During the last two decades, the applications of fluorocarbon based chemicals to provide soil resistant or soil release properties for automotive interior and upholstery have increased tremendously. But, recent studies showed that the soil resistant treatment based on fluorochemicals has detrimental effects on the environment as well as on humans due to the presence of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) content. PFOS and PFOA are toxic, bio accumulative and bio persistent fluoro-organic compounds. This project focus on PFOS and PFOA-free soil resistant chemicals and their application on interior textiles used for automotive. Literature study was done by keeping in mind all the aspects regarding soil and nature of soils, soil resistant mechanism, PFOA and PFOS-free soil resistant chemicals, chemistry of the chemicals, area of the application and the method of application. Experimental application of PFOA and PFOS-free soil resistant chemicals by using different concentrations on 100% Polyester dyed and unfinished fabric was performed with Pad-Dry-Cure method. Experimental application was carried out to evaluate the soil resistant treated samples for soil resistant, clean ability and colour change results. At the end, the comparison of the results of three mentioned evaluations gave us the best possible alternatives. / Program: Magisterutbildning i textilteknologi

Post-operative ileus (POI) is the functional inhibition of propulsive intestinal motility which is a frequent occurrence following abdominal surgery in the horse and in humans. Rodent and human-derived data have shown that manipulation-induced activation of the resident muscularis externa (ME) macrophages in the intestine contributes to the pathophysiology of the disease. Most studies of the disease, specifically in the horse, have focussed on identification of risk factors, descriptive studies of the disease or the assessment of the efficacy of various therapeutic and prophylactic interventions. As a result, the proposed pathogenesis of equine POI is largely reliant on the translation of data from rodent models. The aims of this thesis were to identify macrophage populations in the normal equine gastrointestinal tract (GIT) and to study equine macrophage activation by stimulating equine bone marrow-derived macrophages (eqBMDMs) with lipopolysaccharide (LPS) as a model for intestinal macrophage activation. Firstly, the normal population of macrophages in the equine GIT was determined. Using CD163 as an immunohistochemical marker for macrophages. CD163+ve cells were present in all tissue layers of the equine intestine: mucosa, submucosa, ME and serosa. CD163+ve cells were regularly distributed within the ME, with accumulations adjacent to the myenteric plexus, and therefore to intestinal motility effector cells such as neurons and the Interstitial Cells of Cajal. The differentiation and survival of intestinal macrophages depends upon signals from the macrophage colony-stimulating factor (CSF-1) receptor. LPS translocation from the gut lumen is thought to be a key activator of ME macrophages. To provide a model for gut macrophages, a protocol was optimised to produce pure populations of equine bone marrow-derived macrophages (eqBMDMs) by cultivation of equine bone marrow in CSF-1. Macrophage functionality was assessed using microscopy, flow cytometry and phagocytosis assays. EqBMDMs responded to LPS stimulation with increases in expression of positive control genes, tumour necrosis factor alpha (TNF-α) and Indoleamine 2,3-dioxygenase (IDO1). The same mRNA was subjected to transcriptomic (RNA-Seq) analysis. Differential gene expression and network cluster analysis demonstrated an inflammatory response characterised by the production of pro-inflammatory cytokines such as interleukin 1 beta (IL-1β) and interleukin 6 (IL-6). However, in contrast to rodent macrophages, eqBMDMs failed to produce nitric oxide in response to LPS, showing species-specific variation in innate immune biology. Using these data, we compared gene expression in normal equine intestine and in intestine from horses undergoing abdominal surgery for colic (abdominal pain). Horses undergoing abdominal surgery showed evidence of increased expression of IL-1β, IL-6 and TNF-α in the mucosa and ME when compared to control tissue. Horses with post-operative reflux (POR), a clinical sign of POI, had increased gene expression of IL-1β, IL-6 and TNF-α compared to horses that did not develop POR following abdominal surgery. These preliminary data suggest that there is macrophage activation within the ME of the intestine during abdominal surgery in the horse, and that a greater activation state is present in horses that subsequently develop POR. The final part of this study was to investigate the effect of a long-acting form of CSF- 1, an Fc fusion protein (CSF1-Fc), as a potential treatment for POI using a mouse model. This work, performed in collaboration with another research group, found that mice lacking the C-C chemokine receptor type 2 (CCR2) gene, which is required for monocyte recruitment into tissues, had a longer recovery period following intestinal manipulation (IM) than wild type (WT) mice. With the administration of CSF1-Fc, infiltration of neutrophils to the ME was reduced and the number of macrophages in the ME was increased in both WT and CCR2-/- mice following IM. Administration of CSF1-Fc in CCR2-/- mice improved recovery of gastrointestinal transit three days following IM, to the same extent as WT mice. Network cluster analysis and RT-qPCR of the ME revealed clusters of genes induced and downregulated by CSF1-Fc, with increased expression of anti-inflammatory and pro-resolving genes after IM in WT and CCR2-/- mice following treatment with CSF1-Fc.

This research explores the relationship between intention and actual usage of self-service technology (SST), and investigates the effects of facilitating conditions and customer readiness on customer adoption of SST. In recent years, self-service technologies have created many new service contents; nevertheless, the actual utilization is not actually common yet. Therefore, this research try to explore the relationship between customer readiness and facilitating conditions on the actual use of SST, then focus on narrowing the gap between intention to use SST and actual usage of SST. We believe that this understanding is imperative for service providers to make proactive strategies for fostering customers’ intention and actual usage of the SST. The framework makes it possible to understand and predict customer trial related to using self-service technology by thoroughly examining underlying customer readiness degree and use the internet to illustrate how our framework can be applied to study customer behavior related to a specific self-service technology. To analyze the longitudinal effect, a two-stage survey was conducted and lasted for seven months. As it is well known that behavior intention does not necessary lead to actual behavior, our findings offer proactive strategies to service providers in turning intention into actual usage. Implications are discussed for managerial strategy as well as for future research. The research can be referred as marketing strategy for self-service or kiosk industry, and on academic contribution of narrowing the gap between intention and actual use. It is expected that it is helpful to facilitate self-service development and to enrich customer experience and competitiveness in Taiwan.

<p>Syftet med denna studie är att undersöka och diskutera samtidens porträttering av maskulinitet och avvikelser inom populärkulturen. För att genomföra denna studie analyseras två olika teveserier varav den ena är en dokusåpa och den andra en dramaserie. Båda serierna uppstod vid en och samma tidpunkt på olika delar av världen. Den likhet som fanns mellan dem var att de porträtterade framväxten av en och samma fenomen, nördar som ny manlighet. Analysen genomförs utifrån teoretiska verktyg med grund inom remedering samt teorier om immersivitet och manlighet men även en återkoppling till begreppet freakshow. Uppsatsen är förankrad för att lyfta fram tankar och aspekter kring framväxt av den manliga identiteten men även väcka nya diskussioner.</p> / <p>The purpose of this study is to examine and discuss the current ways of portraying masculinity and deviations within popular culture. For this study, I’ve focused on two different sources, one being a reality-show and the other being a fictional series. Both of these series aired for the first time during 2005, though not in the same country. Despite the distance, both of these series portrayed the appearance of new masculinity, in this case, the fact of being a nerd as a new masculinity. The analysis focuses on examining the series with roots in the remediation theories as well as concepts of the immersive media and masculinity. Also, placing these series in a context where they can be compared to the late freakshow phenomena. This study aims to bring up thoughts around appearances of masculine standards as well as plant seeds for future discussions.</p>

<p>Antibodies have the ability to influence the antibody response against the very antigen they are specific for, in a process called antibody feedback regulation. Depending on the nature of the antigen, the antibody response can be either enhanced or almost completely inhibited. This thesis focuses on the underlying mechanisms of antibody feedback regulation <i>in vivo</i>. </p><p>Antigen-specific IgG can inhibit the antibody response to a particulate antigen. Based on its ability to inhibit B cell activation, the inhibitory FcγRIIB (low affinity receptor for IgG) has been suggested to be involved. Here we show that although FcγRIIB is required for efficient suppression<i> in vitro, </i>it is not required <i>in vivo</i>. Therefore, even though FcγRIIB can inhibit antibody responses, other mechanisms (such as epitope masking and enhanced antigen clearance) play a more dominant role<i> in vivo</i>.</p><p>The antibody response to soluble antigen is greatly enhanced when it is introduced to the immune system in complex with antigen-specific IgG or IgE. We found that FcγRIIB attenuates the magnitude of IgG-mediated enhancement. In mice lacking FcγRIIB, IgG enhanced the antibody response much more efficiently than in normal mice.</p><p>Since B cells require CD4⁺ T cell help in order to become antibody-producing cells, we examined the CD4⁺ T cell response to immune complexes <i>in vivo</i>. Using an adoptive transfer strategy with transgenic ovalbumin (OVA)-specific CD4⁺T cells, we could show that the enhanced OVA-specific IgG response to IgG2a/OVA and IgE/OVA complexes was preceded by a potent OVA-specific CD4⁺ T cell response. IgG2a-mediated enhancement was dependent on activating Fcγ receptors, whereas IgE-mediated enhancement was dependent on CD23, the low affinity receptor for IgE. We identified CD23⁺ B cells as the responsible effector cells for IgE-mediated enhancement<i> in vivo</i>. Taken together, these results show that Fc receptor-mediated antigen presentation is a major mechanism underlying antibody feedback enhancement. </p>

<p>Antibodies, passively administered or actively produced, regulate immune responses to the antigen they recognize. This phenomenon is called antibody-mediated feedback regulation. Feedback regulation can be positive or negative, resulting in >1000-fold enhancement or >99% suppression of the specific antibody response. The outcome depends on size, structure, dose, and route of administration of the antigen as well as on class and subclass of the regulating antibody. This thesis investigates the role of T cells in antibody-mediated feedback enhancement, using both<i> in vivo</i> and <i>in vitro</i> approaches. IgE-antibodies enhance antibody responses to small soluble proteins. This effect is entirely dependent on the low-affinity receptor for IgE, CD23, and most likely depends on increased antigen presentation by CD23⁺ B cells. Strengthening this hypothesis, we show that IgE-mediated CD4⁺ T cell proliferation<i> in vitro</i> required the presence of CD19⁺ CD43^- CD23⁺ B cells. CD23 has also been shown to negatively regulate immune responses. Transgenic mice overexpressing CD23 are known to have impaired responses to antigens in alum. We here demonstrate that they are normal regarding IgE-mediated enhancement. IgG3 enhances antibody responses, and previous data suggested involvement of complement. We found that IgG3-mediated enhancement works well in mice lacking the only Fc-receptor known to bind IgG3, CD64. Although IgG3 could enhance antibody responses it had no major effect on T cell responses. Complement-receptors 1/2 (CR1/2) are required for the initiation of normal antibody responses. Although mice lacking CR1/2 had impaired antibody responses after immunization with sheep erythrocytes, their specific T cell responses were unaffected. The presented data do not support the idea that increased complement-mediated antigen presentation is a major mechanism behind the involvement of complement in antibody responses. They support the hypothesis that antigens forming complement-containing immune complexes may activate specific B cells by co-crosslinking BCR and CR1/2.</p>

Antibodies have the ability to influence the antibody response against the very antigen they are specific for, in a process called antibody feedback regulation. Depending on the nature of the antigen, the antibody response can be either enhanced or almost completely inhibited. This thesis focuses on the underlying mechanisms of antibody feedback regulation in vivo. Antigen-specific IgG can inhibit the antibody response to a particulate antigen. Based on its ability to inhibit B cell activation, the inhibitory FcγRIIB (low affinity receptor for IgG) has been suggested to be involved. Here we show that although FcγRIIB is required for efficient suppression in vitro, it is not required in vivo. Therefore, even though FcγRIIB can inhibit antibody responses, other mechanisms (such as epitope masking and enhanced antigen clearance) play a more dominant role in vivo. The antibody response to soluble antigen is greatly enhanced when it is introduced to the immune system in complex with antigen-specific IgG or IgE. We found that FcγRIIB attenuates the magnitude of IgG-mediated enhancement. In mice lacking FcγRIIB, IgG enhanced the antibody response much more efficiently than in normal mice. Since B cells require CD4+ T cell help in order to become antibody-producing cells, we examined the CD4+ T cell response to immune complexes in vivo. Using an adoptive transfer strategy with transgenic ovalbumin (OVA)-specific CD4+T cells, we could show that the enhanced OVA-specific IgG response to IgG2a/OVA and IgE/OVA complexes was preceded by a potent OVA-specific CD4+ T cell response. IgG2a-mediated enhancement was dependent on activating Fcγ receptors, whereas IgE-mediated enhancement was dependent on CD23, the low affinity receptor for IgE. We identified CD23+ B cells as the responsible effector cells for IgE-mediated enhancement in vivo. Taken together, these results show that Fc receptor-mediated antigen presentation is a major mechanism underlying antibody feedback enhancement.

Antibodies, passively administered or actively produced, regulate immune responses to the antigen they recognize. This phenomenon is called antibody-mediated feedback regulation. Feedback regulation can be positive or negative, resulting in &gt;1000-fold enhancement or &gt;99% suppression of the specific antibody response. The outcome depends on size, structure, dose, and route of administration of the antigen as well as on class and subclass of the regulating antibody. This thesis investigates the role of T cells in antibody-mediated feedback enhancement, using both in vivo and in vitro approaches. IgE-antibodies enhance antibody responses to small soluble proteins. This effect is entirely dependent on the low-affinity receptor for IgE, CD23, and most likely depends on increased antigen presentation by CD23+ B cells. Strengthening this hypothesis, we show that IgE-mediated CD4+ T cell proliferation in vitro required the presence of CD19+ CD43- CD23+ B cells. CD23 has also been shown to negatively regulate immune responses. Transgenic mice overexpressing CD23 are known to have impaired responses to antigens in alum. We here demonstrate that they are normal regarding IgE-mediated enhancement. IgG3 enhances antibody responses, and previous data suggested involvement of complement. We found that IgG3-mediated enhancement works well in mice lacking the only Fc-receptor known to bind IgG3, CD64. Although IgG3 could enhance antibody responses it had no major effect on T cell responses. Complement-receptors 1/2 (CR1/2) are required for the initiation of normal antibody responses. Although mice lacking CR1/2 had impaired antibody responses after immunization with sheep erythrocytes, their specific T cell responses were unaffected. The presented data do not support the idea that increased complement-mediated antigen presentation is a major mechanism behind the involvement of complement in antibody responses. They support the hypothesis that antigens forming complement-containing immune complexes may activate specific B cells by co-crosslinking BCR and CR1/2.

Fibrotic diseases have a poor prognosis with no FDA approved therapies. Monocyte-derived, fibroblast-like cells called fibrocytes participate in the formation of fibrotic lesions. The conserved pentraxin protein serum amyloid P (SAP) inhibits fibrocyte differentiation in cell culture, and injections of SAP significantly reduce fibrosis in several animal models. SAP binds to the receptors for the Fc portion of immunoglobulin G (FcγR), and has been crystallized bound to FcγRIIa. The in vivo activity of SAP appears to be dependent on the common γ chain (FcγR) of activating Fc receptors. The goal of my project is to elucidate the functional domains of SAP and the receptor responsible for SAP bioactivity, which could lead to refinements for SAP as a therapeutic agent and additional drug targets. I found that mutagenesis of the residues critical for SAP binding to FcγRIIa only moderately decreases SAP's ability to inhibit fibrocyte differentiation. In murine cells, deletion of FcγR or FcγRI significantly reduced sensitivity to SAP. Deletion of the combination of FcγRIIb/FcγRIIIa/FcγRIV did not significantly affect sensitivity to SAP, while deletion of just the inhibitory receptor FcγRIIb increased sensitivity to SAP. In human cells, siRNA-mediated reduction of FcγR or FcγRI levels significantly decreased sensitivity to SAP, while reduction of FcγRIIb levels increased sensitivity to SAP. These observations suggest that SAP, at least in part, uses FcγRI and FcγR to inhibit fibrocyte differentiation. I am also interested in how SAP functions in various disease states. SAP is known to be elevated in Alzheimer's disease (AD) and binds to amyloid plaques in the brain, a key hallmark of AD. There is a significant population of individuals that have key hallmarks of AD but show no signs of cognitive impairment, termed non-demented with AD neuropathology (NDAN). I evaluated SAP levels in post mortem samples of hippocampus and frontal cortex in age-matched controls, AD, and NDAN individuals. AD individuals had significantly increased SAP levels, while NDAN samples had no significant difference in SAP levels compared to controls. These results suggest that low levels of SAP in plaques marks the brains of individuals that escape dementia despite the presence of beta amyloid plaques.

Made available in DSpace on 2014-06-12T18:08:02Z (GMT). No. of bitstreams: 2 arquivo8004_1.pdf: 4568730 bytes, checksum: 59b8a548fa5fc647bcee9fe6d1b3e888 (MD5) license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) Previous issue date: 2003 / Conselho Nacional de Desenvolvimento Científico e Tecnológico / Na presente dissertação realizamos estudos através de simulação computacional, utilizando o método Monte Carlo (MC) do antiferromagneto (AF) diluído FexZn1&#8722;xF2, próximo da região de percolação (x = 0.24) e na presença de um campo magnético externo H. O sistema AF FexZn1&#8722;xF2 mostra-se para x = 0.25 com características típicas de um Vidro de Spins (VS s) genuíno, com uma temperatura crítica bem definida. Por meio de um modelo microscópico adequado para a descrição de AF diluídos, em que as razões entre as constantes de trocas medidas no sistema são consideradas, mostramos através da utilização da simulação MC que, para baixas temperaturas, o sistema Fe0.25Zn0.75F2 possui uma forte dependência com a história da medida ou do procedimento numérico utilizado. Os valores obtidos através das medidas da magnetização, quando resfriamos a campo magnético nulo e posteriormente aquecemos com campo magnético não-nulo (ciclo ZFC), são diferentes dos valores quando a medida é feita com resfriamento e aquecimento com campo magnético não nulo ou finito (ciclo FC). Em particular, estudamos a dependência temporal das magnetizações remanentes associadas aos dois ciclos, FC e ZFC, após a retirada do campo magnético. Essa forte dependência com a história evidenciou-se, também, nos resultados que obtivemos para as curvas de histerese e para a linha de Almeida- Thouless, com os resultados sendo comparados com os obtidos experimentalmente e por outros métodos teóricos