914 resultados para Resistance to change


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Plant innate immunity to pathogenic microorganisms is activated in response to recognition of extracellular or intracellular pathogen molecules by transmembrane receptors or resistance proteins, respectively. The defense signaling pathways share components with those involved in plant responses to UV radiation, which can induce expression of plant genes important for pathogen resistance. Such intriguing links suggest that UV treatment might activate resistance to pathogens in normally susceptible host plants. Here, we demonstrate that pre-inoculative UV (254 nm) irradiation of Arabidopsis (Arabidopsis thaliana) susceptible to infection by the biotrophic oomycete Hyaloperonospora parasitica, the causative agent of downy mildew, induces dose- and time-dependent resistance to the pathogen detectable up to 7 d after UV exposure. Limiting repair of UV photoproducts by postirradiation incubation in the dark, or mutational inactivation of cyclobutane pyrimidine dimer photolyase, (6-4) photoproduct photolyase, or nucleotide excision repair increased the magnitude of UV-induced pathogen resistance. In the absence of treatment with 254-nm UV, plant nucleotide excision repair mutants also defective for cyclobutane pyrimidine dimer or (6-4) photoproduct photolyase displayed resistance to H. parasitica, partially attributable to short wavelength UV-B (280–320 nm) radiation emitted by incubator lights. These results indicate UV irradiation can initiate the development of resistance to H. parasitica in plants normally susceptible to the pathogen and point to a key role for UV-induced DNA damage. They also suggest UV treatment can circumvent the requirement for recognition of H. parasitica molecules by Arabidopsis proteins to activate an immune response.

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The current study examined the association between exercise behaviors, disordered eating, and other behaviors to change body shape among fitness center attendees. The participants were 520 adults (245 men, 275 women) who attended fitness centers. Data were gathered using an anonymous questionnaire. Women who attended fitness centers were generally trying to lose weight and improve fitness; men were generally trying to increase their muscles and improve their fitness level. Reasons for exercise predicted the nature of the body change strategies adopted by respondents. Regression analyses demonstrated that exercises performed by people who attend fitness centers are a reflection of whether or not they want to lose weight, increase muscle or improve fitness. All groups were equally likely to engage in health risk behaviors, but the specific nature of these behaviors varied by group. The implications of these findings for health-related messages among people who attend fitness centers are discussed.

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The gene for Rhotekin 2 (RTKN2) was originally identified in a promyelocytic cell line resistant to oxysterol-induced apoptosis. It is differentially expressed in freshly isolated CD4+ T-cells compared with other hematopoietic cells and is down-regulated following activation of the T-cell receptor. However, very little is known about the function of RTKN2 other than its homology to Rho-GTPase effector, rhotekin, and the possibility that they may have similar roles. Here we show that stable expression of RTKN2 in HEK cells enhanced survival in response to intrinsic apoptotic agents; 25-hydroxy cholesterol and camptothecin, but not the extrinsic agent, TNFα. Inhibitors of NF-KappaB, but not MAPK, reversed the resistance and mitochondrial pro-apoptotic genes, Bax and Bim, were down regulated. In these cells, there was no evidence of RTKN2 binding to the GTPases, RhoA or Rac2. Consistent with the role of RTKN2 in HEK over-expressing cells, suppression of RTKN2 in primary human CD4+ T-cells reduced viability and increased sensitivity to 25-OHC. The expression of the pro-apoptotic genes, Bax and Bim were increased while BCL-2 was decreased. In both cell models RTKN2 played a role in the process of intrinsic apoptosis and this was dependent on either NF-KappaB signaling or expression of downstream BCL-2 genes. As RTKN2 is a highly expressed in CD4+ T-cells it may play a role as a key signaling switch for regulation of genes involved in T-cell survival.

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This paper presents findings of an Australian study that investigated how farm- management teams go about learning to manage their businesses, including how they learn in order to make strategic and tactical changes. The Australian farming context is one of increasing complexity and risk that demands greater sophistication and professionalism in farm management. Learning is related to increased capacity to manage successful change. Farm-management teams employ four different learning patterns when making changes to their management and marketing practices. Learning patterns are termed local focussed, people focussed, outward looking and extensive networking. These patterns appear to be related to ongoing learning practices of farm-management teams as well as to learning for change. Local focussed management teams learnt for change by accessing only local sources (including government extension services) or a single individual. People focussed farm-management teams preferred to learn for change principally by seeking information and advice on a one-to-one basis from more than one person, most frequently experts, but often other farmers. The remaining farm businesses accessed a variety of sources. The group classed as extensive networkers accessed a large number of varied sources in learning for change. Others who used a less extensive range were termed outward looking.

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It is widely acknowledged that offender rehabilitation outcomes can be improved by attending to responsivity issues, including the readiness and motivation of offenders to undertake and engage in treatment. The measurement of responsivity, readiness and motivation in offenders, however, has received relatively little research attention. In this paper we focus on anger management programmes and evaluate the utility and psychometric properties of a measure of stages of change in relation to changing anger - the Anger Readiness to Change Questionnaire (ARCQ). Using data from a large sample of offenders undergoing anger management interventions, we investigated the construct validity, convergent validity and predictive validity of the ARCQ. We conclude the ARCQ may have utility as a measure for selecting offenders who are suitable for anger management interventions.

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We evaluated the effect of ambient temperatures between 25 and 43°C on the rate of evaporative water loss (EWL) in eight adult Litoria xanthomera (average body mass = 7.3 ± 0.6 g). Frogs were placed in a cylindrical chamber that permitted them to fully conceal their ventral surfaces using a water-conserving posture. Their EWL was 7.1 ± 0.7 mg g–1 h–1 at 25°C and reached 28.0 ± 2.5 mg g–1 h–1 at 43°C. Agar replicas of the frogs were used to evaluate boundary-layer resistances associated with the EWL measurements and, thus, to permit evaluation of cutaneous resistance to vapour diffusion (rc) in live frogs. The rc of L. xanthomera was stable over the temperature range of 25–35°C, averaging about 28 s cm–1, and then declined stepwise with ambient temperatures above 37°C. The highest rc recorded for each individual over the range of temperatures studied averaged 32.0 ± 1.2 s cm–1. The thermolabile nature of rc demonstrates a well developed thermoregulatory control of EWL in this species, a trait very similar in pattern and extent to that previously measured in the closely related Litoria chloris.

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Heterotrimeric G proteins are involved in the defense response against necrotrophic fungi in Arabidopsis. In order to elucidate the resistance mechanisms involving heterotrimeric G proteins, we analyzed the effects of the Gβ (subunit deficiency in the mutant agb1-2 on pathogenesis-related gene expression, as well as the genetic interaction between agb1-2 and a number of mutants of established defense pathways. Gβ-mediated signaling suppresses the induction of salicylic acid (SA)-, jasmonic acid (JA)-, ethylene (ET)- and abscisic acid (ABA)-dependent genes during the initial phase of the infection with Fusarium oxysporum (up to 48 h after inoculation). However, at a later phase it enhances JA/ET-dependent genes such as PDF1.2 and PR4. Quantification of the Fusarium wilt symptoms revealed that Gβ- and SA-deficient mutants were more susceptible than wild-type plants, whereas JA- and ET-insensitive and ABA-deficient mutants demonstrated various levels of resistance. Analysis of the double mutants showed that the Gβ-mediated resistance to F. oxysporum and Alternaria brassicicola was mostly independent of all of the previously mentioned pathways. However, the progressive decay of agb1-2 mutants was compensated by coi1-21 and jin1-9 mutations, suggesting that at this stage of F. oxysporum infection Gβ acts upstream of COI1 and ATMYC2 in JA signaling.

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Heterotrimeric G proteinshave been previously linked to plant defense; however a role for the Gbg dimer in defense signaling has not been described to date. Using available Arabidopsis (Arabidopsis thaliana) mutants lacking functional Ga or Gb subunits, we show that defense against the necrotrophic pathogens Alternaria brassicicola and Fusarium oxysporum is impaired in Gb-deficient mutants while Ga-deficient mutants show slightly increased resistance compared to wild-type Columbia ecotype plants. In contrast, responses to virulent (DC3000) and avirulent (JL1065) strains of Pseudomonas syringae appear to be independent of heterotrimeric G proteins. The induction of a number of defense-related genes in Gb-deficient mutants were severely reduced in response to A. brassicicola infection. In addition, Gb-deficient mutants exhibit decreased sensitivity to a number of methyl jasmonate-induced responses such as induction of the plant defensin gene PDF1.2, inhibition of root elongation, seed germination, and growth of plants in sublethal concentrations of methyl jasmonate. In all cases, the behavior of the Ga-deficient mutants is coherent with the classic heterotrimeric mechanism of action, indicating that jasmonic acid signaling is influenced by the Gbg functional subunit but not by Ga. We hypothesize that Gbg acts as a direct or indirect enhancer of the jasmonate signaling pathway in plants.

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In recent years there has been increasing recognition internationally that health care is not as safe as it ought to be and that patient safety outcomes need to be improved. To this end, patient safety has become the focus of a world-wide endeavour – endorsed by the World Health Organisation – to reduce the incidence and impact of preventable human errors and related adverse events in health care domains. The emergency department has been identified as a significant site of preventable human errors and adverse events in the health care system, raising important questions about the nature of human error management and patient safety ethics in rapidly changing environments, of which the Emergency Department is a prime example. In Part I of this article series, an overview of the incidence and impact of preventable adverse events in Emergency Department contexts and the development of the global patient safety movement was presented. In this second article brief attention is given to examining some of the ethical tensions that have arisen in response to the patient safety movement and their possible implications for Emergency Department contexts and staff.

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Currently, women occupy less than 20% of places in the ICT courses offered by higher education institutions in Victoria and, as of 2007, women held only 16% of ICT jobs in the state (Multimedia Victoria 2008 p 25). At the secondary school level there has in fact been a marked downturn in girls' interest in such courses, reflecting a more general decline in female participation in ICT courses and careers. Given that there has also been a decline in overall student ICT numbers, there is a strong case to develop programs aimed to convince female students that an ICT career or course is an attractive option for their future. The Digital Divas program is one such course.

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We have developed hematopoietic cells resistant to the cytotoxic effects of oxysterols. Oxysterol-resistant HL60 cells were generated by continuous exposure to three different oxysterols—25-hydroxycholesterol (25-OHC), 7-beta-hydroxycholesterol (7β-OHC) and 7-keto-cholesterol (7κ-C). We investigated the effects of 25-OHC, 7β-OHC, 7κ-C and the apoptotic agent staurosporine on these cells. The effect of the calcium channel blocker nifedipine on oxysterol cytotoxicity was also investigated. Differential display and real-time PCR were used to quantitate gene expression of oxysterol-sensitive and -resistant cells. Our results demonstrate that resistance to the cytotoxic effects of oxysterols is relatively specific to the type of oxysterol, and that the cytotoxicity of 25-OHC but not that of 7β-OHC and 7κ-C, appears to occur by a calcium dependent mechanism. Oxysterol-resistant cells demonstrated no significant difference in the expression of several genes previously implicated in oxysterol resistance, but expressed the bcl-2 gene at significantly lower levels than those observed in control cells. We identified three novel genes differentially expressed in resistant cells when compared to HL60 control cells. Taken together, the results of this study reveal potentially novel mechanisms of oxysterol cytotoxicity and resistance, and indicate that cytotoxicity of 25-OHC, 7β-OHC and 7κ-C occur by independent, yet overlapping mechanisms.

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The thesis study aims to develop a model of readiness to enter treatment to change problem behaviour by addressing the limitations of previous models. The research shows that a model consisting of personal and social factors, mediated by problem recognition and desire for help accurately assesses readiness to enter treatment. The portfolio examines the broad framework of the Multifactor Offender Readiness Model (MORM) which assesses an offender's readiness to engage in treatment. Four case studies are presented.

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This thesis describes the discovery, characterization, and function of a new protein, Rhotekin 2. It is a signaling protein with a significant role in resistance to cell death in human lymphocytes and therefore may be a potential new target in future treatments of immune diseases such a HIV and leukemia.