<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet href="/rss.css" type="text/css"?>
<rdf:RDF xmlns="http://purl.org/rss/1.0/"
    xmlns:cc="http://web.resource.org/cc/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:extra="http://www.w3.org/1999/xhtml"
    xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#">
    <channel rdf:about="http://kinetoplastids.com/feeds/mostaccessed/journal?quantity=&amp;format=rss&amp;version=">
        <title>Kinetoplastid Biology and Disease - Most accessed articles</title>
        <link>http://www.kinetoplastids.com</link>
        <description>The most accessed research articles published by Kinetoplastid Biology and Disease</description>
        <dc:date>2007-06-21T00:00:00Z</dc:date>
        <items>
            <rdf:Seq>
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/2/1/11" />
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/6/1/3" />
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/1/1/3" />
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/2/1/14" />
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/6/1/4" />
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/6/1/5" />
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/1/1/6" />
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/3/1/2" />
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/2/1/9" />
                                <rdf:li rdf:resource="http://www.kinetoplastids.com/content/1/1/2" />
                            </rdf:Seq>
        </items>
        <extra:info rdf:parseType="Literal">
            <html:div style="font:14px Verdana, Geneva, Arial, Helvetica, sans-serif" xmlns:html="http://www.w3.org/1999/xhtml">
                <html:span style="font-weight:bold">
                    This is an RSS newsfeed from BioMed Central
                </html:span>
                <html:br />
                <html:span style="font-size: 12px;">
                    It is intended to be used with an RSS reader. For more information about RSS newsfeeds from BioMed Central, visit
                    <html:br />
                    <html:a href="http://www.biomedcentral.com/info/about/rss/" style="color:#3333CC; font-size:12px;">
                        http://www.biomedcentral.com/info/about/rss/
                    </html:a>
                    <html:br />
                </html:span>
            </html:div>
        </extra:info>
        <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </channel>
        <item rdf:about="http://www.kinetoplastids.com/content/2/1/11">
        <title>Evolution of energy metabolism and its compartmentation in Kinetoplastida</title>
        <description>Kinetoplastida are protozoan organisms that probably diverged early in evolution from other eukaryotes. They are characterized by a number of unique features with respect to their energy and carbohydrate metabolism. These organisms possess peculiar peroxisomes, called glycosomes, which play a central role in this metabolism; the organelles harbour enzymes of several catabolic and anabolic routes, including major parts of the glycolytic and pentosephosphate pathways. The kinetoplastid mitochondrion is also unusual with regard to both its structural and functional properties.In this review, we describe the unique compartmentation of metabolism in Kinetoplastida and the metabolic properties resulting from this compartmentation. We discuss the evidence for our recently proposed hypothesis that a common ancestor of Kinetoplastida and Euglenida acquired a photosynthetic alga as an endosymbiont, contrary to the earlier notion that this event occurred at a later stage of evolution, in the Euglenida lineage alone. The endosymbiont was subsequently lost from the kinetoplastid lineage but, during that process, some of its pathways of energy and carbohydrate metabolism were sequestered in the kinetoplastid peroxisomes, which consequently became glycosomes. The evolution of the kinetoplastid glycosomes and the possible selective advantages of these organelles for Kinetoplastida are discussed. We propose that the possession of glycosomes provided metabolic flexibility that has been important for the organisms to adapt easily to changing environmental conditions. It is likely that metabolic flexibility has been an important selective advantage for many kinetoplastid species during their evolution into the highly successful parasites today found in many divergent taxonomic groups.Also addressed is the evolution of the kinetoplastid mitochondrion, from a supposedly pluripotent organelle, attributed to a single endosymbiotic event that resulted in all mitochondria and hydrogenosomes of extant eukaryotes. Furthermore, indications are presented that Kinetoplastida may have acquired other enzymes of energy and carbohydrate metabolism by various lateral gene transfer events different from those that involved the algal- and &#945;-proteobacterial-like endosymbionts responsible for the respective formation of the glycosomes and mitochondria.</description>
        <link>http://www.kinetoplastids.com/content/2/1/11</link>
                <dc:creator>Veronique Hannaert</dc:creator>
                <dc:creator>Frederic Bringaud</dc:creator>
                <dc:creator>Fred Opperdoes</dc:creator>
                <dc:creator>Paul Michels</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2003, 2:11</dc:source>
        <dc:date>2003-10-28T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-2-11</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>11</prism:startingPage>
        <prism:publicationDate>2003-10-28T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.kinetoplastids.com/content/6/1/3">
        <title>Consultative meeting to develop a strategy 
for treatment of cutaneous leishmaniasis</title>
        <description>Background:
A meeting was organized by Drugs for Neglected Diseases initiative (DNDi) and the Institute Pasteur (IP), Paris, to review the treatment for all forms of cutaneous leishmaniasis (CL) and to propose a strategy for the development of new efficacious and affordable treatments.MethodThe global burden of CL was discussed with respect to financial impact; relation to poverty; the stigma of CL lesions and scars (particularly in young women); lack of effective, affordable, easily implemented tools and political will and resources to implement available control tools; and lack of input from pharmaceutical and biotechnology companies to develop new drugs and vaccines.
Results:
According to the experts from different endemic countries present, the financial and social burdens of CL are high, but we have limited quantitative data. The analysis of published trials indicates that the quality of most trials is poor and requires both improvement and standardization. The available drugs are inadequate. Criteria by which different CL types could be prioritized as target disease were set. These criteria included: severity of the disease; lack of response to available drugs; overall incidence and prevalence of the disease; sequelae of the disease, (including recidivans and mucosal leishmaniasis); the impact of treatment of individuals on control of transmission and lack of other major parties involved in drug development. Based on these, the anthroponotic CL and its sequel &quot;recidivans&quot; caused by L. tropica and CL caused by L. braziliensis and its sequel, mucosal leishmaniasis were considered to be the target diseases.The mechanism for controlling Leishmania infection to reach a stable self healing process is a balanced immune response. Immune stimulation during chemotherapy can enhance cure. There is no adequately effective vaccine, but some encouraging results have been obtained with whole killed Leishmania parasites or imiquimod (an immuno-modulator) plus antimonials. Further studies are needed. One safety/immunogenicity clinical trial is currently ongoing with a Second Generation Vaccine (SGV).Conclusions and recommendationsThere is an urgent need for new treatments for all CL types. CL should be considered as a neglected disease and organizations, such as DNDi, should include it in their list of target diseases. It was agreed that immuno-chemotherapy (with &quot;therapeutic&quot; vaccines or immunomodulators) has a strong potential to make an impact as a new therapy of CL with the view of shortening/reducing duration and dose of drug treatment and preventing resistance. There is also a need for safe, affordable and efficacious new chemotherapeutics. The quality of clinical trials needs to be enhanced and standardized. Short and long-term objectives and activities were defined as a part of meeting recommendations.</description>
        <link>http://www.kinetoplastids.com/content/6/1/3</link>
                <dc:creator>Farrokh Modabber</dc:creator>
                <dc:creator>Pierre Buffet</dc:creator>
                <dc:creator>Els Torreele</dc:creator>
                <dc:creator>Genevieve Milon</dc:creator>
                <dc:creator>Simon Croft</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2007, 6:3</dc:source>
        <dc:date>2007-04-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-6-3</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2007-04-24T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.kinetoplastids.com/content/1/1/3">
        <title>From the cell biology to the development of new chemotherapeutic approaches against trypanosomatids: dreams and reality.</title>
        <description>Members of the Trypanosomatidae family comprise a large number of species that are causative agents of important diseases such as sleeping sickness, Chagas&apos; disease and Leishmaniasis. These organisms are also of biological interest since they are able to change the morphology according to the environment where they live, through a process of reversible cell transformation, and possess structures and organelles that are not found in mammalian cells. This review analyses the process of transformation, which takes place during the life cycle of Trypanosoma cruzi in the vertebrate and invertebrate hosts. Special attention is given to the interaction of the parasite with vertebrate cells. In addition, the present knowledge of structures and organelles such as the nucleus, the plasma membrane, the sub-pellicular microtubules, the flagellum, the kinetoplast-mitochondrion complex, the peroxisome (glycosome), the acidocalcisome and the structures and organelles involved in the endocytic pathway, is reviewed from a cell biology perspective. The possible use of available data for the development of new anti parasite drugs is also discussed.</description>
        <link>http://www.kinetoplastids.com/content/1/1/3</link>
                <dc:creator>Wanderley de Souza</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2002, 1:3</dc:source>
        <dc:date>2002-05-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-1-3</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>1</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2002-05-31T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.kinetoplastids.com/content/2/1/14">
        <title>Physiological consequences of drug resistance in Leishmaniaand their relevance for chemotherapy</title>
        <description>In the early twentieth century, infectious diseases were a leading cause of death worldwide. Through the following years, morbidity and mortality caused by infectious diseases decreased considerably in the developed world, but not in the developing world, where infectious diseases remain an important reason for concern. For example, leishmaniosis has become into a serious Third World problem. This is mainly due to an increasing frequency of drug-resistance in Leishmania and an enhanced risk of co-infection with HIV. Drug-resistance is usually associated with an increased expression of specific P-glycoproteins involved in membrane transport. The present review summarizes information which shows that drug-resistance is also associated with changes in physiological events such as parasite infectivity, incorporation of metabolites, xenobiotics conjugation and traffic, intracellular metabolism, host-parasite interaction, parasite cell shape and promastigote-amastigote differentiation. Furthermore, these events may change in a coordinated manner. An understanding of these physiological events may be helpful for designing chemotherapeutic approaches to multiple cellular targets, identifying strategies to circumvent Leishmania drug-resistance and succesfully treating leishmaniosis.</description>
        <link>http://www.kinetoplastids.com/content/2/1/14</link>
                <dc:creator>Alicia Ponte-Sucre</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2003, 2:14</dc:source>
        <dc:date>2003-10-28T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-2-14</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>14</prism:startingPage>
        <prism:publicationDate>2003-10-28T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.kinetoplastids.com/content/6/1/4">
        <title>Dynamics of infection and competition between two strains of Trypanosoma brucei brucei in the tsetse fly observed using fluorescent markers</title>
        <description>Background:
Genetic exchange occurs between Trypanosoma brucei strains during the complex developmental cycle in the tsetse vector, probably within the salivary glands. Successful mating will depend on the dynamics of co-infection with multiple strains, particularly if intraspecific competition occurs. We have previously used T. brucei expressing green fluorescent protein to study parasite development in the vector, enabling even one trypanosome to be visualized. Here we have used two different trypanosome strains transfected with either green or red fluorescent proteins to study the dynamics of co-infection directly in the tsetse fly.
Results:
The majority of infected flies had both trypanosome strains present in the midgut, but the relative proportion of red and green trypanosome strains varied considerably between flies and between different sections of the midgut in individual flies. Colonization of the paired salivary glands revealed greater variability than for midguts, as each gland could be infected with red and/or green trypanosome strains in variable proportions. Salivary glands with a mixed infection appeared to have a higher density of trypanosomes than glands containing a single strain. Comparison of the numbers of red and green trypanosomes in the proventriculus, salivary exudate and glands from individual flies showed no correlation between the composition of the trypanosome population of the proventriculus and foregut and that of the salivary glands. For each compartment examined (midgut, foregut, salivary glands), there was a significantly higher proportion of mixed infections than expected, assuming the null hypothesis that the development of each trypanosome strain is independent.
Conclusion:
Both the trypanosome strains used were fully capable of infecting tsetse, but the probabilities of infection with each strain were not independent, there being a significantly higher proportion of mixed infections than expected in each of three compartments examined: midgut, proventriculus and salivary glands. Hence there was no evidence of competition between trypanosome strains, but instead co-infection was frequent. Infection rates in co-infected flies were no different to those found routinely in flies infected with a single strain, ruling out the possibility that one strain enhanced infection with the other. We infer that each fly is either permissive or non-permissive of trypanosome infection with at least 3 sequential checkpoints imposed by the midgut, proventriculus and salivary glands. Salivary glands containing both trypanosome strains appeared to contain more trypanosomes than singly-infected glands, suggesting that lack of competition enhances the likelihood of genetic exchange.</description>
        <link>http://www.kinetoplastids.com/content/6/1/4</link>
                <dc:creator>Lori Peacock</dc:creator>
                <dc:creator>Vanessa Ferris</dc:creator>
                <dc:creator>Mick Bailey</dc:creator>
                <dc:creator>Wendy Gibson</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2007, 6:4</dc:source>
        <dc:date>2007-06-06T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-6-4</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>4</prism:startingPage>
        <prism:publicationDate>2007-06-06T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.kinetoplastids.com/content/6/1/5">
        <title>Genetic diversity of Leishmania amazonensis strains isolated in northeastern Brazil as revealed by DNA sequencing, PCR-based analyses and molecular karyotyping</title>
        <description>Background:
Leishmania (Leishmania) amazonensis infection in man results in a clinical spectrum of disease manifestations ranging from cutaneous to mucosal or visceral involvement. In the present study, we have investigated the genetic variability of 18 L. amazonensis strains isolated in northeastern Brazil from patients with different clinical manifestations of leishmaniasis. Parasite DNA was analyzed by sequencing of the ITS flanking the 5.8 S subunit of the ribosomal RNA genes, by RAPD and SSR-PCR and by PFGE followed by hybridization with gene-specific probes.
Results:
ITS sequencing and PCR-based methods revealed genetic heterogeneity among the L. amazonensis isolates examined and molecular karyotyping also showed variation in the chromosome size of different isolates. Unrooted genetic trees separated strains into different groups.
Conclusion:
These results indicate that L. amazonensis strains isolated from leishmaniasis patients from northeastern Brazil are genetically diverse, however, no correlation between genetic polymorphism and phenotype were found.</description>
        <link>http://www.kinetoplastids.com/content/6/1/5</link>
                <dc:creator>Joao Paulo de Oliveira</dc:creator>
                <dc:creator>Flora Fernandes</dc:creator>
                <dc:creator>Angela Cruz</dc:creator>
                <dc:creator>Viviane Trombela</dc:creator>
                <dc:creator>Elisangela Monteiro</dc:creator>
                <dc:creator>Anamaria Camargo</dc:creator>
                <dc:creator>Aldina Barral</dc:creator>
                <dc:creator>Camila de Oliveira</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2007, 6:5</dc:source>
        <dc:date>2007-06-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-6-5</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2007-06-21T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.kinetoplastids.com/content/1/1/6">
        <title>Combating Kinetoplastid diseases</title>
        <description>No description available</description>
        <link>http://www.kinetoplastids.com/content/1/1/6</link>
                <dc:creator>Alberto Davila</dc:creator>
                <dc:creator>Kevin Tyler</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2002, 1:6</dc:source>
        <dc:date>2002-07-05T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-1-6</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>1</prism:volume>
        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2002-07-05T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.kinetoplastids.com/content/3/1/2">
        <title>Chagas&apos; disease and AIDS</title>
        <description>Chagas&apos; disease caused by Trypanosoma cruzi is an opportunistic infection in the setting of HIV/AIDS. Some individuals with HIV and chronic T. cruzi infection may experience a reactivation, which is most commonly manifested by meningoencephalitis. A reactivation myocarditis is the second most common manifestation. These presentations may be difficult to distinguish from toxoplasmosis in individuals with HIV/AIDS. The overlap of HIV and Trypanosoma cruzi infection occurs not only in endemic areas but also in non-endemic areas of North America and Europe where the diagnosis may be even more difficult. The pathological features, diagnosis and the role of cytokines in the pathogenesis of the disease are discussed.</description>
        <link>http://www.kinetoplastids.com/content/3/1/2</link>
                <dc:creator>Anil Vaidian</dc:creator>
                <dc:creator>Louis Weiss</dc:creator>
                <dc:creator>Herbert Tanowitz</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2004, 3:2</dc:source>
        <dc:date>2004-05-13T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-3-2</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>3</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2004-05-13T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.kinetoplastids.com/content/2/1/9">
        <title>Review of the World Class Parasites Book Series</title>
        <description>According to the Series Editors, &quot;The World Class Parasites book series are written for researchers, students and scholars who enjoy reading about excellent research on problems of global significance. Each volume focuses on a parasite, or group of parasites, that has a major impact on human health, or agricultural productivity, and against which we have no satisfactory defense. The volumes are intended to supplement more formal texts that cover taxonomy, life cycles, morphology, vector distribution, symptoms and treatment. They integrate vector, pathogen and host biology and celebrate the diversity of approach that comprises modern parasitological research.&quot;Three volumes deal with kinetoplastid disease: Volume 1 - the African Trypanosomes, Volume 4 - Leishmaniasis, Volume 7 - American Trypanosomiasis. We asked 5 independent experts to assess the quality of these volumes and the extent to which they had met their stated aims.</description>
        <link>http://www.kinetoplastids.com/content/2/1/9</link>
                <dc:creator>Frank Cox</dc:creator>
                <dc:creator>Diane McMahon-Pratt</dc:creator>
                <dc:creator>Kwang-Poo Chang</dc:creator>
                <dc:creator>Samuel Goldenberg</dc:creator>
                <dc:creator>Julio Scharfstein</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2003, 2:9</dc:source>
        <dc:date>2003-10-28T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-2-9</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>9</prism:startingPage>
        <prism:publicationDate>2003-10-28T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.kinetoplastids.com/content/1/1/2">
        <title>PCR identification of Trypanosoma lewisi, a common parasite of laboratory rats</title>
        <description>Trypanosoma (Herpetosoma) lewisi is a trypanosome of the sub-genus Herpetosoma (Stercoraria section), parasite of rats (Rattus rattus and Rattus norvegicus) transmitted by fleas. T. lewisi has a stringent species specificity and cannot grow in other rodents such as mice. Rats are infected principally by oral route, through contamination by flea faeces or ingestion of fleas. Trypanosoma lewisi infections in rat colonies can interfere with research protocols and fleas of wild rats are often the source of such infections. Currently, diagnosis of T. lewisi in rats is performed by microscopic observation of stained blood smears. In the course of a research project at CIRDES, a T. lewisi infection was detected in the rat colony. In this study we evaluated PCR primer sets for their ability to diagnose multiple species of trypanosomes with a single amplification. We show that the use of ITS1 sequence of ribosomal DNA provides an efficient and sensitive assay for detection and identification of T. lewisi infection in rats and recommend the use of this assay for monitoring of T. lewisi infections in rat colonies.</description>
        <link>http://www.kinetoplastids.com/content/1/1/2</link>
                <dc:creator>Marc Desquesnes</dc:creator>
                <dc:creator>Sophie Ravel</dc:creator>
                <dc:creator>Gerard Cuny</dc:creator>
                <dc:source>Kinetoplastid Biology and Disease 2002, 1:2</dc:source>
        <dc:date>2002-05-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-9292-1-2</dc:identifier>
        <prism:publicationName>Kinetoplastid Biology and Disease</prism:publicationName>
        <prism:issn>1475-9292</prism:issn>
        <prism:volume>1</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2002-05-29T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
        <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks" />
    </cc:License>
</rdf:RDF>
