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    <title>Nature Precedings - Tag feed for malaria</title>
    <link>http://precedings.nature.com/tags/malaria</link>
    <description>Recently posted documents tagged with 'malaria'</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
    <dc:language>en</dc:language>
    <prism:publicationName>Nature Precedings</prism:publicationName>
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      <title>Evaluation of CD4+ T Cells in HIV Patients Presenting with Malaria at the University of Ilorin Teaching Hospital Nigeria</title>
      <link>http://precedings.nature.com/documents/3974/version/1</link>
      <description>CD4 count is an important immunological marker of disease progression in HIV seropositive patients. This study was carried out to determine the effect of malaria or fever of unknown origin on the population of CD4+ T lymphocytes of HIV seropositive patients attending the highly active antiretroviral therapy (HAART) clinic of the University of Ilorin Teaching Hospital, Ilorin, Nigeria. 36 subjects were selected for this study. Ongoing history of fever was used as a case definition for malaria and malaria was confirmed from microscopic examination of thick and thin film of blood sample obtained from the patients during presentation with fever. The CD4 count was evaluated during presentation of fever and post-fever using flow cytometry. There was significant decrease in CD4 count of the patients. However, upon classifying the patients into 2 groups &amp;#8211; those that returned to the clinic after a week and those that returned after a month &amp;#8211; a significant increase in CD4 count was noticed in the group that returned after a week, while a significant decrease was noticed in the group that returned after a month (at p value of 95%). Further classification of the patients based on presence of malaria parasite, and body temperature resulted in varying effects on CD4 count post-fever (in the general group, 27 were positive for malaria parasites. Of these 27, there was an increase in CD4 count in 9 (33.3%).  However in the group that returned after a week, all 6 (100%) that were positive for malaria parasites showed increase in CD4 count. Five (26.3%) of the 19 patients that had body temperature within the range of 35.5-37.4oC showed an increase in CD4 count, while 7 (41.2%) the 17 patients that had body temperature of 37.5oC and above showed an increase in CD4 count. The results led to the conclusion that while some components of the immune response to malaria could strengthen the immune system of HIV seropositive patients by increasing their CD4 count, other components will suppress their immunity by decreasing their CD4 count, accelerating the progression to AIDS.    </description>
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      <pubDate>Fri, 13 Nov 2009 13:52:13 UTC</pubDate>
      <dc:title>Evaluation of CD4+ T Cells in HIV Patients Presenting with Malaria at the University of Ilorin Teaching Hospital Nigeria</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3974.1</dc:identifier>
      <dc:date>2009-11-13</dc:date>
      <dc:creator>Olatunji M. Kolawole</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-13T13:52:13Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Microbiology</prism:section>
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      <title>Malaria Diagnosis and the Plasmodium Life Cycle: the BFO Perspective</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3960.1</link>
      <description>Definitive diagnosis of malaria requires the demonstration through laboratory tests of the presence within the patient of malaria parasites or their components. Since malaria parasites can be present even in the absence of malaria, and since symptoms of malaria can be manifested even in the absence of malaria parasites, malaria diagnosis raises important issues for the adequate understanding of disease, etiology and diagnosis. One approach to the resolution of these issues adopts a realist view, according to which the needed clarifications will be derived from a careful representation of the entities on the side of the patient which form the ultimate truthmakers for clinical statements. We address a challenge to this realist approach relating to the diagnosis of malaria, and show how this challenge can be resolved by appeal to Basic Formal Ontology (BFO) and to the Ontology for General Medical Science (OGMS) constructed in its terms.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3960.1</guid>
      <pubDate>Mon, 09 Nov 2009 10:30:10 UTC</pubDate>
      <dc:title>Malaria Diagnosis and the Plasmodium Life Cycle: the BFO Perspective</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3960.1</dc:identifier>
      <dc:date>2009-11-09</dc:date>
      <dc:creator>Werner Ceusters</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-09T10:30:10Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Bioinformatics</prism:section>
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      <title>A set of ontologies to drive tools for the control of vector-borne diseases</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3464.1</link>
      <description>We are developing a set of ontologies that deal with vector-borne diseases and the arthropod vectors that transmit them. For practical reasons (application priorities), we initiated this project with an ontology of insecticide resistance followed by a series of ontologies that describe malaria as well as physiological processes of mosquitoes that are relevant to, and involved in, disease transmission. These will be expanded to encompass other vector-borne diseases as well as non-mosquito vectors. The aim of the whole undertaking, which is worked out in the frame of the international IDO (Infectious Disease Ontology) project, is to provide the community with a set of ontological tools that can be used both in the development of specific databases and, most importantly, in the construction of decision support systems to control these diseases.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3464.1</guid>
      <pubDate>Mon, 27 Jul 2009 20:21:49 UTC</pubDate>
      <dc:title>A set of ontologies to drive tools for the control of vector-borne diseases</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3464.1</dc:identifier>
      <dc:date>2009-07-27</dc:date>
      <dc:creator>Pantelis Topalis</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-27T20:21:49Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Bioinformatics</prism:section>
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      <title>Open Notebook Science &amp;#8211; Falcipain-2 Preliminary Results</title>
      <link>http://dx.doi.org/10.1038/npre.2008.2216.1</link>
      <description>This talk was presented by Jean-Claude Bradley at the American Chemical Society meeting in Philadelphia on August 20, 2008. An introduction to Open Notebook Science is presented followed by an illustration of how ONS can be used in drug discovery. New data relating to the anti-malarial activity of Ugi products on 2 falcipain-2 docking sites is detailed. The docking calculations were provided by Rajarshi Guha and the enzyme and in vitro assays on Plasmodium falciparum were provided by Phil Rosenthal and Jiri Gut. Most of the syntheses were carried out by Khalid Mirza in the Bradley group.Screencast available at: http://video.google.com/videoplay?docid=3251406956070376532&amp;#38;hl=en</description>
      <guid>http://dx.doi.org/10.1038/npre.2008.2216.1</guid>
      <pubDate>Tue, 26 Aug 2008 17:09:10 UTC</pubDate>
      <dc:title>Open Notebook Science &amp;#8211; Falcipain-2 Preliminary Results</dc:title>
      <dc:identifier>doi:10.1038/npre.2008.2216.1</dc:identifier>
      <dc:date>2008-08-26</dc:date>
      <dc:creator>Jean-Claude Bradley</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-08-26T17:09:10Z</prism:publicationDate>
      <prism:category>Presentation</prism:category>
      <prism:section>Chemistry</prism:section>
      <prism:section>Bioinformatics</prism:section>
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      <title>Cerebral malaria admissions in Papua New Guinea may show inter-annual cyclicity: An example of about a 1.5-year cycle for malaria incidence in Burundi</title>
      <link>http://precedings.nature.com/documents/1769/version/1</link>
      <description>Best available descriptions of malaria incidence and mortality dynamics are important to better plan and evaluate the implementation of programs to monitor (e.g., remote sensing) and control the disease, especially in endemic zones. This was stressed recently by Cibulskis et al (2007) in the view of completeness of monthly reporting for cerebral malaria admissions in Papua New Guinea (latitude 6 degree S, 1987-1996). Notably, regardless of the rate of its completeness, the temporal dynamics of admissions was preserved over the years, however, neither raw data nor results on further analyses about eventual inter-annual cyclic components (periods T&gt;1 year) were provided despite obvious graphical patterns for such a specific time structure (chronome). Interestingly, in a recent analysis by Gomez-Elipe et al (2007) on monthly malaria notifications in Burundi, at almost the same latitude (province of Karuzi, &gt;3 degree S, 1997-2001), the data have shown neither trend not periodic oscillations beyond a 6-month (0.5-year) period. Since the graphical representation of both data sets have indicated an eventual existence of inter-annual variations, and because both are located at the same latitude zone, we have further analyzed the data from Burundi for such periodic oscillations. By using a periodogram regression analysis, we discovered a multicomponent cyclic chronome with periods above 12 months (T=17.5-18.0, 27.5 and 65.0-65.5 months, all at p</description>
      <guid>http://precedings.nature.com/documents/1769/version/1</guid>
      <pubDate>Wed, 09 Apr 2008 16:57:13 UTC</pubDate>
      <dc:title>Cerebral malaria admissions in Papua New Guinea may show inter-annual cyclicity: An example of about a 1.5-year cycle for malaria incidence in Burundi</dc:title>
      <dc:identifier>hdl:10101/npre.2008.1769.1</dc:identifier>
      <dc:date>2008-04-09</dc:date>
      <dc:creator>Penka A. Atanassova</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-04-09T16:57:13Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Ecology</prism:section>
      <prism:section>Microbiology</prism:section>
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      <title>The spread of antimalarial drug resistance: A mathematical model with practical implications for ACT drug policies</title>
      <link>http://precedings.nature.com/documents/1539/version/1</link>
      <description>Most malaria-endemic countries are implementing a change in antimalarial drug policy to artemisinin combination therapy (ACT). The impact of different drug choices and implementation strategies is uncertain. A comprehensive model was constructed incorporating important epidemiological and biological factors and used to illustrate the spread of resistance in low and high transmission settings. The model predicts robustly that in low transmission settings drug resistance spreads faster than in high transmission settings, and that in low transmission areas ACTs slows the spread of drug resistance to a partner drug, especially at high coverage rates. This effect decreases exponentially with increasing delay in deploying the ACT and decreasing rates of coverage. A major obstacle to achieving the benefits of high coverage is the current cost of the drugs. This argues strongly for a global subsidy to make ACTs generally available and affordable in endemic areas.</description>
      <guid>http://precedings.nature.com/documents/1539/version/1</guid>
      <pubDate>Thu, 24 Jan 2008 14:53:00 UTC</pubDate>
      <dc:title>The spread of antimalarial drug resistance: A mathematical model with practical implications for ACT drug policies</dc:title>
      <dc:identifier>hdl:10101/npre.2008.1539.1</dc:identifier>
      <dc:date>2008-08-18</dc:date>
      <dc:creator>Wirichada Pongtavornpinyo</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-01-24T14:53:00Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Microbiology</prism:section>
      <prism:section>Pharmacology</prism:section>
      <prism:section>Bioinformatics</prism:section>
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    <item>
      <title>Evolution of malaria virulence in cross-generation transmission through selective immune pressure</title>
      <link>http://precedings.nature.com/documents/203/version/1</link>
      <description>Theoretical arguments and some mathematical models of host-parasite coevolution (e.g. [1- 6]) suggest host immunity as the driving source for the evolution of parasite virulence. Imperfect vaccines in particular, can play the role and recent work [7] sets to test these ideas experimentally, using the mouse malaria model, Plasmodium chabaudi. To this end the authors evolve parasite lines in immunized and nonimmunized (&#8220;na&#239;ve&#8221;) mice using serial passage of infected blood samples. They find parasite lines evolved in immunized mice become more virulent than those evolved in naive mice. Furthermore, this feature persisted even when the evolved strains were transmitted through mosquitoes. Here we develop a mathematical model of parasite dynamics that qualitatively reproduces the experimental results of [7]. Our model accounts for the basic in-host processes: (i) production and depletion of red blood cells (RBC); (ii) immune-modulated parasite growth/ replication, (iii) immune stimulation and clearing of parasite. Besides we introduce multiple parasite strains with variable levels of virulence, and allow random mutations during replication process. The virulence is represented by a single parameter &#8211; immune stimulation threshold. So more virulent strains have higher &#8220;tolerance levels&#8221;, hence increased RBC depletion (anemia). Numeric simulations with our model exhibit, as in [7] the overall evolution of virulence in serial passage of parasite strains, and its enhancement through partial (imperfect) immunization.</description>
      <guid>http://precedings.nature.com/documents/203/version/1</guid>
      <pubDate>Mon, 25 Jun 2007 05:21:52 UTC</pubDate>
      <dc:title>Evolution of malaria virulence in cross-generation transmission through selective immune pressure</dc:title>
      <dc:identifier>hdl:10101/npre.2007.203.1</dc:identifier>
      <dc:date>2009-03-04</dc:date>
      <dc:creator>David E. Gurarie</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2007-06-25T05:21:52Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Immunology</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/203/version/1/files/npre2007203-1.pdf.thumb.png"/>
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    <item>
      <title>Open Notebook Science Using Blogs and Wikis</title>
      <link>http://dx.doi.org/10.1038/npre.2007.39.1</link>
      <description>The first half is a summary of how the Bradley group at Drexel University is doing Open Notebook Science with the UsefulChem project to synthesize and test novel anti-malarial compounds.  Graduate student Dave Strumfels&amp;#8217; code to compute kinetics from JCAMP NMR reaction profiles is then highlighted.  Finally screenshots are shown of a building on Nature Island in Second Life where Beth Ritter-Guth and Eloise Pasteur have helped to set up a poster room with NMR spectra, molecules and an organic chemistry quiz that can be activated by clicking on an obelisk. </description>
      <guid>http://dx.doi.org/10.1038/npre.2007.39.1</guid>
      <pubDate>Tue, 12 Jun 2007 09:47:27 UTC</pubDate>
      <dc:title>Open Notebook Science Using Blogs and Wikis</dc:title>
      <dc:identifier>doi:10.1038/npre.2007.39.1</dc:identifier>
      <dc:date>2007-06-12</dc:date>
      <dc:creator>Jean-Claude Bradley</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2007-06-12T09:47:27Z</prism:publicationDate>
      <prism:category>Presentation</prism:category>
      <prism:section>Chemistry</prism:section>
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