Study of Thermo--Oxidative Stabilization for Strips and Bundles of Polyacrylonitrile Fibers

Stabilization is one of the expensive and critical steps in the manufacture of carbon fibers. It involves complex chemical reactions and physical structure changes. Modeling and simulation are successfully utilized in order to know the stabilization behavior and minimize the cost of experimental tests. In this work a mathematical model of stabilization step is presented for a polyacrylonitrile strip. Differential equations describe the chemical reactions, oxygen diffusion and heat transfer occurring inside the strip. They are resolved by Orthogonal Collocation and Semi implicit Runge - Kutta Method. The results of temperatures and concentrations profiles as a function of the stabilization time are analyzed and compared with a simulation obtained for a bundle of polyacrylonitrile fibers. This investigation indicates that heat transfer in the strip is better than in the bundle and consequently the exothermic reactions are controlled.Os estudos relacionados ao processo de fabricação de fibras de carbono indicam que a etapa de estabilização termo-oxidativa das fibras precursoras é limitante, envolvendo reações químicas complexas e mudanças na estrutura física das fibras. Com o objetivo de se conhecer melhor a etapa de estabilização e eliminar gastos em testes experimentais, a modelagem e a simulação surgem para tentar otimizar este processo. Apresenta-se neste trabalho um modelo matemático para a etapa de estabilização de uma fita de fibras de poliacrilonitrila. As equações do modelo descrevem as principais reações químicas de estabilização, a difusão de oxigênio e a transferência de calor na fita. Para a resolução do modelo foi desenvolvido um programa computacional na linguagem Fortran, utilizando os métodos de Colocação Ortogonal e Runge¾ Kutta Semi-implícito. Foram obtidos resultados de temperaturas e concentrações na fita de fibras de poliacrilonitrila em função do tempo de estabilização e da posição na espessura da fita. Estes resultados foram analisados e comparados com os simulados em um feixe de fibras de poliacrilonitrila e indicaram que a transferência de calor na fita é melhor do que no feixe e conseqüentemente as reações exotérmicas são mais controladas.171179Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP

Changes in Glucose and Glutamine Lymphocyte Metabolisms Induced by Type I Interferon α

In lymphocytes (LY), the well-documented antiproliferative effects of IFN-α are associated with inhibition of protein synthesis, decreased amino acid incorporation, and cell cycle arrest. However, the effects of this cytokine on the metabolism of glucose and glutamine in these cells have not been well investigated. Thus, mesenteric and spleen LY of male Wistar rats were cultured in the presence or absence of IFN-α, and the changes on glucose and glutamine metabolisms were investigated. The reduced proliferation of mesenteric LY was accompanied by a reduction in glucose total consumption (35%), aerobic glucose metabolism (55%), maximal activity of glucose-6-phosphate dehydrogenase (49%), citrate synthase activity (34%), total glutamine consumption (30%), aerobic glutamine consumption (20.3%) and glutaminase activity (56%). In LY isolated from spleen, IFNα also reduced the proliferation and impaired metabolism. These data demonstrate that in LY, the antiproliferative effects of IFNα are associated with a reduction in glucose and glutamine metabolisms

SCI1 Is a Direct Target of AGAMOUS and WUSCHEL and Is Specifically Expressed in the Floral Meristematic Cells

The specified floral meristem will develop a pre-established number of floral organs and, thus, terminate the floral meristematic cells. The floral meristematic pool of cells is controlled, among some others, by WUSCHEL (WUS) and AGAMOUS (AG) transcription factors (TFs). Here, we demonstrate that the SCI1 (Stigma/style cell-cycle inhibitor 1) gene, a cell proliferation regulator, starts to be expressed since the floral meristem specification of Nicotiana tabacum and is expressed in all floral meristematic cells. Its expression is higher in the floral meristem and the organs being specified, and then it decreases from outside to inside whorls when the organs are differentiating. SCI1 is co-expressed with N. tabacum WUSCHEL (NtWUS) in the floral meristem and the whorl primordia at very early developmental stages. Later in development, SCI1 is co-expressed with NAG1 (N. tabacum AG) in the floral meristem and specialized tissues of the pistil. In silico analyses identified cis-regulatory elements for these TFs in the SCI1 genomic sequence. Yeast one-hybrid and electrophoresis mobility shift assay demonstrated that both TFs interact with the SCI1 promoter sequence. Additionally, the luciferase activity assay showed that NAG1 clearly activates SCI1 expression, while NtWUS could not do so. Taken together, our results suggest that during floral development, the spatiotemporal regulation of SCI1 by NtWUS and NAG1 may result in the maintenance or termination of proliferative cells in the floral meristem, respectively.Fil: Cruz, Joelma O.. Universidade de Sao Paulo; BrasilFil: Abramo Barrera San Martin, Juca. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Botánica Darwinion. Academia Nacional de Ciencias Exactas, Físicas y Naturales. Instituto de Botánica Darwinion; Argentina. Universidade de Sao Paulo; BrasilFil: Lubini, Greice. Universidade de Sao Paulo; BrasilFil: Strini, Edward J.. Universidade de Sao Paulo; BrasilFil: Sobral, Rómulo. Universidade do Minho; PortugalFil: Pinoti, Vitor F.. Universidade de Sao Paulo; BrasilFil: Ferreira, Pedro B.. Universidade de Sao Paulo; BrasilFil: Thomé, Vanessa. Universidade de Sao Paulo; BrasilFil: Quiapim, Andréa C.. Universidade de Sao Paulo; BrasilFil: Dornelas, Marcelo C.. Universidade Estadual de Campinas; BrasilFil: Pranchevicius, Maria Cristina S.. Universidade Federal do São Carlos; BrasilFil: Madueño, Francisco. Consejo Superior de Investigaciones Científicas; EspañaFil: Costa, M. Manuela R.. Universidade do Minho; PortugalFil: Goldman, Maria Helena S.. Universidade de Sao Paulo; Brasi

Coinfection with Different Trypanosoma cruzi Strains Interferes with the Host Immune Response to Infection

A century after the discovery of Trypanosoma cruzi in a child living in Lassance, Minas Gerais, Brazil in 1909, many uncertainties remain with respect to factors determining the pathogenesis of Chagas disease (CD). Herein, we simultaneously investigate the contribution of both host and parasite factors during acute phase of infection in BALB/c mice infected with the JG and/or CL Brener T. cruzi strains. JG single infected mice presented reduced parasitemia and heart parasitism, no mortality, levels of pro-inflammatory mediators (TNF-α, CCL2, IL-6 and IFN-γ) similar to those found among naïve animals and no clinical manifestations of disease. On the other hand, CL Brener single infected mice presented higher parasitemia and heart parasitism, as well as an increased systemic release of pro-inflammatory mediators and higher mortality probably due to a toxic shock-like systemic inflammatory response. Interestingly, coinfection with JG and CL Brener strains resulted in intermediate parasitemia, heart parasitism and mortality. This was accompanied by an increase in the systemic release of IL-10 with a parallel increase in the number of MAC-3+ and CD4+ T spleen cells expressing IL-10. Therefore, the endogenous production of IL-10 elicited by coinfection seems to be crucial to counterregulate the potentially lethal effects triggered by systemic release of pro-inflammatory mediators induced by CL Brener single infection. In conclusion, our results suggest that the composition of the infecting parasite population plays a role in the host response to T. cruzi in determining the severity of the disease in experimentally infected BALB/c mice. The combination of JG and CL Brener was able to trigger both protective inflammatory immunity and regulatory immune mechanisms that attenuate damage caused by inflammation and disease severity in BALB/c mice

Regulatory T Cells Phenotype in Different Clinical Forms of Chagas' Disease

CD25High CD4+ regulatory T cells (Treg cells) have been described as key players in immune regulation, preventing infection-induced immune pathology and limiting collateral tissue damage caused by vigorous anti-parasite immune response. In this review, we summarize data obtained by the investigation of Treg cells in different clinical forms of Chagas' disease. Ex vivo immunophenotyping of whole blood, as well as after stimulation with Trypanosoma cruzi antigens, demonstrated that individuals in the indeterminate (IND) clinical form of the disease have a higher frequency of Treg cells, suggesting that an expansion of those cells could be beneficial, possibly by limiting strong cytotoxic activity and tissue damage. Additional analysis demonstrated an activated status of Treg cells based on low expression of CD62L and high expression of CD40L, CD69, and CD54 by cells from all chagasic patients after T. cruzi antigenic stimulation. Moreover, there was an increase in the frequency of the population of Foxp3+ CD25HighCD4+ cells that was also IL-10+ in the IND group, whereas in the cardiac (CARD) group, there was an increase in the percentage of Foxp3+ CD25High CD4+ cells that expressed CTLA-4. These data suggest that IL-10 produced by Treg cells is effective in controlling disease development in IND patients. However, in CARD patients, the same regulatory mechanism, mediated by IL-10 and CTLA-4 expression is unlikely to be sufficient to control the progression of the disease. These data suggest that Treg cells may play an important role in controlling the immune response in Chagas' disease and the balance between regulatory and effector T cells may be important for the progression and development of the disease. Additional detailed analysis of the mechanisms on how these cells are activated and exert their function will certainly give insights for the rational design of procedure to achieve the appropriate balance between protection and pathology during parasite infections