BackgroundHigh unmet need for family planning (32.4%) characterized Burundi in 2010. However, there has not been any study examining the relationship between unmet need and associated factors in Burundi. The present study aims at determining the demographic, socioeconomic and other factors underlying the unmet need for contraception among married women aged 15-49 in Burundi.MethodsThis study used data from the 2010 Burundi Demographic and Health Survey. Total unmet need, unmet need for spacing and for limiting were used as outcomes and demographic, socioeconomic and other factors as independent variables. After a descriptive analysis of the study population (n = 5421), the association between the three outcomes and the independent variables were analysed using logistic regression. Odds ratios with their 95% confidence intervals were calculated with statistical significance at p < 0.05.ResultsThis study showed that the likelihood of total unmet need decreased with age after 35+, with an adjusted Odds Ratio = 0.586 and 95% CI = 0.423-0.811, compared to women aged 15-24. Women with 4-5 and 6+ living children had higher odds [aOR = 1.850 (1.322-2.590) and 2.390 (1.616-3.534) respectively]. Odds of unmet need were lower among women with primary [aOR = 0.741 (0.618-0.888)] and secondary education [aOR = 0.555 (0.399-0.771)]. Women whose husband desired more children than them [aOR = 1.824 (1.411-2.358)] and those ignoring the husband’s desired children [aOR = 2.700 (2.176-3.350)] had higher odds than those desiring the same number as the husband. Women who had experienced the death of 1+ sons had higher odds [aOR = 1.285 (1.038-1.591)]. Middle [aOR = 0.670 (0.530-0.846)] and rich [aOR = 0.664 (0.541-0.817)] compared to poor, women living in the North [aOR = 0.611 (0.412-0.904)] compared to those from Bujumbura, had lower odds. Rural women had higher odds [aOR = 1.373 (1.018-1.852)] and those who had visited a health facility [aOR = 0.765 (0.608-0.961)] or had access to TV [aOR = 0.562 (0.375-0.843)] had lower odds.ConclusionTackling the unmet need for FP in Burundi requires scaling-up male involvement, promoting spousal communication, client-centred services, greater use of media, women’s education, child survival, and pro-poor policies.

Social cues, such as eye gaze and pointing fingers, can increase the prioritisation of specific locations for cognitive processing. A previous study using a manual reaching task showed that, although both gaze and pointing cues altered target prioritisation (reaction times [RTs]), only pointing cues affected action execution (trajectory deviations). These differential effects of gaze and pointing cues on action execution could be because the gaze cue was conveyed through a disembodied head; hence, the model lacked the potential for a body part (i.e., hands) to interact with the target. In the present study, the image of a male gaze model, whose gaze direction coincided with two potential target locations, was centrally presented. The model either had his arms and hands extended underneath the potential target locations, indicating the potential to act on the targets (Experiment 1), or had his arms crossed in front of his chest, indicating the absence of potential to act (Experiment 2). Participants reached to a target that followed a nonpredictive gaze cue at one of three stimulus onset asynchronies. RTs and reach trajectories of the movements to cued and uncued targets were analysed. RTs showed a facilitation effect for both experiments, whereas trajectory analysis revealed facilitatory and inhibitory effects, but only in Experiment 1 when the model could potentially act on the targets. The results of this study suggested that when the gaze model had the potential to interact with the cued target location, the model's gaze affected not only target prioritisation but also movement execution.

At present it is estimated that 25% of the population older than 85 years have significant cognitive impairment. The global prevalence of cognitive impairment and dementia including Alzheimer's disease is expected to rise significantly in proportion to increased life expectancy. Deterioration of memory function and ultimately establishment of Alzheimer's disease (AD) severely debilitates the affected individual, uncompromisingly decreasing the quality of life of both affected patients and their care givers. Moreover, the cost of providing adequate care to patients with AD is a significant burden to both family and the health care providers. Therefore, various attempts have been made to identify means of either delaying the onset of cognitive impairment or improving memory function in patients affected by AD. Among a number of participants, importance of dietary fatty acids in particular omega-3 based fatty acids have gained significant momentum. This article aims to review published evidences for the role of omega-3 in memory function.

The prevalence of diet-induced obesity is increasing amongst adults and children worldwide, predisposing millions of people to an array of health problems that include metabolic syndrome, non-alcoholic fatty liver disease and non-alcoholic steatohepatitis. In this study we used experimental animals to investigate the effects of dietary obesity on markers of hepatic insulin signaling as well as structural changes in hepatocytes. Adult male Wistar rats were randomized and assigned to either a control group or a test group. Controls were fed standard laboratory pelleted diet (chow-fed), while the test group had free access to a highly-palatable diet (HPD). After eight weeks, the HPD-fed animals were subdivided into three subgroups and their diets altered as follows: HPD-to-chow, HPD with the addition of fenofibrate given by oral gavage for a further seven weeks, or HPD with vehicle (1% carboxymethylcellulose at 1 mL/kg body weight) given by oral gavage for a further seven weeks, respectively. Untreated diet-fed animals had significantly higher body weight, liver weight, and all measured metabolic profiles compared with chow-fed and treated diet-fed groups. Expression of kinases IRβ, IRS-1, AKt, eNOS, Shc and ERK1/2 were unaffected by obesity, while IRS-2 and P I3 kinase levels were significantly reduced in untreated HPD animals. Compared with chow-fed animals, steatosis and steatohepatitis were almost doubled in animals from untreated HPD, while removal of HPD and fenofibrate-treatment reduced steatosis by 40% and 80% respectively. These data suggest that diet-induced obesity affects intracellular insulin signaling mechanisms, namely IRS-2 and PI 3-kinase, leading to hepatic insulin resistance. Moreover, diet-induced obesity induces fatty liver, an effect which can be reversed by either removal of the source of obesity or treatment with fenofibrate, a peroxisome proliferator-activated receptor alpha agonist.

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