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Madrid, Spain

Jansa M.,Diabetes Unit | Hernandez C.,Integrated Care Unit | Vidal M.,Diabetes Unit | Nunez M.,Rheumatology Unit | And 4 more authors.
Patient Education and Counseling | Year: 2010

Objective: Determine treatment adherence in patients with multiple chronic conditions (MCC). Methods: A random patient sample ≥15 years, discharged from hospital with ≥1 chronic conditions (CC) was interviewed after 6-12 months. Analysis included variables in 5 dimensions (WHO): socio-demographics, disease, treatment, patient and health system characteristics. Morisky-Green adherence questionnaire was used. High chronic treatment complexity was defined as: >3 pills/day, >6 inhalations/day, >1 injection/day, pharmacological treatment plus diet or self-monitoring techniques. Results: 301 patients were interviewed (62 ± 15 years, 59% males). Despite good treatment information perception (79%), only 3% followed the patient education programme. Poor adherents (82%) were older (64 ± 14 years vs. 55 ± 16 years), had more CC (3.25 ± 2.02 vs. 2.62 ± 2.72), a higher frequency of hypertension (44% vs. 15%), ischaemic heart diseases: (21% vs. 4%), hyperlipidaemia (19% vs. 6%), more pills/day (5.78 ± 4.14 vs. 3.20 ± 4.70) and more complex treatments (95% vs. 70%) (p<0.05). On multivariate analysis number of CC [3.68 (0.75-18.15)], pills/day [2.23 (1.02-4.84)], treatment complexity [4.00 (1.45-11.04)], and hypertension [2.57 (1.06-6.25)] were predictive of poor adherence (OR 95% CI p<0.05). Conclusion: The WHO conceptual framework allows the construction of poor adherence risk profiles in patients with MCC after hospital discharge. Practice implications: Predictive variables of poor adherence could help clinicians detect patients with MCC most likely to present poor adherence. © 2010 Elsevier Ireland Ltd. Source


Lamas J.R.,Rheumatology Service | Rodriguez-Rodriguez L.,Rheumatology Service | Varade J.,Immunology Service | Lopez-Romero P.,CNIC | And 4 more authors.
Journal of Rheumatology | Year: 2010

Objective. To analyze the influence of IL6R rs8192284 polymorphism on the disease activity of rheumatoid arthritis (RA). Methods. Patients with RA (n = 281) were followed for a median of 4.2 years. A total of 1143 disease activity measurements using the 28-joint count Disease Activity Score (DAS28) were performed. A mixed-effect model was used to analyze the measurements. Results. A statistically significant interaction was observed between IL6R rs8192284 polymorphism and the presence of anticyclic citrullinated peptide (anti-CCP) antibodies (p = 0.008). An inverse relationship between the polymorphism and DAS28 was observed depending on anti-CCP status. Conclusion. The anti-CCP status in patients with RA determines the association between the IL6R rs8192284 polymorphism and disease activity. The Journal of Rheumatology Copyright © 2010. All rights reserved. Source


Arduini A.,University of Valencia | Serviddio G.,University of Foggia | Escobar J.,University of Valencia | Tormos A.M.,University of Valencia | And 4 more authors.
American Journal of Physiology - Gastrointestinal and Liver Physiology | Year: 2011

Chronic cholestasis is characterizedby mitochondrial dysfunction, associated with loss of mitochondrialmembrane potential, decreased activities of respiratory chaincomplexes, and ATP production. Our aim was to determine themolecular mechanisms that link long-term cholestasis to mitochondrialdysfunction. We studied a model of chronic cholestasis inducedby bile duct ligation in rats. Key sensors and regulators of theenergetic state and mitochondrial biogenesis, mitochondrial DNA(mtDNA)-to-nuclear DNA (nDNA) ratio (mtDNA/nDNA) relativecopy number, mtDNA deletions, and indexes of apoptosis (BAX,BCL-2, and cleaved caspase 3) and cell proliferation (PCNA) wereevaluated. Our results show that long-term cholestasis is associatedwith absence of activation of key sensors of the energetic state,evidenced by decreased SIRT1 and pyruvate dehydrogenase kinaselevels and lack of AMPK activation. Key mitochondrial biogenesisregulators (PGC-1α and GABP-α) decreased and NRF-1 was nottranscriptionally active. Mitochondrial transcription factor A (TFAM)protein levels increased transiently in liver mitochondria at 2 wk afterbile duct ligation, but they dramatically decreased at 4 wk. ReducedTFAM levels at this stage were mirrored by a marked decrease (65%)in mtDNA/nDNA relative copy number. The blockade of mitochondrialbiogenesis should not be ascribed to activation of apoptosis orinhibition of cell proliferation. Impaired mitochondrial turnover andloss of the DNA stabilizing effect of TFAM are likely the causativeevent involved in the genetic instability evidenced by accumulation ofmtDNA deletions. In conclusion, the lack of stimulation of mitochondrialbiogenesis leads to mtDNA severe depletion and deletions inlong-term cholestasis. Hence, long-term cholestasis should be considereda secondary mitochondrial hepatopathy. © 2011 the American Physiological Society. Source


Nurmi T.,University of Eastern Finland | Mursu J.,University of Eastern Finland | Penalvo J.L.,CNIC | Poulsen H.E.,Copenhagen University | Voutilainen S.,University of Eastern Finland
British Journal of Nutrition | Year: 2010

Intake of lignans has been assessed in different study populations, but so far none of the studies has compared the daily intake of lignans and the urinary excretion of plant and enterolignans. We assessed the intake of lariciresinol, pinoresinol, secoisolariciresinol and matairesinol in 100 Finnish men consuming their habitual omnivorous diet, and measured the 24h urinary excretion of plant and enterolignans to compare the intake and metabolism. Dietary determinants of lignan intake and their urinary excretion were also determined. The mean intake of lignans was 1224 (sd 539) g/d, of which lariciresinol and pinoresinol covered 78%. Almost half (47%) of the intake of lignans was explained by the intake of rye products, berries, coffee, tea and roots. The urinary excretion of plant lignans corresponded to 17% and enterolignans to 92% of the intake of lignans. The urinary excretion of plant lignans was explained 14% by the intake of rye products and intake of coffee, and consequently 3-7% by the intake of water-insoluble fibre. The urinary excretion of enterolactone was explained 11% by the intake of vegetables and rye products, 14% by the intake of water-soluble fibre and only 4% by the intake of lariciresinol. Although the assessed intake of lignans corresponded well with the urinary excretion of lignans, the enterolactone production in the human body depended more on the dietary sources of lignans than the absolute intake of lignans. © 2010 The Author. Source


Sanchez-Fernandez G.,Autonomous University of Madrid | Sanchez-Fernandez G.,Institute Investigacion Sanitaria La Princesa | Cabezudo S.,Autonomous University of Madrid | Cabezudo S.,Institute Investigacion Sanitaria La Princesa | And 8 more authors.
Cellular Signalling | Year: 2014

In the last few years the interactome of Gαq has expanded considerably, contributing to improve our understanding of the cellular and physiological events controlled by this G alpha subunit. The availability of high-resolution crystal structures has led the identification of an effector-binding region within the surface of Gαq that is able to recognise a variety of effector proteins. Consequently, it has been possible to ascribe different Gαq functions to specific cellular players and to identify important processes that are triggered independently of the canonical activation of phospholipase Cβ (PLCβ), the first identified Gαq effector. Novel effectors include p63RhoGEF, that provides a link between G protein-coupled receptors and RhoA activation, phosphatidylinositol 3-kinase (PI3K), implicated in the regulation of the Akt pathway, or the cold-activated TRPM8 channel, which is directly inhibited upon Gαq binding. Recently, the activation of ERK5 MAPK by Gq-coupled receptors has also been described as a novel PLCβ-independent signalling axis that relies upon the interaction between this G protein and two novel effectors (PKCφ and MEK5). Additionally, the association of Gαq with different regulatory proteins can modulate its effector coupling ability and, therefore, its signalling potential. Regulators include accessory proteins that facilitate effector activation or, alternatively, inhibitory proteins that downregulate effector binding or promote signal termination. Moreover, Gαq is known to interact with several components of the cytoskeleton as well as with important organisers of membrane microdomains, which suggests that efficient signalling complexes might be confined to specific subcellular environments. Overall, the complex interaction network of Gαq underlies an ever-expanding functional diversity that puts forward this G alpha subunit as a major player in the control of physiological functions and in the development of different pathological situations. © 2014 Elsevier Inc. Source

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