952 resultados para Fungicides - Physiological effect


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This study investigated the preparation of methyl ester (Biodiesel) from peanut oil by transesterification method and its effect on DI diesel engine. Two parameters were measured during the engine operation: one is engine performance (brake thermal efficiency and brake specific fuel consumption), and the other is the exhaust emissions (NOx and CO). The result showed that, when compared with neat diesel fuel, the brake thermal efficiency of biodiesel blend was almost similar or a slight lower. However, brake specific fuel consumption (bsfc) was a little higher than neat diesel. CO was lower and NOx was little higher with biodiesel blend than that of diesel. The engine performance for B10 and B20 was very similar. At medium and high load conditions the engine emissions for B10 and B20 has no significant variation. Hence, B20 can safely be used in diesel engine without any significant penalty in engine performance and emissions.

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The aims of this study were to examine: (1) the association between sociodemographic and lifestyle factors and sleep quality in a population-based cohort of Australian women and (2) possible influence of reproductive status and mental and physical health factors on these associations. Data on 3,655 women (mean age046.6 years, range 34.3–67.4) were obtained from the Mater Hospital University of Queensland Study of Pregnancy for this cross-sectional study. Self-rated sleep quality was assessed using the Pittsburgh Sleep Quality Index. For the purpose of this study, two cutoff points (scores 5 and 10) were used to divide women into three categories: normal (65.2 %), moderately poor (26.4 %), and very poor sleep quality (8.5 %). Other covariates were measured at 21-year follow-up as well. After adjusting for reproductive status, mental and physical health, there were significant associations between moderately poor sleep quality and education and between very poor sleep quality and unemployment, both measures of socioeconomic status. In addition, work-related exertion was associated with increased rates of moderately poor sleep quality, whereas those women undertaking moderate exercise were less likely to experience very poor sleep quality. Independent associations between sociodemographic factors and exercise with moderately poor and very poor sleep quality were identified. These findings demonstrate the dynamic nature of the association between exercise/exertion, socioeconomic status, and sleep quality and highlight the importance of taking these into consideration when dealing with issues of poor sleep quality in women.

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In this paper two-dimensional (2-D) numerical investigation of flow past four square cylinders in an in-line square configuration are performed using the lattice Boltzmann method. The gap spacing g=s/d is set at 1, 3 and 6 and Reynolds number ranging from Re=60 to 175. We observed four distinct wake patterns: (i) a steady wake pattern (Re=60 and g=1) (ii) a stable shielding wake pattern (80≤Re≤175 and g=1) (iii) a wiggling shielding wake pattern (60≤Re≤175 and g=3) (iv) a vortex shedding wake pattern (60≤Re≤175 and g=6) At g=1, the Reynolds number is observed to have a strong effect on the wake patterns. It is also found that at g=1, the secondary cylinder interaction frequency significantly contributes for drag and lift coefficients signal. It is found that the primary vortex shedding frequency dominates the flow and the role of secondary cylinder interaction frequency almost vanish at g=6. It is observed that the jet between the gaps strongly influenced the wake interaction for different gap spacing and Reynolds number combination. To fully understand the wake transformations the details vorticity contour visualization, power spectra of lift coefficient signal and time signal analysis of drag and lift coefficients also presented in this paper.

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The promise of metabonomics, a new "omics" technique, to validate Chinese medicines and the compatibility of Chinese formulas has been appreciated. The present study was undertaken to explore the excretion pattern of low molecular mass metabolites in the male Wistar-derived rat model of kidney yin deficiency induced with thyroxine and reserpine as well as the therapeutic effect of Liu Wei Di Huang Wan (LW) and its separated prescriptions, a classic traditional Chinese medicine formula for treating kidney yin deficiency in China. The study utilized ultra-performance liquid chromatography/electrospray ionization synapt high definition mass spectrometry (UPLC/ESI-SYNAPT-HDMS) in both negative and positive electrospray ionization (ESI). At the same time, blood biochemistry was examined to identify specific changes in the kidney yin deficiency. Distinct changes in the pattern of metabolites, as a result of daily administration of thyroxine and reserpine, were observed by UPLC-HDMS combined with a principal component analysis (PCA). The changes in metabolic profiling were restored to their baseline values after treatment with LW according to the PCA score plots. Altogether, the current metabonomic approach based on UPLC-HDMS and orthogonal projection to latent structures discriminate analysis (OPLS-DA) indicated 20 ions (14 in the negative mode, 8 in the positive mode, and 2 in both) as "differentiating metabolites".

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Asthma is an incapacitating disease of the respiratory system, which causes extensive morbidity and mortality worldwide. Asthma affects more than 300 million people globally(Masoli et al. 2004). In Australia, it affects 10.2% of the population (Masoli et al. 2004) and causes 60,000 people to be hospitalised annually. Health care expenditure due to asthma in Australia was $606 million in 2004–2005. There are four primary biological factors that function in the initiation and exacerbation of asthma. Airway inflammation is important as it is often the first response to an airway insult, initiating the three other components: bronchoconstriction, mucus hyper-secretion and hyper-reactivity. The mediators involved in asthma are still not well understood, and current anti-inflammatory corticosteroid treatments are not effective with all asthmatics. As there is currently no cure for asthma, and airway inflammation is the primary component of the disease, it is important that we understand and investigate the mediators of airway inflammation to look for a potential cure and to produce better therapeutics to treat the inflammation. Trefoil factors (TFFs) and secretoglobins (SCGBs) are small secreted proteins involved in the mediation of inflammation and epithelial restitution. TFFs are pro-inflammatory and SCGBs anti-inflammatory by nature. The hypothesis of this study is that in response to induced acute airway inflammation, the expression of TFF1 and TFF3 will increase and expression of SCGB1A1 and SCGB3A2 will decrease in non-asthmatics (N-A), asthmatics medicating with bronchodilators (A-BD) and asthmatics medicating with corticosteroids (A-ST). When comparing the three groups, we expect to see higher expression of the TFFs in the A-BD group compared to the N-A and A-ST groups, indicating that inflammation is mediated by TFFs in asthma and that corticosteroid medication controls their expression as part of the control of inflammation. We expect to see the opposite with SCGBs, with a greater decrease in the A-BD group compared to the other two groups, suggesting that the A-BD group has the least anti-inflammatory activity in response to inflammatory insult. Epigenetic modification plays a role in the regulation of genes that initiate disease states such as inflammatory conditions and cancers. Histone acetylation is one such modification, which involves the acetylation of histones in chromatin by histone acetyltransferases (HATs). This increases the transcription of genes involved with inflammation or enrols histone deacetylases (HDACs) to down-regulate the transcription of inflammatory genes. These HATs and HDACs work in a homeostatic fashion; however, in the event of inflammation, increased HAT activity can stimulate further inflammation, which is believed to be the mechanism involved in some inflammatory diseases. This study hypothesises that in response to inflammation, the expression of HDACs (HDAC1-5) will decrease and the expression of HATs (NCOA1-3, HAT-1 and CREBBP) will increase in all groups. When comparing the expression between the groups, it was expected that a greater decrease in HDACs and a greater increase in HATs will be seen in the A-BD group compared to the other two groups. This would identify histone acetylation as a mechanism involved in the inflammatory condition of asthma and indicate that corticosteroids may treat the inflammation in asthma at least in part by controlling histone acetylation. The aim of the project was to compare the expression of inflammatory genes TFF1, TFF3, SCGB1A1 and SCGB3A2, as well as to compare the gene expression of HDAC1-5, NCOA1-3, HAT-1 and CREBBP within and between N-A (n=15), A-BD (n=15) and A-ST (n=15) groups in response to inflammation. This was performed by collecting airway cells and proteins by sputum induction in three sessions. The sessions were coordinated into an initial baseline collection (SI-1), followed by a second session at least one week later (SI-2) and a third session, six hours after SI-2 to collect a sample containing the resultant acute inflammation caused in SI-2 (SI-3). Analysis of the SI-1 and SI-2 samples in all three groups had high amounts of variability between samples. The samples were taken at least one weak apart and the environmental stimuli on each participant outside of the testing sessions could not be controlled. For this reason, the SI-1 samples were not used for analysis; instead SI-2 and SI-3 samples were compared as they were same-day collections, reducing the probability of differences being due to anything other than the sputum induction. The gene expressions of the TFFs, SCGBs, HDACs and HATs were analysed using real-time PCR. Western blot analysis was performed to analyse the protein concentrations of the TFFs and SCGBs in secreted fractions of the sputum collection. Both the secreted and intracellular protein fractions collected from the sputum inductions for pre- and post-inflammation (SI-2, SI-3) samples of the N-A and A-BD groups were analysed using a proteomic method called iTRAQ. This allowed the comparison of the change in protein expression as a result of airway inflammation in each group. This technique was used as a discovery method to identify novel proteins that are modulated by induced acute airway inflammation. Any proteins of interest would then be further validated and used for future research. Inflammation was achieved in the SI-3 samples of the N-A group with a 21% unit increase in % neutrophils compared to SI-2 (p=0.01). The N-A group had a marked 5.5-fold decrease in HDAC1 gene expression in SI-3 compared to SI-2 (p=0.03). No differences were seen in any of the TFFs, SCGBs or any of the rest of the HDACs and HATs. Western blot data did not display any significant changes in the protein levels of the TFFs and SCGBs analysed. However, non-significant analysis of the data displayed increases in TFF1 and TFF3, and decreases in SCGB1A1 and SCGB3A2 for the majority of SI-3 samples compared to SI-2. The A-BD group also presented a marked increase in neutrophils in the SI-3 samples compared to SI-2 (27% unit increase, p=0.04). The A-BD group had a significant increase in TFF3 and SCGB1A1 gene expression concomitant with induced acute airway inflammation. A 7.3-fold increase in TFF3 (p=0.05) in SI-3 indicated that TFF3 is linked to inflammation in asthmatics. A 2.8-fold increase in SCGB1A1 (p=0.03) indicated that this gene is also up-regulated, suggesting that this SCGB is expressed to try to combat induced acute airway inflammation. No significant changes were seen in any of the other genes analysed. Western blot data did not display any significant changes in the protein levels of the TFFs and SCGBs analysed. However, non-significant analysis of the data displayed an increase in TFF1 and TFF3, and a decrease in SCGB1A1 and SCGB3A2 in SI-3, similar to that seen in the N-A group. The A-ST group was different from the A-BD group, characterised by the use of inhaled corticosteroid medication to treat asthma symptoms. Inhaled corticosteroids are known to treat asthma symptoms through the control of inflammation. Therefore, it was expected that corticosteroid medication would also control the expression of TFFs, SCGBs, HATs and HDACs. Gene expression results only identified a 7.6-fold decrease in HDAC2 expression in SI-3 (p=0.001), which is proposed to be due to the up-regulation of HDAC2 protein that is known to be a function of corticosteroid use. Western blot data did not display any significant changes in the protein levels of the TFFs and SCGBs analysed. The gene expression in SI-2 and SI-3 in each group was compared. When comparing the A-BD group to the N-A group, a 9-fold increase in TFF3 (p=0.008) and a 34-fold increase in SCGB1A1 (p=0.03) were seen in the SI-3 samples. Comparisons of the A-ST group to the N-A group had an increased expression in SI-2 samples for HDAC5 (3.6-fold, p=0.04), NCOA2 (8.5-fold, p=0.04), NCOA3 (17-fold, p=0.01), HAT-1 (36-fold, p=0.003) and CREBBP (13-fold, p=0.001). The SI-3 samples in the A-ST group compared to the N-A group had increased expression for HDAC1 (6.4-fold, p=0.04), HDAC5 (5.2-fold, p=0.008), NCOA2 (9.6-fold, p=0.03), NCOA3 (16-fold, p=0.06), HAT-1 (41-fold, p<0.001) and CREBBP (31-fold, p=0.001). Comparisons of the A-ST group to the A-BD group had SI-2 increases in HDAC1 (3.8-fold, p=0.03), NCOA3 (4.5-fold, p=0.03), HAT-1 (5.3-fold, p=0.01) and CREBBP (23-fold, p=0.001), while SI-3 comparisons saw a decrease in HDAC2 (41-fold, p=0.008) and increases in HAT-1 (4.3-fold, p=0.003) and CREBBP (40-fold, p=0.001). Results showed that TFF3 and SCGB1A1 expression is higher in asthmatics than non-asthmatics and that histone acetylation is more active in the A-ST group than either the N-A or A-BD group, which suggests that histone acetylation activity may be positively correlated with asthma severity. The iTRAQ proteomic analysis of the secreted protein samples identified the SCGB1A1 protein and found it to be decreased in both the N-A and A-BD groups post-inflammation, but significantly so only in the A-BD group. Although no significant results were obtained from the western blot data, both groups displayed a decrease in SCGB1A1 concentration in SI-3 samples, suggesting a correlation with the proteomic data. Only 31 peptides were identified from the secreted samples. The intracellular iTRAQ analysis successfully identified 664 peptides, eight of which had differential expression in association with induced acute airway inflammation. Significant increases were seen in the A-BD group in SI-3 compared to SI-2 than in the N-A group in chloride intracellular channel protein 1, keratin-19, eosinophil cationic protein, calnexin, peroxiredoxin-5, and ATP-synthase delta subunit, while decreases were seen in cystatin-A and mucin-5AC. The iTRAQ analysis was only a discovery measure and further validation must be performed. In summary, the expression of TFFs and SCGBs differed between non-asthmatics and asthmatics. It is clear that TFF3 is active in the airway inflammation associated with asthma as indicated by an increase associated with inflammation in the A-BD group compared to the N-A group. Results for HDAC and HAT genes showed high HAT expression in the A-ST group compared to the N-A and A-BD groups, suggesting that histone acetyltransferases may be responsible for the characteristic unregulated inflammatory symptoms of asthmatics taking corticosteroids. Interestingly, corticosteroid medication did not seem to silence the expression of the analysed HAT genes, which indicates that corticosteroids may not control inflammation by direct regulation of HATs, but instead by competition, most probably with HDAC2 protein. As a discovery tool, iTRAQ is a potent method to both identify and compare the concentration of proteins between samples. The method is a powerful first step into the identification of novel proteins that are regulated in response to different treatments.

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Driver sleepiness contributes substantially to fatal and severe crashes and the contribution it makes to less serious crashes is likely to as great or greater. Currently, drivers’ awareness of sleepiness (subjective sleepiness) remains a critical component for the mitigation of sleep-related crashes. Nonetheless, numerous calls have been made for technological monitors of drivers’ physiological sleepiness levels so drivers can be ‘alerted’ when approaching high levels of sleepiness. Several physiological indices of sleepiness show potential as a reliable metric to monitor drivers’ sleepiness levels, with eye blink indices being a promising candidate. However, extensive evaluations of eye blink measures are lacking including the effects that the endogenous circadian rhythm can have on eye blinks. To examine the utility of ocular measures, 26 participants completed a simulated driving task while physiological measures of blink rate and duration were recorded after partial sleep restriction. To examine the circadian effects participants were randomly assigned to complete either a morning or an afternoon session of the driving task. The results show subjective sleepiness levels increased over the duration of the task. The blink duration index was sensitive to increases in sleepiness during morning testing, but was not sensitive during afternoon testing. This finding suggests that the utility of blink indices as a reliable metric for sleepiness are still far from specific. The subjective measures had the largest effect size when compared to the blink measures. Therefore, awareness of sleepiness still remains a critical factor for driver sleepiness and the mitigation of sleep-related crashes.

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We conducted a clinical trial to compare the molecular and cellular responses of human melanocytes and keratinocytes in vivo to solar-simulated ultraviolet radiation (SSUVR) in 57 Caucasian participants grouped according to MC1R genotype. We found that, on average, the density of epidermal melanocytes 14 days after exposure to 2 minimal erythemal dose (MED) SSUVR was twofold higher than baseline (unirradiated) skin. However, the change in epidermal melanocyte counts among people carrying germline MC1R variants (97% increase) was significantly less than those with wild-type MC1R (164% increase; P = 0.01). We also found that sunscreen applied to the skin before exposure to 2 MED SSUVR completely blocked the effects of DNA damage, p53 induction, and cellular proliferation in both melanocytes and keratinocytes.

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This study investigated Nrf2-activating properties of a coffee blend combining raw coffee bean constituents with 5-O-caffeoylquinic acid (CGA) as a lead component with typical roasting products such as N-methylpyridinium (NMP). In cell culture (HT29) the respective coffee extract (CN-CE) increased nuclear Nrf2 translocation and enhanced the transcription of ARE-dependent genes as exemplified for NAD(P)H:quinone oxidoreductase and glutathione-S-transferase (GST)A1, reflected in the protein level by an increase in GST enzyme activity. In a pilot human intervention study (29 healthy volunteers), daily consumption of 750 mL of CN-coffee for 4 weeks increased Nrf2 transcription in peripheral blood lymphocytes on average. However, the transcriptional response pattern of Nrf2/ARE-dependent genes showed substantial interindividual variations. The presence of SNPs in the Nrf2-promoter, reported recently, as well as the detection of GSTT1*0 (null) genotypes in the study collective strengthens the hypothesis that coffee acts as a modulator of Nrf2-dependent gene response in humans, but genetic polymorphisms play an important role in the individual response pattern.

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Saccharification of sugarcane bagasse pretreated at the pilot-scale with different processes (in combination with steam-explosion) was evaluated. Maximum glucan conversion with Celluclast 1.5 L (15–25 FPU/g glucan) was in the following order: glycerol/HCl > HCl > H2SO4 > NaOH, with the glycerol system achieving ∼100% conversion. Surprisingly, the NaOH substrate achieved optimum saccharification with only 8 FPU/g glucan. Glucan conversions (3.6–6%) obtained with mixtures of endo-1,4-β-glucanase (EG) and β-glucosidase (βG) for the NaOH substrate were 2–6 times that of acid substrates. However, glucan conversions (15–60%) obtained with mixtures of cellobiohydrolase (CBH I) and βG on acidified glycerol substrate were 10–30% higher than those obtained for NaOH and acid substrates. The susceptibility of the substrates to enzymatic saccharification was explained by their physical and chemical attributes. Acidified glycerol pretreatment offers the opportunity to simplify the complexity of enzyme mixtures required for saccharification of lignocellulosics.

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The population of Norfolk Island, located off the eastern coast of Australia, possesses an unusual and fascinating history. Most present-day islanders are related to a small number of the 'Bounty' mutineer founders. These founders consisted of Caucasian males and Polynesian females and led to an admixed present-day population. By examining a single large pedigree of 5742 individuals, spanning >200 years, we analyzed the influence of admixture and founder effect on various cardiovascular disease (CVD)-related traits. On account of the relative isolation of the population, on average one-third of the genomes of present-day islanders (single large pedigree individuals) is derived from 17 initial founders. The proportion of Polynesian ancestry in the present-day individuals was found to significantly influence total triglycerides, body mass index, systolic blood pressure and diastolic blood pressure. For various cholesterol traits, the influence of ancestry was less marked but overall the direction of effect for all CVD-related traits was consistent with Polynesian ancestry conferring greater CVD risk. Marker-derived homozygosity was computed and agreed with measures of inbreeding derived from pedigree information. Founder effect (inbreeding and marker-derived homozygosity) significantly influenced height. In conclusion, both founder effect and extreme admixture have substantially influenced the genetic architecture of a variety of CVD-related traits in this population.

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Selenium (Se) is an essential trace element and the clinical consequences of Se deficiency have been well-documented. Se is primarily obtained through the diet and recent studies have suggested that the level of Se in Australian foods is declining. Currently there is limited data on the Se status of the Australian population so the aim of this study was to determine the plasma concentration of Se and glutathione peroxidase (GSH-Px), a well-established biomarker of Se status. Furthermore, the effect of gender, age and presence of cardiovascular disease (CVD) was also examined. Blood plasma samples from healthy subjects (140 samples, mean age = 54 years; range, 20-86 years) and CVD patients (112 samples, mean age = 67 years; range, 40-87 years) were analysed for Se concentration and GSH-Px activity. The results revealed that the healthy Australian cohort had a mean plasma Se level of 100.2 +/- 1.3 microg Se/L and a mean GSH-Px activity of 108.8 +/- 1.7 U/L. Although the mean value for plasma Se reached the level required for optimal GSH-Px activity (i.e. 100 microg Se/L), 47% of the healthy individuals tested fell below this level. Further evaluation revealed that certain age groups were more at risk of a lowered Se status, in particular, the oldest age group of over 81 years (females = 97.6 +/- 6.1 microg Se/L; males = 89.4 +/- 3.8 microg Se/L). The difference in Se status between males and females was not found to be significant. The presence of CVD did not appear to influence Se status, with the exception of the over 81 age group, which showed a trend for a further decline in Se status with disease (plasma Se, 93.5 +/- 3.6 microg Se/L for healthy versus 88.2 +/- 5.3 microg Se/L for CVD; plasma GSH-Px, 98.3 +/- 3.9 U/L for healthy versus 87.0 +/- 6.5 U/L for CVD). These findings emphasise the importance of an adequate dietary intake of Se for the maintenance of a healthy ageing population, especially in terms of cardiovascular health.

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We study the difference in the result of two different risk elicitation methods by linking estimates of risk attitudes to gender, age, personality traits, a decision in a dilemma situation, and physiological states measured by heart rate variability (HRV). Our results indicate that differences between the methods can partly be explained by gender, but not by personality traits. Furthermore, HRV is linked to risktaking in the experiment for at least one of the methods, indicating that more stressed individuals display more risk aversion. Finally, we and that risk attitudes are not predictive of the ability to decide in a dilemma, but personality traits are. Surprisingly, there is also no apparent relationship between the physiological state during the dilemma situation and the ability to make a decision.

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Generally, the magnitude of pollutant emissions from diesel engines is ultimately coupled to the structure of fuel molecules. The presence of oxygen, level of unsaturation and the carbon chain length of respective molecules influence the combustion chemistry. It is speculated that increased oxygen content in the fuel may lead to the increased oxidative potential (Stevanovic, S. 2013). Also, upon the exposure to UV and ozone in the atmosphere, the chemical composition of the exhaust is changed. The presence of an oxidant and UV is triggering the cascade of photochemical reactions as well as the partitioning of semi-volatile compounds between the gas and particle phase. To gain an insight into the relationship between the molecular structures of the esters, their volatile organic content and the potential toxicity of diesel exhaust particulate matter, measurements were conducted on a modern common rail diesel engine. This research also investigates the contribution of atmospheric conditions on the transfer of semi-volatile fraction of diesel exhaust from the gas phase to the particle phase and the extent to which semi-volatile compounds (SVOCs) are related to the oxidative potential, expressed through the concentration of reactive oxygen species (ROS) (Stevanovic, S. 2013)...

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Aim To examine the mediating effect of coping strategies on the consequences of nursing and non-nursing (administrative) stressors on the job satisfaction of nurses during change management. Background Organisational change can result in an increase in nursing and nonnursing- related stressors, which can have a negative impact on the job satisfaction of nurses employed in health-care organisations. Method Matched data were collected in 2009 via an online survey at two timepoints (six months apart). Results Partial least squares path analysis revealed a significant causal relationship between Time 1 administrative and role stressors and an increase in nursing-specific stressors in Time 2. A significant relationship was also identified between job-specific nursing stressors and the adoption of effective coping strategies to deal with increased levels of change-induced stress and strain and the likelihood of reporting higher levels of job satisfaction in Time 2. Conclusions The effectiveness of coping strategies is critical in helping nurses to deal with the negative consequences of organisational change. Implications for nursing management This study shows that there is a causal relationship between change, non-nursing stressors and job satisfaction. Senior management should implement strategies aimed at reducing nursing and nonnursing stress during change in order to enhance the job satisfaction of nurses. Keywords: Australia, change management, job satisfaction, nursing and non-nursing stressors, public and non-profit sector