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    <title>Verloo, P.</title>
    <link>http://repub.eur.nl/res/aut/15190/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Electrophysiological studies of malaria parasite-infected erythrocytes: Current status (Article)</title>
      <link>http://repub.eur.nl/res/pub/35480/</link>
      <pubDate>2007-04-01T00:00:00Z</pubDate>
      <description>The altered permeability characteristics of erythrocytes infected with malaria parasites have been a source of interest for over 30 years. Recent electrophysiological studies have provided strong evidence that these changes reflect transmembrane transport through ion channels in the host erythrocyte plasma membrane. However, conflicting results and differing interpretations of the data have led to confusion in this field. In an effort to unravel these issues, the groups involved recently came together for a week of discussion and experimentation. In this article, the various models for altered transport are reviewed, together with the areas of consensus in the field and those that require a better understanding. </description>
    </item> <item>
      <title>Plasmodium falciparum-activated chloride channels are defective in erythrocytes from cystic fibrosis patients. (Article)</title>
      <link>http://repub.eur.nl/res/pub/13275/</link>
      <pubDate>2004-03-12T00:00:00Z</pubDate>
      <description>An inwardly rectifying anion channel in malaria-infected red blood cells
      has been proposed to function as the "new permeation pathway" for parasite
      nutrient acquisition. As the channel shares several properties with the
      cystic fibrosis transmembrane conductance regulator (CFTR), we tested
      their interrelationship by whole-cell current measurements in Plasmodium
      falciparum-infected and uninfected red blood cells from control and cystic
      fibrosis (CF) patients. A CFTR-like linear chloride conductance as well as
      a malaria parasite-induced and a shrinkage-activated endogenous inwardly
      rectifying chloride conductance with properties identical to the
      malaria-induced channel were all found to be defective in CF erythrocytes.
      Surprisingly, the absence of the inwardly rectifying chloride conductance
      in CF erythrocytes had no gross effect on in vitro parasite growth or new
      permeation pathway activity, supporting an argument against a close
      association between the Plasmodium-activated chloride channel and the new
      permeation pathway. The functional expression of CFTR in red blood cells
      opens new perspectives to exploit the erythrocyte as a readily available
      cell type in electrophysiological, diagnostic, and therapeutic studies of
      CF.</description>
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