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There is convincing evidence that lower socioeconomic position is associated with increased risk of mental disorders. However, the mechanisms involved are not well understood. This study aims to elucidate the causal pathways between socioeconomic position and depression symptoms in South African adults. Two possible causal theories are examined: social causation, which suggests that poor socioeconomic conditions cause mental ill health; and social drift, which suggests that those with poor mental health are more likely to drift into poor socioeconomic circumstances.
The study used longitudinal and cross-sectional observational data on 3904 adults, from a randomised trial carried out in 38 primary health care clinics between 2011 and 2012. Structural equation models and counterfactual mediation analyses were used to examine causal pathways in two directions. First, we examined social causation pathways, with language (a proxy for racial or ethnic category) being treated as an exposure, while education, unemployment, income and depression were treated as sequential mediators and outcomes. Second, social drift was explored with depression treated as a potential influence on health-related quality of life, job loss and, finally, income.
The results suggest that the effects of language on depression at baseline, and on changes in depression during follow-up, were mediated through education and income but not through unemployment. Adverse effects of unemployment and job loss on depression appeared to be mostly mediated through income. The effect of depression on decreasing income appeared to be mediated by job loss.
These results suggest that both social causation and social selection processes operate concurrently. This raises the possibility that people could get trapped in a vicious cycle in which poor socioeconomic conditions lead to depression, which, in turn, can cause further damage to their economic prospects. This study also suggests that modifiable factors such as income, employment and treatable depression are suitable targets for intervention in the short to medium term, while in the longer term reducing inequalities in education will be necessary to address the deeply entrenched inequalities in South Africa.
Rift Valley fever virus (RVFV) is an emerging pathogen of major concern throughout Africa and the Arabian Peninsula, affecting both livestock and humans. In the past recurrent epidemics were reported in Mauritania and studies focused on the analysis of samples from affected populations during acute outbreaks. To verify characteristics and presence of RVFV during non-epidemic periods we implemented a multi-stage serological and molecular analysis. Serum samples of small ruminants, cattle and camels were obtained from Mauritania during an inter-epidemic period in 2012–2013. This paper presents a comparative analysis of potential variations and shifts of antibody presence and the capability of inter-epidemic infections in Mauritanian livestock. We observed distinct serological differences between tested species (seroprevalence: small ruminants 3·8%, cattle 15·4%, camels 32·0%). In one single bovine from Nouakchott, a recent RVF infection could be identified by the simultaneous detection of IgM antibodies and viral RNA. This study indicates the occurrence of a low-level enzootic RVFV circulation in livestock in Mauritania. Moreover, results indicate that small ruminants can preferably act as sentinels for RVF surveillance.
The influence of haemodilution with colloids on somatosensory evoked potentials in non-premedicated volunteers is reported. In seven volunteers (randomized crossover design), blood (20 mL kg−1 within 30 min) was removed and simultaneously replaced by gelatin 3% or hydroxyethylstarch 6%. After 30 min, blood was retransfused within 30 min. Median and posterior tibial nerve somatosensory evoked potentials were recorded from the cortex, second cervical vertebra, Erb's point and 1st lumbar vertebra, respectively. One volunteer experienced a severe allergic reaction to gelatin, therefore only six gelatin trials were evaluated. Haemodilution decreased the haematocrit from 39.8 ± 1.6% (mean ± SD) to 31.1 ± 2.0% (gelatin) and from 40.7 ± 1.7% to 29.8 ± 1.5% (hydroxyethylstarch), respectively. Retransfusion increased haematocrit to 34.4 ± 0.9% (gelatin) and to 34.2 ± 1.3% (hydroxyethylstarch). Neither haemodilution with gelatin nor haemodilution with hydroxyethylstarch or retransfusion influenced evoked potentials. In conclusion, the treatment of blood loss up to 30% of estimated blood volume with gelatin or hydroxyethylstarch will not affect somatosensory evoked potential monitoring provided normovolaemic conditions are maintained.
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