Orientador: Alberto Luiz de Andrade / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Engenharia Quimica / Made available in DSpace on 2018-07-20T05:31:38Z (GMT). No. of bitstreams: 1 Ravagnani_MauroAntoniodaSilvaSa_D.pdf: 3963857 bytes, checksum: 25a55db7dbf16bd53e8bdc0243201327 (MD5) Previous issue date: 1994 / Resumo: Neste trabalho foi desenvolvido um programa computacional para síntese de redes de trocadores de calor incorporando o dimensionamento termohidráulico dos equipamentos. O programa desenvolvido utiliza os conceitos da chamada Tecnologia Pinch ("Pinch Technology"). Para a síntese da rede são definidos inicialmenteos seus objetivos com relação ao custo global mínimo, L / Abstract: In this work a computational program was developed interfacing heat exchanger network synthesis and detailed heat exchanger design. The program uses the concepts of Pinch Technology. To the network synthesis are defined initially the targets with respect to the global minimumcost, optimum ATmin, minimum exchange area, minimum number of units and the hot and cold utilities demand. The network is synthesized using the Pinch Design Method. After these, the network is evolved, identifying and breaking loops without changes in the utilities demand. After the evolution, the exchangers are designed considering pressure drop and fouling, using the Bell-Delaware method. The program was developed in modular form, and the utilization of each module is explained using literature problems. An industrial problem is used to show the applicability of the program developed. The results shown the consistency in the methodology reflecting the importance of the termohidraulic design in the heat exchanger network synthesis / Doutorado / Sistemas de Processos Quimicos e Informatica / Doutor em Engenharia Química

Aged HIV-positive (HIV+) individuals represent a large proportion of the HIV population as life spans are extended significantly by successful antiretroviral therapy. Increased age with HIV infection brings a unique set of central nervous system (CNS) complications including more rapid onset and progression of age-related diseases, loss of protein quality control and accumulation of aberrant proteins, such as hyperphosphorylated Tau (hpTau). In this context, we have discovered a new signaling connection between age-related neurodegeneration and HIV involving the PINCH protein. Particularly interesting new cysteine histidine-rich protein (PINCH), an adaptor protein in neuronal cells is involved in cytoskeletal organization, cell migration and cell survival. While some of the pathophysiological aspects of the PINCH-signaling cascade in tauopathy are largely conserved among neurodegenerative diseases such as Alzheimer’s disease, HIV and others, the presence of the HIV protein Tat impacts specific key points in the PINCH pathway that exacerbate CNS cell dysfunction. In virus-infected cells, Tat regulates viral replication. Even though neurons are not permissive to viral infection, the Tat protein can enter all cell types. Our studies show that Tat interferes with key PINCH signaling partners in neurons. PINCH is robustly expressed by neurons and to a lesser degree by astrocytes in HIV infection of the CNS; whereas, in the healthy CNS, PINCH is nearly undetectable. Similarly, protein phosphatase 1α (PP1α), one of the binding partners of PINCH, is increased in the neurons of HIV encephalitis patients and co-localizes with PINCH in neurons. PINCH is a non-catalytic scaffolding protein that binds integrin-linked kinase (ILK), and PP1α and mediates Akt and GSK3β kinase activities, all of which when disrupted contribute to aberrant Tau phosphorylation. In Tat transgenic mice, increased expression levels of PINCH, PP1α and hpTau were observed. Also, in vivo manipulations of expression levels of PINCH altered the levels of hpTau, where overexpression of PINCH increased hpTau levels in Tat transgenic mouse brains and PINCH knockdown decreased hpTau formation. Furthermore, our studies show that Tat increases levels of hpTau and PINCH, interacts with PP1α and changes the subcellular distribution of PINCH and PP1α in vitro. Tat alters the levels of ILK, Akt and GSK3β, which are key kinases associated with hpTau formation. Furthermore, our preliminary data using expression plasmid for PP1α also shows that overexpression of PP1α decreases Tat-induced aberrant hpTau formation. Our studies address HIV replication-independent functions of Tat in neurons linked to PINCH signaling. These studies address a novel pathway through which Tau may be aberrantly phosphorylated. Thus, understanding new pathways of communication among Tat, PINCH, PP1α, ILK and Tau will open new directions for the study of HIV-associated tauopathy and will provide opportunities for therapeutic interventions in age- and disease-related pathologies. Several studies report associations between the PINCH protein and HIV-associated CNS disease. PINCH is detected in the cerebrospinal fluid (CSF) of HIV patients and changes in levels during disease may be indicative of changes in disease status over time. PINCH binds hpTau in the brain and CSF, but little is known about the relevance of these interactions to HIV CNS disease. In this study, PINCH and hpTau levels were assessed in three separate CSF samples collected longitudinally from 20 HIV+ participants before and after initiating antiretroviral therapy, or before and after a change in the current regimen. Correlational analyses were conducted for CSF levels of PINCH and hpTau and other variables including plasma CD4+ T-cell count, plasma and CSF viral burden, CSF Neopterin, white blood cell (WBC) count, and antiretroviral CNS penetration-effectiveness (CPE). Results suggest that in these HIV participants, changes in CSF levels of PINCH appear to correlate with changes in plasma CD4+ count and with changes in CSF hpTau levels, but not with plasma or CSF viral burden, Neopterin, or WBC, or with anti-retroviral regimen CPE. Furthermore, results from our case matched HIV brain-CSF study confirms that higher levels of PINCH and hpTau are detected in HIV encephalitis brains. Additionally, correlation between PINCH and hpTau levels in brain and other clinical parameters such as age at death, date of death suggesting the era of antiretroviral therapy, CPE score and cognition in HIV patients yielded interesting results that are currently being expanded upon by investigators in the Langford laboratory. Thus, these results suggest that PINCH may be involved in Tauopathy associated neurodegeneration in the HIV CNS disease. Therefore, understanding the contribution of PINCH to HIV-associated Tauopathy may provide a new therapeutic avenue for regulating synaptodendritic dysfunction associated with Tau. Moreover, characterizing the clinical significance of PINCH in the CSF may warrant including PINCH as a member of biomarker panel to assess severity or progression of HIV-associated neurocognitive alterations. / Biomedical Neuroscience

The master’s thesis is focused on familiarization with modern techniques and procedures of process system engineering for identification of energy savings. In this case, process system engineering is applied to the issue of heat exchanger networks and in order to save energy, their retrofit is solved here. The current network pinch method, which uses mathematical programming options, is described for the retrofit of the heat exchanger networks. The method is presented in comparison to older development methods, mainly with the PDM. In addition, the calculation procedure is also developed by this method and in the Maple software environment it is applied to the case of heat exchanger network retrofit in the process of hydrogenation refining of oil. Part of the thesis is an evaluation of the results obtained, including a discussion of the properties of the method used.

The primary objective of fusion research is to realize a thermonuclear fusion power plant. The main method to confine the hot plasma is by using a magnetic field. The reversed-field pinch is a type of magnetic confinement device which suffers from variety of magnetohy- drodynamic (MHD) instabilities. A particular unstable mode that is treated in this work is the resistive wall mode (RWM), which occurs due to the current gradient in the RFP and has growth rates of the order of the magnetic diffusion time of the wall. Application of control engineering tools appears to allow a robust and stable RFP operation.A model-based approach to stabilize the RWMs is pursued in this thesis. The approach consists of empirical modeling of RWMs using a class of subspace identification methodology. The obtained model is then used as a basis for a model based controller. In particular the first experimental results of using a predictive control for RWM stabilization are obtained. It is shown that the formulation of the model based controller allows the user to incorporate several physics relevant phenomena along with the stabilization of RWM. Another use of the model is shown to estimate and compensate the inherent error field. The results are encouraging, and the methods appear to be generically useful as research tools in controlled magnetic confinement fusion. / Fusionsforskningens primära mål är att förverkliga en ny typ av kraftverk baserade på termonukleär fusion. Den viktigaste metoden för att innesluta det heta plasmat är användandet av  magnetfält. ”Reverserat-fält pinch” (RFP) är en typ av anläggning för magnetisk inneslutning av fusionsplasma som uppvisar ett flertal magneto-hydrodynamiska instabiliteter. En specifik instabil mod som behandlas i detta arbete är”resistiv-vägg” moden (RWM). Den orsakas av strömgradienten i RFPn och tillväxer med en tidskonstant som är av samma storleksordning som magnetfältets diffusionstid i det omgivande metallskalet.  Tillämpning av verktyg från reglerteknikområdet förefaller tillåta en robust och stabil RFP drift. I detta arbete används ett modell-baserat tillvägagångssätt för kompensering av RWM. Det innefattar empirisk modellering av RWM med användning av ”subspace” system-identifieringsmetoder. Den erhållna modellen används sedan som grund för en modell-baserad regulator. De första experimentella resultaten från modell-prediktiv kompensering av RWM har erhållits.  I detta arbete har också visats att formuleringen av den modellbaserade regulatorn tillåter användaren att integrera flera relevanta fysikaliska aspekter förutom RWM. Ytterligare en användning av modellen är för att göra uppskattning och kompensering av avvikelser i anläggningens magnetfält, så kallade fält-fel. Resultaten är uppmuntrande, och det förefaller som om de undersökta metoderna är allmänt användbara som verktyg för forskning om magnetisk inneslutning av fusionsplasma. / <p>QC 20170202</p>

In the Xenopus embryo, cell rearrangements during early development require the dynamic modulation of adhesion. Cells primarily use the integrin family of transmembrane receptors for attachment to and interpretation of the extracellular environment. While acting as adhesion receptors, integrins also have bidirectional signalling properties essential for driving cellular movements. The regulation of integrin activity is thought to stem from cytoplasmic assemblies of constitutively expressed molecules. PINCH (Particularly Interesting New cysteine-histidine rich protein), an adapter protein, is part of an IPP complex that has emerged as a key signalling scaffold indispensable for integrin function in vitro. As such, I tested the hypothesis that PINCH regulates integrin function in the Xenopus embryo. Xenopus PINCH was successfully cloned using RT-PCR. The predicted amino acid sequence of PINCH shares a 98% similarity with mammalian orthologs, and comprises of five highly conserved LIM domains. PINCH mRNA and protein are ubiquitously expressed throughout embryogenesis. In situ hybridization indicates that PINCH mRNA is expressed in the blastocoel roof and the pre-involution mesoderm. The localization and temporal expression of PINCH suggests a role in mediating cell adhesive events during gastrulation. A functional approach was used to examine the role of PINCH during gastrulation. I used site-directed mutagenesis to generate non-functional LIM1 (LIM1mut) and LIM4 (LIM4mut) domains that have been proposed to bind ILK and Grb4 respectively. Over-expression of PINCH leads to a delay in blastopore closures, while the expression of both LIM1mut and LIM4mut relieve this inhibition at lower concentrations. Further analysis indicates that PINCH, LIM1mut, and LIM4mut inhibit FN matrix assembly independent of integrin adhesion. Contradictory to in vitro studies, co-immunoprecipitation analysis indicates that endogenous PINCH does not bind ILK, confirming an integrin-independent role during gastrulation. Furthermore, in the embryo PINCH is found at cell boundaries but does not appear to directly modulate cadherin adhesion. As such this thesis provides evidence that PINCH regulates cell intercalation movements independent of integrin and cadherin receptors and raises the possibility that the LIM4 domain is involved in PINCH regulation of cell adhesion during early development.

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 186-193).

No description available.

In the Xenopus embryo, cell rearrangements during early development require the dynamic modulation of adhesion. Cells primarily use the integrin family of transmembrane receptors for attachment to and interpretation of the extracellular environment. While acting as adhesion receptors, integrins also have bidirectional signalling properties essential for driving cellular movements. The regulation of integrin activity is thought to stem from cytoplasmic assemblies of constitutively expressed molecules. PINCH (Particularly Interesting New cysteine-histidine rich protein), an adapter protein, is part of an IPP complex that has emerged as a key signalling scaffold indispensable for integrin function in vitro. As such, I tested the hypothesis that PINCH regulates integrin function in the Xenopus embryo. Xenopus PINCH was successfully cloned using RT-PCR. The predicted amino acid sequence of PINCH shares a 98% similarity with mammalian orthologs, and comprises of five highly conserved LIM domains. PINCH mRNA and protein are ubiquitously expressed throughout embryogenesis. In situ hybridization indicates that PINCH mRNA is expressed in the blastocoel roof and the pre-involution mesoderm. The localization and temporal expression of PINCH suggests a role in mediating cell adhesive events during gastrulation. A functional approach was used to examine the role of PINCH during gastrulation. I used site-directed mutagenesis to generate non-functional LIM1 (LIM1mut) and LIM4 (LIM4mut) domains that have been proposed to bind ILK and Grb4 respectively. Over-expression of PINCH leads to a delay in blastopore closures, while the expression of both LIM1mut and LIM4mut relieve this inhibition at lower concentrations. Further analysis indicates that PINCH, LIM1mut, and LIM4mut inhibit FN matrix assembly independent of integrin adhesion. Contradictory to in vitro studies, co-immunoprecipitation analysis indicates that endogenous PINCH does not bind ILK, confirming an integrin-independent role during gastrulation. Furthermore, in the embryo PINCH is found at cell boundaries but does not appear to directly modulate cadherin adhesion. As such this thesis provides evidence that PINCH regulates cell intercalation movements independent of integrin and cadherin receptors and raises the possibility that the LIM4 domain is involved in PINCH regulation of cell adhesion during early development.

Thesis (Ph. D.)--University of Nevada, Reno, 2007. / "May, 2007." Includes bibliographical references (leaves 213-218). Online version available on the World Wide Web.

abstract: Semiconductor devices are generally analyzed with relatively simple equations or with detailed computer simulations. Most text-books use these simple equations and show device diagrams that are frequently very simplified and occasionally incorrect. For example, the carrier densities near the pinch-off point in MOSFETs and JFETs and the minority carrier density in the base near the reverse-biased base-collector junction are frequently assumed to be zero or near zero. Also the channel thickness at the pinch-off point is often shown to approach zero. None of these assumptions can be correct. The research in thesis addresses these points. I simulated the carrier densities, potentials, electric fields etc. of MOSFETs, BJTs and JFETs at and near the pinch-off regions to determine exactly what happens there. I also simulated the behavior of the quasi-Fermi levels. For MOSFETs, the channel thickness expands slightly before the pinch-off point and then spreads out quickly in a triangular shape and the space-charge region under the channel actually shrinks as the potential increases from source to drain. For BJTs, with collector-base junction reverse biased, most minority carriers diffuse through the base from emitter to collector very fast, but the minority carrier concentration at the collector-base space-charge region is not zero. For JFETs, the boundaries of the space-charge region are difficult to determine, the channel does not disappear after pinch off, the shape of channel is always tapered, and the carrier concentration in the channel decreases progressively. After simulating traditional sized devices, I also simulated typical nano-scaled devices and show that they behave similarly to large devices. These simulation results provide a more complete understanding of device physics and device operation in those regions usually not addressed in semiconductor device physics books. / Dissertation/Thesis / M.S. Electrical Engineering 2011