Publications by authors named "Sara Melville"

Central line associated bloodstream infection (CLABSI) reduction programmes in hospitalised children have been focused in the intensive care setting and little data is available on the efficacy and cost effectiveness of such programmes in other clinical areas. Prospective monitoring of hospital acquired CLABSI rates in all clinical areas was performed at Alder Hey Children's Hospital for a period of three years following the implementation of a central venous line (CVL) care bundle. We observed a decrease in CLABSI rates from 220 in the first year following intervention to 108 per 100,000 patient days (=0.

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The prevalence and pathogenic effects of trypanosomosis were determined in cattle, goats and pigs reared in Kasese, Jinja and Rakai districts, Uganda; presence of trypanosomes was detected by buffy coat technique (BCT). The overall prevalence of trypanosomosis in cattle was 7.6% (144/1,891), 0.

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Background: Soil-transmitted helminth (STH) infections (i.e., Ascaris lumbricoides, hookworm, and Trichuris trichiura) affect more than a billion people.

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Background: Trypanosoma brucei gambiense is the causative agent of chronic Human African Trypanosomiasis or sleeping sickness, a disease endemic across often poor and rural areas of Western and Central Africa. We have previously published the genome sequence of a T. b.

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The gene BRCA2, first identified as a breast cancer susceptibility locus in humans, encodes a protein involved in DNA repair in mammalian cells and mutations in this gene confer increased risk of breast cancer. Here we report a functional characterisation of a Trypanosoma brucei BRCA2 (TbBRCA2) orthologue and show that the protein interacts directly with TbRAD51. A further protein-protein interaction screen using TbBRCA2 identified other interacting proteins, including a trypanosome orthologue of CDC45 which is involved in initiation and progression of the replication fork complex during DNA synthesis.

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African trypanosomes are parasitic protozoa that infect a wide range of mammals, including humans. These parasites remain extracellular in the mammalian bloodstream, where antigenic variation allows them to survive the immune response. The Trypanosoma brucei nuclear genome sequence has been published recently.

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African trypanosomes cause human sleeping sickness and livestock trypanosomiasis in sub-Saharan Africa. We present the sequence and analysis of the 11 megabase-sized chromosomes of Trypanosoma brucei. The 26-megabase genome contains 9068 predicted genes, including approximately 900 pseudogenes and approximately 1700 T.

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A comparison of gene content and genome architecture of Trypanosoma brucei, Trypanosoma cruzi, and Leishmania major, three related pathogens with different life cycles and disease pathology, revealed a conserved core proteome of about 6200 genes in large syntenic polycistronic gene clusters. Many species-specific genes, especially large surface antigen families, occur at nonsyntenic chromosome-internal and subtelomeric regions. Retroelements, structural RNAs, and gene family expansion are often associated with syntenic discontinuities that-along with gene divergence, acquisition and loss, and rearrangement within the syntenic regions-have shaped the genomes of each parasite.

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Mucosal leishmaniasis, which is a sporadic disease in the Sudan, was shown by isoenzyme characterization and PCR to be caused by Leishmania donovani. However, it was not clear if the parasite was exactly the same strain as that causing visceral leishmaniasis (VL), or of a different strain. We utilized a new generation of molecular DNA markers, minisatellites and kinetoplast DNA, for rapid characterization of the parasite.

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The chromosomes of most protozoan parasites cannot be visualized using conventional microscopy because they are too small and do not condense sufficiently at metaphase. Therefore, the development of pulsed field gel electrophoresis allowed the resolution of many parasite karyotypes for the first time. The ability to prepare intact chromosomes in agarose plugs and to isolate individual homologs by electrophoresis has led to many new applications in parasite genomic analysis.

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The ingi (long and autonomous) and RIME (short and nonautonomous) non--long-terminal repeat retrotransposons are the most abundant mobile elements characterized to date in the genome of the African trypanosome Trypanosoma brucei. These retrotransposons were thought to be randomly distributed, but a detailed and comprehensive analysis of their genomic distribution had not been performed until now. To address this question, we analyzed the ingi/RIME sequences and flanking sequences from the ongoing T.

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The African trypanosome, Trypanosoma brucei, causes sleeping sickness in humans in sub-Saharan Africa. Here we report the sequence and analysis of the 1.1 Mb chromosome I, which encodes approximately 400 predicted genes organised into directional clusters, of which more than 100 are located in the largest cluster of 250 kb.

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We report here the sequence of chromosome II from Trypanosoma brucei, the causative agent of African sleeping sickness. The 1.2-Mb pairs encode about 470 predicted genes organised in 17 directional clusters on either strand, the largest cluster of which has 92 genes lined up over a 284-kb region.

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We describe a novel gene family that forms clusters in subtelomeric regions of Trypanosoma brucei chromosomes and partially accounts for the observed clustering of retrotransposons. The ingi and ribosomal inserted mobile element (RIME) non-LTR retrotransposons share 250 bp at both extremities and are the most abundant putatively mobile elements, with about 500 copies per haploid genome. From cDNA clones and subsequently in the T.

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Leishmania spp. and the related kinetoplastid Trypanosoma brucei are single-celled parasites. In Leishmania, the nuclear genome comprises 36 diploid chromosomes and occasional amplified minichromosomes, while the T.

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The genome of the African trypanosome, Trypanosoma brucei, is currently being sequenced, raising the question of how the data generated can be used to determine the function of the large number of genes that will be identified. There is a range of possible approaches, and in this paper we discuss the use of a classical genetic approach coupled with positional cloning based on the ability of trypanosomes to undergo genetic exchange. The genetics of these parasites is essentially similar to a conventional diploid Mendelian system with allelic segregation and an independent assortment of markers on different chromosomes.

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