IntroductionMedia interventions can potentially play a major role in influencing health policies. This integrative systematic review aimed to assess the effects of planned media interventions—including social media—on the health policy-making process.MethodsEligible study designs included randomized and non-randomized designs, economic studies, process evaluation studies, stakeholder analyses, qualitative methods, and case studies. We electronically searched Medline, EMBASE, Communication and Mass Media Complete, Cochrane Central Register of Controlled Trials, and the WHO Global Health Library. We followed standard systematic review methodology for study selection, data abstraction, and risk of bias assessment.ResultsTwenty-one studies met our eligibility criteria: 10 evaluation studies using either quantitative (n = 7) or qualitative (n = 3) designs and 11 case studies. None of the evaluation studies were on social media. The findings of the evaluation studies suggest that media interventions may have a positive impact when used as accountability tools leading to prioritizing and initiating policy discussions, as tools to increase policymakers’ awareness, as tools to influence policy formulation, as awareness tools leading to policy adoption, and as awareness tools to improve compliance with laws and regulations. In one study, media-generated attention had a negative effect on policy advocacy as it mobilized opponents who defeated the passage of the bills that the media intervention advocated for. We judged the confidence in the available evidence as limited due to the risk of bias in the included studies and the indirectness of the evidence.ConclusionThere is currently a lack of reliable evidence to guide decisions on the use of media interventions to influence health policy-making. Additional and better-designed, conducted, and reported primary research is needed to better understand the effects of media interventions, particularly social media, on health policy-making processes, and the circumstances under which media interventions are successful.Trial registrationPROSPERO 2015:CRD42015020243 Electronic supplementary materialThe online version of this article (doi:10.1186/s13012-017-0581-0) contains supplementary material, which is available to authorized users.

Alzheimer’s disease (AD) is the most common neurodegenerative disease. Histological characterization of amyloid plaques and neurofibrillary tangles in the brains of AD patients, alongside genetic studies in individuals suffering the familial form of the disease, has fueled the accumulation of the amyloid-β protein as the initial pathological trigger of disease. Association studies have recently showed that cerebral hypoxia, via both genetic and epigenetic mechanisms, increase amyloid-β deposition by altering expression levels of enzymes involved in the production/degradation of the protein. Furthermore, hypoxia has also been linked to neuronal and glial-cell calcium dysregulation through formation of calcium-permeable pores, dysregulated glutamate signaling, and intracellular calcium-store dysfunction. Hypoxia has also been strongly linked to neuroinflammation; however, this relationship to AD has not been thoroughly discussed in the literature. Here, we highlight and organize critical research evidence showing that in both hypoxic and AD brains, there are similarities in terms of 1) the substances mediating/modulating the neuroinflammatory environment and 2) the immune cells that drive the formation of these substances.

Non-Hodgkin’s lymphoma (NHL) is the sixth-most common cancer in the UK, accounting for around 13,700 new cases every year. Until the late 1990s, treatment relied on intensive chemotherapy, such as CHOP (cyclophosphamide–doxorubicin HCl–vincristine [Oncovin]–prednisone). The use of standard CHOP therapy and its variations had resulted in poor five-year survival rates (as low as 26%), particularly in patients with aggressive NHL. Rituximab (Rituxan) was the first chimeric (mouse/human) monoclonal antibody approved for the treatment of NHL. It was approved by the US Food and Drug Administration in 1997 for indolent forms of NHL. It subsequently received EU approval in June 1998, and was licensed under the trade name Mabthera (Roche, Basel, Switzerland). It then went on to be approved for the first-line treatment of aggressive forms of NHL, such as diffuse large B-cell lymphoma (to be used in combination with CHOP or other anthracycline-based chemotherapy) in 2006. It is directed against the CD20 protein, an antigen found on the surface of B-cell lymphomas. With minimal toxicity, activity as a single-agent (for indolent forms of NHL) and safety when combined with chemotherapy (for aggressive forms), it represents great progress in this field. Here, we analyze how this antibody therapeutic was developed from basic molecular and cellular considerations through to preclinical and clinical evaluations and how it came to be a first-line treatment for NHL, and we discuss the impacts the advent of rituximab had on treatment outcomes for patients with DLBCL compared with the pre-rituximab era.

According to the World Health Organization, 422 million adults worldwide live with diabetes mellitus (DM), a significant portion of whom have type 2 diabetes. The discovery of insulin as a key regulator of glucose metabolism has revolutionized our understanding of DM and provided several therapeutic avenues. Most studies have so far predominantly focused on the role of insulin in type 2 diabetes. However, the balance between insulin and glucagon is essential in ensuring glucose homeostasis. In this review, we begin by evaluating the principal differences between insulin and glucagon with regard to their mechanism and control of their secretion. Next, we discuss their mode of action and effects on metabolism. We further explore how the two hormones impact the natural history of type 2 diabetes. Finally, we outline how current and emerging pharmacological agents attempt to exploit the properties of insulin and glucagon to benefit patients with type 2 diabetes.

ObjectivesA teaching curriculum in health policy may be well established in medical school; however, an emphasis on applying taught principles via participation in health policy roles is less defined. We undertook a study to explore medical student participation in health policy roles.Design and settingAn anonymous online survey via convenience sampling was conducted in the UK.ParticipantsA total of 112 students from six medical schools participated in the study.Outcome measuresThe outcome measures were as follows: medical students’ beliefs about their current knowledge of health policy and their desire to learn more; their current, past and future involvement in a health policy role, and perceived barriers to involvement.ResultsForty-seven percent of participants reported previous teaching on health policy, with the majority scoring themselves 2 out of 5 for knowledge about the topic (38%). Seventy-seven percent of participants expressed a desire to be taught health policy while 73% agreed with compulsory teaching. Ninety-six percent of participants reported no current or previous activity in a health policy role, with 61% willing to undertake a role in the future. The three main barriers to student involvement were: a lack of knowledge about health policy (57%), an unawareness of opportunities available (56%), and a lack of time (43%).ConclusionIn addition to already established teaching programs within medical school, implementation of community-based experiences could improve knowledge of health policy, while providing an opportunity for students to gain experience in health policy committee roles.