Publications
352 results found
Verra F, Simpore J, Warimwe GM, et al., 2007, Haemoglobin C and S role in acquired immunity against Plasmodium falciparum malaria, PLOS One, Vol: 2, ISSN: 1932-6203
Ajala-Agbo T, Komba A, Makani J, et al., 2007, Transcranial doppler in sickle cell disease in Africa, Pages: 74-74, ISSN: 0007-1048
Beeson JG, Ndungu F, Persson KEM, et al., 2007, Antibodies among men and children to placental-binding Plasmodium falciparum-infected erythrocytes that express var2csa, American Journal of Tropical Medicine and Hygiene, Vol: 77, Pages: 22-28
Khor AVS, 2007, A Mal functional variant is associated with protection against invasive pneumococcal disease, bacteremia, malaria and tuberculosis, Nature Genetics, Vol: 39, Pages: 523-528
Khor AVS, 2007, Positive replication and linkage disequilibrium mapping of the chromosome 21q22.1 malaria susceptibility locus, Genes and Immunity, Vol: 8, Pages: 570-576
Ngugi KA, Scott A, Edwards T, et al., 2007, Comparative mortality in people with epilepsy in a rural Kenyan district, Pages: 59-60, ISSN: 0013-9580
Clatworthy MR, Willcocks L, Urban B, et al., 2007, Systemic lupus erythematosus-associated defects in the inhibitory receptor FcγRIIb reduce susceptibility to malaria, Proceedings of the National Academy of Sciences of the United States of America, Vol: 104, Pages: 7169-7174
Atkinson SH, Mwangi TW, Uyoga SM, et al., 2007, The haptoglobin 2-2 genotype is associated with a reduced incidence of Plasmodium falciparum malaria in children on the Coast of Kenya, Clinical Infectious Diseases, Vol: 44, Pages: 802-809
Cordery DV, Kishore U, Kyes S, et al., 2007, Characterization of a Plasmodium falciparum macrophage-migration inhibitory factor homologue, Journal of Infectious Diseases, Vol: 195, Pages: 905-912
Makani J, Williams TN, Marsh K, 2007, Sickle cell disease in Africa: Burden and research priorities, Annals of Tropical Medicine and Parasitology, Vol: 101, Pages: 3-14
Bejon K, 2007, Defining Childhood severe falciparum malaria for intervention studies, PLoS Medicine, Vol: 4, Pages: 1333-1340
Makani J, Meda E, Rwezaula S, et al., 2006, Sickle cell anaemia in East Africa: Preliminary results from a cohort study., Pages: 26B-26B, ISSN: 0006-4971
Golding M, Williams T, Marsh K, et al., 2006, Single nucleotide polymorphisms in trap associate with severe malarial disease: A novel parasite virulence gene, AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE, Vol: 75, Pages: 151-151, ISSN: 0002-9637
Persson KE, McCallum FJ, Reiling L, et al., 2006, Phenotypic variation in P-falciparum invasion of erythrocytes is a mechanism of immune evasion, AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE, Vol: 75, Pages: 283-283, ISSN: 0002-9637
Ajala-Agbo T, Komba A, Williams T, et al., 2006, Associations between oxyhaemoglobin desaturation and haematology in African children with sickle cell anaemia, Pages: 15-15, ISSN: 0007-1048
Ajala-Agbo T, Komba A, Makani J, et al., 2006, Spectrum of cerebral blood flow velocities measured by transcranial Doppler ultrasonography in children with sickle cell disease in Africa, DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY, Vol: 48, Pages: 13-14, ISSN: 0012-1622
Williams TN, 2006, Red blood cell defects and malaria, Molecular and Biochemical Parasitology, Vol: 149, Pages: 121-127
Casals-Pascual DJ, 2006, Suppression of erythropoiesis in malarial anemia is associated with hemozoin in vitro and in vivo, Blood, Vol: 108, Pages: 2569-2577
Casals-Pascual DJ, 2006, Lactate levels in severe malarial anaemia are associated with haemozoin-containing neutrophils and low levels of IL-12, Malaria Journal, Vol: 5
Williams TNAB, 2006, Human red blood cell polymorphisms and malaria, Current Opinion in Microbiology, Vol: 9, Pages: 388-394, ISSN: 1369-5274
Genetic factors are a major determinant of child survival in malaria endemic countries. Identifying which genes are involved and how they affect the malaria disease risk potentially offers a powerful mechanism through which to learn more about the host-parasite relationship. The past few years have seen significant progress towards achieving this goal for some of the best-known malaria resistance genes that determine the structure or function of red blood cells: Gerbich blood group antigen negativity; polymorphisms of the complement receptor genes (most notably CR1); Southeast Asian ovalocytosis; pyruvate kinase deficiency; haemoglobin E; the sickle cell trait; and α-thalassaemia are all examples. The challenge for the future must be to translate such advances into fresh approaches to the prevention and treatment of malaria. © 2006 Elsevier Ltd. All rights reserved.
Polley SD, Conway DJ, Cavanagh DR, et al., 2006, High levels of serum antibodies to merozoite surface protein 2 of Plasmodium falciparum are associated with reduced risk of clinical malaria in coastal Kenya, Vaccine, Vol: 24, Pages: 4233-4246
Wambua S, Mwangi TW, Kortok M, et al., 2006, The effect of α+-thalassaemia on the incidence of malaria and other diseases in children living on the coast of Kenya, PLoS Medicine, Vol: 3, Pages: 643-651
Wambua S, Mwacharo J, Uyoga S, et al., 2006, Co-inheritance of α+-thalassaemia and sickle trait results in specific effects on haematological parameters, British Journal of Haematology, Vol: 133, Pages: 206-209
Urban BC, Shafi MJ, Cordery DV, et al., 2006, Frequencies of peripheral blood myeloid cells in healthy Kenyan children with α+ thalassemia and the sickle cell trait, American Journal of Tropical Medicine and Hygiene, Vol: 74, Pages: 578-584
Urban BC, Cordery D, Shafi MJ, et al., 2006, The frequency of BDCA3-positive dendritic cells is increased in the peripheral circulation of Kenyan children with severe malaria, Infection and Immunity, Vol: 74, Pages: 6700-6706
Jenkins NE, Mwangi TW, Kortok M, et al., 2005, A polymorphism of intercellular adhesion molecule-1 is associated with a reduced incidence of nonmalarial febrile illness in Kenyan children., Clin Infect Dis, Vol: 41, Pages: 1817-1819
An intercellular adhesion molecule-1 polymorphism (ICAM-1(Kilifi)) is present at a high frequency across sub-Saharan Africa, and its presence may increase susceptibility to cerebral malaria. Here, we report that, compared with children in whom wild-type intercellular adhesion molecule-1 is present, the incidence of nonmalarial fever is significantly lower among those homozygous for ICAM-1(Kilifi). We propose that ICAM-1(Kilifi) may be associated with reduced rates of tissue damage and of death due to sepsis.
Makani J, Meda E, Rwezaula S, et al., 2005, Clinical and laboratory features of homozygous sickle cell patients in Tanzania; Malaria, infections and cerebral blood flow velocity., Pages: 23B-23B, ISSN: 0006-4971
Makani J, Ajala-Agbo T, Otieno G, et al., 2005, Cerebral blood flow velocities measured by transcranial Doppler ultrasonography in children with sickle cell disease in Africa., Pages: 23B-23B, ISSN: 0006-4971
Mackinnon MJ, Mwangi TW, Snow RW, et al., 2005, Heritability of malaria in Africa, PLoS Medicine, Vol: 2, Pages: 1253-1259, ISSN: 1549-1277
BackgroundWhile many individual genes have been identified that confer protection against malaria, the overall impact of host genetics on malarial risk remains unknown.Methods and FindingsWe have used pedigree-based genetic variance component analysis to determine the relative contributions of genetic and other factors to the variability in incidence of malaria and other infectious diseases in two cohorts of children living on the coast of Kenya. In the first, we monitored the incidence of mild clinical malaria and other febrile diseases through active surveillance of 640 children 10 y old or younger, living in 77 different households for an average of 2.7 y. In the second, we recorded hospital admissions with malaria and other infectious diseases in a birth cohort of 2,914 children for an average of 4.1 y. Mean annual incidence rates for mild and hospital-admitted malaria were 1.6 and 0.054 episodes per person per year, respectively. Twenty-four percent and 25% of the total variation in these outcomes was explained by additively acting host genes, and household explained a further 29% and 14%, respectively. The haemoglobin S gene explained only 2% of the total variation. For nonmalarial infections, additive genetics explained 39% and 13% of the variability in fevers and hospital-admitted infections, while household explained a further 9% and 30%, respectively.ConclusionGenetic and unidentified household factors each accounted for around one quarter of the total variability in malaria incidence in our study population. The genetic effect was well beyond that explained by the anticipated effects of the haemoglobinopathies alone, suggesting the existence of many protective genes, each individually resulting in small population effects. While studying these genes may well provide insights into pathogenesis and resistance in human malaria, identifying and tackling the household effects must be the more efficient route to reducing the burden of disease in malaria-endemic
Maitland K, Nadel S, Pollard AJ, et al., 2005, Management of severe malaria in children: proposed guidelines for the United Kingdom, British Medical Journal, Vol: 331, Pages: 337-343, ISSN: 0959-8146
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