<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0864-0289</journal-id>
<journal-title><![CDATA[Revista Cubana de Hematología, Inmunología y Hemoterapia]]></journal-title>
<abbrev-journal-title><![CDATA[Rev Cubana Hematol Inmunol Hemoter]]></abbrev-journal-title>
<issn>0864-0289</issn>
<publisher>
<publisher-name><![CDATA[Centro Nacional de Información de Ciencias MédicasEditorial Ciencias Médicas]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0864-02892019000300009</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Introducción del genotipaje molecular de los antigenos plaquetarios]]></article-title>
<article-title xml:lang="en"><![CDATA[Introduction of molecular genotypingof plateles antigens]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Romero Díaz]]></surname>
<given-names><![CDATA[Yisenia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Soler Noda]]></surname>
<given-names><![CDATA[Gilberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Bencomo Hernández]]></surname>
<given-names><![CDATA[Antonio]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto de Hematología e Inmunología  ]]></institution>
<addr-line><![CDATA[La Habana ]]></addr-line>
<country>Cuba</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>09</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>09</month>
<year>2019</year>
</pub-date>
<volume>35</volume>
<numero>3</numero>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_arttext&amp;pid=S0864-02892019000300009&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_abstract&amp;pid=S0864-02892019000300009&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_pdf&amp;pid=S0864-02892019000300009&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN  Introducción: Los antígenos plaquetarios humanos (HPA) se expresan en 6 glucoproteínas plaquetarias diferentes. Se ha descrito que estos antígenos pueden estimular la producción de aloanticuerpos una vez expuestos a plaquetas humanas con diferentes HPA, lo que provoca complicaciones clínicas como la trombocitopenia neonatal aloinmune y la púrpura postransfusional.  Métodos:  Se realizó el estudio a 11 muestras de pacientes en espera de trasplante renal de genotipo de los antígenos HPA-1,2,3 a/b mediante PCR multiplex, mientras que para el estudio de genotipo de los antígenos HPA-5a/b se utilizó la técnica de PCR con secuencia específica de primer. Los productos de ADN amplificados fueron visualizados mediante electroforesis en gel de agarosa y electroforesis capilar.  Resultados: El análisis de los fragmentos de ADN amplificados revelaron resultados similares por ambos métodos. Para los antígenos HPA-1,-2, el 63 % de las muestras fueron homocigóticas para el fenotipo (a) mientras que se observó heterocigocidad en todos los casos para el genotipo HPA-3. En el sistema HPA-5, el 54 % fueron homocigóticas para el fenotipo (a) y el 46 %, heterocigóticas. Para el genotipo del HPA-15, el 4 % fueron homocigóticas para el fenotipo (b) mientras que el 96 % resultaron ser heterocigóticas.  Conclusiones:  Estos resultados muestran similitudes para los genotipos HPA 1, 2,3 a/b, HPA 5a/b y HPA15 a/brespecto a lo planteado en la literatura.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[ABSTRACT  Introduction:  Human platelet antigens (HPA) are expressed in 6 different platelet glycoproteins. It has been described that these antigens can stimulate the production of alloantibodies once exposed to human platelets with different HPA, which causes clinical complications such as neonatal alloimmune thrombocytopenia and postransfusional purpura.  Methods: The study was performed on 11 samples of patients awaiting kidney transplantation of genotype of the HPA-1,2,3 a/b antigens by multiplex PCR, while for the genotype study of the HPA-5a/b antigens was used the PCR technique with primer-specificsequence. The amplified DNA products were visualized by agarose gel electrophoresis and by capillary electrophoresis.  Results: The analysis of DNA fragments amplified by agarose electrophoresis and capillary electrophoresis revealed similar results in both methods. For the HPA-1, -2 antigens, 63% of the samples were homozygous for phenotype (a) while heterozygosity was observed in all cases for the HPA-3 genotype. In the HPA-5 system, 54% were homozygous for the phenotype (a) and 46% were heterozygous. For the genotype of HPA-15, 4% were homozygous for phenotype (b) while 96% proved heterozygous.  Conclusions: These results show similarities for the genotypes HPA 1, 2.3 a/b, HPA 5a/b and HPA15 a/bwith respect to report in literature.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[antígeno]]></kwd>
<kwd lng="es"><![CDATA[genotipo]]></kwd>
<kwd lng="es"><![CDATA[fenotipo]]></kwd>
<kwd lng="es"><![CDATA[HPA 1, 2,3 a/b]]></kwd>
<kwd lng="es"><![CDATA[HPA 5a/b]]></kwd>
<kwd lng="es"><![CDATA[HPA15 a/b]]></kwd>
<kwd lng="en"><![CDATA[antigen]]></kwd>
<kwd lng="en"><![CDATA[genotype]]></kwd>
<kwd lng="en"><![CDATA[fenotype]]></kwd>
<kwd lng="en"><![CDATA[HPA 1, 2,3 a/b]]></kwd>
<kwd lng="en"><![CDATA[HPA 5a/b]]></kwd>
<kwd lng="en"><![CDATA[HPA15 a/b]]></kwd>
</kwd-group>
</article-meta>
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