136 research outputs found

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

    Get PDF
    Introduction L’épilepsie constitue un problĂšme de santĂ© publique au SĂ©nĂ©gal avec une prĂ©valence de 8,3 Ă  14/1000. Elle concerne principalement les enfants. L’objectif de ce travail est d’étudier les aspects biographiques, phĂ©notypiques et Ă©volutifs de la maladie Ă©pileptique dans une cohorte d’enfants au SĂ©nĂ©gal.MĂ©thodologie Il s’agit d’une Ă©tude rĂ©trospective de dossiers d’enfants Ă©pileptiques suivis rĂ©guliĂšrement au CHU de FANN et Ă  l’HĂŽpital d’Enfants Albert Royer, de Juillet 2003 Ă  dĂ©cembre 2010. Les critĂšres d’inclusion Ă©taient: épileptiques ĂągĂ©s de moins de 18 ans, rĂ©guliĂšrement suivis depuis au moins 3 ans, ayant un traitement adaptĂ©, Ă  dose efficace, avec une bonne observance thĂ©rapeutique.RĂ©sultats Nous avons colligĂ© 522 enfants, ĂągĂ©s de 3 mois Ă  16 ans, avec un sex-ratio de 1,7 en faveur des garçons. L’épilepsie Ă©tait idiopathique chez 57% des enfants et non idiopathique chez 43% des patients. Les facteurs étiologiques Ă©taient dominĂ©s par la consanguinitĂ© parentale, les anomalies de la grossesse et de l’accouchement, les infections du systĂšme nerveux central. Dans le groupe des Ă©pilepsies idiopathiques la consanguinitĂ© parentale et l’épilepsie familiale Ă©taient retrouvĂ©es respectivement chez 64 enfants (21,62%) et 20 enfants (6,75%). Neuf enfants (3%) prĂ©sentaient un trouble du langage isolĂ©, alors qu’un seul enfant (0,33%) avait un dĂ©ficit cognitif global. Dans le groupe des Ă©pilepsies non idiopathiques, les signes associĂ©s à l’épilepsie Ă©taient les troubles du langage (15,70%), du comportement (15%) et des dĂ©ficits moteurs (10,32%). 22,41% des enfants scolarisĂ©s avaient des difficultĂ©s d’apprentissage menant parfois Ă  des redoublements scolaires ou une exclusion.Conclusion La classification syndromique Ă  l’épilepsie est nĂ©cessaire pour une bonne prĂ©vision pronostique et thĂ©rapeutique. Le caractĂšre idiopathique ou non en est pour une grande place, corrĂ©lĂ© le plus souvent Ă  une épilepsie familial ou une consanguinitĂ© ou affection pĂ©rinatal ou infectieuse du systĂšme nerveux central.Mots clĂ©s : Epilepsie, syndrome Ă©pileptique, SĂ©nĂ©gal

    Perinatal acquisition of drug-resistant HIV-1 infection: mechanisms and long-term outcome

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Primary-HIV-1-infection in newborns that occurs under antiretroviral prophylaxis that is a high risk of drug-resistance acquisition. We examine the frequency and the mechanisms of resistance acquisition at the time of infection in newborns.</p> <p>Patients and Methods</p> <p>We studied HIV-1-infected infants born between 01 January 1997 and 31 December 2004 and enrolled in the ANRS-EPF cohort. HIV-1-RNA and HIV-1-DNA samples obtained perinatally from the newborn and mother were subjected to population-based and clonal analyses of drug resistance. If positive, serial samples were obtained from the child for resistance testing.</p> <p>Results</p> <p>Ninety-two HIV-1-infected infants were born during the study period. Samples were obtained from 32 mother-child pairs and from another 28 newborns. Drug resistance was detected in 12 newborns (20%): drug resistance to nucleoside reverse transcriptase inhibitors was seen in 10 cases, non-nucleoside reverse transcriptase inhibitors in two cases, and protease inhibitors in one case. For 9 children, the detection of the same resistance mutations in mothers' samples (6 among 10 available) and in newborn lymphocytes (6/8) suggests that the newborn was initially infected by a drug-resistant strain. Resistance variants were either transmitted from mother-to-child or selected during subsequent temporal exposure under suboptimal perinatal prophylaxis. Follow-up studies of the infants showed that the resistance pattern remained stable over time, regardless of antiretroviral therapy, suggesting the early cellular archiving of resistant viruses. The absence of resistance in the mother of the other three children (3/10) and neonatal lymphocytes (2/8) suggests that the newborns were infected by a wild-type strain without long-term persistence of resistance when suboptimal prophylaxis was stopped.</p> <p>Conclusion</p> <p>This study confirms the importance of early resistance genotyping of HIV-1-infected newborns. In most cases (75%), drug resistance was archived in the cellular reservoir and persisted during infancy, with or without antiretroviral treatment. This finding stresses the need for effective antiretroviral treatment of pregnant women.</p

    The promoter of ZmMRP-1, a maize transfer cell-specific transcriptional activator, is induced at solute exchange surfaces and responds to transport demands

    Get PDF
    Transfer cells have specializations that facilitate the transport of solutes across plant exchange surfaces. ZmMRP-1 is a maize (Zea mays) endosperm transfer cell-specific transcriptional activator that plays a central role in the regulatory pathways controlling transfer cell differentiation and function. The present work investigates the signals controlling the expression of ZmMRP-1 through the production of transgenic lines of maize, Arabidopsis, tobacco and barley containing ZmMRP-1promoter:GUS reporter constructs. The GUS signal predominantly appeared in regions of active transport between source and sink tissues, including nematode-induced feeding structures and at sites of vascular connection between developing organs and the main plant vasculature. In those cases, promoter induction was associated with the initial developmental stages of transport structures. Significantly, transfer cells also differentiated in these regions suggesting that, independent of species, location or morphological features, transfer cells might differentiate in a similar way under the influence of conserved induction signals. In planta and yeast experiments showed that the promoter activity is modulated by carbohydrates, glucose being the most effective inducer

    The influence of mosquito resting behaviour and associated microclimate for malaria risk

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>The majority of the mosquito and parasite life-history traits that combine to determine malaria transmission intensity are temperature sensitive. In most cases, the process-based models used to estimate malaria risk and inform control and prevention strategies utilize measures of mean outdoor temperature. Evidence suggests, however, that certain malaria vectors can spend large parts of their adult life resting indoors.</p> <p>Presentation of hypothesis</p> <p>If significant proportions of mosquitoes are resting indoors and indoor conditions differ markedly from ambient conditions, simple use of outdoor temperatures will not provide reliable estimates of malaria transmission intensity. To date, few studies have quantified the differential effects of indoor <it>vs </it>outdoor temperatures explicitly, reflecting a lack of proper understanding of mosquito resting behaviour and associated microclimate.</p> <p>Testing the hypothesis</p> <p>Published records from 8 village sites in East Africa revealed temperatures to be warmer indoors than outdoors and to generally show less daily variation. Exploring the effects of these temperatures on malaria parasite development rate suggested indoor-resting mosquitoes could transmit malaria between 0.3 and 22.5 days earlier than outdoor-resting mosquitoes. These differences translate to increases in transmission risk ranging from 5 to approaching 3,000%, relative to predictions based on outdoor temperatures. The pattern appears robust for low- and highland areas, with differences increasing with altitude.</p> <p>Implications of the hypothesis</p> <p>Differences in indoor <it>vs </it>outdoor environments lead to large differences in the limits and the intensity of malaria transmission. This finding highlights a need to better understand mosquito resting behaviour and the associated microclimate, and to broaden assessments of transmission ecology and risk to consider the potentially important role of endophily.</p

    Antibody isotype analysis of malaria-nematode co-infection: problems and solutions associated with cross-reactivity

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Antibody isotype responses can be useful as indicators of immune bias during infection. In studies of parasite co-infection however, interpretation of immune bias is complicated by the occurrence of cross-reactive antibodies. To confidently attribute shifts in immune bias to the presence of a co-infecting parasite, we suggest practical approaches to account for antibody cross-reactivity. The potential for cross-reactive antibodies to influence disease outcome is also discussed.</p> <p>Results</p> <p>Utilising two murine models of malaria-helminth co-infection we analysed antibody responses of mice singly- or co-infected with <it>Plasmodium chabaudi chabaudi </it>and <it>Nippostrongylus brasiliensis </it>or <it>Litomosoides sigmodontis</it>. We observed cross-reactive antibody responses that recognised antigens from both pathogens irrespective of whether crude parasite antigen preparations or purified recombinant proteins were used in ELISA. These responses were not apparent in control mice. The relative strength of cross-reactive versus antigen-specific responses was determined by calculating antibody titre. In addition, we analysed antibody binding to periodate-treated antigens, to distinguish responses targeted to protein versus carbohydrate moieties. Periodate treatment affected both antigen-specific and cross-reactive responses. For example, malaria-induced cross-reactive IgG1 responses were found to target the carbohydrate component of the helminth antigen, as they were not detected following periodate treatment. Interestingly, periodate treatment of recombinant malaria antigen Merozoite Surface Protein-1<sub>19 </sub>(MSP-1<sub>19</sub>) resulted in increased detection of antigen-specific IgG2a responses in malaria-infected mice. This suggests that glycosylation may have been masking protein epitopes and that periodate-treated MSP-1<sub>19 </sub>may more closely reflect the natural non-glycosylated antigen seen during infection.</p> <p>Conclusions</p> <p>In order to utilize antibody isotypes as a measure of immune bias during co-infection studies, it is important to dissect antigen-specific from cross-reactive antibody responses. Calculating antibody titre, rather than using a single dilution of serum, as a measure of the relative strength of the response, largely accomplished this. Elimination of the carbohydrate moiety of an antigen that can often be the target of cross-reactive antibodies also proved useful.</p
    • 

    corecore