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Background: Promoting Responsible Research and Innovation (RRI) is a major strategy of the “Science with and for Society” work program of the European Union’s Horizon 2020 Framework Programme for Research and Innovation. RRI aims to achieve a better alignment of research and innovation with the values, needs, and expectations of society. The RRI strategy includes the “keys” of public engagement, open access, gender, ethics, and science education. The Structural Transformation to Attain Responsible BIOSciences (STARBIOS2) project promotes RRI in 6 European research institutions and universities from Bulgaria, Germany, Italy, Slovenia, Poland, and the United Kingdom, in partnership with a further 6 institutions from Brazil, Denmark, Italy, South Africa, Sweden, and the United States.Objective: The project aims to attain RRI structural change in 6 European institutions by implementing action plans (APs) and developing APs for 3 non-European institutions active in the field of biosciences; use the implementation of APs as a learning process with a view to developing a set of guidelines on the implementation of RRI; and develop a sustainable model for RRI in biosciences.Methods: The project comprises interrelated research and implementation designed to achieve the aforementioned specific objectives. The project is organized into 6 core work packages and 5 supporting work packages. The core work packages deal with the implementation of institutional APs in 6 European institutions based on the structural change activation model. The supporting work packages include technical assistance, learning process on RRI-oriented structural change, monitoring and assessment, communication and dissemination, and project management.Results: The project is funded by Horizon 2020 and will run for 4 years (May 2016-April 2020). As of June 2018, the initial phase has been completed. The participating institutions have developed and approved APs and commenced their implementation. An observation tool has been launched by the Technical Assistance Team to collect information from the implementation of APs; the Evaluation & Assessment team has started monitoring the advancement of the project. As part of the communication and dissemination strategy, a project website, a Facebook page, and a Twitter account have been launched and are updated periodically. The International Scientific Advisory Committee has been formed to advise on the reporting and dissemination of the project’s results.Conclusions: In the short term, we anticipate that the project will have a considerable impact on the organizational processes and structures, improving the RRI uptake in the participating institutions. In the medium term, we expect to make RRI-oriented organizational change scalable across Europe by developing guidelines on RRI implementation and an RRI model in biosciences. In the long term, we expect that the project would help increase the ability of research institutions to make discoveries and innovations in better alignment with societal needs and values.

Background Most people who receive a kidney transplant die from either cardiovascular disease or cancer before their transplant fails. The most common reason for someone with a kidney transplant to lose the function of their transplanted kidney necessitating return to dialysis is chronic kidney transplant scarring. Immunosuppressant drugs have side effects that increase risks of cardiovascular disease, cancer and chronic kidney transplant scarring. Belatacept may provide sufficient immunosuppression while avoiding unwanted side effects of other immunosuppressant drugs. However, high rates of post‐transplant lymphoproliferative disease (PTLD) have been reported when belatacept is used in particular kidney transplant recipients at high dosage. Objectives 1) Compare the relative efficacy of belatacept versus any other primary immunosuppression regimen for preventing acute rejection, maintaining kidney transplant function, and preventing death. 2) Compare the incidence of several adverse events: PTLD; other malignancies; chronic transplant kidney scarring (IF/TA); infections; change in blood pressure, lipid and blood sugar control. 3) Assess any variation in effects by study, intervention and recipient characteristics, including: differences in pre‐transplant Epstein Barr virus serostatus; belatacept dosage; and donor‐category (living, standard criteria deceased, or extended criteria deceased). Search methods We searched the Cochrane Renal Group's Specialised Register to 1 September 2014 through contact with the Trials' Search Co‐ordinator using search terms relevant to this review. Selection criteria Randomised controlled trials (RCT) that compared belatacept versus any other immunosuppression regimen in kidney transplant recipients were eligible for inclusion. Data collection and analysis Two authors independently extracted data for study quality and transplant outcomes and synthesized results using random effects meta‐analysis, expressed as risk ratios (RR) and mean differences (MD), both with 95% confidence intervals (CI). Subgroup analyses and univariate meta‐regression were used to investigate potential heterogeneity. Main results We included five studies that compared belatacept and calcineurin inhibitors (CNI) that reported data from a total of 1535 kidney transplant recipients. Of the five studies, three (478 participants) compared belatacept and cyclosporin and two (43 recipients) compared belatacept and tacrolimus. Co‐interventions included basiliximab (4 studies, 1434 recipients); anti‐thymocyte globulin (1 study, 89 recipients); alemtuzumab (1 study, 12 recipients); mycophenolate mofetil (MMF, 5 studies, 1509 recipients); sirolimus (1 study, 26 recipients) and prednisone (5 studies, 1535 recipients). Up to three years following transplant, belatacept and CNI‐treated recipients were at similar risk of dying (4 studies, 1516 recipients: RR 0.75, 95% CI 0.39 to 1.44), losing their kidney transplant and returning to dialysis (4 studies, 1516 recipients: RR 0.91, 95% CI 0.61 to 1.38), and having an episode of acute rejection (4 studies, 1516 recipients: RR 1.56, 95% CI 0.85 to 2.86). Belatacept‐treated kidney transplant recipients were 28% less likely to have chronic kidney scarring (3 studies, 1360 recipients: RR 0.72, 95% CI 0.55 to 0.94) and also had better graft function (measured glomerular filtration rate (GFR) (3 studies 1083 recipients): 10.89 mL/min/1.73 m², 95% CI 4.01 to 17.77; estimated GFR (4 studies, 1083 recipients): MD 9.96 mL/min/1.73 m², 95% CI 3.28 to 16.64) than CNI‐treated recipients. Blood pressure was lower (systolic (2 studies, 658 recipients): MD ‐7.51 mm Hg, 95% CI ‐10.57 to ‐4.46; diastolic (2 studies, 658 recipients): MD ‐3.07 mm Hg, 95% CI ‐4.83 to ‐1.31, lipid profile was better (non‐HDL (3 studies 1101 recipients): MD ‐12.25 mg/dL, 95% CI ‐17.93 to ‐6.57; triglycerides (3 studies 1101 recipients): MD ‐24.09 mg/dL, 95% CI ‐44.55 to ‐3.64), and incidence of new‐onset diabetes after transplant was reduced by 39% (4 studies (1049 recipients): RR 0.61, 95% CI 0.40 to 0.93) among belatacept‐treated versus CNI‐treated recipients. Risk of PTLD was similar in belatacept and CNI‐treated recipients (4 studies, 1516 recipients: RR 2.79, 95% CI 0.61 to 12.66) and was no different among recipients who received different belatacept dosages (high versus low dosage: ratio of risk ratios (RRR) 1.06, 95% CI 0.11 to 9.80, test of difference = 0.96) or among those who were Epstein Barr virus seronegative compared with those who were seropositive before their kidney transplant (seronegative versus seropositive; RRR 1.49, 95% CI 0.15 to 14.76, test for difference = 0.73). The belatacept dose used (high versus low), type of donor kidney the recipient received (extended versus standard criteria) and whether the kidney transplant recipient received tacrolimus or cyclosporin made no difference to kidney transplant survival, incidence of acute rejection or estimated GFR. Selective outcome reporting meant that data for some key subgroup comparisons were sparse and that estimates of the effect of treatment in these groups of recipients remain imprecise. Authors' conclusions There is no evidence of any difference in the effectiveness of belatacept and CNI in preventing acute rejection, graft loss and death, but treatment with belatacept is associated with less chronic kidney scarring and better kidney transplant function. Treatment with belatacept is also associated with better blood pressure and lipid profile and a lower incidence of diabetes versus treatment with a CNI. Important side effects (particularly PTLD) remain poorly reported and so the relative benefits and harms of using belatacept remain unclear. Whether short‐term advantages of treatment with belatacept are maintained over the medium‐ to long‐term or translate into better cardiovascular outcomes or longer kidney transplant survival with function remains unclear. Longer‐term, fully reported and published studies comparing belatacept versus tacrolimus are needed to help clinicians decide which patients might benefit most from using belatacept.

My work sought to unravel the process by which targets (usually peptides) are generated or destroyed from intact antigen using a well characterised antigen that is attacked in an autoimmune kidney disease as a model. In doing this I hoped to account for how this process may lead to the survival of self-reactive T cells into the peripheral T cell repertoire as a possible mechanism of tolerance breakdown and the development of autoimmune disease. In the following sections I will introduce the basic concept of tolerance and discuss the possible mechanisms leading to the breakdown of tolerance and development of autoimmunity. Key to my work is the understanding of how antigen is processed and recognised by T cells. This will be covered in detail before considering how alterations in the processing pathway may lead to deviations in the immune response to self. The second section of this chapter will deal with the model of autoimmune kidney disease used for my research, Goodpasture's disease. I hope to highlight its strengths as a model of autoimmunity and cover in some detail what is already known about the immunopathogenesis of the disease including previous research within our own group. I will conclude with how this work lead on to my own research, detailing the aims of the study including an outline of the research approach used.

Additional file 2. Departmental codes.

Additional file 3. Departmental Athena SWAN action plans.

Additional file 1. Overview of the EFFORTI typology of gender equality interventions in research and innovation (source Kalpazidou Schmidt et al. [59]).

Additional file 1. Overview of the EFFORTI typology of gender equality interventions in research and innovation (source Kalpazidou Schmidt et al. [59]).

A high and increasing proportion of people in the United Kingdom are living with a long-term condition (DH, 2005a). The National Health Service is facing the challenge of increased pressure on its service provision. Government Policy has placed emphasis on supporting individuals to self-care (Department of Health, 2005a, c). However, there are specific challenges associated with living with a long-term condition, and in particular the psychosocial aspects of illness when set alongside a clinical approach to care (Gabe et al, 2004, Bury et al, 2005) It has been argued that disclosure of illness may in itself be a self-care strategy (Munir et al, 2005). However, to date individuals‟ experiences of disclosure of long-term conditions are neither clearly defined nor its role in managing a long-term condition fully understood. The aims of the study were to explore the role of disclosure in the management of a long-term health condition. The study drew on constructivist grounded theory (Charmaz, 2006) undertaking thirty-five in-depth qualitative interviews (fifteen people living with epilepsy, and twenty people living with type 1 diabetes) recruited from patient support groups and clinical nurse specialist‟s clinics. This study identified that strategies of disclosure are not necessarily fixed but may be subject to change over time. “Learning about disclosure” is an integral part of living with a long-term condition. Three key disclosure roles were identified: (1) access to self-care and social support, (2) non-disclosure (concealment) of the condition to protect one‟s identity from stigma. (3) redressing myths about the condition in advance: to avoid perceived stigma.\ud The findings provide important insights that could enable health care professionals to develop more of an emphasis on including disclosure as an issue when talking to \ud patients about managing type 1 diabetes and epilepsy and this is also relevant to a broad spectrum of long-term conditions.

Additional file 2. Departmental codes.

Additional file 3. Departmental Athena SWAN action plans.