1000 resultados para pyrethroids resistance


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Popular culture has a strong influence on youth, and the creation of meanings associated with youth. Representations within popular culture, specifically film, branch beyond entertainment and become discourses that construct how we perceive our world. Youth resistance is commonly represented in films geared towards the teenage gene{ation. Yet, the discourse of resistance has positioned females as non-resistors. This thesis addresses representations of teenage girl resistance within popular culture due to the strong influence film has on teenage girls today. This thesis will specificaIJy examine three films directed at North American teenage girls: Thirteen, Ghost World and The Sisterhood of the Travelling Pants. Through a feminist poststructurallens utilizing discourse analysis, this thesis will examine teenage girl resistance as it is represented in the aforementioned films. This thesis repositions teenage girl resistance as a multi-dimensional concept, allowing for resistance to branch beyond the traditional meaning associated with it.

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In animals, both stress resistance and longevity appear to be influenced by the insulin/insulin-like growth factor-l signaling (lIS) pathway, the basic organization of which is highly conserved from invertebrates to vertebrates. Reduced lIS or genetic disruption of the lIS pathway leads to the activation of forkhead box transcription factors, which is thought to upregulate the expression of genes involved in enhancing stress resistance, including perhaps key antioxidant enzymes as well as DNA repair enzymes. Enhanced antioxidant and DNA repair capacities may underlie the enhanced cellular stress resistance observed in long-lived animals, however little data is available that directly supports this idea. I used three. experimental approaches to test the association of intracellular antioxidant and DNA base excision repair (BER) capacities with stress resistance and longevity: (1) a comparison of multiple vertebrate endotherm species of varying body masses and longevities; (2) a comparison of long-lived Snell dwarf mice and their normallittermates; and (3) a comparison of hypometabolic animals undergoing hibernation or estivation with their active counterparts. The activities of the five major intracellular antioxidant enzymes as well as the two rate-limiting enzymes in the BER pathway, apurininc/apyrimidinic (AP) endonuclease and polymerase ~, were measured. These measurements were performed in one or more of the following: (1) cultured dermal fibroblasts; (2) brain tissue; (3) heart tissue; (4) liver tissue. My results indicate that antioxidant enzymes are not universally upregulated in association with enhanced stress resistance and longevity. I also did not find that BER enzyme activity was positively correlated with longevity, in an inter-species context, though there was evidence for enhanced BER in long-lived Snell dwarf mice. Thus, while there were instances in which enhanced antioxidant and BER enzyme activities were associated with increased stress resistance and/or longevity, this was not universally the case, indicating that other mechanisms must be involved. These results suggest the need to re-examine existing 'oxidative stress' hypotheses of longevity and probe further into the molecular physiology of longevity to discover its mechanistic basis.

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It has been proposed that phages can be used commercially as a biopesticide for the control of fire blight caused by the phytopathogen Erwinia amylovora. The aim of these studies was to investigate two common bacterial resistance mechanisms, lysogeny and exopolysaccharide production and their influence on phage pathogenesis. A multiplex real-time PCR protocol was designed to monitor and quantify Podoviridae and Myoviridae phages. This protocol is compatible with known E. amylovora and Pantoea agglomerans rtPCR primers/probes which allowed simultaneous study of both phage and bacterial targets. Using in vitro positive phage selection, bacteriophage insensitive derivatives were isolated within sensitive populations of E. amylovora. Prophage screening with real-time PCR and mitomycin C induction determined that the insensitive derivatives harboured the temperate Podoviridae phage ΦEaTlOO. Lysogenic conversion resulted in resistance to secondary homologous phage infections. Prophage screening of environmental samples of E. amylovora and P. agglomerans collected from various locations in Canada, United States and Europe did not demonstrate lysogeny. Therefore, lysogeny is rare or absent while these bacterial species reside on the plant. Recombineering was used to construct exopolysaccharide deficient E. amylovora mutants. The EPS amylovoran mutants became resistant to Podoviridae and certain Siphoviridae phages. Increasing amylovoran production increased phage population growth, presumably by increasing the total number of bacterial cell surface receptors which promoted increased phage infections. In contrast, amylovoran did not playa role in Myoviridae infections, nor did production of the EPS levan for any phage pathogenesis.

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Fire blight is a disease caused by the phytopathogenic bacterium Erwinia amylovora, an economically important pathogen in the commercial production of apples and pears. Bacteriophages have been proposed as a commercial biopesticide to relieve the pressures on apple and pear production and provide alternatives to existing biological control options. This work reports on the investigation of host resistance in the development of a phage biopesticide. Exopolysaccharide (EPS) deficient bacterial mutants were generated through recombineering to investigate the role of EPS in bacteriophage adsorption and infection. The mutants that were deficient in amylovoran production were avirulent and resistant to infection by phages of the Podoviridae and some of the Siphoviridae family. Levan deficient bacterial mutants resulted in reduced phage titers in some phages from the Myoviridae family. Exopolysaccharide mimetic monosaccharides were used to demonstrate that levan and amylovoran play an important role in phage attack of E. amylovora.

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Arabidopsis thaliana is an established model plant system for studying plantpathogen interactions. The knowledge garnered from examining the mechanism of induced disease resistance in this model system can be applied to eliminate the cost and danger associated with current means of crop protection. A specific defense pathway, known as systemic acquired resistance (SAR), involves whole plant protection from a wide variety of bacterial, viral and fungal pathogens and remains induced weeks to months after being triggered. The ability of Arabidopsis to mount SAR depends on the accumulation of salicylic acid (SA), the NPRI (non-expressor of pathogenesis related gene 1) protein and the expression of a subset of pathogenesis related (PR) genes. NPRI exerts its effect in this pathway through interaction with a closely related class of bZIP transcription factors known as TGA factors, which are named for their recognition of the cognate DNA motif TGACG. We have discovered that one of these transcription factors, TGA2, behaves as a repressor in unchallenged Arabidopsis and acts to repress NPRI-dependent activation of PRJ. TGA1, which bears moderate sequence similarity to TGA2, acts as a transcriptional activator in unchallenged Arabidopsis, however the significance of this activity is J unclear. Once SAR has been induced, TGAI and TGA2 interact with NPRI to form complexes that are capable of activating transcription. Curiously, although TGAI is capable of transactivating, the ability of the TGAI-NPRI complex to activate transcription results from a novel transactivation domain in NPRI. This transactivation domain, which depends on the oxidation of cysteines 521 and 529, is also responsible for the transactivation ability of the TGA2-NPRI complex. Although the exact mechanism preventing TGA2-NPRI interaction in unchallenged Arabidopsis is unclear, the regulation of TGAI-NPRI interaction is based on the redox status of cysteines 260 and 266 in TGAl. We determined that a glutaredoxin, which is an enzyme capable of regulating a protein's redox status, interacts with the reduced form of TGAI and this interaction results .in the glutathionylation of TGAI and a loss of interaction with NPRl. Taken together, these results expand our understanding of how TGA transcription factors and NPRI behave to regulate events and gene expression during SAR. Furthermore, the regulation of the behavior of both TGAI and NPRI by their redox status and the involvement of a glutaredoxin in modulating TGAI-NPRI interaction suggests the redox regulation of proteins is a general mechanism implemented in SAR.

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In challenging normative social relations, queer cultural studies has shied away from deploying historical materialist theoretical tools. My research addresses this gap by drawing these two literatures into conversation. I do so by investigating how global economic relations provide an allegorical and material context for the regulation, representation and re-imagining of working-class queer childhood through anti- capitalist queer readings of three films: Kes, Billy Elliot, and Boys Village. I deploy this reading practice to investigate how these films represent heteronormative capitalism’s systematic extermination of the life possibilities of working class children, how children resist forces of normalisation by creating queer times and spaces, and how nostalgia engenders a spatio-temporal understanding of queerness through a radical utopianism. My analysis foregrounds visual cultural productions as sites for understanding how contemporary social worlds exclude queer working class children, who struggle to insert themselves into and thereby shift the grounds of normative social relations.

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While billions of farmed animals are immobilized within agribusiness, every year some of these animals manage to break free. This thesis examines the stories of those who flee slaughterhouses and the public response to these individuals. My objective is to understand how animals resist and the role that their stories play in disrupting the ways that humans, particularly as consumers, are distanced from the violence of animal enterprises. Included are six vignettes that allow for an in-depth case study of those who have escaped within New York State. Located in the interdisciplinary field of critical animal studies, my inquiry draws upon new animal geographies, transnational feminisms, and critical discourse analysis. This contribution provides discussion of farmed animal resistance in particular and compares experiences and representations of their resistance from both the “view from below,” which is learned through the animals’ caretakers, and a “view from above,” which is gleaned from their representations in corporate-driven mainstream media.

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Glutaredoxins are oxidoreductases capable of reducing protein disulfide bridges and glutathione mixed disulfides through the process of deglutathionylation and glutathionylation. Lately, redox-mediated modifications of functional cysteine residues of TGA1 and TGA8 transcription factors have been postulated. Namely, GRX480 and ROXY1 glutaredoxins have been previously shown to interact with TGA proteins and have been suggested to regulate redox state of these proteins. TGA1, together with TGA2, is involved in systemic acquired resistance (SAR) establishment in the plant Arabidopsis thaliana through PR1 (Pathogenesis related 1) gene activation. They both form an enhanceosome complex with the NPR1 protein (non-expressor of pathogenesis related gene 1) which leads to PR1 transcription. Although TGA1 is capable of activating PR1 transcription, the ability of the TGA1 NPR1 enhanceosome complex to assembly is based on the redox status of TGA1. We identified GRX480 as a glutathionylating enzyme that catalyzes the TGA1 glutathione disulfide transferase reaction with a Km of around 20μM GSSG (oxidized glutathione). Out of four cysteine residues found within TGA1, C172 and C266 were found to be glutathionylated by this enzyme. We also confirmed TGA1 glutathionylation in vivo and showed that this modification takes place while TGA1 is associated with the PR1 promoter enzymatically via GRX480. Furthermore, we show that glutathionylation via GRX480 abolishes TGA1's interaction with NPR1 and consequently prevents the TGA1-NPR1 transcription activation of PR1. When glutathionylated, TGA1 is recruited to the PR1 promoter and acts as a repressor. Therefore, glutathionylation is a mechanism that prevents TGA1 NPR1 interaction, allowing TGA1 to function as a repressor of PR1 transcription. Surprisingly, GRX480 was not able to deglutathionylate proteins demonstrating the irreversible nature of the reaction. Moreover, we demonstrate that other members of CC-class glutaredoxins, namely ROXY1 and ROXY2, can also catalyze protein glutathionylation. The TGA8 protein was previously shown to interact with NPR1 analogs, BOP1 and BOP2 proteins. However, unlike the case of TGA1 NPR1 interaction, here we demonstrate that TGA8-BOP1 interaction is not redox regulated and that TGA8 glutathionylation by ROXY1 and ROXY2 enzymes does not abolish this interaction in vitro. However, TGA8 glutathionylation results in TGA8 oligomer disassembly into smaller complexes and monomers. Our results suggest that CC-Grxs are unable to reduce mixed disulfides, instead they efficiently catalyze the opposite reaction which distinguishes them from traditional glutaredoxins. Therefore, they should not be classified as glutaredoxins but as protein glutathione disulfide transferases.

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During infection, the model plant Arabidopsis thaliana is capable of activating long lasting defence responses both in tissue directly affected by the pathogen and in more distal tissue. Systemic acquired resistance (SAR) is a type of systemic defence response deployed against biotrophic pathogens resulting in altered plant gene expression and production of antimicrobial compounds. One such gene involved in plant defence is called pathogenesis-related 1 (PR1) and is under the control of several protein regulators. TGA II-clade transcription factors (namely TGA2) repress PR1 activity prior to infection by forming large oligomeric complexes effectively blocking gene transcription. After pathogen detection, these complexes are dispersed by a mechanism unknown until now and free TGA molecules interact with the non-expressor of pathogenesis-related gene 1 (NPR1) protein forming an activating complex enabling PR1 transcription. This study elucidates the TGA2 dissociation mechanism by introducing protein kinase CK2 into this process. This enzyme efficiently phosphorylates TGA2 resulting in two crucial events. Firstly, the DNA-binding ability of this transcription factor is completely abolished explaining how the large TGA2 complexes are quickly evicted from the PR1 promoter. Secondly, a portion of TGA2 molecules dissociate from the complexes after phosphorylation which likely makes them available for the formation of the TGA2-NPR1 activating complex. We also show that phosphorylation of a multiserine motif found within TGA2’s N terminus is responsible for the change of affinity to DNA, while modification of a single threonine in the leucine zipper domain seems to be responsible for deoligomerization. Despite the substantial changes caused by phosphorylation, TGA2 is still capable of interacting with NPR1 and these proteins together form a complex on DNA promoting PR1 transcription. Therefore, we propose a change in the current model of how PR1 is regulated by adding CK2 which targets TGA2 displacing it’s complexes from the promoter and providing solitary TGA2 molecules for assembly of the activating complex. Amino acid sequences of regions targeted by CK2 in Arabidopsis TGA2 are similar to those found in TGA2 homologs in rice and tobacco. Therefore, the molecular mechanism that we have identified may be conserved among various plants, including important crop species, adding to the significance of our findings.

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The purpose of this study was to examine the acute hormonal responses to a bout of resistance versus plyometric exercise in young male athletes. Specifically, changes in salivary cortisol, testosterone and testosterone-to-cortisol ratio from pre- to post-exercise between the two different exercise protocols were examined. Twenty-six peri-pubertal active boys participated in this cross-over study, completing two exercise sessions. During each session, participants first completed a 30 min control period, which did not include any exercise, and then was randomly assigned to perform a 45 min of either a resistance exercise or a plyometric exercise protocol. All participants crossed over to perform the other exercise protocol during their second exercise session, a week later. Four saliva samples during each protocol were taken at: baseline, pre-exercise, 5 min post-exercise and 30 min post-exercise. Significant increases in testosterone values were reported 5 min post-exercise following the resistance protocol, but not the plyometric protocol. Both exercise protocols resulted in significant cortisol decreases overtime, as well as significant testosterone-to-cortisol ratio increases. The post-exercise increases in salivary testosterone and testosterone-to-cortisol ratio followed the typical exercise induced anabolic response seen in adults. However, the post-exercise decrease in salivary cortisol was different than the typical adult response indicating an insufficient stimulus for this age group maybe due to their stage of the biological development. Thus, in the adolescent boys, exercise appears to change the anabolic to catabolic balance in favor of anabolism.

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Many position stands and review papers have refuted the myths associated with resistance training (RT) in children and adolescents. With proper training methods, RT for children and adolescents can be relatively safe and improve overall health. The objective of this position paper and review is to highlight research and provide recommendations in aspects of RT that have not been extensively reported in the pediatric literature. In addition to the well-documented increases in muscular strength and endurance, RT has been used to improve function in pediatric patients with cystic fibrosis, cerebral palsy and burn victims. Increases in children’s muscular strength have been attributed primarily to neurological adaptations due to the disproportionately higher increase in muscle strength than in muscle size. Although most studies using anthropometric measures have not shown significant muscle hypertrophy in children, more sensitive measures such as magnetic resonance imaging and ultrasound have suggested hypertrophy may occur. There is no minimum age for RT for children. However the training and instruction must be appropriate for children and adolescents involving a proper warm-up, cool-down and an appropriate choice of exercises. It is recommended that low-to-moderate intensity resistance should be utilized 2-3 times per week on non-consecutive days, with 1-2 sets initially, progressing to 4 sets of 8-15 repetitions for 8-12 exercises. These exercises can include more advanced movements such as Olympic style lifting, plyometrics and balance training, which can enhance strength, power, co-ordination and balance. However specific guidelines for these more advanced techniques need to be established for youth. In conclusion, a RT program that is within a child’s or adolescent’s capacity, involves gradual progression under qualified instruction and supervision with appropriately sized equipment can involve more advanced or intense RT exercises which can lead to functional (i.e. muscular strength, endurance, power, balance and co-ordination) and health benefits.

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This study examined the effect of 8-weeks of resistance (RT) and plyometric (PLYO) training on maximal strength, power and jump performance compared with no added training (CON), in young male soccer players. Forty-one 11-13 year-old soccer players were divided into three groups (RT, PLYO, CON). All participants completed 5 isometric knee extensions at 90° and 5 isokinetic knee extensions at 240°/s pre- and post-training. Peak torque (PT), peak rate of torque development (pRTD), electromechanical-day (EMD), rate of muscle activation (Q30), muscle cross-sectional area (mCSA) and jump performance were examined. Both RT and PLYO resulted in significant (p < 0.05) increases in PT, pRTD and jump performance. RT resulted in significantly greater increases in both isometric and isokinetic PT, while PLYO resulted in significantly greater increases in isometric pRTD and jump performance compared with CON (p < 0.05). Q30 increased to a greater extent in PLYO (20%) compared with RT (5%) and CON (-5%) (p = 0.1). In conclusion, 8-weeks of RT and PLYO resulted in significant improvements in muscle strength and jump performance. RT appears to be more effective at eliciting increases in maximal strength while PLYO appears to enhance explosive strength, mediated by possible increases in the rate of muscle activation.

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Affiliation: Faculté de pharmacie, Université de Montréal & Institut de recherches cliniques de Montréal

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La leucémie lymphoblastique aiguë des cellules Pré-B (B-ALL) reste le type de cancer le plus souvent diagnostiqué chez les enfants. Des études ont montré que des déterminants génétiques jouent un rôle important dans la susceptibilité/résistance au développement de ce cancer. À cet égard, les gènes Killer-cell Immunoglobulin-like Receptor (KIR) sont d'une importance particulière. Ces gènes sont fortement polymorphiques et codent pour des récepteurs qui contrôlent l’activité fonctionnelle des cellules Natural Killer (NK). Notre hypothèse est que les gènes activateurs des KIR s’associent avec la résistance innée pour développer la B-ALL. Afin d'évaluer cette hypothèse, nous avons entrepris une étude de cas-contrôles chez des enfants canadiens-français dans laquelle nous avons utilisé l'ADN génomique de 100 patients atteints de B-ALL ainsi que l’ADN de 245 individus sains. La présence ou l'absence de chaque gène KIR a été détectée par PCR en utilisant des amorces de séquences spécifiques. Nous avons trouvé que la présence des gènes KIR activateurs est significativement diminuée chez les enfants leucémiques par rapport aux témoins. En outre, le nombre de ces gènes a aussi montré une association significative linéaire avec la résistance au développement d’une B-ALL. Cela suggère des effets additifs de ces gènes permettant de conférer une protection contre ce cancer. Ces résultats pourraient être utiles afin de déceler de façon précoce les enfants ayant un risque de développer cette leucémie. Enfin, des stratégies thérapeutiques basées sur les récepteurs KIR pourraient être envisagées et s'avérer utiles concernant le traitement de ce cancer chez les enfants.

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Antimicrobial resistance is a growing public health concern and is associated with the over or inappropriate use of antimicrobials in both humans and agriculture. While there has been recognition of this problem on the part of agricultural and public health authorities, there has nonetheless been significant difficulty in translating policy recommendations into practical guidelines. In this paper, we examine the process of public health policy development in Quebec agriculture, with a focus on the case of pork production and the role of food animal veterinarians in policy making. We argue that a tendency to employ strictly techno-scientific risk analyses of antimicrobial use ignores the fundamental social, economic and political realities of key stakeholders and so limits the applicability of policy recommendations developed by government advisory groups. In particular, we suggest that veterinarians’ personal and professional interests, and their ethical norms of practice, are key factors to both the problem of and the solution to the current over-reliance on antimicrobials in food production.