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Lleida, Spain

Sanchez-De-La-Torre M.,University of Santa Maria in Ecuador | Sanchez-De-La-Torre M.,Research Center Biomedica En Red Of Enfermedades Respiratorias Ciberes | Nadal N.,University of Santa Maria in Ecuador | Nadal N.,Primary Care Unit of Lleida | And 19 more authors.
Thorax | Year: 2015

Objective To evaluate whether follow-up of patients with obstructive sleep apnoea (OSA) undergoing CPAP treatment could be performed in primary care (PC) settings. Design Non-inferiority, randomised, prospective controlled study. Settings Sleep unit (SU) at the University Hospital and in 8 PC units in Lleida, Spain. Participants Patients with OSA were randomised to be followed up at the SU or PC units over a 6-month period. Main outcomes measured The primary outcome was CPAP compliance at 6 months. The secondary outcomes were Epworth Sleep Scale (ESS) score, EuroQoL, patient satisfaction, body mass index (BMI), blood pressure and cost-effectiveness. Results We included 101 patients in PC ((mean±SD) apnoea-hypopnoea index (AHI) 50.8±22.9/h, age 56.2 ±11 years, 74% male) and 109 in the SU (AHI 51.4 ±24.4/h, age 55.8±11 years, 77% male)). The CPAP compliance was (mean (95% CI) 4.94 (4.47 to 5.5) vs 5.23 (4.79 to 5.66) h, p=0.18) in PC and SU groups, respectively. In the SU group, there were greater improvements in ESS scores (mean change 1.79, 95% CI +0.05 to +3.53, p=0.04) and patient satisfaction (-1.49, 95% CI -2.22 to -0.76); there was a significant mean difference in BMI between the groups (0.57, 95% CI +0.01 to +1.13, p=0.04). In the PC setting, there was a cost saving of 60%, with similar effectiveness, as well as a decrease in systolic blood pressure (-5.32; 95% CI -10.91 to +0.28, p=0.06). Conclusions For patients with OSA, treatment provided in a PC setting did not result in worse CPAP compliance compared with a specialist model and was shown to be a cost-effective alternative. Source


Arcidiacono M.V.,University of Washington | Yang J.,University of Washington | Fernandez E.,IRB Lleida | Fernandez E.,University of Lleida | Dusso A.,University of Washington
Nephrology Dialysis Transplantation | Year: 2015

Background In secondary hyperparathyroidism (SHPT), enhanced parathyroid levels of transforming growth factor- (TGF) increase EGF receptor (EGFR) activation causing parathyroid hyperplasia, high parathyroid hormone (PTH) and also reductions in vitamin D receptor (VDR) that limit vitamin D suppression of SHPT. Since anti-EGFR therapy is not an option in human SHPT, we evaluated ADAM17 as a therapeutic target to suppress parathyroid hyperplasia because ADAM17 is required to release mature TGF, the most potent EGFR-activating ligand. Methods Computer analysis of the ADAM17 promoter identified TGF and C/EBP' 2 as potential regulators of the ADAM17 gene. Their regulation of ADAM17 expression, TGF /EGFR-driven growth and parathyroid gland (PTG) enlargement were assessed in promoter-reporter assays in A431 cells and corroborated in rat and human SHPT, using erlotinib as anti-EGFR therapy to suppress TGF signals, active vitamin D to induce C/EBP' 2 or the combination. Results While TGF induced ADAM17-promoter activity by 2.2-fold exacerbating TGF /EGFR-driven growth, ectopic C/EBP' 2 expression completely prevented this vicious synergy. Accordingly, in advanced human SHPT, parathyroid ADAM17 levels correlated directly with TGF and inversely with C/EBP' 2. Furthermore, combined erlotinib + calcitriol treatment suppressed TGF /EGFR-cell growth and PTG enlargement more potently than erlotinib in part through calcitriol induction of C/EBP' 2 to inhibit ADAM17-promoter activity, mRNA and protein. Importantly, in rat SHPT, the correction of vitamin D deficiency effectively reversed the resistance to paricalcitol induction of C/EBP' 2 to suppress ADAM17 expression and PTG enlargement, reducing PTH by 50%. Conclusion In SHPT, correction of vitamin D and calcitriol deficiency induces parathyroid C/EBP' 2 to efficaciously attenuate the severe ADAM17/TGF synergy, which drives PTG enlargement and high PTH. © The Author 2014. Source


Arcidiacono M.V.,University of Washington | Arcidiacono M.V.,University of Lleida | Yang J.,University of Washington | Fernandez E.,IRB Lleida | And 3 more authors.
Nephrology Dialysis Transplantation | Year: 2015

Background In chronic kidney disease (CKD), parathyroid hyperplasia contributes to high serum parathyroid hormone (PTH) and also to an impaired suppression of secondary hyperparathyroidism by calcium, vitamin D and fibroblast growth factor 23 (FGF23). In rats, systemic inhibition of epidermal growth factor receptor (EGFR) activation markedly attenuated uremia-induced parathyroid hyperplasia and vitamin D receptor (VDR) loss, hence restoring the response to vitamin D. Therefore, we propose that parathyroid-specific EGFR inactivation should prevent CKD-induced parathyroid hyperplasia. Methods A dominant-negative human EGFR mutant, which forms non-functional heterodimers with full-length endogenous EGFR, was successfully targeted to the parathyroid glands (PTGs) of FVB/N mice, using the 5' €2 regulatory sequence of the PTH promoter. The parathyroid phenotype and serum chemistries of wild-type (WT) and transgenic mice were examined after 14 weeks of either sham operation or 75% renal mass reduction (NX). Results Both genotypes had similar morphology and body weight, and NX-induction enhanced similarly serum blood urea nitrogen compared with sham-operated controls. However, despite similar serum calcium, phosphate and FGF23 levels in NX mice of both genotypes, parathyroid EGFR inactivation sufficed to completely prevent the marked increases in PTG enlargement, serum PTH and in parathyroid levels of transforming growth factor-, a powerful EGFR-activator, and the VDR reductions observed in WT mice. Conclusion In CKD, parathyroid EGFR activation is essential for parathyroid hyperplasia and VDR loss, rendering this transgenic mouse a unique tool to scrutinize the pathogenesis of parathyroid and multiple organ dysfunction of CKD progression unrelated to parathyroid hyperplasia. © The Author 2014. Source


Barbe F.,Hosp Universitari Arnau Of Vilanova And Santa Maria | Barbe F.,Research Center Biomedica En Red Of Enfermedades Respiratorias Ciberes | Sanchez-De-la-torre A.,Hosp Universitari Arnau Of Vilanova And Santa Maria | Sanchez-De-la-torre A.,Research Center Biomedica En Red Of Enfermedades Respiratorias Ciberes | And 17 more authors.
European Respiratory Journal | Year: 2015

The goal of this study was to evaluate the influence of obstructive sleep apnoea on the severity and short-term prognosis of patients admitted for acute coronary syndrome. Obstructive sleep apnoea was defined as an apnoea-hypopnoea index (AHI) >15 h-1. We evaluated the acute coronary syndrome severity (ejection fraction, Killip class, number of diseased vessels, and plasma peak troponin) and short-term prognosis (length of hospitalisation, complications and mortality). We included 213 patients with obstructive sleep apnoea (mean±SD AHI 30±14 h-1, 61±10 years, 80% males) and 218 controls (AHI 6±4 h-1, 57±12 years, 82% males). Patients with obstructive sleep apnoea exhibited a higher prevalence of systemic hypertension (55% versus 37%, p<0.001), higher body mass index (29±4 kg·m-2 versus 26±4 kg·m-2, p<0.001), and lower percentage of smokers (61% versus 71%, p=0.04). After adjusting for smoking, age, body mass index and hypertension, the plasma peak troponin levels were significantly elevated in the obstructive sleep apnoea group (831±908 ng·L-1 versus 987±884 ng·L-1, p=0.03) and higher AHI severity was associated with an increased number of diseased vessels (p=0.04). The mean length of stay in the coronary care unit was higher in the obstructive sleep apnoea group (p=0.03). This study indicates that obstructive sleep apnoea is related to an increase in the peak plasma troponin levels, number of diseased vessels, and length of stay in the coronary care unit. Copyright © ERS 2015. Source


Vilaplana J.,University of Lleida | Solsona F.,University of Lleida | Teixido I.,University of Lleida | Mateo J.,University of Lleida | And 2 more authors.
Journal of Supercomputing | Year: 2014

The ability to deliver guaranteed QoS (Quality of Service) is crucial for the commercial success of cloud platforms. This paper presents a model based on queuing theory to study computer service QoS in cloud computing. Cloud platforms are modeled with an open Jackson network that can be used to determine and measure the QoS guarantees the cloud can offer regarding the response time. The analysis can be performed according to different parameters, such as the arrival rate of customer services and the number and service rate of processing servers, among others. Detailed results for the model are presented. When scaling the system and depending on the types of bottleneck in the system, we show how our model can provide us with the best option to guarantee QoS. The results obtained confirm the usefulness of the model presented for designing real cloud computing systems. © 2014 Springer Science+Business Media New York. Source

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