In this article we use the example of race/ethnic inequalities in severe mental illness to demonstrate the utility of a novel integrative approach to theorising the role of racism in generating inequality. Ethnic minority people in the UK are at much greater risk than White British people of being diagnosed with a severe – psychosis related – mental illness, and this is particularly the case for those with Black Caribbean or Black African origins. There is entrenched dispute about how we might understand the drivers of this inequality. To address this dispute we build on, and to a certain extent refine, established approaches to theorising structural and institutional racism, and integrate this within a theoretical framework that also incorporates racist/discriminatory interactions (interpersonal racism). We argue that this provides a conceptually robust and thorough analysis of the role of inter‐related dimensions of racism in shaping risks of severe mental illness, access to care, and policy and practice responses. This analysis carries implications for a broader, but integrated, understanding of the fundamental drives of race/ethnic inequalities in health and for an anti‐racism public health agenda.

Background To investigate and address the evidence gap on the effectiveness of co-creation/production in international health research. Methods An initial systematic search of previous reviews published by 22 July 2017 in Medline, Embase, PsycINFO, Scopus and Web of Science. We extracted reported aims, elements and outcomes of co-creation/production from 50 reviews; however, reviews rarely tested effectiveness against intended outcomes. We therefore checked the reference lists in 13 included systematic reviews that cited quantitative studies involving the public/patients in the design and/or implementation of research projects to conduct meta-analyses on their effectiveness using standardized mean difference (SMD). Results Twenty-six primary studies were included, showing moderate positive effects for community functions (SMD = 0.56, 95%CI = 0.29–0.84, n = 11) and small positive effects for physical health (SMD = 0.25, 95%CI = 0.07–0.42, n = 9), health-promoting behaviour (SMD = 0.14, 95%CI = 0.03–0.26, n = 11), self-efficacy (SMD = 0.34, 95%CI = 0.01–0.67, n = 3) and health service access/receipt (SMD = 0.36, 95%CI = 0.21–0.52, n = 12). Non-academic stakeholders that co-created more than one research stage showed significantly favourable mental health outcomes. However, co-creation was rarely extended to later stages (evaluation/dissemination), with few studies specifically with ethnic minority groups. Conclusions The co-creation of research may improve several health-related outcomes and public health more broadly, but research is lacking on its longer term effects.

The influence of the gut microbiota on traumatic brain injury (TBI) is presently unknown. This knowledge gap is of paramount clinical significance as TBI patients are highly susceptible to alterations in the gut microbiota by antibiotic exposure. Antibiotic-induced gut microbial dysbiosis established prior to TBI significantly worsened neuronal loss and reduced microglia activation in the injured hippocampus with concomitant changes in fear memory response. Importantly, antibiotic exposure for 1 week after TBI reduced cortical infiltration of Ly6Chigh monocytes, increased microglial pro-inflammatory markers, and decreased T lymphocyte infiltration, which persisted through 1 month post-injury. Moreover, microbial dysbiosis was associated with reduced neurogenesis in the dentate gyrus 1 week after TBI. By 3 months after injury (11 weeks after discontinuation of the antibiotics), we observed increased microglial proliferation, increased hippocampal neuronal loss, and modulation of fear memory response. These data demonstrate that antibiotic-induced gut microbial dysbiosis after TBI impacts neuroinflammation, neurogenesis, and fear memory and implicate gut microbial modulation as a potential therapeutic intervention for TBI.

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Background Large-vessel vasculopathy (LVV) increases stroke risk in pediatric sickle cell disease (SCD) beyond the baseline elevated stroke risk in this vulnerable population. The mechanisms underlying this added risk and its unique impact on the developing brain are not established. Methods We analyzed magnetic resonance imaging (MRI) and angiography (MRA) scans of 66 children with SCD and infarcts by infarct density heatmaps and Jacobian determinants, a metric utilized to delineate focal volume change, to investigate if infarct location, volume, frequency, and cerebral atrophy differed among hemispheres with and without LVV. Results Infarct density heatmaps demonstrated infarct “hot spots” within the deep white matter internal borderzone region in both LVV and non-LVV hemispheres, but with greater infarct density and larger infarct volumes in LVV hemispheres (2.2 mL vs 0.25 mL, p <0.001). Additional scattered cortical infarcts in the internal carotid artery territory occurred in LVV hemispheres, but were rare in non-LVV hemispheres. Jacobian determinants revealed greater atrophy in gray and white matter of the parietal lobes of LVV compared to non-LVV hemispheres. Conclusion LVV in SCD appears to increase ischemic vulnerability in the borderzone region, as demonstrated by the increased frequency and extent of infarction within deep white matter, and increase risk of focal atrophy. Scattered infarctions across the LVV-affected hemispheres suggest additional stroke etiologies of vasculopathy (i.e. thrombo-embolism) in addition to chronic hypoxia-ischemia.