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Gonzalez-Mateo G.,Hospital Universitario La Paz | Jimenez-Heffernan J.,Hospital Universitario Of La Princesa | Selgas R.,Hospital Universitario La Paz | Aguilera Peralta A.,Institute Investigacion Sanitaria Princesa IP
International Journal of Nephrology | Year: 2013

Mesothelial-to-mesenchymal transition (MMT) is an autoregulated physiological process of tissue repair that in uncontrolled conditions, such as peritoneal dialysis (PD), can lead to peritoneal fibrosis. The maximum expression of sclerotic peritoneal syndromes (SPS) is the encapsulating peritoneal sclerosis (EPS) for which no specific treatment exists. The SPS includes a wide range of peritoneal fibrosis that appears progressively and is considered as a reversible process, while EPS does not. EPS is a serious complication of PD characterized by a progressive intra-abdominal inflammatory process that results in bridles and severe fibrous tissue formation which cover and constrict the viscera. Recent studies show that transdifferentiated mesothelial cells isolated from the PD effluent correlate very well with the clinical events such as the number of hemoperitoneum and peritonitis, as well as with PD function (lower ultrafiltration and high Cr-MTC). In addition, in peritoneal biopsies from PD patients, the MMT correlates very well with anatomical changes (fibrosis and angiogenesis). However, the pathway to reach EPS from SPS has not been fully and completely established. Herein, we present important evidence pointing to the MMT that is present in the initial peritoneal fibrosis stages and it is perpetual over time, with at least theoretical possibility that MMT initiated the fibrosing process to reach EPS. © 2013 Jesús Loureiro et al.


Ancochea J.,Institute Investigacion Sanitaria Princesa IP | Miravitlles M.,Institute dinvestigacions Biomediques August Pi i Sunyer IDIBAPS | Garcia-Rio F.,Servicio de Neumologia | Munoz L.,Servicio de Neumologia | And 3 more authors.
Archivos de Bronconeumologia | Year: 2013

Introduction: The distribution of chronic obstructive pulmonary disease (COPD) in women, and its underdiagnosis and determinants in the general population, have not been well described. The EPI-SCAN study is an epidemiologic, observational study conducted at 11 Spanish centers on the general population aged 40 to 80. Patients and method: This paper describes the rates and extrapolates the population burden from the 3,802 participants of the EPI-SCAN study. Results: With 2,005 female and 1,797 male participants, there was a lower prevalence of COPD in women (5.7%; 95%. CI, 4.7-6.7) than in men (15.1%; 95%. CI, 13.5-16.8; P. <. .05). Among the 386 participants with COPD, 114 (29.5%) were women, who were younger, currently smoked less and had lower tobacco smoke exposure, while reporting a lower level of education (P. <. .05). As for the respiratory symptoms, there were no differences between sexes for cough, dyspnea or wheezing, but the women with COPD reported sputum less frequently (P. <. .05). There were no differences in the spirometric severity of COPD between women and men. Overall, 73% of the patients with a spirometric COPD criteria were underdiagnosed, and this percentage is unevenly distributed by sex, being 1.27 times more frequent in women (86.0%) than in men (67.6%) (P. <. .05). By extrapolating the rates of prevalence and underdiagnosis of COPD to the general population, we estimate that there are 628,102 Spanish women between the ages of 40 and 80 with COPD, 540,168 of whom still have not been diagnosed. Conclusions: There is a greater underdiagnosis of COPD in women than in men in Spain. © 2012 SEPAR.


Cabaleiro T.,Hospital Universitario Of La Princesa | Lopez-Rodriguez R.,Institute Investigacion Sanitaria Princesa IP | Lopez-Rodriguez R.,Institute Salud Carlos III | Ochoa D.,Hospital Universitario Of La Princesa | And 4 more authors.
Human Psychopharmacology | Year: 2013

Objective: The pharmacokinetics of olanzapine and response to treatment could be affected by polymorphisms in genes coding for drug-metabolizing enzymes, transporters, or receptors. The aim of this study was to identify genetic markers predictive of pharmacokinetics, pharmacodynamics, and adverse effects of olanzapine. Methods: Sixty-three healthy volunteers receiving a single 5-mg oral dose of olanzapine were genotyped for 39 genetic variants that could be related to the response to olanzapine. All genetic variants were analyzed by PharmaChip, but DRD2 Taq1A polymorphism was determined by real-time polymerase chain reaction. Olanzapine was measured using high-performance liquid chromatography combined with tandem mass spectrometry. The relationship of gender and polymorphisms with olanzapine pharmacokinetics, the change in prolactin levels, and the incidence of adverse effects were evaluated by multiple regression analysis. Results: The pharmacokinetics of olanzapine was influenced by polymorphisms in CYP3A5, GSTM3, and GRIN2B. Prolactin levels were affected by gender and polymorphisms in DRD2 and 5-HTR2A. Polymorphisms in CYP2C9, TPMT, UGT1A1, MDR1, and 5-HTR2A were related to some adverse effects of olanzapine. Conclusions: Several polymorphisms can explain differences in the pharmacokinetics, pharmacodynamics, and safety of olanzapine in healthy subjects. Whether these genetic factors influence the risk of therapeutic failure or tolerability in patients remains to be established. Copyright © 2013 John Wiley & Sons, Ltd.


Martinez-deMena R.,Institute Investigaciones Biomedicas IIB | Anedda A.,Institute Investigacion Sanitaria Princesa IP | Cadenas S.,Institute Investigacion Sanitaria Princesa IP | Cadenas S.,Autonomous University of Madrid | Obregon M.-J.,Institute Investigaciones Biomedicas IIB
Molecular and Cellular Endocrinology | Year: 2015

TSH receptor (TSHR) is present in the thyroid and other tissues, as adipose tissue. In brown adipose tissue (BAT) TSH increases UCP1 expression and lipolysis. We have studied the regulation of Tshr mRNA expression and the effect of TSH on Ucp1 and Dio2 mRNA, on D2 activity and O2 consumption in rat brown adipocytes and the TSH signaling pathways. Tshr increased during brown adipocyte differentiation, was up-regulated by insulin and low TSH concentrations and down-regulated by high TSH concentrations, T3 and/or NE. TSH increased basal Ucp1 mRNA in a dose-dependent way acting synergistically with T3, while had no effect when NE was present. High TSH concentrations increased basal Dio2 mRNA (12-fold) and were synergistic with T3 (100-fold), but decreased Dio2 mRNA in T3+NE-treated cells. TSH increased D2 activities in T3-treated cells and inhibition of ERK pathway decreased the TSH effect by 55%. In T3+NE treated-cells TSH decreased D2 activity by 50%, in a dose-dependent manner. TSH activated Akt and Erk phosphorylation, while inhibition of PKA promoted Akt phosphorylation. TSH inhibited leptin mRNA. TSH increased O2 consumption by 20% and T3 enhanced its effect. Tshr is expressed in brown adipocytes and is regulated by insulin, TSH, T3 and NE. TSH increases basal and T3-stimulated Ucp1 and Dio2 expression and D2 activity only when T3 is present, but decreases Dio2 mRNA and D2 activity stimulated by NE+T3. TSH increases O2 consumption, confirming the role of TSH in the maintenance of thermogenesis. © 2015 Elsevier Ireland Ltd.


Garcia-Iglesias P.,Institute Universitari Parc Tauli | Villoria A.,Institute Universitari Parc Tauli | Suarez D.,Autonomous University of Barcelona | Brullet E.,Institute Universitari Parc Tauli | And 9 more authors.
Alimentary Pharmacology and Therapeutics | Year: 2011

Background Determining the risk of rebleeding after endoscopic therapy for peptic ulcer bleeding (PUB) may be useful for establishing additional haemostatic measures in very high-risk patients. Aim To identify predictors of rebleeding after endoscopic therapy. Methods Bibliographic database searches were performed to identify studies assessing rebleeding after endoscopic therapy for PUB. All searches and data abstraction were performed in duplicate. A parameter was considered to be an independent predictor of rebleeding when it was detected as prognostic by multivariate analyses in ≥2 studies. Pooled odds ratios (pOR) were calculated for prognostic variables. Results Fourteen studies met the prespecified inclusion criteria. Pre-endoscopic predictors of rebleeding were: (i) Haemodynamic instability: significant in 9 of 13 studies evaluating the variable (pOR: 3.30, 95% CI: 2.57-4.24); (ii) Haemoglobin value: significant in 2 of 10 (pOR: 1.73, 95% CI: 1.14-2.62) and (iii) Transfusion: significant in two of six (pOR not calculable). Endoscopic predictors of rebleeding were: (i) Active bleeding: significant in 6 of 12 studies (pOR: 1.70, 95% CI: 1.31-2.22); (ii) Large ulcer size: significant in 8 of 12 studies (pOR: 2.81, 95% CI: 1.98-4.00); (iii) Posterior duodenal ulcer location: significant in four of eight studies (pOR: 3.83, 95% CI: 1.38-10.66) and (iv) High lesser gastric curvature ulcer location: significant in three of eight studies (pOR: 2.86; 95% CI: 1.69-4.86). Conclusions Major predictors for rebleeding in patients receiving endoscopic therapy are haemodynamic instability, active bleeding at endoscopy, large ulcer size, ulcer location, haemoglobin value and the need for transfusion. These risk factors may be useful for guiding clinical management in patients with PUB. © 2011 Blackwell Publishing Ltd.

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