983 resultados para Reproductive Strategies


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Purpose – The purpose of this paper is to develop an effective methodology for implementing lean manufacturing strategies and a leanness evaluation metric using continuous performance measurement (CPM). Design/methodology/approach – Based on five lean principles, a systematic lean implementation methodology for manufacturing organizations has been proposed. A simplified leanness evaluation metric consisting of both efficiency and effectiveness attributes of manufacturing performance has been developed for continuous evaluation of lean implementation. A case study to validate the proposed methodology has been conducted and proposed CPM metric has been used to assess the manufacturing leanness. Findings – Proposed methodology is able to systematically identify manufacturing wastes, select appropriate lean tools, identify relevant performance indicators, achieve significant performance improvement and establish lean culture in the organization. Continuous performance measurement matrices in terms of efficiency and effectiveness are proved to be appropriate methods for continuous evaluation of lean performance. Research limitations/implications – Effectiveness of the method developed has been demonstrated by applying it in a real life assembly process. However, more tests/applications will be necessary to generalize the findings. Practical implications – Results show that applying the methods developed, managers can successfully identify and remove manufacturing wastes from their production processes. By improving process efficiency, they can optimize their resource allocations. Manufacturers now have a validated step by step methodology for successfully implementing lean strategies. Originality/value – According to the authors’ best knowledge, this is the first known study that proposed a systematic lean implementation methodology based on lean principles and continuous improvement techniques. Evaluation of performance improvement by lean strategies is a critical issue. This study develops a simplified leanness evaluation metric considering both efficiency and effectiveness attributes and integrates it with the lean implementation methodology.

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Background Parents are at risk for physical inactivity; however, few studies have designed physical activity (PA) interventions specifically applied to individuals with young children. To ensure the effectiveness of interventions, it may be useful to first elicit the needs from the target population and incorporate salient strategies identified to the design and delivery of a resultant intervention. We aimed to explore strategies for what to include in and how to best deliver a program designed to increase parental PA. Methods Twelve parents (6 mothers, 6 fathers) of children younger than 5 years participated in focus group discussions exploring strategies for an intervention program designed to increase parental PA. Results A range of themes such as Focus on the Children and Flexible Life/Family Plans imbedded in strategies such as persuasion and information, problem-solving, skill building, and environmental approaches were identified. In addition, a range of strategies for how to best deliver a parental PA intervention evidenced in emerging themes such as Diverse and Brief and Individualized Approach was discussed. Conclusions Future research should continue to adopt a ground up, community-based approach to the development and implementation of interventions for this at-risk group to ensure sustained involvement in regular PA.

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PROBLEM Estradiol regulates chemokine secretion from uterine epithelial cells, but little is known about estradiol regulation in vivo or the role of estrogen receptors (ERs). METHOD CCL20 and CXCL1 present in reproductive washes following treatment with selective estrogen receptor modulators (SERMs) were compared with that during estrous and following estradiol-treated ovariectomized BALB/c mice. Cellular regulation was determined using isolated vaginal and uterine epithelial/stromal cells in vitro. RESULTS Uterine and vaginal chemokine secretion is cyclically regulated with CCL20 at low levels but CXCL1 at high levels during high estradiol, generally mimicking estradiol effect in vivo. ERα but not ERβ regulated CCL20/CXCL1 secretion by uterine epithelial cells in vitro and vaginal CCL20 in vivo. Estradiol/SERMs failed to alter uterine CCL20 secretion in ovariectomized mice. Diminished uterine epithelial ERα staining following ovariectomy corresponded with estradiol unresponsiveness of uterine tissue. CONCLUSION Estrogen receptors α regulates CCL20/CXCL1 secretion in the female reproductive tract, and ERα antagonists directly oppose the regulation by estradiol. Understanding ER-mediated antimicrobial chemokine expression is important to elucidate cyclic susceptibility to sexually transmitted pathogens.

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The studies presented in this review explore three distinct areas with potential for inhibiting HIV infection in women. Based on emerging information from the physiology, endocrinology and immunology of the female reproductive tract (FRT), we propose unique 'works in progress' for protecting women from HIV. Various aspects of FRT immunity are suppressed by estradiol during the menstrual cycle, making women more susceptible to HIV infection. By engineering commensal Lactobacillus to secrete the anti-HIV molecule Elafin as estradiol levels increase, women could be protected from HIV infection. Selective estrogen response modifiers enhance barrier integrity and enhance secretion of protective anti-HIV molecules. Finally, understanding the interactions and regulation of FRT endogenous antimicrobials, proteases, antiproteases, etc., all of which are under hormonal control, will open new avenues to therapeutic manipulation of the FRT mucosal microenvironment. By seeking new alternatives to preventing HIV infection in women, we may finally disrupt the HIV pandemic.

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This review examines the multiple levels of pre-existing immunity in the upper and lower female reproductive tract. In addition, we highlight the need for further research of innate and adaptive immune protection of mucosal surfaces in the female reproductive tract. Innate mechanisms include the mucus lining, a tight epithelial barrier and the secretion of antimicrobial peptides and cytokines by epithelial and innate immune cells. Stimulation of the innate immune system also serves to bridge the adaptive arm resulting in the generation of pathogen-specific humoral and cell-mediated immunity. Less understood are the multiple components that act in a coordinated way to provide a network of ongoing protection. Innate and adaptive immunity in the human female reproductive tract are influenced by the stage of menstrual cycle and are directly regulated by the sex steroid hormones, progesterone and estradiol. Furthermore, the effect of hormones on immunity is mediated both directly on immune and epithelial cells and indirectly by stimulating growth factor secretion from stromal cells. The goal of this review is to focus on the diverse aspects of the innate and adaptive immune systems that contribute to a unique network of protection throughout the female reproductive tract.

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The immune system in the female reproductive tract (FRT) does not mount an attack against HIV or other sexually transmitted infections (STI) with a single endogenously produced microbicide or with a single arm of the immune system. Instead, the body deploys dozens of innate antimicrobials to the secretions of the female reproductive tract. Working together, these antimicrobials along with mucosal antibodies attack many different viral, bacterial and fungal targets. Within the FRT, the unique challenges of protection against sexually transmitted pathogens coupled with the need to sustain the development of an allogeneic fetus have evolved in such a way that sex hormones precisely regulate immune function to accomplish both tasks. The studies presented in this review demonstrate that estradiol and progesterone secreted during the menstrual cycle act both directly and indirectly on epithelial cells and other immune cells in the reproductive tract to modify immune function in a way that is unique to specific sites throughout the FRT. As presented in this review, studies from our laboratory and others demonstrate that the innate immune response is under hormonal control, varies with the stage of the menstrual cycle, and as such is suppressed at mid-cycle to optimize conditions for successful fertilization and pregnancy. In doing so, a window of STI vulnerability is created during which potential pathogens including HIV enter the reproductive tract to infect host targets.

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Successful control of sexually transmitted diseases (STDs) through vaccination will require the development of vaccine strategies that target protective immunity to both the female and male reproductive tracts (MRT). In the male, the immune privileged nature of the male reproductive tract provides a barrier to entry of serum immunoglobulins into the male reproductive ducts, thereby preventing the induction of protective immunity using conventional injectable vaccination techniques. In this study we investigated the potential of intranasal (IN) immunization to elicit anti-chlamydial immunity in BALB/c male mice. Intranasal immunization with Chlamydia muridarum major outer membrane protein (MOMP) admixed with cholera toxin (CT) resulted in high levels of MOMP-specific IgA in prostatic fluids (PF) and MOMP-specific IgA-secreting cells in the prostate. Prostatic fluid IgA inhibited in vitro infection of McCoy cells with C. muridarum. Using RT-PCR we also show that mRNA for the polymeric immunoglobulin receptor (PIgR), which transports IgA across mucosal epithelia, is expressed only in the prostate but not in other regions of the male reproductive ducts upstream of the prostate. These data suggest that using intranasal immunization to target IgA to the prostate may protect males against STDs while at the same time maintaining the state of immune privilege within the MRT.

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Objective The 2010–2011 Queensland floods resulted in the most deaths from a single flood event in Australia since 1916. This article analyses the information on these deaths for comparison with those from previous floods in modern Australia in an attempt to identify factors that have contributed to those deaths. Haddon's Matrix, originally designed for prevention of road trauma, offers a framework for understanding the interplay between contributing factors and helps facilitate a clearer understanding of the varied strategies required to ensure people's safety for particular flood types. Methods Public reports and flood relevant literature were searched using key words ‘flood’, ‘fatality’, ‘mortality’, ‘death’, ‘injury’ and ‘victim’ through Google Scholar, PubMed, ProQuest and EBSCO. Data relating to reported deaths during the 2010–2011 Queensland floods, and relevant data of previous Australian flood fatality (1997–2009) were collected from these available sources. These sources were also used to identify contributing factors. Results There were 33 deaths directly attributed to the event, of which 54.5% were swept away in a flash flood on 10 January 2011. A further 15.1% of fatalities were caused by inappropriate behaviours. This is different to floods in modern Australia where over 90% of deaths are related to the choices made by individuals. There is no single reason why people drown in floods, but rather a complex interplay of factors. Conclusions The present study and its integration of research findings and conceptual frameworks might assist governments and communities to develop policies and strategies to prevent flood injury and fatalities.

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Victim/survivors of human trafficking involving partner migration employ diverse help-seeking strategies, both formal and informal, to exit their exploitative situations. Drawing on primary research conducted by Lyneham and Richards (forthcoming), the authors highlight the importance of educating the community and professionals from a wide range of sectors—including health, mental health, child protection, social welfare, social work, domestic violence, migration, legal and law enforcement services—about human trafficking and the help-seeking strategies of victims/survivors in order to support them to leave exploitative situations. Enhancing Australia’s knowledge of victim/survivors’ help-seeking strategies will better inform government and community responses to this crime, improve detection and identification of human trafficking matters and subsequent referral to appropriate victim services.

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Background Chlamydia trachomatis infection results in reproductive damage in some women. The process and factors involved in this immunopathology are not well understood. This study aimed to investigate the role of primary human cellular responses to chlamydial stress response proteases and chlamydial infection to further identify the immune processes involved in serious disease sequelae. Results Laboratory cell cultures and primary human reproductive epithelial cultures produced IL-6 in response to chlamydial stress response proteases (CtHtrA and CtTsp), UV inactivated Chlamydia, and live Chlamydia. The magnitude of the IL-6 response varied considerably (up to 1000 pg ml-1) across different primary human reproductive cultures. Thus different levels of IL-6 production by reproductive epithelia may be a determinant in disease outcome. Interestingly, co-culture models with either THP-1 cells or autologous primary human PBMC generally resulted in increased levels of IL-6, except in the case of live Chlamydia where the level of IL-6 was decreased compared to the epithelial cell culture only, suggesting this pathway may be able to be modulated by live Chlamydia. PBMC responses to the stress response proteases (CtTsp and CtHtrA) did not significantly vary for the different participant cohorts. Therefore, these proteases may possess conserved innate PAMPs. MAP kinases appeared to be involved in this IL-6 induction from human cells. Finally, we also demonstrated that IL-6 was induced by these proteins and Chlamydia from mouse primary reproductive cell cultures (BALB/C mice) and mouse laboratory cell models. Conclusions We have demonstrated that IL-6 may be a key factor for the chlamydial disease outcome in humans, given that primary human reproductive epithelial cell culture showed considerable variation in IL-6 response to Chlamydia or chlamydial proteins, and that the presence of live Chlamydia (but not UV killed) during co-culture resulted in a reduced IL-6 response suggesting this response may be moderated by the presence of the organism.

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The overall aim of this research project was to provide a broader range of value propositions (beyond upfront traditional construction costs) that could transform both the demand side and supply side of the housing industry. The project involved gathering information about how building information is created, used and communicated and classifying building information, leading to the formation of an Information Flow Chart and Stakeholder Relationship Map. These were then tested via broad housing industry focus groups and surveys. The project revealed four key relationships that appear to operate in isolation to the whole housing sector and may have significant impact on the sustainability outcomes and life cycle costs of dwellings over their life cycle. It also found that although a lot of information about individual dwellings does already exist, this information is not coordinated or inventoried in any systematic manner and that national building information files of building passports would present value to a wide range of stakeholders.

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Enormous progress has been made towards understanding the role of specific factors in the process of epithelial-mesenchymal transition (EMT); however, the complex underlying pathways and the transient nature of the transition continues to present significant challenges. Targeting tumour cell plasticity underpinning EMT is an attractive strategy to combat metastasis. Global gene expression profiling and high-content analyses are among the strategies employed to identify novel EMT regulators. In this review, we highlight several approaches to systematically interrogate key pathways involved in EMT, with particular emphasis on the features of multiparametric, high-content imaging screening strategies that lend themselves to the systematic discovery of highly significant modulators of tumour cell plasticity.

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Objective Recently, a number of studies have identified self-employed Protective Behavioral Strategies (PBS) as effective in decreasing the level of alcohol-related harm among young people. However, much of the published research has ignored important gender differences, such as women's increased tendency to rely on PBS that are social in nature. To further the understanding of women's PBS, the current study sought to investigate the nature and correlates of the strategies young women employ to keep their friends safe when drinking (i.e., peer-directed PBS). Method A scale measuring peer-directed PBS was developed and administered in conjunction with existing measures of alcohol consumption, personal PBS, and peer attachment. Participants consisted of 422 women aged 18–30 years, recruited among psychology students and the general public. Results Exploratory factor analysis revealed two clusters of peer-directed PBS; those that were aimed at reducing intoxication among one's friends and those that were designed to minimize alcohol-related harms. Further analysis found a positive relationship between women's tendency to implement personal and peer-directed PBS and that risky drinkers were less likely to engage in personal or peer-directed PBS (either type). Conclusion Findings indicate that personal and peer-directed PBS are related behaviors that are less frequently adopted by risky drinkers.

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The PI3K/AKT/mTOR pathway regulates cell growth and proliferation and is often dysregulated in cancer due to mutation, amplification, deletion, methylation and post-translational modifications. We and others have shown that activation of this pathway in non-small cell lung cancer (NSCLC) leads to a more aggressive disease which correlates to poor prognosis for patients. A multitude of selective inhibitors are in development which target key regulators in this pathway, however the success of PI3K targeted inhibition has been hampered by a high rate of innate and acquired resistance. Response to PI3K inhibition may be improved by co-targeting potential mediators of resistance, such as related cell surface receptors or other intracellular signaling pathways which cross-talk with the PI3K pathway. Inhibition of the PI3K pathway may also overcome radioresistance, chemoresistance and immune evasion in NSCLC. The identification of appropriate patient cohorts who will benefit from PI3K co-targeted inhibition strategies will be key to the success of these inhibitors.