The ACA training programme to improve communication between general practitioners and their palliative care patients: development and applicability

<p>Abstract</p> <p>We describe the development of a new training programme on GP-patient communication in palliative care, and the applicability to GPs and GP Trainees. This ‘ACA training programme’ focuses on <b> <it>A</it> </b><it>vailability</it> of the GP for the patient, <b> <it>C</it> </b><it>urrent issues</it> that should be raised by the GP, and <b> <it>A</it> </b><it>nticipating</it> various scenarios. Evaluation results indicate the ACA training programme to be applicable to GPs and GP Trainees. The ACA checklist was appreciated by GPs as useful both in practice and as a learning tool, whereas GP Trainees mainly appreciated the list for use in practice.</p

Expression of CD11c Is Associated with Unconventional Activated T Cell Subsets with High Migratory Potential

Ajudes rebudes: Marie Curie Career Integration Grant; Dexeus Foundation for Women's Health Research; i Contratos Ramón y CajalCD11c is an α integrin classically employed to define myeloid dendritic cells. Although there is little information about CD11c expression on human T cells, mouse models have shown an association of CD11c expression with functionally relevant T cell subsets. In the context of genital tract infection, we have previously observed increased expression of CD11c in circulating T cells from mice and women. Microarray analyses of activated effector T cells expressing CD11c derived from naïve mice demonstrated enrichment for natural killer (NK) associated genes. Here we find that murine CD11c+ T cells analyzed by flow cytometry display markers associated with non-conventional T cell subsets, including γδ T cells and invariant natural killer T (iNKT) cells. However, in women, only γδ T cells and CD8+ T cells were enriched within the CD11c fraction of blood and cervical tissue. These CD11c+ cells were highly activated and had greater interferon (IFN)-γ secretory capacity than CD11c- T cells. Furthermore, circulating CD11c+ T cells were associated with the expression of multiple adhesion molecules in women, suggesting that these cells have high tissue homing potential. These data suggest that CD11c expression distinguishes a population of circulating T cells during bacterial infection with innate capacity and mucosal homing potential

Ecology and Transmission of Buruli Ulcer Disease: A Systematic Review

Buruli ulcer is a neglected emerging disease that has recently been reported in some countries as the second most frequent mycobacterial disease in humans after tuberculosis. Cases have been reported from at least 32 countries in Africa (mainly west), Australia, Southeast Asia, China, Central and South America, and the Western Pacific. Large lesions often result in scarring, contractual deformities, amputations, and disabilities, and in Africa, most cases of the disease occur in children between the ages of 4–15 years. This environmental mycobacterium, Mycobacterium ulcerans, is found in communities associated with rivers, swamps, wetlands, and human-linked changes in the aquatic environment, particularly those created as a result of environmental disturbance such as deforestation, dam construction, and agriculture. Buruli ulcer disease is often referred to as the “mysterious disease” because the mode of transmission remains unclear, although several hypotheses have been proposed. The above review reveals that various routes of transmission may occur, varying amongst epidemiological setting and geographic region, and that there may be some role for living agents as reservoirs and as vectors of M. ulcerans, in particular aquatic insects, adult mosquitoes or other biting arthropods. We discuss traditional and non-traditional methods for indicting the roles of living agents as biologically significant reservoirs and/or vectors of pathogens, and suggest an intellectual framework for establishing criteria for transmission. The application of these criteria to the transmission of M. ulcerans presents a significant challenge

Species-Specific Therapy of Acute Lymphoid Leukemia

Forty years ago, Farber and associates described temporary remissions of acute leukemia in children produced by folic acid antagonists [13]. This ignited the hope that this most frequent and always fatal childhood cancer might be curable by drugs. Twenty years ago, Aur and as-sociates completed accession of patients to total therapy study V, the first treat-ment protocol to result in 50 % cure of acute lymphoid leukemia (ALL) [3]. Their results stand 20 years later (Fig. 1), and have been reproduced throughout the world in many thousands of children [6]. More important, recent national vital statistics of the United States and the United Kingdom indicate a 50 % reduc-tion in childhood leukemia mortality [4, 29]. Further, the cured children generally enjoy a normal life-style without need for medication. In the past 20 years, efforts have been directed at improving the cure rate of ALL while simplifying curative treat-ment, reducing its side effects, and im-proving its availability and accessibility. In a Stohlman Lecture at Wilsede 10 years ago the following statement was made [32]:- The most significant opportunity for improving the treatment of acute lymphoid leukemia in the past five years has been its biological and clini-cal classification by immunological cell surface markers. This allows spe-cies identification of the leukemia cells, the first step toward developing specific cytocidal or cytostatic therapy

Genetic network identifies novel pathways contributing to atherosclerosis susceptibility in the innominate artery

Abstract Background Atherosclerosis, the underlying cause of cardiovascular disease, results from both genetic and environmental factors. Methods In the current study we take a systems-based approach using weighted gene co-expression analysis to identify a candidate pathway of genes related to atherosclerosis. Bioinformatic analyses are performed to identify candidate genes and interactions and several novel genes are characterized using in-vitro studies. Results We identify 1 coexpression module associated with innominate artery atherosclerosis that is also enriched for inflammatory and macrophage gene signatures. Using a series of bioinformatics analysis, we further prioritize the genes in this pathway and identify Cd44 as a critical mediator of the atherosclerosis. We validate our predictions generated by the network analysis using Cd44 knockout mice. Conclusion These results indicate that alterations in Cd44 expression mediate inflammation through a complex transcriptional network involving a number of previously uncharacterized genes