The prevalence of self-reported underuse of medications due to cost for the elderly: Results from seven European urban communities

Background: The aim of this study was to evaluate the prevalence of self-reported underuse of medications due to procurement costs amongst older persons from seven European urban communities. Methods: The data were collected in a cross-sectional study (“ABUEL, Elder abuse: A multinational prevalence survey”) in 2009. Randomly selected people aged 60–84 years (n = 4,467) from seven urban communities: Stuttgart (Germany), Athens (Greece), Ancona (Italy), Kaunas (Lithuania), Porto (Portugal), Granada (Spain) and Stockholm (Sweden) were interviewed. Response rate - 45.2 %. Ethical permission was received in each country. Results: The results indicate that 3.6 % (n = 162) of the respondents self-reported refraining from buying prescribed medications due to cost. The highest prevalence of this problem was identified in Lithuania (15.7 %, n = 99) and Portugal (4.3 %, n = 28). Other countries reported lower percentages of refraining from buying medications (Germany – 2.0 %, Italy – 1.6 %, Sweden – 1.0 %, Greece – 0.6 %, Spain – 0.3 %). Females refrained more often from buying medications than males (2.6 % vs. 4.4 %, p < 0.0001). The prevalence of this refraining tended to increase with economic hardship. Discussion: These differences between countries can be only partly described by the financing of health-care systems. In spite of the presence of cost reimbursement mechanisms, patients need to make co-payments (or in some cases to pay the full price) for prescribed medications. This indicates that the purchasing power of people in 10.1186/s12913-015-1089-4 the particular country can play a major role and be related with the economic situation in the country. Lithuania, which has reported the highest refrain rates, had the lowest gross domestic product (at the time of conducting this study) of all participating countries in the study. Conclusions: Refraining from buying the prescribed medications due to cost is a problem for women and men in respect to ageing people in Europe. Prevalence varies by country, sex, and economic hardship.The ABUEL was supported by the Executive Agency for Health and Consumers (EAHC) (Grant No., A/2007123) and participating institutions

Principles of all-inclusive public health: developing a public health leadership curriculum

This article describes the way in which the international Leadership in European Public Health Initiative (LEPHIE) course was developed, outlines its content, and describes how the earlier DELTAH project informed its development. The project, funded by the EC Leonardo da Vinci Lifelong Learning programme between 2004 and 2007 is now being operationalised in a number of European countries and continues to attract growing interest amongst those still striving to develop their public health systems

The ADAMTS (A Disintegrin and Metalloproteinase with Thrombospondin motifs) family

The ADAMTS (A Disintegrin and Metalloproteinase with Thrombospondin motifs) enzymes are secreted, multi-domain matrix-associated zinc metalloendopeptidases that have diverse roles in tissue morphogenesis and patho-physiological remodeling, in inflammation and in vascular biology. The human family includes 19 members that can be sub-grouped on the basis of their known substrates, namely the aggrecanases or proteoglycanases (ADAMTS1, 4, 5, 8, 9, 15 and 20), the procollagen N-propeptidases (ADAMTS2, 3 and 14), the cartilage oligomeric matrix protein-cleaving enzymes (ADAMTS7 and 12), the von-Willebrand Factor proteinase (ADAMTS13) and a group of orphan enzymes (ADAMTS6, 10, 16, 17, 18 and 19). Control of the structure and function of the extracellular matrix (ECM) is a central theme of the biology of the ADAMTS, as exemplified by the actions of the procollagen-N-propeptidases in collagen fibril assembly and of the aggrecanases in the cleavage or modification of ECM proteoglycans. Defects in certain family members give rise to inherited genetic disorders, while the aberrant expression or function of others is associated with arthritis, cancer and cardiovascular disease. In particular, ADAMTS4 and 5 have emerged as therapeutic targets in arthritis. Multiple ADAMTSs from different sub-groupings exert either positive or negative effects on tumorigenesis and metastasis, with both metalloproteinase-dependent and -independent actions known to occur. The basic ADAMTS structure comprises a metalloproteinase catalytic domain and a carboxy-terminal ancillary domain, the latter determining substrate specificity and the localization of the protease and its interaction partners; ancillary domains probably also have independent biological functions. Focusing primarily on the aggrecanases and proteoglycanases, this review provides a perspective on the evolution of the ADAMTS family, their links with developmental and disease mechanisms, and key questions for the future

Quality of medical training and emigration of physicians from India

<p>Abstract</p> <p>Background</p> <p>Physician 'brain drain' negatively impacts health care delivery. Interventions to address physician emigration have been constrained by lack of research on systematic factors that influence physician migration. We examined the relationship between the quality of medical training and rate of migration to the United States and the United Kingdom among Indian medical graduates (1955–2002).</p> <p>Methods</p> <p>We calculated the fraction of medical graduates who emigrated to the United States and the United Kingdom, based on rankings of medical colleges and universities according to three indicators of the quality of medical education (a) student choice, (b) academic publications, and (c) the availability of specialty medical training.</p> <p>Results</p> <p>Physicians from the top quintile medical colleges and of universities were 2 to 4 times more likely to emigrate to the United States and the United Kingdom than graduates from the bottom quintile colleges and universities.</p> <p>Conclusion</p> <p>Graduates of institutions with better quality medical training have a greater likelihood of emigrating. Interventions designed to counter loss of physicians should focus on graduates from top quality institutions.</p

Driving vascular endothelial cell fate of human multipotent Isl1+ heart progenitors with VEGF modified mRNA

Distinct families of multipotent heart progenitors play a central role in the generation of diverse cardiac, smooth muscle and endothelial cell lineages during mammalian cardiogenesis. The identification of precise paracrine signals that drive the cell-fate decision of these multipotent progenitors, and the development of novel approaches to deliver these signals in vivo, are critical steps towards unlocking their regenerative therapeutic potential. Herein, we have identified a family of human cardiac endothelial intermediates located in outflow tract of the early human fetal hearts (OFT-ECs), characterized by coexpression of Isl1 and CD144/vWF. By comparing angiocrine factors expressed by the human OFT-ECs and non-cardiac ECs, vascular endothelial growth factor (VEGF)-A was identified as the most abundantly expressed factor, and clonal assays documented its ability to drive endothelial specification of human embryonic stem cell (ESC)-derived Isl1+ progenitors in a VEGF receptor-dependent manner. Human Isl1-ECs (endothelial cells differentiated from hESC-derived ISL1+ progenitors) resemble OFT-ECs in terms of expression of the cardiac endothelial progenitor- and endocardial cell-specific genes, confirming their organ specificity. To determine whether VEGF-A might serve as an in vivo cell-fate switch for human ESC-derived Isl1-ECs, we established a novel approach using chemically modified mRNA as a platform for transient, yet highly efficient expression of paracrine factors in cardiovascular progenitors. Overexpression of VEGF-A promotes not only the endothelial specification but also engraftment, proliferation and survival (reduced apoptosis) of the human Isl1+ progenitors in vivo. The large-scale derivation of cardiac-specific human Isl1-ECs from human pluripotent stem cells, coupled with the ability to drive endothelial specification, engraftment, and survival following transplantation, suggest a novel strategy for vascular regeneration in the heart

Zebrafish hoxd4a Acts Upstream of meis1.1 to Direct Vasculogenesis, Angiogenesis and Hematopoiesis

10.1371/journal.pone.0058857PLoS ONE83

Chromatin remodelling complex dosage modulates transcription factor function in heart development

Dominant mutations in cardiac transcription factor genes cause human inherited congenital heart defects (CHDs); however, their molecular basis is not understood. Interactions between transcription factors and the Brg1/Brm-associated factor (BAF) chromatin remodelling complex suggest potential mechanisms; however, the role of BAF complexes in cardiogenesis is not known. In this study, we show that dosage of Brg1 is critical for mouse and zebrafish cardiogenesis. Disrupting the balance between Brg1 and disease-causing cardiac transcription factors, including Tbx5, Tbx20 and Nkx2–5, causes severe cardiac anomalies, revealing an essential allelic balance between Brg1 and these cardiac transcription factor genes. This suggests that the relative levels of transcription factors and BAF complexes are important for heart development, which is supported by reduced occupancy of Brg1 at cardiac gene promoters in Tbx5 haploinsufficient hearts. Our results reveal complex dosage-sensitive interdependence between transcription factors and BAF complexes, providing a potential mechanism underlying transcription factor haploinsufficiency, with implications for multigenic inheritance of CHDs

RSF Governs Silent Chromatin Formation via Histone H2Av Replacement

Human remodeling and spacing factor (RSF) consists of a heterodimer of Rsf-1 and hSNF2H, a counterpart of Drosophila ISWI. RSF possesses not only chromatin remodeling activity but also chromatin assembly activity in vitro. While no other single factor can execute the same activities as RSF, the biological significance of RSF remained unknown. To investigate the in vivo function of RSF, we generated a mutant allele of Drosophila Rsf-1 (dRsf-1). The dRsf-1 mutant behaved as a dominant suppressor of position effect variegation. In dRsf-1 mutant, the levels of histone H3K9 dimethylation and histone H2A variant H2Av were significantly reduced in an euchromatic region juxtaposed with heterochromatin. Furthermore, using both genetic and biochemical approaches, we demonstrate that dRsf-1 interacts with H2Av and the H2Av-exchanging machinery Tip60 complex. These results suggest that RSF contributes to histone H2Av replacement in the pathway of silent chromatin formation