Work ethics and general work attitudes in adolescents are related to quality of life, sense of coherence and subjective health – a Swedish questionnaire study

BACKGROUND: Working life is an important arena in most people's lives, and the working line concept is important for the development of welfare in a society. For young people, the period before permanent establishment in working life has become longer during the last two decades. Knowledge about attitudes towards work can help us to understand young people's transition to the labour market. Adolescents are the future workforce, so it seems especially important to notice their attitudes towards work, including attitudes towards the welfare system. The aim of this study was to describe and analyse upper secondary school students' work attitudes, and to explore factors related to these attitudes. METHODS: The sample consisted of 606 upper secondary school students. They all received a questionnaire including questions about quality of life (QOL), sense of coherence (SOC), subjective health and attitudes towards work. The response rate was 91%. A factor analysis established two dimensions of work attitudes. Multivariate analyses were carried out by means of logistic regression models. RESULTS: Work ethics (WE) and general work attitudes (GWA) were found to be two separate dimensions of attitudes towards work. Concerning WE the picture was similar regardless of gender or study programme. Males in theoretical programmes appeared to have more unfavourable GWA than others. Multivariate analyses revealed that good QOL, high SOC and good health were significantly related to positive WE, and high SOC was positively related to GWA. Being female was positively connected to WE and GWA, while studying on a practical programme was positively related to GWA only. Among those who received good parental support, GWA seemed more favourable. CONCLUSION: Assuming that attitudes towards work are important to the working line concept, this study points out positive factors of importance for the future welfare of the society. Individual factors such as female gender, good QOL, high SOC and good health as well as support from both parents, positive experience of school and work contacts related positively to attitudes towards work. Further planning and supportive work have to take these factors into account

CDK2 and PKA Mediated-Sequential Phosphorylation Is Critical for p19INK4d Function in the DNA Damage Response

DNA damage triggers a phosphorylation-based signaling cascade known as the DNA damage response. p19INK4d, a member of the INK4 family of CDK4/6 inhibitors, has been reported to participate in the DNA damage response promoting DNA repair and cell survival. Here, we provide mechanistic insight into the activation mechanism of p19INK4d linked to the response to DNA damage. Results showed that p19INK4d becomes phosphorylated following UV radiation, β-amyloid peptide and cisplatin treatments. ATM-Chk2/ATR-Chk1 signaling pathways were found to be differentially involved in p19INK4d phosphorylation depending on the type of DNA damage. Two sequential phosphorylation events at serine 76 and threonine 141 were identified using p19INK4d single-point mutants in metabolic labeling assays with 32P-orthophosphate. CDK2 and PKA were found to participate in p19INK4d phosphorylation process and that they would mediate serine 76 and threonine 141 modifications respectively. Nuclear translocation of p19INK4d induced by DNA damage was shown to be dependent on serine 76 phosphorylation. Most importantly, both phosphorylation sites were found to be crucial for p19INK4d function in DNA repair and cell survival. In contrast, serine 76 and threonine 141 were dispensable for CDK4/6 inhibition highlighting the independence of p19INK4d functions, in agreement with our previous findings. These results constitute the first description of the activation mechanism of p19INK4d in response to genotoxic stress and demonstrate the functional relevance of this activation following DNA damage

Deficiency in trefoil factor 1 (TFF1) increases tumorigenicity of human breast cancer cells and mammary tumor development in TFF1-knockout mice

Although trefoil factor 1 (TFF1; previously named pS2) is abnormally expressed in about 50% of human breast tumors, its physiopathological role in this disease has been poorly studied. Moreover, controversial data have been reported. TFF1 function in the mammary gland therefore needs to be clarified. In this study, using retroviral vectors, we performed TFF1 gain- or loss-of-function experiments in four human mammary epithelial cell lines: normal immortalized TFF1-negative MCF10A, malignant TFF1-negative MDA-MB-231 and malignant TFF1-positive MCF7 and ZR75.1. The expression of TFF1 stimulated the migration and invasion in the four cell lines. Forced TFF1 expression in MCF10A, MDA-MB-231 and MCF7 cells did not modify anchorage-dependent or -independent cell proliferation. By contrast, TFF1 knockdown in MCF7 enhanced soft-agar colony formation. This increased oncogenic potential of MCF7 cells in the absence of TFF1 was confirmed in vivo in nude mice. Moreover, chemically induced tumorigenesis in TFF1-deficient (TFF1-KO) mice led to higher tumor incidence in the mammary gland and larger tumor size compared with wild-type mice. Similarly, tumor development was increased in the TFF1-KO ovary and lung. Collectively, our results clearly show that TFF1 does not exhibit oncogenic properties, but rather reduces tumor development. This beneficial function of TFF1 is in agreement with many clinical studies reporting a better outcome for patients with TFF1-positive breast primary tumors