Malnutrition is estimated to contribute to more than one third of all child deaths, although it is rarely listed as the direct cause. Contributing to more than half of deaths in children worldwide; child malnutrition was associated with 54% of deaths in children in developing countries in 2001. Poverty remains the major contributor to this ill. The vicious cycle of poverty, disease and illness aggravates this situation. Grooming undernourished children causes children to start life at mentally sub optimal levels. This becomes a serious developmental threat. Lack of education especially amongst women disadvantages children, especially as far as healthy practices like breastfeeding and child healthy foods are concerned. Adverse climatic conditions have also played significant roles like droughts, poor soils and deforestation. Sociocultural barriers are major hindrances in some communities, with female children usually being the most affected. Corruption and lack of government interest and investment are key players that must be addressed to solve this problem. A multisectorial approach is vital in tackling this problem. Improvement in government policy, fight against corruption, adopting a horizontal approach in implementing programmes at community level must be recognized. Genetically modified foods to increase food production and to survive adverse climatic conditions could be gateways in solving these problems. Socio cultural peculiarities of each community are an essential base line consideration for the implementation of any nutrition health promotion programs.

BackgroundThe interaction between intestinal parasites and malaria is still not clear. Data in published literature are conflicting. We studied the effect of intestinal parasitic infection (IPI) on the clinical outcome of malaria in coinfected children.MethodsIn a cross sectional study performed between October 2014 and September 2015, children infected with malaria, as demonstrated by the presence of asexual parasites in Giemsa stained blood films, were enrolled. Stool samples were obtained from participants and subjected to the formol-ether concentration technique for the detection of intestinal parasites. The Complete blood count was performed using an automated haematology analyser (Mindray, BC-2800). The risk ratio, Pearson’s chi-square and the student T test were all performed as part of the statistical analyses. Statistical significance was set at p < 0.05.ResultsIn all, 405 children successfully took part in the study. The children were between 1 week and 120 months of age (mean ± SD = 41.5 ± 33.5). Coinfection with intestinal parasites was observed in 11.6%. The rate of severe malaria (SM) attack in this study was 10.9%. SM was not observed to be associated with age (p = 0.377) or gender (p = 0.387), meanwhile coinfection with intestinal parasites was associated with age (p = 0.003). Among SM cases, IPI prevalence was higher in children with mild (WHO group 3) severe malaria (p = 0.027). Overall, IPI was not observed to be associated with SM (p = 0.656) or malaria parasite density (p = 0.185) or haemoglobin concentration (p = 0.205). The main clinical features of SM observed were hyperpyrexia (68.2%), severe malarial anaemia (61.4%), and multiple convulsion (52.3%).ConclusionIPI was not observed to be associated with the severity of malaria, the malaria parasite density, and the haemoglobin concentration in coinfected children in Cameroon. The clinical outcome of malaria in children coinfected with intestinal parasites may depend on the geographical setting after all.

Background Chronic obstructive pulmonary disease (COPD) is characterized by a progressive and abnormal inflammatory response in the lungs, mainly caused by cigarette smoking. Animal models exposed to cigarette smoke (CS) are used to mimic human COPD but the use of different CS protocols makes it difficult to compare the immunological and structural consequences of using a nose-only or whole-body CS exposure system. We hypothesized that when using a standardized CS exposure protocol based on particle density and CO (carbon monoxide) levels, the whole-body CS exposure system would generate a more severe inflammatory response than the nose-only system, due to possible sensitization by uptake of CS-components through the skin or via grooming. Methods In this study focusing on early COPD, mice were exposed twice daily 5 days a week to CS either with a nose-only or whole-body exposure system for 14 weeks to assess lung function, remodeling and inflammation. Results At sacrifice, serum cotinine levels were significantly higher in the whole-body (5.3 (2.3–6.9) ng/ml) compared to the nose-only ((2.0 (1.8–2.5) ng/ml) exposure system and controls (1.0 (0.9–1.0) ng/ml). Both CS exposure systems induced a similar degree of lung function impairment, while inflammation was more severe in whole body exposure system. Slightly more bronchial epithelial damage, mucus and airspace enlargement were observed with the nose-only exposure system. More lymphocytes were present in the bronchoalveolar lavage (BAL) and lymph nodes of the whole-body exposure system while enhanced IgA and IgG production was found in BAL and to a lesser extent in serum with the nose-only exposure system. Conclusion The current standardized CS-exposure protocol resulted in a higher internal load of serum cotinine in the whole-body exposure system, which was associated with more inflammation. However, both exposure systems resulted in a similar lung function impairment. Data also highlighted differences between the two models in terms of lung inflammation and remodelling, and potential sensitization to CS. Researchers should be aware of these differences when designing their future studies for an early intervention in COPD.

Endothelial erosion of atherosclerotic plaques and resulting thrombosis causes approximately 30% of acute coronary syndromes (ACS). As changes in the haemodynamic environment strongly influence endothelial function and contribute to plaque development, we reconstructed the coronary artery geometries of plaques with thrombi overlying intact fibrous caps from 17 ACS patients and performed computational fluid dynamic analysis. The results demonstrated that erosions frequently occur within areas of stenosis exposed to elevated flow. We recapitulated this flow environment in vitro, exposing human coronary artery endothelial cells to elevated flow and modelled smoking (a risk factor for erosion) by exposure to a combination of aqueous cigarette smoke extract and TNFα. This treatment induced endothelial detachment, which increased with pharmacological activation of the antioxidant system controlled by transcription factor Nrf2 (encoded by NFE2L2). The expression of Oxidative Stress Growth INhibitor genes OSGIN1 and OSGIN2 increased under these conditions and also in the aortas of mice exposed to cigarette smoke. Sustained high level expression of OSGIN1+2 resulted in cell cycle arrest, induction of senescence, loss of focal adhesions and actin stress fibres, and dysregulation of autophagy. Overexpression of either Nrf2 or OSGIN1+2 induced cell detachment, which did not depend on apoptosis, and could be partially rescued by inhibition of HSP70 using VER-155008, or AMP kinase activation using metformin. These findings demonstrate that under elevated flow, smokinginduced hyperactivation of Nrf2 can trigger endothelial cell detachment, highlighting a novel mechanism that could contribute to ACS involving endothelial erosion overlying stenotic plaques.

Background: Chronic Obstructive Pulmonary Disease (COPD) is characterized by a progressive and abnormal inflammatory response in the lungs, mainly caused by cigarette smoking. Animal models exposed to cigarette smoke (CS) are used to mimic human COPD but the use of different CS protocols makes it difficult to compare the immunological and structural consequences of using a nose-only or whole-body CS exposure system. We hypothesized that when using a standardized CS exposure protocol based on particle density and CO (carbon monoxide) levels, the whole-body CS exposure system would generate a more severe inflammatory response than the nose-only system, due to possible sensitization, uptake of gases through the skin or uptake of tar particles stuck on the skin via grooming. Methods: In this study focusing on early COPD, mice were exposed twice daily 5 days a week to CS either with a nose-only or whole-body exposure system for 14 weeks to assess lung remodeling and inflammation. Data was analyzed with a one-way ANOVA with Bonferroni post-hoc test or Kruskal-Wallis with Dunn’s test for multiple comparison depending on respectively parametric or non-parametric datasets.Results: Both CS exposure systems induced a similar degree of lung function impairment and morphological alterations. Interestingly, an enhanced lymphoid presence in the bronchoalveolar lavage and lymph nodes with a higher mRNA expression of interleukin 6 and keratinocyte chemoattractant in the lungs were found with the whole-body system. Conclusion: Our data indicate that the inflammatory outcomes are more severe in the whole-body CS exposure compared to the nose-only system, but lung remodeling and lung function impairment are similarly affected. These observations can assist researchers to make an appropriate choice between the two CS exposure systems in designing their future studies in early drug interventions.