Investigation of decoupling capacitor connection methods using PEEC and study of alien crosstalk from a BroadR-Reach® protocol based system

Power Distribution Network (PDN) for Printed Circuit Board (PCB) design requires proper power integrity analysis. In order to deliver a low-ripple DC voltage from a Voltage Regulator Module (VRM) to an Integrated Circuit (IC), a certain target input impedance should be achieved. Developing simple physics-based equivalent circuit models are essential for understanding how a system works and making crucial design decisions. In this work, the input impedance of a decoupling capacitor due to traces, pads and via discontinuities are investigated using the Physics-based Model Size Reduction (PMSR) method. Various decoupling capacitor connection methods are compared and design guidelines are provided for reducing the equivalent inductance to meet target impedance requirements. It is shown that a shared pad having 179 pH equivalent Labove loop inductance is a better design choice as compared to a doublet or shared via design with 218 pH and 406 pH Labove loop inductance respectively. The second part of this thesis relates to BroadR-Reach® technology, a point-to-point Ethernet Physical Layer (PHY) standard, which is used in automotive applications. This technology allows full-duplex communication between two devices over a single, Unshielded Twisted wire Pair (UTP) cable. Here, alien crosstalk in a 6 UTP bundle is investigated for meeting electromagnetic compatibility requirements. The performance of Alien Near-End and Far-End Crosstalk of two different UTPs with and without an inline Circular Plastic Connector (CPC) are compared to standard limits. An inline connector in the middle of a 15 m 6 UTP cable bundle, with a 25 cm untwisted region fails the PSANEXT standard limit by 4 dB at 100 MHz, while the same bundle without the connector passes the standard by a margin of 8 dB at 100 MHz --Abstract, page iii

Predicting Radiated Emissions from a Complex Transportation System Wiring Harness

Low frequency radiated emissions problems are often caused by common mode currents flowing on wiring harnesses. The ability to predict radiated emissions problems early in the design process can save both time and money and result in a better product. Methods have previously been reported for rapidly characterizing common-mode sources driving a harness and then using these equivalent sources to predict radiated emissions. These methods are extended in the following paper to predict radiated emissions from a complex 32-wire harness bundle connected to an engine control unit. Rapid experimental characterization of the common mode sources is enabled using an equivalent cable bundle approximation of the original harness, where wires with roughly equivalent source and load impedances are lumped together and treated as a single equivalent wire. Sources driving the equivalent bundle were found using a specialized measurement fixture. Only a few measurements are required, even if there are many wires associated with the source and they originate at different ports on the component. Full-wave models of the equivalent harness were built and along with the equivalent source were used to predict radiated emissions. This model was able to predict radiated emissions from 20-300 MHz with reasonable accuracy, with peak emissions typically predicted within about 6 dB of measurements, when using multiple different harness lengths and routings

ალცჰაიმერის მქონე პაციენტების და მათი ოჯახის წევრების სოციალური პრობლემები

Alzheimer’s is one of the most proliferated disease in the world. It’s possible to diagnose this disease and even in Georgia it’s possible to do so, but the country’s healthcare system can’t offer anything else to its society and usually, the one who takes care of the diseased one is the Family Member of the patient. This is why our research focus was to determine the situation in the families of the diseased ones in Georgia. Particulary, our goal was to research the problems and the requirements of the people with alzhaimer’s and their families using qualitative method, in particular Biographical-Narrative interview, using which was gathered required data. Analysis of the data showed the small role government plays in the life of a diseased one and it only limits itself with a pension and the only responsible ones for the medical examination and other economical or social factors, which sums up itself with the lack of governmental services or about not enough information about them at all, is the families of the diseased ones. On the other hand, families of the diseased ones, do not have information about NGOs at all or they just are not interested in the programs offered by them.ალცჰაიმერი მსოფლიოში ერთ-ერთი გავრცელებული დაავადებაა. დღესდღეობით მისი განკურნება შეუძლებელია. ძირითადად ტარდება სიმპტომური მკურნალობა. ავადმყოფებს და მათი ოჯახის წევრებს სამედიცინო პერსონალი ეხმარება სნეულებასთან შეგუებაში. კვლევის მიზანია ალცჰაიმერით დაავადებულ ადამიანთა და მათი ოჯახის წევრთა პრობლემებისა და საჭიროებების კვლევა რესპონდენტთა ინტერპრეტაციისა და აღქმის საფუძველზე. კვლევის ფარგლებში, თვისებრივი მეთოდის, კერძოდ კი ბიოგრაფიულ-ნარატიული ინტერვიუს გამოყენებით შეგროვდა მონაცემები. კვლევის შედეგების მიხედვით გამოიკვეთა სახელმწიფოს უმნიშვნელო როლი პაციენტთა ცხოვრებაში. შესაბამისად, ოჯახს უწევს სრულად აიღოს პასუხისმგებლობა პაციენტის ზრუნვაზე. ამასთან, ისინი ნაკლებად არიან ინფორმირებულნი სხვადასხვა არასამთავრო ორგანიზაციების მიერ შეთავაზებული პროგრამებით

AKONE - Aliens Know One : diseño e implementación de un videojuego tipo shooter en Unity

En el mundo de los videojuegos cabe destacar la unión de tres factores muy importantes; el diseño del juego, el arte y la programación. En mi TFG (Trabajo Final de Grado) he optado por desarrollar un prototipo del juego de género shooter en la cual participen estos tres factores. La evolución del proyecto ha sido notable en cuanto a la fase de aprendizaje, investigación y conexión entre distintas herramientas que han facilitado a unificar todo el proceso. El trabajo de un ingeniero informático frente a este tipo de proyecto es sin duda la adaptación al medio y la capacidad de resolución de problemas demostrando el uso de su ingenio. AKONE ha sido el resultado.In the world of video games it should be noted that the union of three factors: game design, art, and programming; is very important. As a final thesis, it has been decided to develop a playable demo in which those three factors are very present. The evolution of the project has been notable in terms of these phases: learning, investigation and connection between various tools that made all the composition much easier. The work of and engineer among these type of projects is without a doubt the adaptation to the environment and the capacity to solve problems showing the use of its inventiveness. AKONE is the final result.En el món dels videojocs cal destacar la unió de tres factors molt importants; el disseny del joc, l'art i la programació. En el meu TFG (Treball Final de Grau) he optat per desenvolupar un prototip del joc de gènere shooter en la qual participen aquests tres factors. L'evolució del projecte ha estat notable pel que fa a la fase d'aprenentatge, investigació i connexió entre diferents eines que han facilitat a unificar tot el procés. La feina d'un enginyer informàtic front a aquest tipus de projecte és sens dubte l'adaptació al medi i la capacitat de resolució de problemes demostrant l'ús del seu enginy. AKONE ha estat el resultat

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1

DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The C terminal binding protein–interacting protein (CtIP) is phosphorylated in G2 by cyclin-dependent kinases to initiate resection and promote HR. CtIP also exerts functions during NHEJ, although the mechanism phosphorylating CtIP in G1 is unknown. In this paper, we identify Plk3 (Polo-like kinase 3) as a novel DSB response factor that phosphorylates CtIP in G1 in a damage-inducible manner and impacts on various cellular processes in G1. First, Plk3 and CtIP enhance the formation of ionizing radiation-induced translocations; second, they promote large-scale genomic deletions from restriction enzyme-induced DSBs; third, they are required for resection and repair of complex DSBs; and finally, they regulate alternative NHEJ processes in Ku−/− mutants. We show that mutating CtIP at S327 or T847 to nonphosphorylatable alanine phenocopies Plk3 or CtIP loss. Plk3 binds to CtIP phosphorylated at S327 via its Polo box domains, which is necessary for robust damage-induced CtIP phosphorylation at S327 and subsequent CtIP phosphorylation at T847

Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1

DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The C terminal binding protein–interacting protein (CtIP) is phosphorylated in G2 by cyclin-dependent kinases to initiate resection and promote HR. CtIP also exerts functions during NHEJ, although the mechanism phosphorylating CtIP in G1 is unknown. In this paper, we identify Plk3 (Polo-like kinase 3) as a novel DSB response factor that phosphorylates CtIP in G1 in a damage-inducible manner and impacts on various cellular processes in G1. First, Plk3 and CtIP enhance the formation of ionizing radiation-induced translocations; second, they promote large-scale genomic deletions from restriction enzyme-induced DSBs; third, they are required for resection and repair of complex DSBs; and finally, they regulate alternative NHEJ processes in Ku−/− mutants. We show that mutating CtIP at S327 or T847 to nonphosphorylatable alanine phenocopies Plk3 or CtIP loss. Plk3 binds to CtIP phosphorylated at S327 via its Polo box domains, which is necessary for robust damage-induced CtIP phosphorylation at S327 and subsequent CtIP phosphorylation at T847

The process of displacing the single-stranded DNA-binding protein from single-stranded DNA by RecO and RecR proteins

The regions of single-stranded (ss) DNA that result from DNA damage are immediately coated by the ssDNA-binding protein (SSB). RecF pathway proteins facilitate the displacement of SSB from ssDNA, allowing the RecA protein to form protein filaments on the ssDNA region, which facilitates the process of recombinational DNA repair. In this study, we examined the mechanism of SSB displacement from ssDNA using purified Thermus thermophilus RecF pathway proteins. To date, RecO and RecR are thought to act as the RecOR complex. However, our results indicate that RecO and RecR have distinct functions. We found that RecR binds both RecF and RecO, and that RecO binds RecR, SSB and ssDNA. The electron microscopic studies indicated that SSB is displaced from ssDNA by RecO. In addition, pull-down assays indicated that the displaced SSB still remains indirectly attached to ssDNA through its interaction with RecO in the RecO-ssDNA complex. In the presence of both SSB and RecO, the ssDNA-dependent ATPase activity of RecA was inhibited, but was restored by the addition of RecR. Interestingly, the interaction of RecR with RecO affected the ssDNA-binding properties of RecO. These results suggest a model of SSB displacement from the ssDNA by RecF pathway proteins

RecO-mediated DNA homology search and annealing is facilitated by SsbA

Bacillus subtilis RecO plays a central role in recombinational repair and genetic recombination by (i) stimulating RecA filamentation onto SsbA-coated single-stranded (ss) DNA, (ii) modulating the extent of RecA-mediated DNA strand exchange and (iii) promoting annealing of complementary DNA strands. Here, we report that RecO-mediated strand annealing is facilitated by cognate SsbA, but not by a heterologous one. Analysis of non-productive intermediates reveals that RecO interacts with SsbA-coated ssDNA, resulting in transient ternary complexes. The self-interaction of ternary complexes via RecO led to the formation of large nucleoprotein complexes. In the presence of homology, SsbA, at the nucleoprotein, removes DNA secondary structures, inhibits spontaneous strand annealing and facilitates RecO loading onto SsbA–ssDNA complex. RecO relieves SsbA inhibition of strand annealing and facilitates transient and random interactions between homologous naked ssDNA molecules. Finally, both proteins lose affinity for duplex DNA. Our results provide a mechanistic framework for rationalizing protein release and dsDNA zippering as coordinated events that are crucial for RecA-independent plasmid transformation

CtIP tetramer assembly is required for DNA-end resection and repair.

Mammalian CtIP protein has major roles in DNA double-strand break (DSB) repair. Although it is well established that CtIP promotes DNA-end resection in preparation for homology-dependent DSB repair, the molecular basis for this function has remained unknown. Here we show by biophysical and X-ray crystallographic analyses that the N-terminal domain of human CtIP exists as a stable homotetramer. Tetramerization results from interlocking interactions between the N-terminal extensions of CtIP's coiled-coil region, which lead to a 'dimer-of-dimers' architecture. Through interrogation of the CtIP structure, we identify a point mutation that abolishes tetramerization of the N-terminal domain while preserving dimerization in vitro. Notably, we establish that this mutation abrogates CtIP oligomer assembly in cells, thus leading to strong defects in DNA-end resection and gene conversion. These findings indicate that the CtIP tetramer architecture described here is essential for effective DSB repair by homologous recombination.We thank M. Kilkenny for help with the collection of X-ray diffraction data, A. Sharff and P. Keller for help with X-ray data processing and J.D. Maman for assistance with SEC-MALS. This work was supported by a Wellcome Trust Senior Research Fellowship award in basic biomedical sciences (L.P.), an Isaac Newton Trust research grant (L.P. and O.R.D.) and a Cambridge Overseas Trust PhD studentship (M.D.S.). Research in the laboratory of S.P.J. is funded by Cancer Research UK (CRUK; programme grant C6/A11224), the European Research Council and the European Community Seventh Framework Programme (grant agreement no. HEALTH-F2-2010-259893 (DDResponse)). Core funding is provided by Cancer Research UK (C6946/A14492) and the Wellcome Trust (WT092096). S.P.J. receives his salary from the University of Cambridge, supplemented by CRUK. J.V.F. is funded by Cancer Research UK programme grant C6/A11224 and the Ataxia Telangiectasia Society. R.B. and J.C. are funded by Cancer Research UK programme grant C6/A11224. Y.G. and M.D. are funded by the European Research Council grant DDREAM.This is the accepted manuscript of a paper published in Nature Structural & Molecular Biology, 22, 150–157 (2015) doi: 10.1038/nsmb.293