Public health education in Europe: old and new challenges

The purpose of this article is to discuss some of the current challenges faced by European schools of public health. Perhaps most remarkable on the continent is the diversity, the magnitude, and the rapidity of the developments in public health education since the Second World War. This article discusses its evolution, its main characteristics and the underlying rationale with several examples. Further, it addresses specific aspects of the future development, namely the collaboration of academic schools with practice-oriented institutions, as well as the interactions between the constituent disciplines of public health. The Bologna process on post-graduate education in Europe has had an important impact on the overall design of most schools. There is a willingness to develop public health in each country of the European region and there is a need to develop common strategies to reach high standards in teaching, training and researching in all disciplines related to public health.

Interactions between cancer stem cells and their niche govern metastatic colonization.

Metastatic growth in distant organs is the major cause of cancer mortality. The development of metastasis is a multistage process with several rate-limiting steps. Although dissemination of tumour cells seems to be an early and frequent event, the successful initiation of metastatic growth, a process termed 'metastatic colonization', is inefficient for many cancer types and is accomplished only by a minority of cancer cells that reach distant sites. Prevalent target sites are characteristic of many tumour entities, suggesting that inadequate support by distant tissues contributes to the inefficiency of the metastatic process. Here we show that a small population of cancer stem cells is critical for metastatic colonization, that is, the initial expansion of cancer cells at the secondary site, and that stromal niche signals are crucial to this expansion process. We find that periostin (POSTN), a component of the extracellular matrix, is expressed by fibroblasts in the normal tissue and in the stroma of the primary tumour. Infiltrating tumour cells need to induce stromal POSTN expression in the secondary target organ (in this case lung) to initiate colonization. POSTN is required to allow cancer stem cell maintenance, and blocking its function prevents metastasis. POSTN recruits Wnt ligands and thereby increases Wnt signalling in cancer stem cells. We suggest that the education of stromal cells by infiltrating tumour cells is an important step in metastatic colonization and that preventing de novo niche formation may be a novel strategy for the treatment of metastatic disease.

Apprendre ensemble pourtravailler ensemble: l'education interprofessionnelle, un mythe ou une réalité [Learning together to work together: interprofessional education, a myth or reality?].

This article offers a review of the literature on interprofessional education (EIP), a form of education which brings together members of two or more professions in a joint training. In this course, participants gain knowledge through other professionals and about them. The goal of EIP is to improve collaboration between health professionals and the quality of patient care. The EIP is booming worldwide and seems for from a mere fad. This expansion can be explained by several factors: the increasing importance attributed to the quality of care and patient safety, care changes (aging population and increasing chronic diseases) and the shortage of health professionals. The expectations of the EIP are large, while the evidence supporting its effectiveness is being built.

Functional education of invariant NKT cells by dendritic cell tuning of SHP-1.

Invariant NKT (iNKT) cells play key roles in host defense by recognizing lipid Ags presented by CD1d. iNKT cells are activated by bacterial-derived lipids and are also strongly autoreactive toward self-lipids. iNKT cell responsiveness must be regulated to maintain effective host defense while preventing uncontrolled stimulation and potential autoimmunity. CD1d-expressing thymocytes support iNKT cell development, but thymocyte-restricted expression of CD1d gives rise to Ag hyperresponsive iNKT cells. We hypothesized that iNKT cells require functional education by CD1d(+) cells other than thymocytes to set their correct responsiveness. In mice that expressed CD1d only on thymocytes, hyperresponsive iNKT cells in the periphery expressed significantly reduced levels of tyrosine phosphatase SHP-1, a negative regulator of TCR signaling. Accordingly, heterozygous SHP-1 mutant mice displaying reduced SHP-1 expression developed a comparable population of Ag hyperresponsive iNKT cells. Restoring nonthymocyte CD1d expression in transgenic mice normalized SHP-1 expression and iNKT cell reactivity. Radiation chimeras revealed that CD1d(+) dendritic cells supported iNKT cell upregulation of SHP-1 and decreased responsiveness after thymic emigration. Hence, dendritic cells functionally educate iNKT cells by tuning SHP-1 expression to limit reactivity.

The Europeanisation of the measurement of diversity in education: a soft instrument of public policy

Faced with an increasing number of data and rankings, the author questions the roles of the different groups of actors who were originally involved in questioning the use of statistical indicators as a means of addressing issues of access to higher education. The comparison and nature of these international (UNESCO, OECD, EUROSTAT) and national (Germany, England, France, Switzerland) indicators in matters of inequalities of access to higher education question the tension between the discourses and the indicators they generate, and their recording at the national level. Who says what and with what consequences? What range of actors are involved in this process? What kind of power relations forms them? The author discusses how the issue of inequalities of access to higher education got on to the agendas of European organisations, identifies the policies that were defined, and sets them against an array of indicators, showing the discrepancy between the discourses and what the indicators reveal, the gap between the recommendations and the available tools. Why is there such a contrast? What are the mechanisms at work? Is it a technical or a political problem? What does this discrepancy reveal as far as national specificities within the construction of social inequalities are concerned?

Cancer Cell-Associated MT1-MMP Promotes Blood Vessel Invasion and Distant Metastasis in Triple-Negative Mammary Tumors.

Functional roles for the cancer cell-associated membrane type I matrix metalloproteinase (MT1-MMP) during early steps of the metastatic cascade in primary tumors remain unresolved. In an effort to determine its significance, we determined the in vivo effects of RNAi-mediated downregulation in mammary cancer cells on the migration, blood and lymphatic vessel invasion (LVI), and lymph node and lung metastasis. We also correlated the expression of cancer cell MT1-MMP with blood vessel invasion (BVI) in 102 breast cancer biopsies. MT1-MMP downregulation in cancer cells decreased lung metastasis without affecting primary tumor growth. The inhibition of lung metastasis correlated with reduced cancer cell migration and BVI. Furthermore, cancer cell-expressed MT1-MMP upregulated the expression of MT1-MMP in vascular endothelial cells, but did not affect MT1-MMP expression in lymphatic endothelial cells, LVI, or lymph node metastasis. Of clinical importance, we observed that elevated MT1-MMP expression correlated with BVI in biopsies from triple-negative breast cancers (TNBC), which have a poor prognosis and high incidence of distant metastasis, relative to other breast cancer subtypes. Together, our findings established that MT1-MMP activity in breast tumors is essential for BVI, but not LVI, and that MT1-MMP should be further explored as a predictor and therapeutic target of hematogenous metastasis in TNBC patients. Cancer Res; 71(13); 4527-38. ©2011 AACR.