Working co-operatively for sustainable and just food system transformation

Co-operative ways of working can be understood as people-centred approaches. This article considers how co-operative ways of working have the potential to support the scaling-out of sustainable and just food systems in the context of Wales through people-centred change. Drawing upon a series of interviews with stakeholders involved in the sustainable and the co-operative food sector within Wales and international case studies, opportunities and challenges facing the scaling-out of sustainable and just food systems are considered. Findings demonstrate the potential of co-operative and community-based approaches to sustainable production, processing, distribution, and trading of healthy food that is affordable, culturally appropriate, and based upon an ethic of justice and care for land, workers, and animals. Community supported agriculture, incubator farms, food hubs, and platform co-operatives are identified as key mechanisms for sustainable and just food systems. Capacity building through education, information, and training are further critical foundations for co-operative and people-centred ways of working. In order to accelerate sustainable and just food futures, community-based participation, networks for training, access to resources and land, and transformative forms of governance, including legislative change, are key. We conclude by highlighting implications for future research into policy transfer and food system transformation

Abnormal infant islet morphology precedes insulin resistance in PCOS-like monkeys.

Polycystic ovary syndrome (PCOS) is prevalent in reproductive-aged women and confounded by metabolic morbidities, including insulin resistance and type 2 diabetes. Although the etiology of PCOS is undefined, contribution of prenatal androgen (PA) exposure has been proposed in a rhesus monkey model as premenopausal PA female adults have PCOS-like phenotypes in addition to insulin resistance and decreased glucose tolerance. PA female infants exhibit relative hyperinsulinemia, suggesting prenatal sequelae of androgen excess on glucose metabolism and an antecedent to future metabolic disease. We assessed consequences of PA exposure on pancreatic islet morphology to identify evidence of programming on islet development. Islet counts and size were quantified and correlated with data from intravenous glucose tolerance tests (ivGTT) obtained from dams and their offspring. Average islet size was decreased in PA female infants along with corresponding increases in islet number, while islet fractional area was preserved. Infants also demonstrated an increase in both the proliferation marker Ki67 within islets and the beta to alpha cell ratio suggestive of enhanced beta cell expansion. PA adult females have reduced proportion of small islets without changes in proliferative or apoptotic markers, or in beta to alpha cell ratios. Together, these data suggest in utero androgen excess combined with mild maternal glucose intolerance alter infant and adult islet morphology, implicating deviant islet development. Marked infant, but subtle adult, morphological differences provide evidence of islet post-natal plasticity in adapting to changing physiologic demands: from insulin sensitivity and relative hypersecretion to insulin resistance and diminished insulin response to glucose in the mature PCOS-like phenotype

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Circulating Tumour Necrosis Factor is highly correlated with brainstem serotonin transporter availability in humans

Preclinical studies demonstrate that pro-inflammatory cytokines increase serotonin transporter availability and function, leading to depressive symptoms in rodent models. Herein we investigate associations between circulating inflammatory markers and brainstem serotonin transporter (5-HTT) availability in humans. We hypothesised that higher circulating inflammatory cytokine concentrations, particularly of tumour necrosis factor (TNF-α), would be associated with greater 5-HTT availability, and that TNF-α inhibition with etanercept (sTNFR:Fc) would in turn reduce 5-HTT availability. In 13 neurologically healthy adult women, plasma TNF-α correlated significantly with 5-HTT availability (rho=0.6; p=0.03) determined by [123I] -beta-CIT SPECT scanning. This association was replicated in an independent sample of 12 patients with psoriasis/psoriatic arthritis (rho=0.76; p=0.003). Indirect effects analysis, showed that there was a significant overlap in the variance explained by 5-HTT availability and TNF-α concentrations on BDI scores. Treatment with etanercept for 6-8 weeks was associated with a significant reduction in 5-HTT availability (Z= 2.09; p=0.03; r=0.6) consistent with a functional link. Our findings confirm an association between TNF-α and 5-HTT in both the basal physiological and pathological condition. Modulation of both TNF-α and 5-HTT by etanercept indicate the presence of a mechanistic pathway whereby circulating inflammatory cytokines are related to central nervous system substrates underlying major depression

Brain-stem serotonin transporter availability in maternal uniparental disomy and deletion Prader–Willi syndrome

Prader–Willi syndrome (PWS) is a rare condition because of the deletion of paternal chromosomal material (del PWS), or a maternal uniparental disomy (mUPD PWS), at 15q11-13. Affective psychosis is more prevalent in mUPD PWS. We investigated the relationship between the two PWS genetic variants and brain-stem serotonin transporter (5-HTT) availability in adult humans. Mean brain-stem 5-HTT availability determined by [123I]-beta-CIT single photon emission tomography was lower in eight adults with mUPD PWS compared with nine adults with del PWS (mean difference −0.93, t = −2.85, P = 0.014). Our findings confirm an association between PWS genotype and brain-stem 5-HTT availability, implicating a maternally expressed/paternally imprinted gene, that is likely to account for the difference in psychiatric phenotypes between the PWS variants

Shaping more resilient and just food systems: Lessons from the COVID-19 Pandemic

The COVID-19 pandemic has highlighted weaknesses in global food systems, as well as opening windows of opportunity for innovation and transformation. While the nature and extent of this crisis is rare, extreme climatic events will increase in magnitude and frequency, threatening similar societal impacts. It is therefore critical to identify mechanisms for developing food systems that are resilient to such impacts. We examine impacts of the crisis on UK food systems and how these further entrenched social inequalities. We present data on the experiences and actions of producers, consumers, and community organisers. The data were collected by adapting ongoing research to include surveys, interviews and online workshops focused on the pandemic. Actors’ responses to the pandemic foreshadow how enduring change to food systems can be achieved. We identify support required to enable these transformations and argue that it is vital that these opportunities are em-bedded in food justice principles which promote people-centred approaches to avoid exacerbating injustices prevalent pre-crisis. Learning from these experiences therefore provides insights for how to make food systems elsewhere more resilient and just

COVID-19: Understanding novel pathogens in coupled social–ecological systems

The emergence of SARS-CoV-2 and the spread of COVID-19 is explored using a social-ecological systems (SES) framework. From an SES perspective, the pandemic is the outcome of feedback loops and cascading interactions within an anthropologically disturbed system. However, the SES framework tends to overemphasize human agency as drivers of system disequilibrium. Drawing on posthumanism theory in social science, the agency of the non-human world also plays a critical role in disturbances in SES. Non-human agency is incorporated into the SES framework, applying it to the emergence of SARS-CoV-2 and the spread of COVID-19, and public health responses. The paper is interdisciplinary, and a non-systematic literature review was combined with Socratic dialogue to examine how human-induced changes trigger feedbacks in SES, such as SARS-CoV-2. The non-human world, embedded within a coupled system of material relations; the natural/biological element, that finds expression in the emergence of SARS-CoV-2 and in generating the genome novel recombinant, which aligns with the conceptualization of the non-human as “vibrant”, all play a role in shaping systems dynamics. This calls into question the anthropocentric view that human agency has the capacity to drive ecosystem dynamics. The implications for SES theory are discussed and we conclude with a case for a new ethics of interdependency to better serve SES analysis. The implications for practice, particularly considering projected future novel virus outbreaks, are discussed