastructure and expectations of retail businesses and institutions of the town of Igualda about it. This qualitative case study finds out that the current equipment and level of uses of ICTs are low and that the current situation of the town stores is receptive to a potential introduction of open source software.

Contribution to Asterisk Open Source Project

With this final master thesis we are going to contribute to the Asterisk open source project. Asterisk is an open source project that started with the main objective of develop an IP telephony platform, completely based on Software (so not hardware dependent) and under an open license like GPL. This project was started on 1999 by the software engineer Mark Spencer at Digium. The main motivation of that open source project was that the telecommunications sector is lack of open solutions, and most of the available solutions are based on proprietary standards, which are close and not compatible between them. Behind the Asterisk project there is a company, Digum, which is the project leading since the project was originated in its laboratories. This company has some of its employees fully dedicated to contribute to the Asterisk project, and also provide the whole infrastructure required by the open source project. But the business of Digium isn't based on licensing of products due to the open source nature of Asterisk, but it's based on offering services around Asteriskand designing and selling some hardware components to be used with Asterisk. The Asterisk project has grown up a lot since its birth, offering in its latest versions advanced functionalities for managing calls and compatibility with some hardware that previously was exclusive of proprietary solutions. Due to that, Asterisk is becoming a serious alternative to all these proprietaries solutions because it has reached a level of maturity that makes it very stable. In addition, as it is open source, it can be fully customized to a givenrequirement, which could be impossible with the proprietaries solutions. Due to the bigness that is reaching the project, every day there are more companies which develop value added software for telephony platforms, that are seriously evaluating the option of make their software fully compatible withAsterisk platforms. All these factors make Asterisk being a consolidated project but in constant evolution, trying to offer all those functionalities offered by proprietaries solutions. This final master thesis will be divided mainly in two blocks totally complementaries. In the first block we will analyze Asterisk as an open source project and Asterisk as a telephony platform (PBX). As a result of this analysis we will generate a document, written in English because it is Asterisk project's official language, which could be used by future contributors as an starting point on joining Asterisk. On the second block we will proceed with a development contribution to the Asterisk project. We will have several options in the form that we do the contribution, such as solving bugs, developing new functionalities or start an Asterisk satellite project. The type of contribution will depend on the needs of the project on that moment.