S Coulibaly

University of Bamako, Bammaco, Bamako, Mali

Are you S Coulibaly?

Claim your profile

Publications (6)12.24 Total impact

  • Journal of Neurology 11/2012; 260(1). DOI:10.1007/s00415-012-6738-5 · 3.84 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: As genetic advances become incorporated into health care delivery, disparities between developing and developed countries may become greater. By addressing genetic health care needs and specific differences of developing countries, these disparities may be mitigated. We sought to describe the attitudes and knowledge of subjects with hereditary neurological diseases in Mali before and after receiving genetic testing and counseling for the first time. A questionnaire of attitudes and knowledge items was adapted and piloted for use in Mali. We found that the majority of subjects had positive attitudes toward genetic testing and counseling, both before and afterwards. Subjects responded to approximately half of the knowledge questions regarding hereditary transmission correctly before and after genetic testing and counseling. Neither overall attitudes nor knowledge scores changed significantly from baseline. Concerns about confidentiality were expressed by the majority of subjects. These findings indicate that, despite limited knowledge of patterns of inheritance, Malians understood the sensitive nature of this information and were favorable toward receiving genetic testing and counseling for diagnostic and prognostic purposes.
    Journal of community genetics 03/2011; 2(1):33-42. DOI:10.1007/s12687-011-0038-0
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We identified a family in Mali with two sisters affected by spastic paraplegia. In addition to spasticity and weakness of the lower limbs, the patients had marked atrophy of the distal upper extremities. Homozygosity mapping using single nucleotide polymorphism arrays showed that the sisters shared a region of extended homozygosity at chromosome 19p13.11-q12 that was not shared by controls. These findings indicate a clinically and genetically distinct form of hereditary spastic paraplegia with amyotrophy, designated SPG43.
    Neurogenetics 07/2010; 11(3):313-8. DOI:10.1007/s10048-009-0230-0 · 2.66 Impact Factor
  • A. S. Diabate · S. Coulibaly · N. S. Dede · A. C. Aké · M. Kojok · L. N. Gui · P. Yapo
    Journal de Radiologie 10/2009; 90(10):1467-1467. DOI:10.1016/S0221-0363(09)75756-7 · 0.57 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The island of Bioko is part of the Republic of Equatorial Guinea and is the only island in the World to have endemic onchocerciasis. The disease is hyperendemic and shows a forest-type epidemiology with low levels of blindness and high levels of skin disease, and the whole population of 68,000 is estimated to be at risk. Control of onchocerciasis began in 1990 using ivermectin and this yielded significant clinical benefits but transmission was not interrupted. Feasibility and preparatory studies carried out between 1995 and 2002 confirmed the probable isolation of the vector on the island, the high vectorial efficiency of the Bioko form of Simulium yahense, the seasonality of river flow, blackfly breeding and biting densities, and the distribution of the vector breeding sites. It was proposed that larviciding should be carried out from January to April, when most of the island's rivers were dry or too low to support Simulium damnosum s.l., and that most rivers would not need to be treated above 500 m altitude because they were too small to support the breeding of S. damnosum s.l. Larviciding (with temephos) would need to be carried out by helicopter (because of problems of access by land), supplemented by ground-based delivery. Insecticide susceptibility trials showed that the Bioko form was highly susceptible to temephos, and insecticide carry was tested in the rivers by assessing the length of river in which S. damnosum s.l. larvae were killed below a temephos dosing point. Regular fly catching points were established in 1999 to provide pre-control biting densities, and to act as monitoring points for control efforts. An environmental impact assessment concluded that the proposed control programme could be expected to do little damage, and a large-scale larviciding trial using ground-based applications of temephos (Abate 20EC) throughout the northern (accessible) part of the island was carried out for five weeks from 12 February 2001. Following this, a first attempt to eliminate the vectors was conducted using helicopter and ground-based applications of temephos from February to May 2003, but this was not successful because some vector populations persisted and subsequently spread throughout the island. A second attempt from January to May 2005 aimed to treat all flowing watercourses and greatly increased the number of treatment points. This led to the successful elimination of the vector. The last biting S. damnosum s.l. was caught in March 2005 and none have been found since then for more than 3 years.
    Acta tropica 10/2009; 111(3):211-8. DOI:10.1016/j.actatropica.2009.03.007 · 2.52 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We studied a Malian family with parental consanguinity and two of eight siblings affected with late-childhood-onset progressive myoclonus epilepsy and cognitive decline, consistent with the diagnosis of Lafora disease. Genetic analysis showed a novel homozygous single-nucleotide variant in the NHLRC1 gene, c.560A>C, producing the missense change H187P. The changed amino acid is highly conserved, and the mutation impairs malin's ability to degrade laforin in vitro. Pathological evaluation showed manifestations of Lafora disease in the entire brain, with particularly severe involvement of the pallidum, thalamus, and cerebellum. Our findings document Lafora disease with severe manifestations in the West African population. Electronic supplementary material The online version of this article (doi:10.1007/s10048-009-0190-4) contains supplementary material, which is available to authorized users.
    Neurogenetics 04/2009; 10(4):319-23. DOI:10.1007/s10048-009-0190-4 · 2.66 Impact Factor