Publications by authors named "Pablo Binder"

This paper reviews the current problems and prospects to overcome circular water economy management challenges in European countries. The geopolitical paradigm of water, the water economy, water innovation, water management and regulation in Europe, environmental and safety concerns at water reuse, and technological solutions for water recovery are all covered in this review, which has been prepared in the frame of the COST ACTION (CA, 20133) FULLRECO4US, Working Group (WG) 4. With a Circular Economy approach to water recycling and recovery based on this COST Action, this review paper aims to develop novel, futuristic solutions to overcome the difficulties that the European Union (EU) is currently facing.

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Background Prolonged activation of angiotensin II is the main mediator that contributes to the development of heart diseases, so converting angiotensin II into angiotensin 1-7 has emerged as a new strategy to attenuate detrimental effects of angiotensin II. Prolylcarboxypeptidase is a lysosomal pro-X carboxypeptidase that is able to cleave angiotensin II at a preferential acidic pH optimum. However, insufficient attention has been given to the cardioprotective functions of prolylcarboxylpeptidase.

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The ever-increasing demand for phosphorus fertilisers for securing global food production, coupled with finite phosphate rock reserves, is one of the emerging problems in the world. Indeed, phosphate rock is listed as an EU critical raw material, triggering attention to find an alternative source to substitute the use of this limited resource. Cheese whey, characterized by a high content of organic matter and phosphorus, represents a promising feedstock for phosphorus recovery and recycling.

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Endoplasmic Reticulum (ER) stress and oxidative stress have been highly implicated in the pathogenesis of cardiac hypertrophy and heart failure (HF). However, the mechanisms involved in the interplay between these processes in the heart are not fully understood. The present study sought to determine a causative link between Pak2-dependent UPR activation and oxidative stress Nrf2 regulation under pathological ER stress.

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Myocardial inflammation contributes to cardiomyopathy in diabetic patients through incompletely defined underlying mechanisms. In both human and time-course experimental samples, diabetic hearts exhibited abnormal ER, with a maladaptive shift over time in rodents. Furthermore, as a cardiac ER dysfunction model, mice with cardiac-specific p21-activated kinase 2 (PAK2) deletion exhibited heightened myocardial inflammatory response in diabetes.

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Cardiovascular disease is the leading cause of mortality worldwide and there is an increasing need to identify new therapeutic targets that could be used to prevent or treat these diseases. Due to recent scientific advances, non-coding RNAs are widely accepted as important regulators of cellular processes, and the identification of an axis of interaction between long non-coding RNAs (lncRNAs) and micro RNAs (miRNAs) has provided another platform through which cardiovascular disease could be targeted therapeutically. Increasing evidence has detailed the importance of these non-coding RNAs, both individually and in an axis of regulation, in the processes and diseases involving the heart.

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Myocardial insulin resistance contributes to heart failure in response to pathological stresses, therefore, a therapeutic strategy to maintain cardiac insulin pathways requires further investigation. We demonstrated that insulin receptor substrate 1 (IRS1) was reduced in failing mouse hearts post-myocardial infarction (MI) and failing human hearts. The mice manifesting severe cardiac dysfunction post-MI displayed elevated in the myocardium.

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Rationale: Secreted and membrane-bound proteins, which account for 1/3 of all proteins, play critical roles in heart health and disease. The endoplasmic reticulum (ER) is the site for synthesis, folding, and quality control of these proteins. Loss of ER homeostasis and function underlies the pathogenesis of many forms of heart disease.

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Unlabelled: The endoplasmic reticulum (ER) serves several essential cellular functions including protein synthesis, protein folding, protein translocation, calcium homoeostasis and lipid biosynthesis. Physiological or pathological stimuli, which disrupt ER homoeostasis and disturb its functions, lead to an accumulation of misfolded and unfolded proteins, a condition referred to as ER stress. ER stress triggers the unfolded protein response to restore the homoeostasis of ER, through activating transcriptional and translational pathways.

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We studied the acquisition of dehydroascorbic acid by rat hepatocytes, H4IIE rat hepatoma cells and Xenopus laevis oocytes. Transport kinetics and competition and inhibition studies revealed that rat hepatocytes transport oxidized dehydroascorbic acid through a single functional component possessing the functional and kinetic properties expected for the glucose transporter GLUT2. On the other hand, rat hepatoma cells showed expression of at least two dehydroascorbic acid transporters with the expected functional and kinetic properties expected for GLUT1 and GLUT2.

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