Publications by authors named "M Cantero"

Background: Telemedicine is a means of providing efficient treatment for children with complex chronic conditions and/or subsidiary palliative paediatric care.

Aim: To evaluate how satisfied families and healthcare professionals are with a telemedicine programme.

Methodology: This is a qualitative study of narrative design.

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Background: The immunomodulatory oligodeoxynucleotide (ODN) IMT504 might harbor antifibrotic properties within the liver.

Methods: Fibrosis models were induced in mice through thioacetamide (TAA) administration and bile-duct ligation. Cre-loxP mice were utilized to identify GLAST + Wnt1 + bone marrow stromal progenitors (BMSPs) and to examine their contribution with cells in the liver.

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Background: Mesenchymal stromal cells (MSCs) tropism for tumours allows their use as carriers of antitumoural factors and in vitro transcribed mRNA (IVT mRNA) is a promising tool for effective transient expression without insertional mutagenesis risk. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine with antitumor properties by stimulating the specific immune response. The aim of this work was to generate modified MSCs by IVT mRNA transfection to overexpress GM-CSF and determine their therapeutic effect alone or in combination with doxorubicin (Dox) in a murine model of hepatocellular carcinoma (HCC).

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The Adult Attachment Questionnaire-Revised and its psychometric properties are presented for dimensional and categorical evaluation of adult attachment style. Eight items were added to the original questionnaire (CAA; Melero and Cantero, 2008) that expanded avoidance dimension assessment and sensitivity evaluation. The exploratory factor analysis EFA led to 35 items grouped in 4 affective dimensions.

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Inherited hearing impairment is a remarkably heterogeneous monogenic condition, involving hundreds of genes, most of them with very small (< 1%) epidemiological contributions. The exception is GJB2, the gene encoding connexin-26 and underlying DFNB1, which is the most frequent type of autosomal recessive non-syndromic hearing impairment (ARNSHI) in most populations (up to 40% of ARNSHI cases). DFNB1 is caused by different types of pathogenic variants in GJB2, but also by large deletions that keep the gene intact but remove an upstream regulatory element that is essential for its expression.

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