Nuestros investigadores

Paula Aranaz Oroz

Departamento

Publicaciones científicas más recientes (desde 2010)

Autores: Lucio Ollauri, David; Martínez Oharriz, María Cristina; Jaras, G., ; et al.
Revista: EUROPEAN JOURNAL OF PHARMACEUTICS AND BIOPHARMACEUTICS
ISSN 0939-6411  Vol. 121  2017  págs. 104 - 112
The aim of this work was to evaluate the capability of zein nanoparticles as oral carriers for glibenclamide (GB). Nanoparticles were prepared by a desolvation procedure in the presence of lysine as stabilizer. A central composite design was used to optimize this preparative process. Under the selected conditions, nanoparticles displayed a size of about 190 nm, a surface charge of ¿37 mV and a payload of 45 ¿g GB/mg. Small-angle neutron scattering and X-ray diffraction techniques suggested an internal fractal-like structure, based on the repetition of spherical blocks of zein units (about 20 nm) grouped to form the nanoparticles. This structure, stabilized by lysine molecules located at the surface, would determine the release of GB (molecularly trapped into the nanoparticles) by a pure diffusion mechanism. Moreover, GB-loaded nanoparticles induced a significant hypolipidemic effect with a reduction of about 15% in the fat content of C. elegans worms. In addition, did not induce any significant modification in the lifespan of worms. In summary, the employment of zein nanoparticles as delivery systems of glibenclamide may be an interesting approach to develop new oral formulations of this antidiabetic drug.
Autores: Aranaz Oroz, Paula; Romo Hualde, Ana; Zabala Navó, María; et al.
Revista: FOOD & FUNCTION
ISSN 2042-6496  2017 
Obesity and type 2-diabetes are becoming a worldwide health problem, remarking the importance of alternative therapies to tackle their progression. Here, we hypothesized that supplementation of diet with 6 % w/w of a freeze-dried strawberry-blueberry (5:1) powder (FDSB) could exert beneficial metabolic effects in Wistar rats. FDSB-supplemented animals experienced significantly reduced body weight gain, food efficiency and visceral adiposity accumulation in two independent experiments. FDSB supplementation also contributed to lower area under the curve after an intraperitoneal GTT and reduced serum insulin levels and insulin resistance index (IR-HOMA) in HFS diet-fed animals, together with reduced plasma MCP-1 inflammation marker concentrations. Gene expression analysis in retroperitoneal adipocytes from experiment 1 and 3T3-L1 cells showed that FDSB inhibited adipogenesis and lipogenesis through down-regulation of Pparg, Cebpa, Lep, Fasn, Scd-1 and Lpl gene expression. Untargeted metabolomics identified the cis isomer ofresveratrol-3-glucoside-sulphate as a metabolite differentially increased in FDSB-treated serum samples, which corresponds to a strawberry metabolite that could be considered a serum biomarker of FDSB-intake. Our results suggest that FDSB powder might be useful for treatment/prevention of obesity-related diseases.
Autores: Eder-Azanza, L., ; Hurtado Rudi, Cristina; Navarro-Herrera, D., ; et al.
Revista: HAEMATOLOGICA
ISSN 0390-6078  Vol. 102  Nº 8  2017  págs. e328 - e331
Autores: Erquiaga Martínez, Ignacio; Hurtado Rudi, Cristina; Aranaz Oroz, Paula; et al.
Revista: BIOTECHNIQUES
ISSN 0736-6205  Vol. 56  Nº 6  2014  págs. 327 - 329
When studying mutations in DNA samples, determining whether novel sequence changes are somatic mutations or germline polymorphisms can be difficult. Here we describe a novel and very simple approach for identification of somatic mutations and loss of heterozygosity (LoH) events in DNA samples where no matched tissue sample is available. Our method makes use of heterozygous polymorphisms that are located near the putative mutation to trace both germinal alleles.
Autores: Eder Azanza, L., ; Navarro Herrera, D., ; Aranaz Oroz, Paula; et al.
Revista: LEUKEMIA
ISSN 0887-6924  Vol. 28  Nº 10  2014  págs. 2106 - 2109
Autores: Fernández Mercado, Marta; Pellagatti, A., ; Di Genua, C., ; et al.
Revista: BRITISH JOURNAL OF HAEMATOLOGY
ISSN 0007-1048  Vol. 163  Nº 2  2013  págs. 235 - 239
Whole exome sequencing was performed in a patient with myelodysplastic syndrome before and after progression to acute myeloid leukaemia. Mutations in several genes, including SETBP1, were identified following leukaemic transformation. Screening of 328 patients with myeloid disorders revealed SETBP1 mutations in 14 patients (4 center dot 3%), 7 of whom had -7/del(7q) and 3 had i(17)(q10), cytogenetic markers associated with shortened overall survival and increased risk of leukaemic evolution. SETBP1 mutations were frequently acquired at the time of leukaemic evolution, coinciding with increase of leukaemic blasts. These data suggest that SETBP1 mutations may play a role in MDS and chronic myelomonocytic leukaemia disease progression.
Autores: Aranaz Oroz, Paula; Miguéliz Basterra, Itziar; Hurtado Rudi, Cristina; et al.
Revista: LEUKEMIA AND LYMPHOMA
ISSN 1042-8194  Vol. 54  Nº 2  2013  págs. 428 - 431
Autores: Aranaz Oroz, Paula; Hurtado Rudi, Cristina; Erquiaga Martínez, Ignacio; et al.
Revista: Haematologica-journal of Hematology
ISSN 1138-0381  Vol. 97  Nº 8  2012  págs. 1234 -1241
Autores: Hurtado Rudi, Cristina; Erquiaga Martínez, Ignacio; Aranaz Oroz, Paula; et al.
Revista: Leukemia Research
ISSN 0145-2126  Vol. 35  Nº 11  2011  págs. 1537 - 1539
Autores: Euba Rementeria, Begoña; Vizmanos Pérez, José Luis; García-Granero Marquez, Marta; et al.
Revista: Leukemia & Lymphoma
ISSN 1042-8194  Vol. 53  Nº 6  2011  págs. 1230-1233
Autores: Erquiaga Martínez, Ignacio; Ormazábal Goicoechea, Cristina; Hurtado Rudi, Cristina; et al.
Revista: LEUKEMIA AND LYMPHOMA
ISSN 1042-8194  Vol. 51  Nº 9  2010  págs. 1720 - 1726
Hematological malignancies with eosinophilia are often associated with fusions in PDGFRA, PDGFRB, or FGFR1 genes. RT-PCR has proved to be useful for finding new PDGFRA gene fusions, but some studies have shown overexpression of the TK domain which cannot be explained by the existence of such aberrations. This fact could be related to the expression of alternative PDGFRA transcripts. We show that quantification of the expression of three different PDGFRA fragments discriminates between PDGFRA alternative transcripts and fusion genes, and we have tested this novel methodological approach in a group of eosinophilia cases. Our data show that alternative PDGFRA transcripts should be taken into account when screening for PDGFRA aberrations, such as gene fusions, by RT-PCR. Expression from an internal PDGFRA promoter seems to be a frequent event, in both normal and leukemic samples, and is probably related to physiological conditions, but it could have a role in other tumors. Even so, we show that our RQ-PCR methodology can discriminate expression of alternative transcripts from the presence of X-PDGFRA fusion genes.
Autores: Aranaz Oroz, Paula; Ormazábal Goicoechea, Cristina; Hurtado Rudi, Cristina; et al.
Revista: CANCER GENETICS AND CYTOGENETICS
ISSN 0165-4608  Vol. 199  Nº 1  2010  págs. 1 - 8
BCR/ABL1-negative chronic myeloproliferative neoplasms (CMPNs) are a heterogeneous group of clonal hematological malignancies. Over recent years, some genetic events in tyrosine lcinase (TK) genes have been described as causal events of these diseases. To identify new genetic aberrations underlying these diseases, we used denaturing high performance liquid chromatography and fluorescence in situ hybridization (FISH) to analyze 17 genes from two receptor-TK families (III and IV) and from three cytoplasmic-TK families (Syk, Abl, and Jak) on samples from 44 BCR/ABL1-negative and JAK2(V617F)-negative CMPN patients with different clinical phenotypes. Although screening by FISH did not reveal novel chromosomal aberrations, several sequence changes were detected. None of them were frequent events, but we identified a new potential activating mutation in the FERM domain of JAK2(R340Q). None of the germline JAK2(V617F) singlenucleotide polymorphisms detected differed in distribution between patients and control subjects. In summary, data presented here show that these genes are not frequently mutated or rearranged in CMPNs, suggesting that molecular events causing these disorders must be located in other genes.