Etude de l’activité antioxydante des extraits des feuilles de Vitex doniana (Verbenacea)

L’objectif de la présente étude était d’évaluer l’activité antioxydante des extraits des feuilles de Vitex doniana par spectrophotométrie en utilisant les méthodes de piégeage des radicaux libres 2,2-diphényl-1- picryl-hydrazyle (DPPH•) et acide 2,2’-azino-bis-(3-éthylbenzothiazoline-6-sulfonique) (ABTS+•). Une extraction éthanolique des feuilles de Vitex doniana a été effectuée au Soxhlet. L’extrait sec recueilli a été redissout dans de l’eau puis fractionné en utilisant successivement de l’hexane, du dichlorométhane et de l’acétate d’éthyle. Les propriétés antioxydantes de l’extrait éthanolique et celles de ses différentes fractions ont été évaluées aux concentrations de 2,5 ; 10 ; 100 et 200 μg/mL. Les pourcentages d’inhibition (PI) expriment l’effet antioxydant mesuré. L’extrait éthanolique et ses différentes fractions ont présenté une activité de piégeage des deux radicaux libres. Lors des tests d’inhibition de l’absorbance du radical DPPH•, les PI ont varié de (18,15±0,01)% pour la fraction hexanique (2,5 μg/mL) à (92,45±0,01)% pour la fraction d’acétate d’éthyle (100 μg/mL). Avec le radical ABTS+•, les PI ont varié de (52,76±0,05)% pour la fraction hexanique (2,5 μg/mL) à (98,27±0,12)% pour la fraction d’acétate d’éthyle (100 μg/mL). Ainsi, l’extrait éthanolique des feuilles de Vitex doniana et ses différentes fractions possèdent un pouvoir antioxydant significatif.Mots clés : Activité antioxydante, DPPH, ABTS, Vitex doniana

Epilespie de l’enfant et de l’adolescent au Senegal

Introduction L’épilepsie constitue un problème de santé publique au Sénégal avec une prévalence de 8,3 à 14/1000. Elle concerne principalement les enfants. L’objectif de ce travail est d’étudier les aspects biographiques, phénotypiques et évolutifs de la maladie épileptique dans une cohorte d’enfants au Sénégal.Méthodologie Il s’agit d’une étude rétrospective de dossiers d’enfants épileptiques suivis régulièrement au CHU de FANN et à l’Hôpital d’Enfants Albert Royer, de Juillet 2003 à décembre 2010. Les critères d’inclusion étaient: épileptiques âgés de moins de 18 ans, régulièrement suivis depuis au moins 3 ans, ayant un traitement adapté, à dose efficace, avec une bonne observance thérapeutique.Résultats Nous avons colligé 522 enfants, âgés de 3 mois à 16 ans, avec un sex-ratio de 1,7 en faveur des garçons. L’épilepsie était idiopathique chez 57% des enfants et non idiopathique chez 43% des patients. Les facteurs étiologiques étaient dominés par la consanguinité parentale, les anomalies de la grossesse et de l’accouchement, les infections du système nerveux central. Dans le groupe des épilepsies idiopathiques la consanguinité parentale et l’épilepsie familiale étaient retrouvées respectivement chez 64 enfants (21,62%) et 20 enfants (6,75%). Neuf enfants (3%) présentaient un trouble du langage isolé, alors qu’un seul enfant (0,33%) avait un déficit cognitif global. Dans le groupe des épilepsies non idiopathiques, les signes associés à l’épilepsie étaient les troubles du langage (15,70%), du comportement (15%) et des déficits moteurs (10,32%). 22,41% des enfants scolarisés avaient des difficultés d’apprentissage menant parfois à des redoublements scolaires ou une exclusion.Conclusion La classification syndromique à l’épilepsie est nécessaire pour une bonne prévision pronostique et thérapeutique. Le caractère idiopathique ou non en est pour une grande place, corrélé le plus souvent à une épilepsie familial ou une consanguinité ou affection périnatal ou infectieuse du système nerveux central.Mots clés : Epilepsie, syndrome épileptique, Sénégal

Hybridized zoonotic schistosoma infections result in hybridized morbidity profiles: a clinical morbidity study amongst co-infected human populations of Senegal

Hybridization of infectious agents is a major emerging public and veterinary health concern at the interface of evolution, epidemiology, and control. Whilst evidence of the extent of hybridization amongst parasites is increasing, their impact on morbidity remains largely unknown. This may be predicted to be particularly pertinent where parasites of animals with contrasting pathogenicity viably hybridize with human parasites. Recent research has revealed that viable zoonotic hybrids between human urogenital Schistosoma haematobium with intestinal Schistosoma species of livestock, notably Schistosoma bovis, can be highly prevalent across Africa and beyond. Examining human populations in Senegal, we found increased hepatic but decreased urogenital morbidity, and reduced improvement following treatment with praziquantel, in those infected with zoonotic hybrids compared to non-hybrids. Our results have implications for effective monitoring and evaluation of control programmes, and demonstrate for the first time the potential impact of parasite hybridizations on host morbidity

Resistance to DDT and Pyrethroids and Increased kdr Mutation Frequency in An. gambiae after the Implementation of Permethrin-Treated Nets in Senegal

Introduction: The aim of this study was to evaluate the susceptibility to insecticides of An. gambiae mosquitoes sampled in Dielmo (Senegal), in 2010, 2 years after the implementation of Long Lasting Insecticide-treated Nets (LLINs) and to report the evolution of kdr mutation frequency from 2006 to 2010. Methods: WHO bioassay susceptibility tests to 6 insecticides were performed on adults F0, issuing from immature stages of An. gambiae s.l., sampled in August 2010. Species and molecular forms as well as the presence of L1014F and L1014S kd

Kdr-based insecticide resistance in Anopheles gambiae s.s populations in

<p>Abstract</p> <p>Background</p> <p>The spread of insecticide resistance in the malaria mosquito, <it>Anopheles gambiae </it>is a serious threat for current vector control strategies which rely on the use of insecticides. Two mutations at position 1014 of the S₆transmembrane segment of domain II in the voltage gated sodium channel, known as <it>kdr </it>(<it>knockdown resistance</it>) mutations leading to a change of a Leucine to a Phenylalanine (L1014F) or to a Serine (L1014S) confer resistance to DDT and pyrethroid insecticides in the insect. This paper presents the current distribution of the <it>kdr </it>alleles in wild <it>Anopheles gambiae </it>populations in Cameroon.</p> <p>Results</p> <p>A total of 1,405 anopheline mosquitoes were collected from 21 localities throughout Cameroon and identified as <it>An. gambiae </it>(N = 1,248; 88.8%), <it>An. arabiensis </it>(N = 120; 8.5%) and <it>An. melas </it>(N = 37; 2.6%). Both <it>kdr </it>alleles 1014F and 1014S were identified in the M and S molecular forms of <it>An. gambiae </it>s.s. The frequency of the 1014F allele ranged from 1.7 to 18% in the M-form, and from 2 to 90% in the S-form. The 1014S allele ranged from 3-15% in the S-form and in the M-form its value was below 3%. Some specimens were found to carry both resistant <it>kdr </it>alleles.</p> <p>Conclusion</p> <p>This study provides an updated distribution map of the <it>kdr </it>alleles in wild <it>An. gambiae </it>populations in Cameroon. The co-occurrence of both alleles in malaria mosquito vectors in diverse ecological zones of the country may be critical for the planning and implementation of malaria vector control interventions based on IRS and ITNs, as currently ongoing in Cameroon.</p

Transcriptional Profiling in Pathogenic and Non-Pathogenic SIV Infections Reveals Significant Distinctions in Kinetics and Tissue Compartmentalization

Simian immunodeficiency virus (SIV) infection leads to AIDS in experimentally infected macaques, whereas natural reservoir hosts exhibit limited disease and pathology. It is, however, unclear how natural hosts can sustain high viral loads, comparable to those observed in the pathogenic model, without developing severe disease. We performed transcriptional profiling on lymph node, blood, and colon samples from African green monkeys (natural host model) and Asian pigtailed macaques (pathogenic model) to directly compare gene expression patterns during acute pathogenic versus non-pathogenic SIV infection. The majority of gene expression changes that were unique to either model were detected in the lymph nodes at the time of peak viral load. Results suggest a shift toward cellular stress pathways and Th1 profiles during pathogenic infection, with strong and sustained type I and II interferon responses. In contrast, a strong type I interferon response was initially induced during non-pathogenic infection but resolved after peak viral load. The natural host also exhibited controlled Th1 profiles and better preservation of overall cell homeostasis. This study identified gene expression patterns that are specific to disease susceptibility, tissue compartmentalization, and infection duration. These patterns provide a unique view of how host responses differ depending upon lentiviral infection outcome

Losartan Slows Pancreatic Tumor Progression and Extends Survival of SPARC-Null Mice by Abrogating Aberrant TGFβ Activation

Pancreatic adenocarcinoma, a desmoplastic disease, is the fourth leading cause of cancer-related death in the Western world due, in large part, to locally invasive primary tumor growth and ensuing metastasis. SPARC is a matricellular protein that governs extracellular matrix (ECM) deposition and maturation during tissue remodeling, particularly, during wound healing and tumorigenesis. In the present study, we sought to determine the mechanism by which lack of host SPARC alters the tumor microenvironment and enhances invasion and metastasis of an orthotopic model of pancreatic cancer. We identified that levels of active TGFβ1 were increased significantly in tumors grown in SPARC-null mice. TGFβ1 contributes to many aspects of tumor development including metastasis, endothelial cell permeability, inflammation and fibrosis, all of which are altered in the absence of stromal-derived SPARC. Given these results, we performed a survival study to assess the contribution of increased TGFβ1 activity to tumor progression in SPARC-null mice using losartan, an angiotensin II type 1 receptor antagonist that diminishes TGFβ1 expression and activation in vivo. Tumors grown in SPARC-null mice progressed more quickly than those grown in wild-type littermates leading to a significant reduction in median survival. However, median survival of SPARC-null animals treated with losartan was extended to that of losartan-treated wild-type controls. In addition, losartan abrogated TGFβ induced gene expression, reduced local invasion and metastasis, decreased vascular permeability and altered the immune profile of tumors grown in SPARC-null mice. These data support the concept that aberrant TGFβ1-activation in the absence of host SPARC contributes significantly to tumor progression and suggests that SPARC, by controlling ECM deposition and maturation, can regulate TGFβ availability and activation

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