907 resultados para Cancer prevention


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The school environment plays an important role in shaping adolescent outcomes, and research increasingly demonstrates the need to target the school social context in health promotion programs. This paper describes the research process undertaken to design a school connectedness component of an injury prevention program for early adolescents, Skills for Preventing Injury in Youth (SPIY). The connectedness component takes the form of a professional development workshop for teachers on increasing students’ connectedness to school, and this paper describes the research process used to construct program material. It also describes the methods used to encourage teachers’ implementation of connectedness strategies following program delivery. A multi-stage process of data collection included, (i) surveys with 540 Grade 9 students to examine links between school connectedness and risk-related injury, (ii) a systematic literature review of previously-evaluated school connectedness programs to determine key strategies that encourage implementation fidelity and program effectiveness, and (iii) interviews with 14 high school teachers to understand current use of connectedness strategies and ideas for program design. Findings from each stage are discussed in terms of how results informed the program design. The survey data provided information from which to frame program content, and the results of the systematic review demonstrated effective program strategies. The teacher interview data also provided program content incorporating target participants’ views and aligning with their priorities, which is important to ensure effective implementation of program strategies. A comprehensive design process provides an understanding of methods for, and may encourage, teachers’ future implementation of program strategies.

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High-risk adolescents are a population most vulnerable to harm from injury due to increased engagement in risk taking behaviour. There is a gap in the literature regarding how universal school based injury prevention programs apply to high-risk adolescents. This study involves a component of the process evaluation of a school based injury prevention program, as it relates to high-risk adolescents (13-14 years)...

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Macrophage inhibitory cytokine-1 (MIC-1/GDF15), a divergent member of the TGF-β superfamily, is over-expressed by many common cancers including those of the prostate (PCa) and its expression is linked to cancer outcome. We have evaluated the effect of MIC-1/GDF15 overexpression on PCa development and spread in the TRAMP transgenic model of spontaneous prostate cancer. TRAMP mice were crossed with MIC-1/GDF15 overexpressing mice (MIC-1fms) to produce syngeneic TRAMPfmsmic-1 mice. Survival rate, prostate tumor size, histopathological grades and extent of distant organ metastases were compared. Metastasis of TC1-T5, an androgen independent TRAMP cell line that lacks MIC-1/GDF15 expression, was compared by injecting intravenously into MIC-1fms and syngeneic C57BL/6 mice. Whilst TRAMPfmsmic-1 survived on average 7.4 weeks longer, had significantly smaller genitourinary (GU) tumors and lower PCa histopathological grades than TRAMP mice, more of these mice developed distant organ metastases. Additionally, a higher number of TC1-T5 lung tumor colonies were observed in MIC-1fms mice than syngeneic WT C57BL/6 mice. Our studies strongly suggest that MIC-1/GDF15 has complex actions on tumor behavior: it limits local tumor growth but may with advancing disease, promote metastases. As MIC-1/GDF15 is induced by all cancer treatments and metastasis is the major cause of cancer treatment failure and cancer deaths, these results, if applicable to humans, may have a direct impact on patient care.

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Tumour necrosis factor (TNF) is a pleiotropic cytokine with dual roles in cancer biology including prostate cancer (PCa). On the one hand, there is evidence that it stimulates tumour angiogenesis, is involved in the initiation of PCa from an androgen-dependent to a castrate resistant state, plays a role in epithelial to mesenchymal plasiticity, and may contribute to the aberrant regulation of eicosanoid pathways. On the other hand, TNF has also been reported to inhibit neovascularisation, induce apoptosis of PCa cells, and stimulate anti-tumour immunity. Much of the confusion surrounding its seemingly paradoxical roles in cancer biology stems from the dependence of its effects on the biological model within which TNF is investigated. This review will address some of these issues, and also discuss on the therapeutic implications.

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Paraffin sections (n = 168, 27 benign, 16 low malignant potential [LMP] and 125 malignant tumours) from epithelial ovarian tumours were evaluated immunohistochemically for expression of retinoblastoma gene product (pRB) and p53 protein, and the relationship among pRB, p53 and cyclin-dependent kinase inhibitor 2 (CDKN2) gene product p16INK4A (p16) was analysed, following our previous study of p16. Forty-one percent of the benign, 50% of the LMP and most (71%) of the malignant tumours showed high pRB expression. High expression of pRB (>50% pRB-positive cells) significantly correlated with non-mucinous histological subtypes. Reduced pRB expression, substage and residual disease were significant predictors for poor prognosis in stage I patients. All the benign and most of the LMP (81%) tumours were in either the p53-negative or low p53-positive category, but nearly half of the malignant tumours had high p53 expression. High p53 accumulation was found in non-mucinous, high grade and late stage tumours. For well-differentiated carcinomas, high p53 expression was a predictor of poor prognosis. However, even though high p53 expression was not associated with histological subtype, stage or the presence of residual disease, high p53 expression was not an independent predictor when all clinical parameters were combined. For all ovarian cancers, a close correlation was found between high p53 and high p16 expression. The relationship between the expression of pRB and p16 depended on tumour stage. In stage I tumours, high pRB was associated with low p16 reactivity. On the other hand, most advanced tumours showed both high pRB and high p16 reactivity. Int. J. Cancer 74:407–415, 1997. © 1997 Wiley-Liss, Inc.

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Paraffin sections from 190 epithelial ovarian tumours, including 159 malignant and 31 benign epithelial tumours, were analysed immunohistochemically for expression of cyclin-dependent kinase inhibitor 2 (CDKN2A) gene product p16INK4A (p16). Most benign tumours showed no p16 expression in the tumour cells, whereas only 11% of malignant cancers were p16 negative. A high proportion of p16-positive tumour cells was associated with advanced stage and grade, and with poor prognosis in cancer patients. For FIGO stage 1 tumours, a high proportion of p16-positive tumour cells was associated with poorer survival, suggesting that accumulation of p16 is an early event of ovarian tumorigenesis. In contrast to tumour cells, high expression of p16 in the surrounding stromal cells was not associated with the stage and grade, but was associated with longer survival. When all parameters were combined in multivariate analysis, high p16 expression in stromal cells was not an independent predictor for survival, indicating that low p16 expression in stromal cells is associated with other markers of tumour progression. High expression of p16 survival in the stromal cells of tumours from long-term survivors suggests that tumour growth is limited to some extent by factors associated with p16 expression in the matrix.

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Background/objectives This study estimates the economic outcomes of a nutrition intervention to at-risk patients compared with standard care in the prevention of pressure ulcer. Subjects/methods Statistical models were developed to predict ‘cases of pressure ulcer avoided’, ‘number of bed days gained’ and ‘change to economic costs’ in public hospitals in 2002–2003 in Queensland, Australia. Input parameters were specified and appropriate probability distributions fitted for: number of discharges per annum; incidence rate for pressure ulcer; independent effect of pressure ulcer on length of stay; cost of a bed day; change in risk in developing a pressure ulcer associated with nutrition support; annual cost of the provision of a nutrition support intervention for at-risk patients. A total of 1000 random re-samples were made and the results expressed as output probability distributions. Results The model predicts a mean 2896 (s.d. 632) cases of pressure ulcer avoided; 12 397 (s.d. 4491) bed days released and corresponding mean economic cost saving of euros 2 869 526 (s.d. 2 078 715) with a nutrition support intervention, compared with standard care. Conclusion Nutrition intervention is predicted to be a cost-effective approach in the prevention of pressure ulcer in at-risk patients.

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To enhance workplace safety in the construction industry it is important to understand interrelationships among safety risk factors associated with construction accidents. This study incorporates the systems theory into Heinrich’s domino theory to explore the interrelationships of risks and break the chain of accident causation. Through both empirical and statistical analyses of 9,358 accidents which occurred in the U.S. construction industry between 2002 and 2011, the study investigates relationships between accidents and injury elements (e.g., injury type, part of body, injury severity) and the nature of construction injuries by accident type. The study then discusses relationships between accidents and risks, including worker behavior, injury source, and environmental condition, and identifies key risk factors and risk combinations causing accidents. The research outcomes will assist safety managers to prioritize risks according to the likelihood of accident occurrence and injury characteristics, and pay more attention to balancing significant risk relationships to prevent accidents and achieve safer working environments.

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Destruction of cancer cells by genetically modified viral and nonviral vectors has been the aim of many research programs. The ability to target cytotoxic gene therapies to the cells of interest is an essential prerequisite, and the treatment has always had the potential to provide better and more long-lasting therapy than existing chemotherapies. However, the potency of these infectious agents requires effective testing systems, in which hypotheses can be explored both in vitro and in vivo before the establishment of clinical trials in humans. The real prospect of off-target effects should be eliminated in the preclinical stage, if current prejudices against such therapies are to be overcome. In this review we have set out, using adenoviral vectors as a commonly used example, to discuss some of the key parameters required to develop more effective testing, and to critically assess the current cellular models for the development and testing of prostate cancer biotherapy. Only by developing models that more closely mirror human tissues will we be able to translate literature publications into clinical trials and hence into acceptable alternative treatments for the most commonly diagnosed cancer in humans.

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The publication of the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric Association, 1994) introduced the notion that a life-threatening illness can be a stressor and catalyst for Posttraumatic Stress Disorder (PTSD). Since then a solid body of research has been established investigating the post-diagnosis experience of cancer. These studies have identified a number of short and long-term life changes resulting from a diagnosis of cancer and associated treatments. In this chapter, we discuss the psychosocial response to the cancer experience and the potential for cancer-related distress. Cancer can represent a life-threatening diagnosis that may be associated with aggressive treatments and result in physical and psychological changes. The potential for future trauma through the lasting effects of the disease and treatment, and the possibility of recurrence, can be a source of continued psychological distress. In addition to the documented adverse repercussions of cancer, we also outline the recent shift that has occurred in the psycho-oncology literature regarding positive life change or posttraumatic growth that is commonly reported after a diagnosis of cancer. Adopting a salutogenic framework acknowledges that the cancer experience is a dynamic psychosocial process with both negative and positive repercussions. Next, we describe the situational and individual factors that are associated with posttraumatic growth and the types of positive life change that are prevalent in this context. Finally, we discuss the implications of this research in a therapeutic context and the directions of future posttraumatic growth research with cancer survivors. This chapter will present both quantitative and qualitative research that indicates the potential for personal growth from adversity rather than just mere survival and return to pre-diagnosis functioning. It is important to emphasise however, that the presence of growth and prevalence of resilience does not negate the extremely distressing nature of a cancer diagnosis for the patient and their families and the suffering that can accompany treatment regimes. Indeed, it will be explained that for growth to occur, the experience must be one that quite literally shatters previously held schemas in order to act as a catalyst for change.