Aggravation de l’anémie et polymorphisme de l’haptoglobine au cours de la drépanocytose au Sénégal

La drépanocytose homozygote s’accompagne d’une augmentation de l’hémoglobine (Hb) plasmatique, susceptible d’exposer les hématies à un stress oxydant. L’haptoglobine présente trois phénotypes majeurs (Hp1-1, Hp 2-1 et Hp 2-2) susceptibles de fixer l’hémoglobine extracellulaire avec une efficacité différente. L’objectif de ce travail est de voir si la connaissance du phénotype d’Hp pouvait constituer un élément prédictifde l’anémie sévère. Pour cela, il a été recruté 68 drépanocytaires  homozygotes, âgés de 5 à 31 ans. Pour chaque patient, un témoin de même sexe et de même âge ± 2 ans a été recruté. Le phénotypage de l’Hp a été réalisé par électrophorèse sur gel de polyacrylamide. Les résultats du dosage de l’Hb font ressortir que les taux d’Hb sont significativement différentes chez les patients comparées à celles des témoins (p = 0,001). Lorsque la répartition a été faite en fonction du phénotype d’Hp, une différence statistiquement significative a étéretrouvée entre le phénotype Hp1-1 et le phénotype Hp2-2 (p < 0,001) chez les patients et non chez les témoins. Les résultats de cette étude préliminaire suggéreraient que la connaissance du phénotype d’Hp seraitun facteur prédictif de l’anémie sévère au cours de la drépanocytose.Mots clés : Drépanocytose, anémie, phénotypes d’haptoglobine

Détermination du débit de filtration glomérulaire (DFG) au cours du diabète : Cockroft et Gault, MDRD ou CKD-EPI ?

Plusieurs paramètres peuvent être étudiés pour évaluer le rein. Parmi ceux-ci, le débit de filtration glomérulaire (DFG) a été déterminé avec les formules de Cockroft et Gault (CG), du Modification of Diet in Renal Disease (MDRD) et du Chronic Kidney Disease EPIdemiology Collaboration (CKD-EPI) et la formule la mieux adaptée pour le diabétique a été recherchée. Chez 59 diabétiques de type 1 (DT1) et 70 diabétiques de type 2 (DT2), le DFG a été déterminé avec les formules de CG, du MDRD et du CKD-EPI. Avec l’analyse statistique, les seuils de significativité ont été fixés pour p<0,05 ; T0α>1,96 et Z0α>1,96. Le MDRD est superposable au CKD-EPI chez les DT1 et DT2. Chez les DT1, le DFG moyen et la corrélation entre 1/créatininémie et DFG ne varient pas si CG ou CKD-EPI ; cependant, les sujets à DFG réduit (< 90 ml/min/1,73 m²) sont plus nombreux avec CG plutôt qu’avec CKD-EPI (66,10% vs 47,46% ; T0α=2,05). Chez les DT2, le DFG moyen et la proportion de sujets à DFG réduit sont indépendants de la formule utilisée, mais la corrélation entre 1/créatininémie et DFG est plus forte si CKD-EPI que CG (0,961 vs 0,632 ; Z0α=7,02). Ainsi, la formule la mieux adaptée pour la détermination du DFG serait CG chez les DT1 et CKD-EPI chez les DT2, sachant que CKD-EPI est équivalent à MDRD quel que soit le type de diabète.Mots clés : Cockroft et Gault - MDRD - CKD-EPI – débit de filtration glomérulaire (DFG) – diabète

Accounting for Equity Considerations in Cost-Effectiveness Analysis : A Systematic Review of Rotavirus Vaccine in Low- and Middle-Income Countries

Additional file 3: Appendix C. Full data table of results

An African Muslim Saint and his Followers in France

This paper explores the practice of Islam among a relatively understudied group of Muslim migrants in France, the Halpulaaren, some of whom have been living in France for more than three decades. Drawing on field research in Senegal, Mali and France, the author considers the contexts for Halpulaaren migration to France, including the West African background to such migration and the situation migrants face in France. The author focuses on a Halpulaaren Muslim religious leader from Senegal, Mansour Baro, who has a reputation as a living Muslim saint, and his followers in France. Tierno Mansour is one of a handful of the most esteemed leaders of the Tijaniyya Sufi order in Senegal. The appeal of this saint, who annually visits Europe, for his followers in France is examined in order to try and understand some of the ways of being Muslim in the shadow of the global city with both its promises and constraints. [Journal abstract]ASC – Publicaties niet-programma gebonde

Mitotic Spindle Proteomics in Chinese Hamster Ovary Cells

Mitosis is a fundamental process in the development of all organisms. The mitotic spindle guides the cell through mitosis as it mediates the segregation of chromosomes, the orientation of the cleavage furrow, and the progression of cell division. Birth defects and tissue-specific cancers often result from abnormalities in mitotic events. Here, we report a proteomic study of the mitotic spindle from Chinese Hamster Ovary (CHO) cells. Four different isolations of metaphase spindles were subjected to Multi-dimensional Protein Identification Technology (MudPIT) analysis and tandem mass spectrometry. We identified 1155 proteins and used Gene Ontology (GO) analysis to categorize proteins into cellular component groups. We then compared our data to the previously published CHO midbody proteome and identified proteins that are unique to the CHO spindle. Our data represent the first mitotic spindle proteome in CHO cells, which augments the list of mitotic spindle components from mammalian cells

Primate TNF Promoters Reveal Markers of Phylogeny and Evolution of Innate Immunity

Background. Tumor necrosis factor (TNF) is a critical cytokine in the immune response whose transcriptional activation is controlled by a proximal promoter region that is highly conserved in mammals and, in particular, primates. Specific single nucleotide polymorphisms (SNPs) upstream of the proximal human TNF promoter have been identified, which are markers of human ancestry. Methodology/Principal findings. Using a comparative genomics approach we show that certain fixed genetic differences in the TNF promoter serve as markers of primate speciation. We also demonstrate that distinct alleles of most human TNF promoter SNPs are identical to fixed nucleotides in primate TNF promoters. Furthermore, we identify fixed genetic differences within the proximal TNF promoters of Asian apes that do not occur in African ape or human TNF promoters. Strikingly, protein-DNA binding assays and gene reporter assays comparing these Asian ape TNF promoters to African ape and human TNF promoters demonstrate that, unlike the fixed differences that we define that are associated with primate phylogeny, these Asian ape-specific fixed differences impair transcription factor binding at an Sp1 site and decrease TNF transcription induced by bacterial stimulation of macrophages. Conclusions/significance. Here, we have presented the broadest interspecies comparison of a regulatory region of an innate immune response gene to date. We have characterized nucleotide positions in Asian ape TNF promoters that underlie functional changes in cell type- and stimulus-specific activation of the TNF gene. We have also identified ancestral TNF promoter nucleotide states in the primate lineage that correspond to human SNP alleles. These findings may reflect evolution of Asian and African apes under a distinct set of infectious disease pressures involving the innate immune response and TNF

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Anomalies of coronary artery origin: About two cases

Anomalies of coronary artery origin are congenital malformations characterized by the abnormal birth of a coronary artery from the controlateral coronary aortic sinus (birth of the left coronary artery from the right sinus or birth of the right coronary artery from the left sinus). The artery concerned has an abnormal initial path between the aorta and the pulmonary artery; this segment is most often intramural, in the aortic wall. They are rare with a prevalence (0.1% to 0.3% of the population). They pose a high risk of sudden stress death related to exercise myocardial ischemia. The most common mode of discovery is aborted sudden death, but sometimes fortuitously. The contribution of multi-round CT is described for the positive diagnosis of these anatomical variations, sometimes delicate in coronary angiography, but also for the distinction between “benign” and “malignant” forms, potentially responsible for myocardial ischemia. Treatment is usually surgical in symptomatic forms. We report the cases of two patients with coronary connection abnormalities discovered in adulthood