What has economics got to do with it? The impact of socioeconomic factors on mental health and the case for collective action

A clear link exists between social and economic inequality and poor mental health. There is a social gradient in mental health, and higher levels of income inequality are linked to higher prevalence of mental illness. Despite this, in the late 20th and early 21st century, psychiatric and psychological perspectives have dominated mental health research and policy, obscuring root socioeconomic contributors. Drawing on contemporary research on the social determinants of mental health, with particular reference to Europe and the U.S., this paper argues that a sharper focus on socioeconomic factors is required in research and policy to address inequalities in mental health. Current attempts to move this direction include: evaluation of the impact of economic policies on mental health, community-based partnerships, increased professional awareness and advocacy on socioeconomic factors. This necessitates greater understanding of the barriers to such actions. This paper argues that advancing ‘upstream’ approaches to population mental health requires an interdisciplinary research vision that supports greater understanding of the role of socioeconomic factors. It also demands collective cross-sectoral action through changes in social and economic policy, as well as economic frameworks that move beyond an exclusive focus on economic growth to embrace collective and societal wellbeing

Understanding and promoting student mental health in Scottish higher education - a mapping exercise

There has been an increase in the incidence of mental health difficulties among HE students over the past decade. Official statistics show that the proportion of undergraduates declaring a mental health difficulty on entry to HE rose from 5 in every 10,000 in 1994-5 to 30 in every 10,000 in 2004-5. Incidence of severe psychological problems has increased, and student mental health is generally worse than that of the general population (for agematched populations). Anxiety and depression are the most commonly noted difficulties. The research review identified a relationship between mental health and the following factors: finances, accommodation, academic issues, university systems and social factors. Academic issues, and specifically coursework, emerged as particularly related to stress levels and mental health issues

Exploring metabolic pathway disruption in the subchronic phencyclidine model of schizophrenia with the generalized singular value decomposition

The quantification of experimentally-induced alterations in biological pathways remains a major challenge in systems biology. One example of this is the quantitative characterization of alterations in defined, established metabolic pathways from complex metabolomic data. At present, the disruption of a given metabolic pathway is inferred from metabolomic data by observing an alteration in the level of one or more individual metabolites present within that pathway. Not only is this approach open to subjectivity, as metabolites participate in multiple pathways, but it also ignores useful information available through the pairwise correlations between metabolites. This extra information may be incorporated using a higher-level approach that looks for alterations between a pair of correlation networks. In this way experimentally-induced alterations in metabolic pathways can be quantitatively defined by characterizing group differences in metabolite clustering. Taking this approach increases the objectivity of interpreting alterations in metabolic pathways from metabolomic data. We present and justify a new technique for comparing pairs of networks - in our case these networks are based on the same set of nodes and there are two distinct types of weighted edges. The algorithm is based on the Generalized Singular Value Decomposition (GSVD), which may be regarded as an extension of Principle Components Analysis to the case of two data sets. We show how the GSVD can be interpreted as a technique for reordering the two networks in order to reveal clusters that are exclusive to only one. Here we apply this algorithm to a new set of metabolomic data from the prefrontal cortex (PFC) of a translational model relevant to schizophrenia, rats treated subchronically with the N-methyl-D-Aspartic acid (NMDA) receptor antagonist phencyclidine (PCP). This provides us with a means to quantify which predefined metabolic pathways (Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolite pathway database) were altered in the PFC of PCP-treated rats. Several significant changes were discovered, notably: 1) neuroactive ligands active at glutamate and GABA receptors are disrupted in the PFC of PCP-treated animals, 2) glutamate dysfunction in these animals was not limited to compromised glutamatergic neurotransmission but also involves the disruption of metabolic pathways linked to glutamate; and 3) a specific series of purine reactions Xanthine Inosine adenylosuccinate is also disrupted in the PFC of PCP-treated animals. Network reordering via the GSVD provides a means to discover statistically validated differences in clustering between a pair of networks. In practice this analytical approach, when applied to metabolomic data, allows us to quantify the alterations in metabolic pathways between two experimental groups. With this new computational technique we identified metabolic pathway alterations that are consistent with known results. Furthermore, we discovered disruption in a novel series of purine reactions that may contribute to the PFC dysfunction and cognitive deficits seen in schizophrenia

Relationship between diffusion capacity and small airway abnormality in COPDGene.

Impaired single breath carbon monoxide diffusing capacity (DLCO) is associated with emphysema. Small airways disease (SAD) may be a precursor lesion to emphysema, but the relationship between SAD and DLCO is undescribed. We hypothesized that in mild COPD, functional SAD (fSAD) defined by computed tomography (CT) and Parametric Response Mapping methodology would correlate with impaired DLCO. Using data from ever-smokers in the COPDGene cohort, we established that fSAD correlated significantly with lower DLCO among both non-obstructed and GOLD 1-2 subjects. The relationship between DLCO with CT-defined emphysema was present in all GOLD stages, but most prominent in severe disease. TRIAL REGISTRATION: NCT00608764. Registry: COPDGene. Registered 06 February 2008, retrospectively registered

Climate‐related variations in mixing dynamics in an Alaskan arctic lake

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/109805/1/lno2009546part22401.pd

Understanding citizenship within a health and social care context in Scotland using community based participatory research methods

Community based participatory research (CBPR) principles were used to develop a conceptual framework of citizenship for people experiencing mental health problems and/or other life disrupting events in Scotland. This case study illustrates the use of a participatory methodology replicating an approach adopted as part of an international collaboration in understanding citizenship across diverse social and cultural contexts. Reflecting on the approach taken, we argue that it encourages the development of a model of citizenship that is entirely grounded in the perspectives and lived experiences of the participants. We consider the importance of ‘meaningfully’ engaging peer researchers throughout the research process, exploring the methodological issues, challenges and opportunities when working in partnership. The importance of adopting a reflexive approach throughout the research approach is emphasised. We consider how the need for adequate resources, preparatory work, training and research management is key to the success of a CBPR approach with peer researchers. Finally, we suggest making appropriate adaptations to any research methodology when working with diverse populations, particularly the ‘seldom heard’ groups within society, in order to inform health and social policy and practice

Citizens defining citizenship : a model grounded in lived experience and its implications for research, policy and practice

Citizenship is gaining currency in health and social care internationally as a way of making sense of the lived experiences of people with major life disruptions who face exclusion, marginalisation and discrimination, but the concept is often contested, poorly defined and understood. This paper charts the development of an empirical model of citizenship within Scotland, UK. A mixed method, community based participatory research approach using 10 focus groups (n = 77), concept mapping exercises (n = 45) and statement clarity and relevant ratings (n = 242) was used to develop a model of citizenship that is grounded in the lived experience of participants, which is absent from current conceptualisations of citizenship. Multidimensional scaling and hierarchical cluster analysis revealed five core domains emerging from our work: 'building relationships', 'autonomy and acceptance', 'access to services and supports', 'shared values and social roles' and 'civic rights and responsibilities' representing the personal meanings of citizenship for participants. We argue that the value of this model is that is draws upon the personal understandings and experiences of participants who emphasised the "banal ordinariness" of its core elements. We suggest that the model makes an original contribution by clearly illustrating the practical applicability of citizenship as a concept thus enhancing existing theories of citizenship. Our model highlights the interplay between the relational and structural aspects of citizenship and acknowledging the barriers that marginalised groups face in claiming their citizenship rights. It offers a call to action for policy makers and practitioners to set goals that contribute to the social inclusion of those who have experienced major life disruptions

Chronic otitis media is initiated by a bulla cavitation defect in the FBXO11 mouse model

Auditory bulla cavitation defects are a cause of otitis media, but the normal cellular pattern of bulla mesenchyme regression and its failure are not well understood. In mice, neural-crest-derived mesenchyme occupies the bulla from embryonic day 17.5 (E17.5) to postnatal day 11 (P11) and then regresses to form the adult air-filled bulla cavity. We report that bulla mesenchyme is bordered by a single layer of non-ciliated epithelium characterized by interdigitating cells with desmosome cell junctions and a basal lamina, and by Bpifa1 gene expression and laminin staining of the basal lamina. At P11-P12, the mesenchyme shrinks: mesenchyme-associated epithelium shortens, and mesenchymal cells and extracellular matrix collagen fibrils condense, culminating in the formation of cochlea promontory mucosa bordered by compact non-ciliated epithelial cells. FBXO11 is a candidate disease gene in human chronic otitis media with effusion and we report that a bulla cavitation defect initiates the pathogenesis of otitis media in the established mouse model Jeff (Fbxo11Jf/+). Persistent mesenchyme in Fbxo11Jf/+ bullae has limited mesenchymal cell condensation, fibrosis and hyperplasia of the mesenchyme-associated epithelium. Subsequent modification forms fibrous adhesions that link the mucosa and the tympanic membrane, and this is accompanied by dystrophic mineralization and accumulation of serous effusion in the bulla cavity. Mouse models of bulla cavitation defects are important because their study in humans is limited to post-mortem samples. This work indicates new diagnostic criteria for this otitis media aetiology in humans, and the prospects of studying the molecular mechanisms of murine bulla cavitation in organ culture

Role of Ectodysplasin signalling in middle ear and nasal pathology in rat and mouse models of hypohidrotic ectodermal dysplasia

Patients with mutations in the ectodysplasin receptor signalling pathway genes – the X-linked ligand ectodysplasin-A (EDA), the receptor EDAR or the receptor adapter EDARADD – have hypohidrotic ectodermal dysplasia (HED). In addition to having impaired development of teeth, hair, eccrine sweat glands, and salivary and mammary glands, HED patients have ear, nose and throat disease. The mouse strains Tabby (EdaTa) and downless (Edardl-J/dl-J) have rhinitis and otitis media due to loss of submucosal glands in the upper airway. We report that prenatal correction of EDAR signalling in EdaTa mice with the agonist anti-EDAR antibody rescues the auditory-tube submucosal glands and prevents otitis media, rhinitis and nasopharyngitis. The sparse- and wavy-haired (swh) rat strain carries a mutation in the Edaradd gene and has similar cutaneous HED phenotypes to mouse models. We report that auditory-tube submucosal glands are smaller in the homozygous mutant Edaraddswh/swh than those in unaffected heterozygous Edaraddswh/+ rats, and that this predisposes them to otitis media. Furthermore, the pathogenesis of otitis media in the rat HED model differs from that in mice, as otitis media is the primary pathology, and rhinitis is a later-onset phenotype. These findings in rodent HED models imply that hypomorphic as well as null mutations in EDAR signalling pathway genes may predispose to otitis media in humans. In addition, this work suggests that the recent successful prenatal treatment of X-linked HED (XLHED) in humans may also prevent ear, nose and throat disease, and provides diagnostic criteria that distinguish HED-associated otitis media from chronic otitis media with effusion, which is common in children