Objective This study aimed to investigate pregnancy outcomes in Somali-born women compared with those women born in each of the six receiving countries: Australia, Belgium, Canada, Finland, Norway and Sweden.Design Meta-analyses of routinely collected data on confinements and births.Setting National or regional perinatal datasets spanning 3-6 years between 1997 and 2004 from six countries.Sample A total of 10 431 Somali-born women and 2 168 891 receiving country-born women.Methods Meta-analyses to compare outcomes for Somali-born and receiving country-born women across the six countries.Main outcome measures Events of labour (induction, epidural use and proportion of women using no analgesia), mode of birth (spontaneous vaginal birth, operative vaginal birth and caesarean section) and infant outcomes (preterm birth, birthweight, Apgar at 5 minutes, stillbirths and neonatal deaths).Results Compared with receiving country-born women, Somaliborn women were less likely to give birth preterm (pooled OR 0.72, 95% CI 0.64-0.81) or to have infants of low birthweight (pooled OR 0.89, 95% CI 0.82-0.98), but there was an excess of caesarean sections, particularly in first births (pooled OR 1.41, 95% CI 1.25-1.59) and an excess of stillbirths (pooled OR 1.86, 95% CI 1.38-2.51).Conclusions This analysis has identified a number of disparities in outcomes between Somali-born women and their receiving country counterparts. The disparities are not readily explained and they raise concerns about the provision of maternity care for Somali women postmigration. Review of maternity care practices followed by implementation and careful evaluation of strategies to improve both care and outcomes for Somali women is needed.

Significance Statement Many experimental approaches require housing rodents in individual cages, a stressful condition for social animals, even in an enriched environment context. Using the pilocarpine (pilo) model of epilepsy in rats and mice, we report that singly housing animals develop a more severe phenotype in terms of stress and epilepsy as compared to animals maintaining social contact. We propose that social isolation adds a degree of complexity for the interpretation of data, which may be particularly relevant for preclinical studies.

No abstract

The retinal circadian clock is crucial for optimal regulation of retinal physiology and function, yet its cellular location in mammals is still controversial. We used laser microdissection to investigate the circadian profiles and phase relations of clock gene expression and Period gene induction by light in the isolated outer (rods/cones) and inner (inner nuclear and ganglion cell layers) regions in wild-type and melanopsin-knockout (Opn 4 (-/-) ) mouse retinas. In the wild-type mouse, all clock genes are rhythmically expressed in the photoreceptor layer but not in the inner retina. For clock genes that are rhythmic in both retinal compartments, the circadian profiles are out of phase. These results are consistent with the view that photoreceptors are a potential site of circadian rhythm generation. In mice lacking melanopsin, we found an unexpected loss of clock gene rhythms and of the photic induction of Per1-Per2 mRNAs only in the outer retina. Since melanopsin ganglion cells are known to provide a feed-back signalling pathway for photic information to dopaminergic cells, we further examined dopamine (DA) synthesis in Opn 4 (-/-) mice. The lack of melanopsin prevented the light-dependent increase of tyrosine hydroxylase (TH) mRNA and of DA and, in constant darkness, led to comparatively high levels of both components. These results suggest that melanopsin is required for molecular clock function and DA regulation in the retina, and that Period gene induction by light is mediated by a melanopsin-dependent, DA-driven signal acting on retinal photoreceptors.

Many experimental approaches require housing rodents in individual cages, including in epilepsy research. However, rats and mice are social animals; and individual housing constitutes a stressful situation. The goal of the present study was to determine the effects of individual housing as compared to conditions maintaining social contact on stress markers and epilepsy. Control male mice socially housed during pretest and then transferred to individual cages for six weeks displayed anhedonia, increased anxiety and biological markers of stress as compared to pretest values or mice kept socially housed during six weeks. Pilocarpine-treated mice housed together showed increased levels of anhedonia, anxiety and stress markers as well as decreased cognitive performance as compared to the control group. The differences were more significant in pilocarpine-treated mice housed individually. Anxiety correlated linearly with cognitive performance and stress markers independently of the experimental conditions. In the male rat pilocarpine model, seizures were sixteen times more frequent in singly housed animals as compared to animals kept in pairs. Daily interactions with an experimenter in otherwise singly housed animals was sufficient to produce results identical to those found in animals kept in pairs. We propose that social isolation produces a severe phenotype in terms of stress and seizure frequency as compared to animals maintaining social contact (at least in these two models), a factor that needs to be taken into account for data interpretation, in particular for preclinical studies.Significance StatementMany experimental approaches require housing rodents in individual cages, a stressful condition for social animals, even in an enriched environment context. Using the pilocarpine model of epilepsy in rats and mice, we report that singly housing animals develop a more severe phenotype in terms of stress and epilepsy as compared to animals maintaining social contact. We propose that social isolation adds a degree of complexity for the interpretation of data, which may be particularly relevant for preclinical studies.