Determinants of Mortality in Children under Five Years of Age with Severe Acute Malnutrition Admitted to the Yalgado Ouédraogo Teaching Hospital (Burkina Faso)

Background: To determine critical factors associated with severely malnourished children under five this case-control study was conducted. Methods: The data of a total of 433 children aged 0-59 months and admitted to the Hospital Yalgado Ouedraogo, (CHU – YO) between January 31, 2009 to January 31, 2013, were included in the analysis: 72 for the case group and 361 for the control group. Clinical and treatment records were accessed and data were analyzed. Results: For clinical signs, determinants of mortality were diarrhea [OR = 4.6; (95%CI 2.6-8.2], anorexia [OR = 2.7; (95%CI 1.4-5.0] and hepatomegaly [OR = 2.6; (95%CI 1.4-4.8]. For infections, determinants of mortality were pediatric HIV/AIDS [OR = 10.9; (95%CI 5.6-21.5] and digestive illnesses [OR = 5.1 (95%CI 2.8-9.4)]. Regarding the complications of malnutrition, determinants of mortality were severe dehydration [OR = 16.4 (95%CI 8.0-33.5)], skin lesions [OR = 14.3 (95%CI 6.4 -31.9)], heart failure [OR = 6.8 (95%CI 2.5-19.0)] and severe anemia [OR = 3.2(95%CI 1.4-7.1)]. For biochemical indicators, low serum sodium [OR = 0.7(95%CI 0.5-1.0)] and potassium levels [OR = 0.9(95%CI 0.9-1.0)] were the critical factors. In addition the risk of death was associated with low value of MUAC [OR = 0.9 (95% CI 0.8-0.9)]. Conclusions: The risk of death of children with severe acute malnutrition varies according to different factors studied

Transgenic neuronal overexpression reveals that stringently regulated p23 expression is critical for coordinated movement in mice

<p>Abstract</p> <p>Background</p> <p>p23 belongs to the highly conserved p24 family of type I transmembrane proteins, which participate in the bidirectional protein transport between the endoplasmic reticulum and Golgi apparatus. Mammalian p23 has been shown to interact with γ-secretase complex, and modulate secretory trafficking as well as intramembranous processing of amyloid precursor protein in cultured cells. Negative modulation of β-amyloid production by p23 in cultured cell lines suggested that elevation of p23 expression in neurons might mitigate cerebral amyloid burden.</p> <p>Results</p> <p>We generated several lines of transgenic mice expressing human p23 in neurons under the control of <it>Thy-1.2 </it>promoter. We found that even a 50% increase in p23 levels in the central nervous system of mice causes post-natal growth retardation, severe neurological problems characterized by tremors, seizure, ataxia, and uncoordinated movements, and premature death. The severity of the phenotype closely correlated with the level of p23 overexpression in multiple transgenic lines. While the number and general morphology of neurons in Hup23 mice appeared to be normal throughout the brain, abnormal non-Golgi p23 localization was observed in a subset of neurons with high transgene expression in brainstem. Moreover, detailed immunofluorescence analysis revealed marked proliferation of astrocytes, activation of microglia, and thinning of myelinated bundles in brainstem of Hup23 mice.</p> <p>Conclusions</p> <p>These results demonstrate that proper level of p23 expression is critical for neuronal function, and perturbing p23 function by overexpression initiates a cascade of cellular reactions in brainstem that leads to severe motor deficits and other neurological problems, which culminate in premature death. The neurological phenotype observed in Hup23 mice highlights significant adverse effects associated with manipulating neuronal expression of p23, a previously described negative modulator of γ-secretase activity and β-amyloid production. Moreover, our report has broader relevance to molecular mechanisms in several neurodegenerative diseases as it highlights the inherent vulnerability of the early secretory pathway mechanisms that ensure proteostasis in neurons.</p

Crystal constructions in Number Theory

Weyl group multiple Dirichlet series and metaplectic Whittaker functions can be described in terms of crystal graphs. We present crystals as parameterized by Littelmann patterns and we give a survey of purely combinatorial constructions of prime power coefficients of Weyl group multiple Dirichlet series and metaplectic Whittaker functions using the language of crystal graphs. We explore how the branching structure of crystals manifests in these constructions, and how it allows access to some intricate objects in number theory and related open questions using tools of algebraic combinatorics

Differential Dynamics of Transposable Elements during Long-Term Diploidization of Nicotiana Section Repandae (Solanaceae) Allopolyploid Genomes

PubMed ID: 23185607This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited