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While there is a broad literature analysing the effects of migration on health, important knowledge gaps persist particularly on the causal effects of forced displacement on health outcomes. We undertake a scoping review of applied epidemiological, statistical and econometric studies examining causal health impacts of forced displacement, which initially identified 1454 studies from the health and social sciences disciplines published up to May 2021. Our study makes two key contributions. First, we offer a comprehensive overview of the evidence generated, methodologies adopted and analytical challenges faced by current research examining the causal relationship between forced displacement and health. Second, we present concrete examples of how key challenges around study design and estimation approaches influence the strength of the evidence-base on the topic, using as a case study the broad domain of reproductive health. We find that, beyond the increased mortality risk that can be attributed to forced displacement, most of the available empirical evidence for a wide range of health outcomes is prone to substantial bias, making it difficult to draw firm conclusions. Our synthesis of credible studies conducted in different settings indicates that current research practice in the field could be strengthened through selection of valid control groups and application of more appropriate causal inference methods. Our findings are useful to promote the generation of further evidence on the topic that can reliably inform the design of policies to protect the health of displaced populations.

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OBJECTIVE: To assess the relationship between biomarkers of oxidative stress (OS) and the length of stay in intensive care units (LSICU) in septic children. METHODS: Clinical parameters and biomarkers of OS were measured in 16 children admitted for sepsis in an intensive care unit. The associations between biomarkers of OS and the LSICU were assessed by linear correlation. Multiple linear regression models were constructed to adjust other variables. RESULTS: The mean of LSICU was 7.13 ± 4.17 days. LSICU was associated with the catalase activity (rho =0.56, p-value =0.024) and the ferric reducing ability of plasma (FRAP, r = 0.73, p-value =0.001). However, only FRAP at ICU admission was independently associated with LSICU, which rose 0.21 days for each 10 µmol/l of increase in the FRAP level. CONCLUSION: We conclude for first time that FRAP level at ICU admission is independently associated with LSICU in pediatric patients.

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AIM: To estimate the impact of tobacco use, sedentary lifestyle, obesity and alcohol consumption on type 2 diabetes mellitus (T2DM) prevalence in the Chilean population. METHODS: The study-included 5,293 subjects with fasting glycaemia levels from the nationwide cross-sectional health survey in 2010, commissioned by the Ministry of Health, Chile. Crude and Adjusted Odds Ratio to T2DM and its corresponding 95% confidence interval were estimated through logistic regressions. Attributable fractions and population attributable fractions were estimated. RESULTS: T2DM prevalence was 9.5%. Sedentary lifestyles and obesity were significant risk factors for T2DM. 52,4% of T2DM could be avoided if these individuals were not obese, and at a population level, 23% of T2DM could be preventable if obesity did not exist. A 64% of T2DM is explained by sedentariness, and if people would become active, a 62,2% of the cases of diabetes could be avoided. INTERPRETATION: About 79% of T2DM cases in Chile could be prevented with cost-effective strategies focused on preventing sedentary lifestyle and obesity. It's therefore urgent to implement evidence-based public health polices, aimed to decrease the prevalence of T2DM, by controlling its risk factors and consequently, reducing the complications from T2DM.

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PURPOSE: Percutaneous coronary angioplasty (PCA) has been demonstrated to reduce mortality and morbidity and thereby improve the prognosis of patients undergoing acute myocardial infarctions (AMIs). However, this procedure paradoxically increases the initial damage as the result of a condition known as 'myocardial reperfusion injury'. Oxidative stress may contribute to the mechanism of this injury. The goal of the present study was to ascertain whether high plasma ascorbate levels could ameliorate the reperfusion injuries that occur after the successful restoration of blood flow. METHODS: Patients from three clinical centers of the public health system were included in the study. The groups were formed by either-sex patients with a diagnosis of ST-segment elevation myocardial infarction with an indication for primary PCA. Only the patients who presented with their first myocardial infarction were enrolled. Ascorbate was administered through an infusion given prior to the restoration of the coronary flow, which was then followed by oral treatment with vitamin C (500 mg/12 hours) plus vitamin E (400 IU/day) for 84 days. The left ventricular ejection fraction (LVEF) was determined by using cardiac magnetic resonance on days 6 and 84 following the onset of the reperfusion. In addition, the microvascular function was assessed by an angiographic evaluation using the Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion grade (TMPG). The results were grouped according to the plasma ascorbate concentration achieved immediately following the onset of reperfusion into either the HA group (high ascorbate, >1 mmol/l) or the LA group (low ascorbate, <1 mmol/l). The biochemical parameters were analyzed throughout the protocol. RESULTS: The LVEF of the HA group was significantly higher than that of the LA group, values on day 84 in the HA group were 33% higher than those of the LA group. The amelioration of the LVEF was accompanied by an improvement in the microvascular dysfunction, after PCA, 95% of the patients in the HA group achieved a TMPG of 2-3, in the LA group only 79% of patients showed a TMPG of 2-3. CONCLUSIONS: These data are consistent with the protective effect of high plasma levels of ascorbate against the oxidative challenge caused by reperfusion injury in patients subjected to PCA following an AMI. Further studies are needed to elucidate the mechanism accounting for this beneficial antioxidant effect.

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Cardiovascular diseases are a leading cause of mortality and morbidity worldwide, with hypertension being a major risk factor. Numerous studies support the contribution of reactive oxygen and nitrogen species in the pathogenesis of hypertension, as well as other pathologies associated with ischemia/reperfusion. However, the validation of oxidative stress-related biomarkers in these settings is still lacking and novel association of these biomarkers and other biomarkers such as endothelial progenitor cells, endothelial microparticles, and ischemia modified albumin, is just emerging. Oxidative stress has been suggested as a pathogenic factor and therapeutic target in early stages of essential hypertension. Systolic and diastolic blood pressure correlated positively with plasma F2-isoprostane levels and negatively with total antioxidant capacity of plasma in hypertensive and normotensive patients. Cardiac surgery with extracorporeal circulation causes an ischemia/reperfusion event associated with increased lipid peroxidation and protein carbonylation, two biomarkers associated with oxidative damage of cardiac tissue. An enhancement of the antioxidant defense system should contribute to ameliorating functional and structural abnormalities derived from this metabolic impairment. However, data have to be validated with the analysis of the appropriate oxidative stress and/or nitrosative stress biomarkers.

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Acute myocardial infarction (AMI) is the leading cause of mortality worldwide. Major advances in the treatment of acute coronary syndromes and myocardial infarction, using cardiologic interventions, such as thrombolysis or percutaneous coronary angioplasty (PCA) have improved the clinical outcome of patients. Nevertheless, as a consequence of these procedures, the ischemic zone is reperfused, giving rise to a lethal reperfusion event accompanied by increased production of reactive oxygen species (oxidative stress). These reactive species attack biomolecules such as lipids, DNA, and proteins enhancing the previously established tissue damage, as well as triggering cell death pathways. Studies on animal models of AMI suggest that lethal reperfusion accounts for up to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented. Although a number of strategies have been aimed at to ameliorate lethal reperfusion injury, up to date the beneficial effects in clinical settings have been disappointing. The use of antioxidant vitamins could be a suitable strategy with this purpose. In this review, we propose a systematic approach to the molecular basis of the cardioprotective effect of antioxidant vitamins in myocardial ischemia-reperfusion injury that could offer a novel therapeutic opportunity against this oxidative tissue damage.

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