809 research outputs found
A DNA-Inspired Synthetic Ion Channel Based on G-C Base Pairing
No full textA dinucleoside containing guanosine and cytidine at the end groups has been prepared using a modular one-pot azide-alkyne cycloaddition. Single channel analysis showed that this dinucleoside predominantly forms large channels with 2.9 nS conductance for the transport of potassium ions across a phospholipid bilayer. Transmission electron microscopy, atomic force microscopy, and circular dichroism spectroscopy studies reveal that this dinucleoside can spontaneously associate through Watson-Crick canonical H-bonding and pi-pi stacking to form stable supramolecular nanostructures. Most importantly, the ion channel activity of this G-C dinucleoside can be inhibited using the nucleobase cytosine
Clock multiplication techniques for high-speed I/Os
Get PDFGeneration of a low-jitter, high-frequency clock from a low-frequency reference clock using classical analog phase-locked loops (PLLs) requires a large loop filter capacitor and power hungry oscillator. Digital PLLs can help reduce area but their jitter performance is severely degraded by quantization error. In this dissertation different clock multiplication techniques have been explored that can be suitable for high-speed wireline systems. With the emphasis on ring oscillator based architecture using cascaded stages, three possible architectures are explored.
First, a scrambling TDC (STDC) is presented to improve deterministic jitter (DJ) performance when used with a low-frequency reference clock. A cascaded architecture with digital multiplying delay locked loop as the first stage and hybrid analog/digital PLL as the second stage is used to achieve low random jitter in a power efficient manner. Fabricated in a 90nm CMOS process, the prototype frequency synthesizer consumes 4.76mW power from a 1.0V supply and generates 160MHz and 2.56 GHz output clocks from a 1.25MHz crystal reference frequency. The long-term absolute jitter of the 60MHz digital MDLL and 2.56 GHz digital PLL outputs are 2.4 psrms and 4.18 psrms, while the peak-to-peak jitter is 22.1 ps and 35.2 ps, respectively. The proposed frequency synthesizer occupies an active die area of 0.16mm2 and achieves power efficiency of 1.86 mW/GHz.
Second, a hybrid phase/current-mode phase interpolator (HPC-PI) is presented to improve phase noise performance of ring oscillator-based fractional-N PLLs. The proposed HPC-PI alleviates the bandwidth trade-off between VCO phase noise suppression and ΔΣ quantization noise suppression. By combining the phase detection and interpolation functions into an XOR phase detector/interpolator (XOR PD-PI) block, accurate quantization error cancellation is achieved without using calibration. Use of a digital MDLL in front of the fractional-N PLL helps in alleviating the bandwidth limitation due to reference frequency and enables bandwidth extension even further. The extended bandwidth helps in suppressing the ring-VCO phase noise and lowering the in-band noise floor. Fabricated in 65nm CMOS process, the prototype generates fractional frequencies from 4.25 to 4.75 GHz, with an in-band phase noise floor of -104 dBc/Hz and 1.5 psrms integrated jitter. The clock multiplier achieves power efficiency of 2.4mW/GHz and FoM of -225.8 dB.
Finally, an efficient clock generation, recovery, and distribution techniques for flexible-rate transceivers are presented. Using a fixed-frequency low-jitter clock provided by an integer-N PLL, fractional frequencies are generated/recovered locally using multi-phase fractional clock multipliers. Fabricated in a 65nm CMOS, the prototype transceiver can be programmed to operate at any rate from 3-to-10 Gb/s. At 10 Gb/s, integrated jitter of the Tx output and recovered clock is 360 fsrms and 758 fsrms, respectively.Submission published under a 24 month embargo labeled 'U of I Access', the embargo will last until 2019-05-01The student, Romesh Kumar Nandwana, accepted the attached license on 2017-04-17 at 15:09.The student, Romesh Kumar Nandwana, submitted this Dissertation for approval on 2017-04-17 at 15:42.This Dissertation was approved for publication on 2017-04-19 at 08:46.DSpace SAF Submission Ingestion Package generated from Vireo submission #10816 on 2017-08-10 at 15:05:48Made available in DSpace on 2017-08-10T20:32:59Z (GMT). No. of bitstreams: 3
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Role of SOCS proteins in FLT3-ITD and BCR/ABL mediated leukemogenesis
No full textAcute myeloid/lymphoid leukemia is a fatal hematological malignancy characterized by accumulation of nonfunctional, immature blasts, which interferes with the production of normal blood cells. Activating mutations of receptor tyrosine kinases are common genetic lesions in leukemia. FLT3-ITD is a frequent activating mutation found in AML patients, leading to uncontrolled proliferation of leukemic blasts. FLT3-ITD directly activates STAT5, leading to the induction of STAT5 target gene expression like PIM kinases and SOCS genes. STAT5 and PIM kinases have been shown to play a crucial role in the FLT3-ITD mediated transformation. On the other hand, the role of SOCS proteins in FLT3-ITD mediated transformation has not been studied to date. SOCS proteins are part of a negative feedback mechanism that controls Jak kinases downstream of cytokine receptors. One of the SOCS family members, SOCS1 has been reported to suppress oncogenecity of several activating kinases implicated in hematologic malignancies. In this thesis the role of these SOCS proteins in FLT3-ITD mediated transformation (in vitro) and leukemogenesis (in vivo) is systematically explored. Expression of FLT3-ITD in cell lines of myeloid (32D) and lymphoid (Ba/F3) origin, led to CIS, SOCS1 and SOCS2 expression. FLT3-ITD expression in primary murine bone marrow stem/progenitor cells led to a 59 fold induction of SOCS1 expression. Furthermore, FLT3-ITD positive AML cell lines (MV4-11, MOLM-13) show kinase dependent CIS, SOCS1, and SOCS3 expression. Importantly SOCS1 is highly expressed in AML patients with FLT3-ITD compared to healthy individuals. SOCS1 protein was expressed in FLT3-ITD transduced murine bone marrow stem cells and SOCS1 expression was abolished with kinase inhibition in MOLM-13 cell line. In conclusion, SOCS1 was highly regulated by FLT3-ITD in myeloid, lymphoid cell lines, in bone marrow stem/progenitors and in AML patient samples. SOCS1 co-expression did not affect FLT3-ITD mediated signaling and proliferation, but abolished IL-3 mediated proliferation and protected 32D cells from interferon-α and interferon-γ mediated growth inhibition. FLT3-ITD expressing 32D cells showed diminished STAT1 activation in response to interferons (α and γ). Alone, SOCS1 strongly inhibited cytokine induced colony formation of bone marrow stem and progenitors, but not FLT3-ITD induced colony formation. Most importantly, in the presence of growth inhibitory interferon-γ, SOCS1 co-expression with FLT3-ITD led to increased colony formation compared to FLT3-ITD alone. Taken together, FLT3-ITD induced and exogenously expressed SOCS1, shielded cells from external cytokines, signals, while not affecting FLT3-ITD induced proliferation/signaling. In further experiments the in vivo effects of SOCS1 were studied in a bone marrow transplantation model. SOCS1 bone marrow transplants were unable to engraft/proliferate in mice. FLT3-ITD was shown to induce a myeloproliferative disease. Both control (empty vector), SOCS1 transplanted mice were normal and did not show any disease phenotype. FLT3-ITD alone and SOCS1 co-expressing FLT3-ITD developed either myeloproliferative disease or acute lymphoblastic leukemia with equal distribution. SOCS1 co-expression with FLT3-ITD led to a decreased latency. Mice transplanted with FLT3-ITD alone and SOCS1 co-expressing FLT3-ITD displayed enlarged spleens, liver and hypercellular bone marrow indicating infiltration of leukemic cells. Mice were also anemic and showed decreased platelet counts. Importantly SOCS1 co-expression particularly shortened the latency of myeloproliferative disease but not of acute lymphoblastic leukemia. In summary, in the context of FLT3-ITD, SOCS1 acts as a ‘conditional oncogene’ and cooperates with FLT3-ITD in the development of myeloproliferative disease. With these data we propose the following model: FLT3-ITD induces SOCS gene expression, which shields cells against proliferation and differentiation signals from cytokines, while not affecting FLT3-ITD mediated proliferative signals. This leaves cells under the dictate of FLT3-ITD thereby contributing to leukemogenesis. Similar to FLT3-ITD, BCR/ABL (P190) (an oncogenic fusion kinase often found in acute lymphoblastic leukemia) induces SOCS gene expression in K562 and long-term cultured cells from patients with acute lymphoblastic leukemia. SOCS1 co-expression does not affect BCR/ABL mediated proliferation while abrogating IL-3 mediated proliferation. These findings suggest that SOCS proteins may play a general co-operative role in the context of oncogenes which aberrantly activate STAT3/5 independently of JAK kinases. This study reveals a novel molecular mechanism of FLT3-ITD mediated leukemogenesis and suggests SOCS genes as potential therapeutic targets.Akute Leukämien sind unbehandelt tödlich verlaufende, hämatologische Erkrankungen, bei denen es zu einer Anreicherung unreifer und funktionsloser Blasten im Knochenmark kommt, was wiederum mit der gesunden Hämatopoese interferiert. Ursache dieser Leukämien sind chomosomale Translokationen oder Funtionsgewinn- bzw. Funktionsverlustmutationen. Die Mehrheit dieser Mutationen tritt in Genen auf, die Proliferation und/oder Differenzierung regulieren. Im Rahmen dieser Dissertation wurde die Rolle einer dieser Mutationen der Rezeptortyrosinkinase FLT3 in der Leukämogenese bearbeitet, genannt FLT3-ITD (interne Tandemduplikation). FLT3 wird in frühen hämatopoetischen Stamm- und Progenitorzellen exprimiert und spielt eine wichtige Rolle für das Überleben und die Proliferation lymphatischer und myeloischer Linien. Die Bindung des FLT3 Liganden an den Wildtyp-FLT3 Rezeptor führt zur dessen Dimerisierung und Aktivierung, wobei diese Aktivierung wiederum unterschiedliche Signalwege wie z.B. PI3K/Akt und Erk aktiviert. FLT3-ITD ist eine aktivierende Mutation der FLT3 Rezeptortyrosinkinase, die bei etwa 25 % der AML-Patienten gefunden wird und zur unkontrollierten Proliferation leukämischer Blasten führt. Diese Mutation führt zu einer Ligand-unabhängigen, konstitutiv aktiven Form des Rezeptors, so dass die nachfolgenden Signalwege (PI3K/Akt, Erk und STAT5) permanent angeschaltet sind. Ein Genexpressionsprofil in FLT3-ITD exprimierenden 32D Zellen im Vergleich zu Ligand aktivierten Wildtyp-FLT3 exprimierenden Zellen zeigt eine erhöhte Expression von STAT5 Zielgenen wie PIM Kinasen und SOCS Proteinen. Interessanterweise aktiviert FLT3-ITD STAT5 dabei unabhängig von Jak und Src Kinasen und verleiht IL-3 abhängigen Zelllinien wie 32D und Ba/F3 ein Faktor unabhängiges Wachstum. Weiterhin verursacht eine FLT3-ITD Expression im Gegensatz zum Wildtyp-FLT3 in Maustransplantationsexperimenten eine myeloproliferative Erkrankung. Vergleichbar mit FLT3-ITD ist BCR/ABL auch ein onkogenes Fusionsprotein, das durch eine Translokation zwischen den Chromosomen 9 und 22, bezeichnet als t(9;22), zustande kommt. Das BCR/ABL Protein wird in ca. 90 % aller chronischen myeloischen Leukämien (CML) und in 10-20 % aller akuten lymphatischen Leukämien (ALL) gefunden. Wie FLT3-ITD verleiht auch BCR/ABL 32D und Ba/F3 Zellen ein IL-3 unabhängiges Wachstum. Außerdem führt es zu einer konstitutiven Aktivierung der PI3K/AKT, Ras/MAPK und STAT5 Signalwege. Die BCR/ABL vermittelte Aktivierung von STAT5 erfolgt hierbei entweder durch direkte Phosphorylierung oder über die Src Kinase HCK. Im Knochenmarktransplantationsmodell induziert BCR/ABL eine myeloproliferative Erkrankung, die einer CML ähnelt. Die Produktion hämatopoetischer Zellen unterliegt einer strengen Kontrolle durch hämatopoetische Zytokine. Die Zytokinrezeptoren besitzen keine intrinsische Kinaseaktivität. Die Signalweiterleitung erfolgt hier über Jak Kinasen. Auf diese Weise kontrollieren Zytokinrezeptoren wichtige Prozesse des Immunsystems und der Blutzellhomöostase. SOCS Proteine sind Teil eines negativen Rückkopplungsmechanismus, der die Aktivierung von STAT Proteinen durch Zytokinrezeptoren kontrolliert. SOCS Proteine binden an Jak Kinasen und inhibieren deren Kinaseaktivität über verschiedene Mechanismen, was zur Termination der Zytokinsignale führt. Von einem Mitglied der SOCS Familie, SOCS1, ist bekannt, dass es durch die Hemmung einiger aktivierender Kinasen bei hämatologischen Erkrankungen tumorsupressive Eigenschaften hat. Die Rolle der SOCS Proteine in der FLT3-ITD vermittelten Transformation ist bis heute nicht hinreichend analysiert. Insbesondere ist unklar wie transformierte Zellen der strengen Kontrolle des Zytokinnetzwerks entgehen können, das normalerweise die korrekte Funktion hämatopoetischer Zellen garantiert. In der vorliegenden Arbeit wurde die Rolle von SOCS Proteinen in der FLT3-ITD vermittelten Transformation (in vitro) und Leukämieentstehung (in vivo) systematisch untersucht. Weiterhin wurde die SOCS Genexpression und die Folgen der BCR/ABL vermittelten Transformation analysiert. Schlussfolgerung 1: FLT3-ITD induziert die Expression von SOCS Genen in Zelllinien und murinen Knochenmarkzellen; SOCS1 ist in Patienten mit FLT3-ITD induziert. Zunächst wurden bestehende microarray Daten durch quantitative real time PCR validiert. Die Expression von FLT3-ITD in myeloischen (32D) und lymphatischen (Ba/F3) Zelllinien induziert die Expression von CIS, SOCS1 und SOCS2. In primärem murinen Knochenmarksstamm-/progenitorzellen führt die Expression von FLT3-ITD zu einem sehr starken Anstieg der SOCS1 Expression (59-fach). Zudem zeigen Zelllinien, die von FLT3-ITD positiven AML-Patienten gewonnen wurden (MV4-11, MOLM-13), eine Kinase abhängige CIS, SOCS1 und SOCS3 Expression. Interessanterweise wird außerdem SOCS1 im Knochenmark von AML-Patienten mit FLT3-ITD Mutationen im Vergleich zu Kontrollen von gesunden Spender stark überexprimiert. Das SOCS1 Protein wird ferner in FLT3-ITD transduziertem murinen Knochenmark exprimiert und die Expression geht in MOLM-13 Zellen nach Behandlung mit Kinaseinhibitoren verloren. Zusammenfassend wird die Expression von SOCS1 in hohem Maße durch FLT3-ITD in myeloischen und lymphatischen Zelllinien sowie in hämatopoetischen Stamm- und Progenitorzellen und AML-Patienten hochreguliert. Schlussfolgerung 2: Die SOCS1 Expression verhindert Zytokinrezeptor vermittelte Effekte aber nicht die FLT3-ITD induzierte Signalgebung und Proliferation. Aufgrund der hohen SOCS1 Induktion durch FLT3-ITD im primären murinen Knochenmark und in Patientenproben wurde dessen Rolle in der FLT3-ITD vermittelten Transformation untersucht. Die Koexpression von SOCS1 beeinträchtigt nicht die durch FLT3-ITD induzierten Signalwege (MAPK/ERK, PI3K/AKT und STAT5) oder die Proliferation, jedoch unterbindet es die IL-3 vermittelte Proliferation und schützt 32D Zellen vor der Wachstumshemmung durch Interferon α und γ. So zeigten FLT3-ITD exprimierende 32D Zellen eine verminderte STAT1-Aktivierung durch Interferon α und γ. In einem kompetitiven Proliferationsassay wirkte die SOCS1 Expression alleine wachtumsinhibierend, koexprimiert mit FLT3-ITD trat allerdings der gegenteilige Effekt auf. Im murinen Knochenmark führte SOCS1 zu einer starken Hemmung der Zytokin induzierten Kolonienbildung hämatopoetischer Stamm- und Progenitorzellen, jedoch nicht der FLT3-ITD induzierten Kolonienbildung, was auf eine SOCS1 Resistenz von FLT3-ITD hindeutet. Interessanterweise führte SOCS1 in Anwesenheit des wachstumhemmenden Interferons γ zu einer Verstärkung der FLT3-ITD induzierten Kolonienbildung. Zusammenfassend führt die FLT3-ITD induzierte oder exogene SOCS1 Expression zu einer Abschirmung der Zellen von exogenen Zytokinsignalen, während die FLT3-ITD vermittelten, zellulären Effekte unbeeinflusst bleiben. Schlussfolgerung 3: SOCS1 Expression verstärkt die myeloproliferative Erkrankung, die durch FLT3-ITD induziert wird: SOCS1 als „konditionales Onkogen“. Für FLT3-ITD wurde bereits die Entstehung einer myeloproliferativen Erkrankung und einer akuten lymphozytischen B- und T-Zellleukämie im murinen Knochenmark gezeigt. Im transgenen Mausmodell löst FLT3-ITD entweder eine myeloproliferative oder eine lymphatische Erkrankung aus. In dieser Arbeit wurde die Rolle von SOCS1 in der FLT3-ITD vermittelten Leukämie im Knochmarktransplantationsmodell in vivo untersucht. Die Übertragung der in vitro gefundenen Effekte von SOCS1 auf FLT3-ITD in das Mausmodell in vivo zeigte, dass es bei der Transplantation von SOCS1 exprimierendem Knochenmark nicht zu einem Anwachsen oder zur Proliferation in der Maus kommt, was einen kompetitiven Wachstumsnachteil dieser Zellen demonstriert. SOCS1 und FLT3-ITD koexprimierende Transplantate zeigten jedoch eine höhere Proliferationsrate in vivo als ausschließlich Flt3-ITD exprimierende Zellen. Sowohl Kontroll- als auch SOCS1 transplantierte Mäuse waren unauffällig und ohne erkennbaren Phänotyp. Mäuse mit Flt3-ITD transduzierten oder FLT3-ITD und SOCS1 koexprimierenden Transplantaten entwickelten zu gleichen Teilen entweder eine myeloproliferative Erkrankung oder eine akute lymphatische Leukämie. Die Koexpression von SOCS1 mit FLT3-ITD führte zu einer verkürzten Latenzzeit. Mäuse mit FLT3-ITD transduzierten Transplantaten (mit oder ohne SOCS1) zeigten vergrößerte Milzen und Lebern sowie ein hyperzelluläres Knochenmark als Anhaltspunkt für eine Infiltration mit leukämischen Blasten. Ferner waren die Mäuse anämisch und hatte eine verminderte Thrombozytenzahl. Interessanterweise verkürzte die Koexpression von SOCS1 die Latenzzeit für die myeloproliferative Erkrankung, aber nicht für die akute lymphatische Leukämie. Zusammenfassend wirkt SOCS1 im Zusammenhang mit FLT3-ITD als konditionales Onkogen und kooperiert mit FLT3-ITD bei der Entstehung der myeloproliferativen Erkrankung. Schlußfolgerung 4: SOCS Gene werden durch BCR/ABL induziert. SOCS1 Expression beeinflusst nicht die BCR/ABL vermittelte Transformation. Eine Aktivierung von STAT5 wurde im Zusammenhang mit mehreren hämatologischen, malignen Erkrankungen, die durch onkogene Kinasen ausgelöst wurden, beobachtet. Da BCR/ABL STAT5 stark aktiviert, wurde die SOCS Genexpression in BCR/ABL positiven Zelllinien und im Knochenmark mittels quantitativer PCR analysiert. Im Vergleich zu BCR/ABL negativen ALL Zellen wurde in BCR/ABL positiven, primären ALL Zellen eine Induktion von CIS, SOCS2 und SOCS3 beobachtet. Die Inhibition der ABL Kinaseaktivität in BCR/ABL positiven, primären ALL Zellen durch Zugabe von Imatinib führte zu einer Verminderung der SOCS Expression, was eine Kinase abhängige Expression dieser Proteine demonstriert. Ebenso konnte auch in der BCR/ABL positiven Zelllinie K562 durch die Inhibition der ABL Kinaseaktivität mittels Imatinib eine Reduktion von CIS, SOCS1 und SOCS3 demonstriert werden. Die Expression von BCR/ABL im primären murinen Knochenmark induzierte eine hohe Expression von CIS, SOCS1 und SOCS3. Die Koexpression von SOCS1 beeinflusste nicht die BCR/ABL vermittelte Proliferation, während aber die IL-3 vermittelte Proliferation unterdrückt wurde, was auf eine SOCS1 Resistenz von BCR/ABL deutet. Mit diesen Ergebnissen schlagen wir ein Modell vor, bei dem FLT3-ITD die Expression von SOCS Genen induziert, welche wiederum die Zelle von pro- oder antiproliferativen sowie Differenzierungssignalen exogener Zytokine abschirmen, ohne die FLT3-ITD vermittelten Signale zu beeinflussen. So verbleibt die Zelle einzig unter der Kontrolle von FLT3-ITD, was zur Leukämieentstehung beiträgt. Dieses Model erklärt das ‚SOCS Paradoxon’, in dem die scheinbar gegensätzlichen Ergebnisse der erhöhten Expression der Tumorsupressorproteine der SOCS Familie im Kontext mit onkogenen Kinasen wie FLT3-ITD stehen. Die vorliegende Untersuchung zeigt einen neuen molekularen Mechanismus der FLT3-ITD vermittelten Leukämieentstehung. Mechanistisch setzen SOCS Proteine die externe Kontrolle durch Zytokine außer Kraft und wirken so positiv in der Leukämogenese. Dies deutet auf eine Rolle von SOCS Proteinen als mögliche therapeutische Zielstrukturen hin. Diese Beobachtungen legen nahe, dass SOCS Proteine generell mit Onkogenen kooperieren, die eine aberrante Aktivierung von STAT3/5 unabhängig von JAK Kinasen, induzieren
Event-driven simulation of mixed-signal systems
Get PDFSubmission published under a 24 month embargo labeled 'U of I Access', the embargo will last until 2022-05-01This thesis presents a method of performing fast and accurate simulation for mixed-signal systems. The first section introduces traditional simulation methods for mixed-signal systems and their drawbacks. The second section shows a new way to perform such simulation in a fast and accurate way, using the event-driven simulation method. For illustrative purposes, a type-2 charge-pump phase-locked loop is implemented. The third section is an extension to the second one: nonlinear effect is also included in the system.The student, Yongxin Li, accepted the attached license on 2020-04-09 at 09:52.The student, Yongxin Li, submitted this Thesis for approval on 2020-04-09 at 10:02.This Thesis was approved for publication on 2020-04-10 at 10:32.DSpace SAF Submission Ingestion Package generated from Vireo submission #14947 on 2020-08-25 at 17:27:14Made available in DSpace on 2020-08-26T23:51:27Z (GMT). No. of bitstreams: 2
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At the Crossroads: Multidiscipline Integration and Coordination in an EPC Contract: A Resurgence of Challenges and Strategic Improvement Opportunities
Get PDFMaster's thesis in Industrial Asset ManagementOver the years, the faculty of Project management contributed excellent methodologies through a set of constituted guidelines that are applicable for smooth execution of projects in every industry. They are broadly based on initiating, planning, organizing, executing, and monitoring & controlling the process groups as a single entity. The implementation of project management methodologies is carried out through project management knowledge in specialized areas such as integration, scope, time, cost, quality, human resource, communications and risk. Projects are governed by factors that have major influence in directing the success or failures. Broadly cost, time & quality have been identified as key important success factors for projects. However, the factors are also governed by the complexity of projects and risk involved in project execution.
Over the decades the EPC contractors are trying to find solutions to cope up to the complexities colligated with significant risks in project execution. Extensive research is done by every contractor with an objective to integrate schedule and time management functions in an EPC project. Many scholars and researchers used different methodologies such as utility theory, scheduling milestones, cost milestones, performance index, cost accounting etc.
However, the focus has been primarily on the construction phase of the project and most often ignores the fact that success delivery of a project is a synchronous and integrated effort of all the disciplines involved in project execution.
This research is carried out to identify the critical success factors in EPC projects and establish the essential factors requisite for efficient execution. In a quest to define a framework that essentially facilitates identifying the critical success factors and their key influencing factors, a systematic investigation of established facts were used. The journey in search of knowledge through previously established researches and scholarly work culminated into the design and development of a framework methodology congenial to the current research environment. Collaboration with the research unit specialist groups and individuals helped to develop a survey questionnaire. The required data was acquired from selected participants of the EPC contractor organization that is specialized in offering EPC services in the oil & gas industry. The data was collected based on convenience statistical sampling technique. Acquired data was analyzed through univariate, bivariate, multivariate statistical techniques and identified the critical factors that require attention of the management of the organization under research. The findings indicated concurrence of established project success factors i.e. scope, time and cost with critical success factors identified and defined in the research. The results of analysis identified factors that are significantly affecting the efficiency of multidiscipline integration and co-ordination.
The research established that an integrated control system is necessary to the management as a tool that investigates and provides answers from the project stakeholders. Such a system provides the reflection of the factors that are directly or indirectly impacting the cost, schedule and quality constraints of a project.
Research Faculty Supervisor: Professor. Jayantha.P. Liyanage, Ph.D,
Professor & Chair, Centre for Industrial Asset Management (CIAM),
Faculty of Science & Technology, University of Stavanger
Research External Supervisors: Nils Erik Olsen and Eivind Eliassen
Researcher and Author: Pavan Kumar Akella
M.Sc Student, Faculty of Science & Technology,
University of Stavange
Loss of susceptibility as a novel breeding strategy for durable and broad-spectrum resistance
Get PDFRecent studies on plant immunity have suggested that a pathogen should suppress induced plant defense in order to infect a plant species, which otherwise would have been a nonhost to the pathogen. For this purpose, pathogens exploit effector molecules to interfere with different layers of plant defense responses. In this review, we summarize the latest findings on plant factors that are activated by pathogen effectors to suppress plant immunity. By looking from a different point of view into host and nonhost resistance, we propose a novel breeding strategy: disabling plant disease susceptibility genes (S-genes) to achieve durable and broad-spectrum resistanc
RC relaxational oscillator with high supply rejection
Get PDFA low power RC relaxation oscillator with very low voltage and temperature sensitivities is presented. Supply sensitivity is reduced by using a self-regulation loop that biases the oscillator near its zero-voltage coefficient point. Fabricated in a 65nm CMOS process, the prototype 1.5MHz oscillator consumes 6μW from 1V supply and achieves better than ±50ppm/ ̊C and ±1500ppm/V temperature and voltage sensitivities, respectively.Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2020-05-01The student, Tianyu Wang, accepted the attached license on 2018-04-25 at 16:33.The student, Tianyu Wang, submitted this Thesis for approval on 2018-04-25 at 16:37.This Thesis was approved for publication on 2018-04-26 at 08:25.DSpace SAF Submission Ingestion Package generated from Vireo submission #12497 on 2018-08-31 at 17:30:30Made available in DSpace on 2018-09-04T20:47:31Z (GMT). No. of bitstreams: 2
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Clock distribution network techniques
Get PDFClock distribution networks are essential to synchronous systems. The design of these networks affects the system performance dramatically and sometimes determines whether the chip can function properly or not. This thesis first describes in detail how a synchronous system works. Based on the design metrics such as the clock skew requirement and power requirement, different clock distribution network topologies are then presented, including the popular H tree, grid and serpentine structures. Finally, commonly used techniques for improving clock skew, jitter and power are discussed and conclusions are offered.Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2022-08-01The student, Shuang Chen, accepted the attached license on 2020-06-26 at 16:40.The student, Shuang Chen, submitted this Thesis for approval on 2020-06-26 at 16:50.This Thesis was approved for publication on 2020-06-29 at 15:08.DSpace SAF Submission Ingestion Package generated from Vireo submission #15473 on 2020-10-02 at 15:49:41Made available in DSpace on 2020-10-07T22:48:09Z (GMT). No. of bitstreams: 2
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Previous issue date: 2020-06-29Embargo set by: Seth Robbins for item 116297
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Reason: Author requested closed access (OA after 2yrs) in Vireo ETD systemEmbargo set by: Seth Robbins for item 116297
Lift date: 2022-10-07T22:50:13Z
Reason: Author requested closed access (OA after 2yrs) in Vireo ETD systemAuthor requested closed access (OA after 2yrs) in Vireo ETD systemLimite
Energy-efficient wireline transceivers
Get PDFPower-efficient wireline transceivers are highly demanded by many applications in high performance computation and communication systems. Apart from transferring a wide range of data rates to satisfy the interconnect bandwidth requirement, the transceivers have very tight power budget and are expected to be fully integrated. This thesis explores enabling techniques to implement such transceivers in both circuit and system levels. Specifically, three prototypes will be presented: (1) a 5Gb/s reference-less clock and data recovery circuit (CDR) using phase-rotating phase-locked loop (PRPLL) to conduct phase control so as to break several fundamental trade-offs in conventional receivers; (2) a 4-10.5Gb/s continuous-rate CDR with novel frequency acquisition scheme based on bang-bang phase detector (BBPD) and a ring oscillator-based fractional-N PLL as the low noise wide range DCO in the CDR loop; (3) a source-synchronous energy-proportional link with dynamic voltage and frequency scaling (DVFS) and rapid on/off (ROO) techniques to cut the link power wastage at system level. The receiver/transceiver architectures are highly digital and address the requirements of new receiver architecture development, wide operating range, and low power/area consumption while being fully integrated. Experimental results obtained from the prototypes attest the effectiveness of the proposed techniques.Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2018-12-01The student, Guanghua Shu, accepted the attached license on 2016-09-28 at 11:50.The student, Guanghua Shu, submitted this Dissertation for approval on 2016-09-28 at 15:42.This Dissertation was approved for publication on 2016-09-30 at 13:20.DSpace SAF Submission Ingestion Package generated from Vireo submission #10172 on 2017-02-28 at 14:40:52Made available in DSpace on 2017-03-01T17:00:54Z (GMT). No. of bitstreams: 3
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Previous issue date: 2016-09-30Embargo set by: Seth Robbins for item 98665
Lift date: 2019-03-01T17:02:22Z
Reason: Author requested closed access (OA after 2yrs) in Vireo ETD systemEmbargo set by: Seth Robbins for item 98665
Lift date: 2019-03-01T17:03:32Z
Reason: Author requested closed access (OA after 2yrs) in Vireo ETD systemEmbargo set by: Seth Robbins for item 98665
Lift date: 2019-03-01T17:05:02Z
Reason: Author requested closed access (OA after 2yrs) in Vireo ETD systemEmbargo set by: Seth Robbins for item 98665
Lift date: 2019-03-01T17:06:55Z
Reason: Author requested closed access (OA after 2yrs) in Vireo ETD systemLimited Restriction Lifted for Item 98665 on 2019-03-02T10:15:18Z
Toxicity of Bacillus thuringiensis-Derived Pesticidal Proteins Cry1Ab and Cry1Ba against Asian Citrus Psyllid, Diaphorina citri (Hemiptera)
Get PDFThe Asian citrus psyllid (ACP), Diaphorina citri Kuwayama (Hemiptera), is an important pest of citriculture. The ACP vectors a bacterium that causes huanglongbing (HLB), a devastating and incurable disease of citrus. The bacterium Bacillus thuringiensis (Bt) produces multiple toxins with activity against a diverse range of insects. In efforts to provide additional control methods for the ACP vector of HLB, we identified pesticidal proteins derived from Bt for toxicity against ACP. The trypsin proteolytic profiles of strain-derived toxins were characterized. Strain IBL-00200, one of six strains with toxins shown to have basal activity against ACP was selected for liquid chromatography-mass spectrometry (LC-MS/MS) identification of the individual Cry toxins expressed. Toxicity assays with individual toxins derived from IBL-00200 were then performed. The activated form of the Cry toxins Cry1Ab and Cry1Ba were toxic to ACP with LC50 values of approximately 120 µg/mL. Disruption of the midgut epithelium was associated with the toxicity of both the IBL-00200-derived toxin mixture, and with Cry1Ba. With further optimization of the efficacy of Cry1Ab and Cry1Ba, these toxins may have practical utility against ACP. Bt toxins with activity against ACP may provide an additional tool for management of ACP and the associated HLB disease, thereby providing a more sustainable and environmentally benign approach than repeated application of broad-spectrum insecticides.This article is published as Fernandez-Luna, Maria Teresa, Pavan Kumar, David G. Hall, Ashaki D. Mitchell, Michael B. Blackburn, and Bryony C. Bonning. "Toxicity of Bacillus thuringiensis-Derived Pesticidal Proteins Cry1Ab and Cry1Ba against Asian Citrus Psyllid, Diaphorina citri (Hemiptera)." Toxins 11, no. 3 (2019): 173. doi: 10.3390/toxins11030173.</p
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