No description available.

O presente trabalho investigou como a natureza de um líquido iônico pode influenciar a formação e o crescimento de nanopartículas de [Rh(0)], bem como estabeleceu o desempenho catalítico das nanopartículas obtidas em reações de hidrogenação de arenos. A simples redução de compostos de ródio RhCl3.3H2O, [Rh(cod)Cl]2 e [Rh(cod)2]X (X = BF4 -, CF3SO3 - e cod = 1,5-ciclooctadieno), dispersas em líquidos iônicos tetrafluoroborato (BF4 -), hexafluorofosfato (PF6 -) e trifluorometanosulfonato (CF3SO3 -) de 1- n-butil-3-metilimidazólio (BMI+), com hidrogênio molecular, rendeu nanopartículas de [Rh(0)], isoladas como pó escuro. As nanopartículas de [Rh(0)] formadas nos três líquidos iônicos foram caracterizadas por Microscopia Eletrônica de Transmissão (MET), Difração de Raios X (DRX) e Espectroscopia de Fotoelétrons de Raios X (XPS). O tamanho médio e a dispersão de tamanho destas nanopartículas depende pouco do precursor de ródio e mais do líquido iônico empregado. O tamanho médio das nanopartículas geradas em BMI.BF4 centram-se em 2,8 nm e em contraste, tamanhos médios maiores foram observados para nanopartículas de [Rh(0)] obtidas em BMI.PF6 (4,7 nm) e em BMI.CF3SO3 (5,0 nm). A atividade catalítica destas nanopartículas em reações de hidrogenação de arenos depende tanto da natureza do precursor quanto do líquido iônico empregado para prepará-las. Independentemente da natureza do líquido iônico, nanopartículas progressivamente mais ativas foram obtidas, primeiro, mudando o precursor na seqüência [Rh(cod)Cl]2 < [Rh(cod)2]CF3SO3 < RhCl3.3H2O < [Rh(cod)2]BF4 e, segundo, mudando o líquido iônico na sequência BMI.CF3SO3 < BMI.PF6 < BMI.BF4. É digno de nota, que as nanopartículas de [Rh(0)] obtidas pela combinação de [Rh(cod)2]BF4 / BMI.BF4 mostraram, na hidrogenação do benzeno, atividade catalítica similar à amostra de Rh/C.

O presente trabalho investigou como a natureza de um líquido iônico pode influenciar a formação e o crescimento de nanopartículas de [Rh(0)], bem como estabeleceu o desempenho catalítico das nanopartículas obtidas em reações de hidrogenação de arenos. A simples redução de compostos de ródio RhCl3.3H2O, [Rh(cod)Cl]2 e [Rh(cod)2]X (X = BF4 -, CF3SO3 - e cod = 1,5-ciclooctadieno), dispersas em líquidos iônicos tetrafluoroborato (BF4 -), hexafluorofosfato (PF6 -) e trifluorometanosulfonato (CF3SO3 -) de 1- n-butil-3-metilimidazólio (BMI+), com hidrogênio molecular, rendeu nanopartículas de [Rh(0)], isoladas como pó escuro. As nanopartículas de [Rh(0)] formadas nos três líquidos iônicos foram caracterizadas por Microscopia Eletrônica de Transmissão (MET), Difração de Raios X (DRX) e Espectroscopia de Fotoelétrons de Raios X (XPS). O tamanho médio e a dispersão de tamanho destas nanopartículas depende pouco do precursor de ródio e mais do líquido iônico empregado. O tamanho médio das nanopartículas geradas em BMI.BF4 centram-se em 2,8 nm e em contraste, tamanhos médios maiores foram observados para nanopartículas de [Rh(0)] obtidas em BMI.PF6 (4,7 nm) e em BMI.CF3SO3 (5,0 nm). A atividade catalítica destas nanopartículas em reações de hidrogenação de arenos depende tanto da natureza do precursor quanto do líquido iônico empregado para prepará-las. Independentemente da natureza do líquido iônico, nanopartículas progressivamente mais ativas foram obtidas, primeiro, mudando o precursor na seqüência [Rh(cod)Cl]2 < [Rh(cod)2]CF3SO3 < RhCl3.3H2O < [Rh(cod)2]BF4 e, segundo, mudando o líquido iônico na sequência BMI.CF3SO3 < BMI.PF6 < BMI.BF4. É digno de nota, que as nanopartículas de [Rh(0)] obtidas pela combinação de [Rh(cod)2]BF4 / BMI.BF4 mostraram, na hidrogenação do benzeno, atividade catalítica similar à amostra de Rh/C.

Syftet med vår studie var att, utifrån en läromedelsanalys, belysa hur olika läromedlen presenterar räknesättet subtraktion med tiotalsövergång inom talområdet 0–20. Studien syftade likaså till att undersöka vilka representationsformer som används i matematikböckernas uppgifter för att representera subtraktion samt identifiera kritiska aspekter som kan förekomma. Representationsformerna som användes är bild, konkret modell, symbol, språk och verklighet. Studien utgick från en kvalitativ metod där analyserna utfördes med hjälp av innehållsanalyser. Läromedelsanalyserna genomfördes utifrån variationsteorin där stor vikt lades vid att undersöka vilka representationsformer som förekommer i läroböckerna samt på vilka sätt de framställer matematikområdet subtraktion med tiotalsövergång. Det urval som gjorts för studien var läromedel för årskurs 1 samt att båda skulle vara publicerade efter Läroplan för grundskolan, förskoleklassen och fritidshemmet 2011. Resultatet visade att läromedlen hade en bred variation av representationsformer men att den konkreta modellen inte återfinns i något av läromedlen. De representationsformer som var mest framtränade för att förtydliga subtraktionsbegreppet var språk och symbol. Representationsformerna bild och verklighet förekom likaså i relativt stor utsträckning. Utifrån analyserna av läromedlen kan resultatet bidra till en medvetenhet kring eventuella brister samt hur dessa kan kompletteras i undervisningen, i koppling till subtraktion med tiotalsövergång.

Let A be an m x n, (0, 1)-matrix. A submatrix of A is odd if the sum of its entries is an odd integer and even otherwise. The maximum number of 2 x 2 odd submatrices in a (0, 1)-matrix is related to the existence of Hadamard matrices and bounds on Turán numbers. Pinelis [On the minimal number of even submatrices of 0-1 matrices, Designs, Codes and Cryptography, 9:85-93, 1994] exhibits an asymptotic formula for the minimum possible number of p x q even submatrices of an m x n (0, 1)-matrix. Assuming the Hadamard conjecture, specific techniques are provided on how to assign the 0's and 1's, in order to yield the maximum number of 2 x 2 odd submatrices in an m x n (0, 1)-matrix. Moreover, formulas are determined that yield the exact maximum counts with one exception, in which case upper and lower bounds are given. These results extend and refine those of Pinelis.

No description available.

<P> A study has been made of the transformation of deoxidation products in the Fe-V-0 system in the temperature range 1545 -1640°C, using galvanic cells with solid electrolytes. The cells used were in the form of Zr02 (caO) immersion probes and Th02(Y2o2) crucible assemblies. The fields of study of Fev2o4(spinel) and v2o3 were established with respect to oxygen activity and temperature. </p> / Thesis / Master of Engineering (MEngr)

<p> 0-GlcNAc modification is a single N-acetylglucosamine (GlcNAc) modification on Ser or Thr residue on protein. The addition and removal of the 0GlcNAc molecule are controlled by two enzymes (OGT and NCOAT). In this study, I expressed and purified the two enzymes involved in the 0-GlcNAc modification. A method was developed for the synthesis and purification of the peptide substrate YSDSPSTST for in vitro glycosylation and characterized the OGT enzyme activity by the in vitro glycosylation and H3 labeling. A method was developed based on detection of glycosylation peptide by mass spectrometry after separation by capillary liquid chromatography (CapLC). The optimization of mass spectrometry parameters was done using synthesized standard glycopeptide YSDSPSgTST ("Sg" represents 0-GlcNAc modified Serine). The in vitro modification site was determined by CID after alkaline J3-elimination. Furthers experiment could include detection of 0-GlcNAc modification of protein substrate both in vitro and in vivo. This will give a better understanding of the dynamics of 0-GlcNAc modification. </p> / Thesis / Master of Science (MSc)

Cells respond to their environment through dynamic posttranslational modification of their existing proteins. There are more than 20 posttranslational modifications that occur on eukaryotic proteins. Several of these modifications, with phosphorylation being the hallmark, participate in signal transduction. Generally, glycosylation is not thought to participate directly in signaling. Complex N-and 0-linked glycosylation occurs on membrane-bound or secreted proteins that are synthesized in the endoplasmic reticulum and Golgi apparatus. The lumenal or extracellular localization ofthese glycans restricts their potential for dynamic responsiveness to signals. In contrast, 0-GlcNAc is a simple monosaccharide modification that is abundant on serine or threonine residues ofnucleocytoplasmic proteins. An 0-GlcNAc site consensus motif has not yet been identified. However, many attachment sites are identical to those used by serine/threonine) kinases, and a neural network program has been developed to predict 0GlcNAc sites. The dynamic glycosylation of serine or threonine residues on nuclear and cytosolic proteins by 0-linked beta-N-acetylglucosamine (0-GlcNAc) is abundant in all multicellular eukaryotes. On several proteins, 0-GlcNAc and 0-phosphate alternatively occupy the same or adjacent sites, leading to the hypothesis that one function of this saccharide is to transiently block phosphorylation. Many proteins have been identified that carry this modification, including transcription factors, cytoskeletal proteins, nuclear pore proteins, oncogene products, and tumor suppressors. 0-GlcNAc appears to modify a large number of nucleocytoplasmic proteins· One of important regulatory proteins on which this project concentrates is β-catenin. Here, we examined where does this type ofposttranslational modification takes place on the protein. Our results indicated that P-catenin is 0-glycosylated on both the N-terminus and Cterminus, but not at the ARMADILLO segment. Further, we show that the known phosphorylation sites located at theN-terminal "destruction box" of this protein are not involved in 0-glycosylation. Furthermore, we demonstrated that the threonines adjacent to phosphorylation-site Threonin41 are not essential in 0-glycosylation process. In addition, treatment ofprostate cancer lines with PUGNAc, a non-cytotoxic reversible inhibitor ofOGlcNAcase, caused a decrease in the expression oftransfected P-catenin in the nucleus with increasing cellular 0-glycosylation ofthe protein suggesting that 0-glycosylation was hindering P-catenin's nuclear translocation. Additional studies showed that 0-glycosylation of P-catenin decreased transcriptional activity of a TopFlash reporter plasmid. In summary, our results show that P-catenin is 0-glycosylated on theN-and C-terminus, but not on ARMADILLO segment, and that phosphorylation sites are not the critical for 0-glycosylation. Furthermore, our data show that 0-glycosylation of P-catenin may represent a novel mechanism important in the regulation of the nuclear localization and transcriptional activity of P-catenin. / Thesis / Master of Science (MSc)

Herpes simplex virus 1 (HSV-1) is a double-stranded DNA virus, often acquired during childhood, that currently infects more than 50% of the human population. The symptoms of infection are herpetic lesions that frequently appear throughout a host's life in response to stress in the orofacial or genital region. As a pathogen, HSV-1 replicates rapidly in epithelial cells, but it is also capable of infecting neurons where it can pursue a lytic or latent infection. Latency is a state of viral quiescence where the virus can persist indefinitely yet remain poised to reactivate. Latency is unique to herpesviruses and key to HSV's success, but the molecular mechanisms that govern this state are unclear. A virus-encoded E3-ubiquitin ligase, Infected Cell protein 0 (ICP0), is often correlated with latency establishment but is detected in opposition to the state of latency. During lytic infection, ICP0 has many biological roles but primarily catalyzes the addition of ubiquitin to target substrate, marking proteins for degradation or altering their function. This ubiquitination ability allows ICP0 to alter the intracellular environment making neurons conducive to lytic or latent HSV-1 infection. ICP0's neuron-specific targets, however, are unknown, representing a significant gap in knowledge. Through the studies presented in this dissertation, we identified some of the neuron-specific ubiquitination targets of ICP0 in neurons. We utilized primary adult sensory neurons of the dorsal root ganglia and HSV-1 viral strains KOS, wild-type virus encoding a fully functional ICP0, and HSV-1 n212, encoding a truncated ICP0 protein, to illuminate the mechanisms involved in establishing and maintaining HSV latency. By using adult primary neurons and functional HSV-1 strains with and without ICP0, we were able to show that ICP0 regulates host and viral proteins during the initial onset of neuronal infection. We also show that based on neuronal conditions set forth before HSV-1 initial infection, host proteins will influence HSV-1 viral proteins to repress viral gene expression, thereby promoting the establishment of latency. / Doctor of Philosophy / Herpes simplex virus (HSV-1) is a virus, often acquired during childhood, that more than 50% of people have. Those who are infected with HSV-1 often have cold sores that appear in response to stress on the face or on the genitals. As a virus, HSV-1 replicates around the eyes, nose, and mouth but can also infect neurons where it can continue to replicate or establish latency. Latency is when the virus is inside the neurons but is unnoticeable and can reappear in response to stress. The state of latency is unique to herpesviruses and key to the success of HSV-1, but scientists are unsure of how it works. A protein made by the virus, Infected Cell Protein 0 (ICP0), is often correlated with the state of latency but is often present when the virus is not latent. ICP0 does a lot to support HSV-1, but it primarily destroys proteins that prevent the virus from replicating. By destroying proteins that prevent HSV-1 replication, ICP0 can help the virus make more viruses. The proteins that are destroyed by ICP0 are currently unknown, which represents a significant gap in knowledge. Through the research conducted in this dissertation, we identified some of the proteins that ICP0 destroys in neurons. We utilized neurons from the dorsal root ganglia and HSV-1 viral strain KOS, which encoded a functional ICP0, and n212, which encodes a nonfunctional ICP0, to study the mechanisms used by the virus to infect neurons. By using HSV-1 viruses with and without ICP0, we were able to show what proteins ICP0 destroys during infection in neurons. We were also able to show that HSV-1's ability to establish latency is dependent on how the neurons handle the initial onset of infection. Overall, a combination of host and viral proteins coordinates the virus's ability to establish latency and persist within a host.