Incidence and dietary risk factors of goitre in children in a rural area/ D.R.Congo

Background: Although deficiency in dietary iodine remains the main cause of endemic and sporadic goitre, naturally occurring goitrogens in foods are additional factors that play a major role in developing goitre. In this study we focused on the relationship of different potential goitrogenous food and the development of goitre in preschool children in the rural area of Bwamanda, Democratic Republic of the Congo (DRC). Objectives: First, to do a semi-systematic literature review on the incidence of goitre and the role of dietary pattern in its genesis. Second, describe the incidence of goitre in preschool children in DRC in relation to age, sex, and season. Third, examine the effects of specific food items on occurrence of goitre in these children. Methods: For the 1st objective, we used a semi- systematic method to search for relevant published articles to the topic area. We searched four online databases, three online journals, five authors and the reference lists of the identified key articles. We did a secondary analysis of the data from an original dynamic population study which was done in the rural area of Bwamanda, DRC. That study included an open cohort of 5657 children which was followed up every 3 months throughout six survey rounds, during a period of three years from 1989- 1991. All the investigations and clinical examination were done by trained doctors and interviewers at special under five clinics in the study setting. Incidence of goitre among the children who were at risk of developing goitre was calculated for 5 survey intervals. The incidence of goitre was also assessed in relation to season, sex and age of the children. For the 3rd specific objective, seven food items were selected to be investigated for their potential goitrogenic effects. The exposed group was those children who ate these foods and the unexposed group was the children who didn’t eat these foods. Age, sex, height for age Z-score (HAZ), and weight for length Z-score (WLZ) were considered as potential confounders. All selected food items and confounders were analysed using logistic regression analysis. Results: Four studies were included in the semi-systematic literature review; the conclusion was similar in all of them with iodine deficiency being the main cause of goitre in man, and cassava consumption being an important factor in addition to that. Incidence of goitre was different in each survey interval and it was higher in rainy season. The incidence of goitre increased significantly when children got older but being a male or a female was statistically unrelated. Eating cassava leaves, cassava tubers and maize played a major role in developing goitre especially in older children, while nuts reduced the risk of developing goitre in those children. Banana, fish and papaya had non-significant contributions. iv Conclusion: This study confirms that goitre incidence in children (0-5years) in a rural area in Central Africa is significantly related with age as the older children had more risk to develop goitre than the younger children, but it had no relation to gender. The incidence of goitre increased also during rainy seasons. This is the 1st longitudinal analysis showing the relationship between consumption of specific food items and the development of goitre in children (0-5 years) in a rural area in central Africa, where cassava and maize found to be important contributory factors while nuts may have a protective role in developing goitre in those children.Master of philosophy in international healthMAMD-INTHINTH39

Towards An Effective Urban Growth Management Strategy In Qatar (1)

Control and management of urban growth is currently a subject of intense debate in both professional and academic planning circles, as suburban sprawl, pollution, and the decline of the urban environment particularly in city centres have become more sensitive public issues. The desire to control growth versus an increasing public need for housing and other related facilities has created a serious dilemma for planning agencies in their efforts to facilitate for better living environment. Growth management can be defined as the mitigation of the impacts of growth in order to improve or maintain the quality of life in a community. By clearly articulating the values of the community and identifying those items that contribute to the quality of life through the creation of a growth management strategy and implementation plan, it is possible to establish an effective approach to manage future growth. Increasing demands for urban growth with decreasing satisfaction in the resulting quality of life is the dilemma of most countries including the State of Qatar. The inefficient use of economic and physical resources results in development that generates new problems, such as sprawl, traffic congestion and rising demands for increased government spending on new infrastructure and services. The lack of comprehensive planning and development control may also results in infrastructure installation costs that are much higher than what they would be with a growth management strategy in place. The land allocation policies that are uncoordinated with physical development plans in Qatar exacerbate the problem by directing development to areas without appropriate infrastructure and services. This paper aim at reviews the current problems associated with the lack of an urban growth management strategy in the State of Qatar and outlines the process of creating a comprehensive system to effectively handle urban growth. The paper will also attempt to formulate an outline for an effective strategy to mitigate the impacts of growth in order to maintain and improve the quality of life in the State of Qatar

E2F6 initiates stable epigenetic silencing of germline genes during embryonic development.

In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes; however, the molecular mechanisms of this specificity remain unclear. Here, we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6), is critical to target and initiate epigenetic silencing at germline genes in early embryogenesis. Genome-wide, E2F6 binds preferentially to CpG islands in embryonic cells. E2F6 cooperates with MGA to silence a subgroup of germline genes in mouse embryonic stem cells and in embryos, a function that critically depends on the E2F6 marked box domain. Inactivation of E2f6 leads to a failure to deposit CpG island DNA methylation at these genes during implantation. Furthermore, E2F6 is required to initiate epigenetic silencing in early embryonic cells but becomes dispensable for the maintenance in differentiated cells. Our findings elucidate the mechanisms of epigenetic targeting of germline genes and provide a paradigm for how transient repression signals by DNA-binding factors in early embryonic cells are translated into long-term epigenetic silencing during mouse development

The cancer preventative agent resveratrol is converted to the anticancer agent piceatannol by the cytochrome P450 enzyme CYP1B1

Resveratrol is a cancer preventative agent that is found in red wine. Piceatannol is a closely related stilbene that has antileukaemic activity and is also a tyrosine kinase inhibitor. Piceatannol differs from resveratrol by having an additional aromatic hydroxy group. The enzyme CYP1B1 is overexpressed in a wide variety of human tumours and catalyses aromatic hydroxylation reactions. We report here that the cancer preventative agent resveratrol undergoes metabolism by the cytochrome P450 enzyme CYP1B1 to give a metabolite which has been identified as the known antileukaemic agent piceatannol. The metabolite was identified by high performance liquid chromatography analysis using fluorescence detection and the identity of the metabolite was further confirmed by derivatisation followed by gas chromatography–mass spectrometry studies using authentic piceatannol for comparison. This observation provides a novel explanation for the cancer preventative properties of resveratrol. It demonstrates that a natural dietary cancer preventative agent can be converted to a compound with known anticancer activity by an enzyme that is found in human tumours. Importantly this result gives insight into the functional role of CYP1B1 and provides evidence for the concept that CYP1B1 in tumours may be functioning as a growth suppressor enzyme

Calpain-mediated cleavage of Beclin-1 and autophagy deregulation following retinal ischemic injury in vivo

Autophagy is the major intracellular degradation pathway that regulates long-lived proteins and organelles turnover. This process occurs at basal levels in all cells but it is rapidly upregulated in response to starvation and cellular stress. Although being recently implicated in neurodegeneration, it remains still unclear whether autophagy has a detrimental or protective role. In this study, we investigated the dynamics of the autophagic process in retinal tissue that has undergone transient ischemia, an experimental model that recapitulates features of ocular pathologies, including glaucoma, anterior ischemic optic neuropathy and retinal vessels occlusion. Retinal ischemia, induced in adult rats by increasing the intraocular pressure, was characterized by a reduction in the phosphatidylethanolamine-modified form of LC3 (LC3II) and by a significant decrease in Beclin-1. The latter event was associated with a proteolytic cleavage of Beclin-1, leading to the accumulation of a 50-kDa fragment. This event was prevented by intravitreal treatment with the non-competitive N-methyl-D-aspartate antagonist MK801 and calpain inhibitors or by calpain knockdown. Blockade of autophagy by pharmacological inhibition or Beclin-1 silencing in RGC-5 increased cell death, suggesting a pro-survival role of the autophagic process in this neuronal cell type. Altogether, our results provide original evidence for calpain-mediated cleavage of Beclin-1 and deregulation of basal autophagy in the rat retina that has undergone ocular ischemia/reperfusion injury

Autophagy–physiology and pathophysiology

“Autophagy” is a highly conserved pathway for degradation, by which wasted intracellular macromolecules are delivered to lysosomes, where they are degraded into biologically active monomers such as amino acids that are subsequently re-used to maintain cellular metabolic turnover and homeostasis. Recent genetic studies have shown that mice lacking an autophagy-related gene (Atg5 or Atg7) cannot survive longer than 12 h after birth because of nutrient shortage. Moreover, tissue-specific impairment of autophagy in central nervous system tissue causes massive loss of neurons, resulting in neurodegeneration, while impaired autophagy in liver tissue causes accumulation of wasted organelles, leading to hepatomegaly. Although autophagy generally prevents cell death, our recent study using conditional Atg7-deficient mice in CNS tissue has demonstrated the presence of autophagic neuron death in the hippocampus after neonatal hypoxic/ischemic brain injury. Thus, recent genetic studies have shown that autophagy is involved in various cellular functions. In this review, we introduce physiological and pathophysiological roles of autophagy

New and Common Haplotypes Shape Genetic Diversity in Asian Tiger Mosquito Populations from Costa Rica and Panama

The Asian tiger mosquito, Aedes albopictus (Skuse) (Diptera: Culicidae), is a vector of several human pathogens. Ae. albopictus is also an invasive species that, over recent years, has expanded its range out of its native Asia. Ae. albopictus was suspected to be present in Central America since the 1990s, and its presence was confirmed by most Central American nations by 2010. Recently, this species has been regularly found, yet in low numbers, in limited areas of Panama and Costa Rica (CR). Here, we report that short sequences (?558 bp) of the mitochondrial cytochrome oxidase subunit 1 (COI) and NADH dehydrogenase subunit 5 genes of Ae. albopictus, had no haplotype diversity. Instead, there was a common haplotype for each gene in both CR and Panama. In contrast, a long COI sequence (?1,390 bp) revealed that haplotype diversity (±SD) was relatively high in CR (0.72 ± 0.04) when compared with Panama (0.33 ± 0.13), below the global estimate for reported samples (0.89 ± 0.01). The long COI sequence allowed us to identify seven (five new) haplotypes in CR and two (one new) in Panama. A haplotype network for the long COI gene sequence showed that samples from CR and Panama belong to a single large group. The long COI gene sequences suggest that haplotypes in Panama and CR, although similar to each other, had a significant geographic differentiation (Kst = 1.33; P < 0.001). Thus, most of our results suggest a recent range expansion in CR and Panama

Imprinting disorders: a group of congenital disorders with overlapping patterns of molecular changes affecting imprinted loci.

Congenital imprinting disorders (IDs) are characterised by molecular changes affecting imprinted chromosomal regions and genes, i.e. genes that are expressed in a parent-of-origin specific manner. Recent years have seen a great expansion in the range of alterations in regulation, dosage or DNA sequence shown to disturb imprinted gene expression, and the correspondingly broad range of resultant clinical syndromes. At the same time, however, it has become clear that this diversity of IDs has common underlying principles, not only in shared molecular mechanisms, but also in interrelated clinical impacts upon growth, development and metabolism. Thus, detailed and systematic analysis of IDs can not only identify unifying principles of molecular epigenetics in health and disease, but also support personalisation of diagnosis and management for individual patients and families.All authors are members of the EUCID.net network, funded by COST (BM1208). TE is funded by the German Ministry of research and education (01GM1513B). GPdN is funded by I3SNS Program of the Spanish Ministry of Health (CP03/0064; SIVI 1395/09), Instituto de Salud Carlos III (PI13/00467) and Basque Department of Health (GV2014/111017).This is the final version of the article. It first appeared from BioMed Central via http://dx.doi.org/10.1186/s13148-015-0143-