CIBER ISCIII

Barcelona, Spain

CIBER ISCIII

Barcelona, Spain

The Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition is a public research consortium which was founded on November 28, 2006 financed by the Instituto de Salud Carlos III and the Ministerio de Ciencia e Innovación .The CIBERObn gathers 25 investigation groups from different Spanish Hospitals, Universities and Research Centres. Its mission is to promote a better knowledge about the mechanisms contributing to obesity development in order to reduce its incidence and prevalence, as well as its complications, in addition to nutrition-related diseases.The CIBERObn is structured into 8 scientific programs intended to increase the collaboration between researchers, to strengthen synergies and to boost new research lines. Programs are as follows: Nutrition: effects of different types of diet and nutrients on human health. Adipobiology: identification of new signals released by the adipose tissue which are involved in the regulation of energy homeostasis. Obesity and Cancer: role of those proteins associated with cell cycle on metabolic control and obesity development. Obesity and Cardiovascular risk: hemodynamic, metabolic and inflammatory factors associated to cardiac and vascular diseases in obesity. Neurocognitive and Environmental Factors: environmental and emotional factors in nutrition and obesity disorders. Obesity in Childhood-Adolescence Period: biochemical, hormonal, metabolic, genetic, proteomic and body-composition study in children and adolescents. Biomarkers: new strategies, therapeutic and prevention technologies, biomarkers of obesity. Biological Models and Therapeutic Targets: development and validation of experimental models and therapeutic targets in case of obesity.Additionally, CIBERObn lays a particular emphasis on translational research, specially focusing on research transfer to clinical applications and practices. To this end, two cross-cutting programs have been created: Staff Training and Recruitment, which is intended to train our staff according to our research lines and priorities “Fat Bank” Structural Program: biobank infrastructure connecting the above mentioned programs in a cross way by contributing with common solutions.The Fat Bank is a strategic platform of the CIBERobn which offers the Scientific Community different kinds of biological material which are associated to thorough metabolic phenotyping. This information is entered by means of a tailor-made individualised software. This fat-bank- launched in 2009- currently contains 3000 samples of biologic material from more than 300 individuals. In 2009, 287 indexed articles were published. Their average impact factor is 4.05, which is very high for this subject area. Of them, 67 belong to the first decile and 105 more belong to the first quartile of the subject area of indexed journals. They accumulate a total impact factor of 1,165. Provisional data of 2010 show an increase of 10%, highly improving the international visibility of the consortium. Wikipedia.

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Surmeier D.J.,Northwestern University | Obeso J.A.,University of San Pablo - CEU | Obeso J.A.,CIBER ISCIII | Halliday G.M.,University of Sydney | Halliday G.M.,University of New South Wales
Nature Reviews Neuroscience | Year: 2017

Intracellular α-synuclein (α-syn)-rich protein aggregates called Lewy pathology (LP) and neuronal death are commonly found in the brains of patients with clinical Parkinson disease (cPD). It is widely believed that LP appears early in the disease and spreads in synaptically coupled brain networks, driving neuronal dysfunction and death. However, post-mortem analysis of human brains and connectome-mapping studies show that the pattern of LP in cPD is not consistent with this simple model, arguing that, if LP propagates in cPD, it must be gated by cell-or region-Autonomous mechanisms. Moreover, the correlation between LP and neuronal death is weak. In this Review, we briefly discuss the evidence for and against the spreading LP model, as well as evidence that cell-Autonomous factors govern both α-syn pathology and neuronal death. © 2017 Macmillan Publishers Limited, part of Springer Nature.All rights reserved.


Patent
University of Seville and Ciber Isciii | Date: 2016-09-14

The invention relates to an intelligent bioimpedance sensor for biomedical applications, which can carry out bioimpedance measurements in a plurality of configurable frequencies, process data in order to obtain the modulus and the phase of the bioimpedance (or real and imaginary part of the bioimpedance) in each of the frequencies, and wirelessly transmit the results of the processing, configured by means of a device that is in contact with the biological means to be measured by means of a series of electrodes in such a way that the device injects electrical current, via said electrodes, into the biological means, in the different frequencies, and measures the tension generated by the circulation of said current based on the joint operation of various subsystems.


Miravitlles M.,CIBER ISCIII
Current Opinion in Pharmacology | Year: 2012

Since the end of the 1980s augmentation therapy with alpha-1 antitrypsin (AAT) from human plasma has been available for specific treatment of emphysema due to AAT deficiency. Intravenous augmentation therapy has demonstrated to be safe and weekly infusions of AAT have demonstrated to result in plasma AAT concentration above those considered protective for the lungs. Randomized, placebo-controlled clinical trials have confirmed a reduction in the decline in lung density in patients receiving augmentation therapy. This is the first example of an antiprotease effective in restoring the protease/antiprotease imbalance in the lungs and changing the natural history of congenital emphysema. On the basis of the results obtained with the long-term infusion of AAT, there is growing interest in the possible use of antiprotease treatment in patients with smokers COPD. However, no drugs are yet available to increase antiprotease protection of the lower airways of smokers. © 2012 Elsevier Ltd. All rights reserved.


Navarro X.,Autonomous University of Barcelona | Navarro X.,CIBER ISCIII
European Journal of Neuroscience | Year: 2016

Peripheral nerve injuries usually lead to severe loss of motor, sensory and autonomic functions in the patients. Due to the complex requirements for adequate axonal regeneration, functional recovery is often poorly achieved. Experimental models are useful to investigate the mechanisms related to axonal regeneration and tissue reinnervation, and to test new therapeutic strategies to improve functional recovery. Therefore, objective and reliable evaluation methods should be applied for the assessment of regeneration and function restitution after nerve injury in animal models. This review gives an overview of the most useful methods to assess nerve regeneration, target reinnervation and recovery of complex sensory and motor functions, their values and limitations. The selection of methods has to be adequate to the main objective of the research study, either enhancement of axonal regeneration, improving regeneration and reinnervation of target organs by different types of nerve fibres, or increasing recovery of complex sensory and motor functions. It is generally recommended to use more than one functional method for each purpose, and also to perform morphological studies of the injured nerve and the reinnervated targets. © 2016 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.


Bove J.,CIBER ISCIII | Perier C.,CIBER ISCIII
Neuroscience | Year: 2012

Animal experimentation in the Parkinson's disease (PD) field is a classic example of how the use of animal models to study diseases can have a significant impact on human health. Among the different neurotoxin-based animal models of PD that are presently available, the 6-hydroxydopamine (6-OHDA) and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models have been established and validated as useful models for the development of therapeutic strategies aimed to treat motor symptoms and to study alterations of the basal ganglia that occur in this disease. The 6-OHDA rat model and the MPTP primate model have contributed enormously to translate animal experimentation into clinical practice, including pharmacological treatments and deep brain stimulation of the subthalamic nucleus. These models, along with the MPTP mouse model, are helping to elucidate the pathogenic mechanism of neurodegeneration in PD. The roles of oxidative stress, apoptosis, mitochondrial dysfunction, inflammation, and impairment of the protein degradation pathways have also come under careful consideration thanks to these models. The more recently developed paraquat and rotenone rodent models are also contributing to our understanding of neuronal cell death. However, none of the neuroprotective strategies that have worked in the pre-clinical stage have thus far been successfully translated to a clinical setting to treat PD patients. At the same time, the lack of any effective neuroprotective strategy for PD is preventing the validation of any one particular model as a screening tool for such neuroprotective strategies. Therefore, it seems that we are trapped in a vicious circle that casts doubt on the suitability of the neurotoxin-based models for this purpose. Here, we discuss how epidemiological data may help to validate a specific model with data linking a lower risk of developing PD with nutritional/consumption habits or with a specific chronic drug therapy.This article is part of a Special Issue entitled: Neuroscience Disease Models. © 2012 IBRO.


Martinez-Vicente M.,CIBER ISCIII | Martinez-Vicente M.,Autonomous University of Barcelona
Seminars in Cell and Developmental Biology | Year: 2015

Neuronal homeostasis depends on the proper functioning of quality control systems like autophagy. This mechanism is responsible of the clearance of misfolded proteins, aggregates and the turnover of organelles within the neuron. Autophagic dysfunction has been described in many neurodegenerative diseases. It can occur at several steps of the autophagic machinery and can contribute to the formation of intracellular aggregates and ultimately to neuronal death. Accordingly restoring autophagy activity in affected neurons can be an attractive therapeutic approach to fight neurodegeneration. In this review we summarize the present encouraging strategies that have been achieved with pharmacological and genetic treatments aimed to induce neuronal autophagy in experimental models of neurodegenerative diseases. © 2015 Elsevier Ltd.


Lott I.T.,University of California at Irvine | Dierssen M.,CIBER ISCIII
The Lancet Neurology | Year: 2010

Improvements in medical interventions for people with Down's syndrome have led to a substantial increase in their longevity. Diagnosis and treatment of neurological complications are important in maintaining optimal cognitive functioning. The cognitive phenotype in Down's syndrome is characterised by impairments in morphosyntax, verbal short-term memory, and explicit long-term memory. However, visuospatial short-term memory, associative learning, and implicit long-term memory functions are preserved. Seizures are associated with cognitive decline and seem to cause additional decline in cognitive functioning, particularly in people with Down's syndrome and comorbid disorders such as autism. Vision and hearing disorders as well as hypothyroidism can negatively impact cognitive functioning in people with Down's syndrome. Dementia that resembles Alzheimer's disease is common in adults with Down's syndrome. Early-onset dementia in adults with Down's syndrome does not seem to be associated with atherosclerotic complications. © 2010 Elsevier Ltd. All rights reserved.


Quirce S.,CIBER ISCIII
Current Opinion in Allergy and Clinical Immunology | Year: 2014

PURPOSE OF REVIEW: To evaluate recent data on the causative role of specific IgE antibodies, as well as the performance of IgE diagnostic tests, in allergic occupational asthma induced by high (HMW) or low-molecular-weight (LMW) agents. RECENT FINDINGS: Skin prick testing (SPT) and specific IgE assays are useful to document allergy to most HMW allergens and some LMW agents. These tests, however, are limited by the lack of standardized and commercially available reagents. There is a wide variability among the quality of occupational allergen extracts used for SPT and the sensitivity of several SPT solutions is low. In addition, many individuals with allergen-specific serum IgE and/or positive SPT to specific HMW allergens do not have clinical symptoms. Sensitization or allergenic cross-reactivity to allergens or epitopes from unrelated sources may interfere in the diagnosis of IgE-mediated allergy, giving rise to false-positive results, particularly when cross-reactive carbohydrate determinants (CCDs) are involved. The immune responses to these ubiquitous structures may interfere with the diagnosis of occupational allergy. Component-resolved diagnosis of IgE-mediated allergic diseases (occupational and nonoccupational) using panels of native or recombinant allergens, or micro-arrayed allergens, have been proposed to identify specific molecules responsible for these disorders and to overcome false-positive in-vitro test results. SUMMARY: Improvement and standardization of SPT solutions for occupational allergens are highly recommended. More refined diagnostic tools than specific IgE measurements are being developed, such as inhibition assays of IgE binding to CCDs with specific carbohydrate molecules, and component-resolved diagnosis. © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins.


Ratera I.,CIBER ISCIII | Veciana J.,CIBER ISCIII
Chemical Society Reviews | Year: 2012

The literature has shown numerous contributions on the synthesis and physicochemical properties of persistent organic radicals but there are a lesser number of reports about their use as building blocks for obtaining molecular magnetic materials exhibiting an additional and useful physical property or function. These materials show promise for applications in spintronics as well as bistable memory devices and sensing materials. This critical review provides an up-to-date survey to this new generation of multifunctional magnetic materials. For this, a detailed revision of the most common families of persistent organic radicals - nitroxide, triphenylmethyl, verdazyl, phenalenyl, and dithiadiazolyl - so far reported will be presented, classified into three different sections: materials with magnetic, conducting and optical properties. An additional section reporting switchable materials based on these radicals is presented (257 references).


Canton R.,CIBER ISCIII | Morosini M.-I.,CIBER ISCIII
FEMS Microbiology Reviews | Year: 2011

Within a susceptible wild-type population, a small fraction of cells, even <10-9, is not affected when challenged by an antimicrobial agent. This subpopulation has mutations that impede antimicrobial action, allowing their selection during clinical treatment. Emergence of resistance occurs in the frame of a selective compartment termed a mutant selection window (MSW). The lower margin corresponds to the minimum inhibitory concentration of the susceptible cells, whereas the upper boundary, named the mutant prevention concentration (MPC), restricts the growth of the entire population, including that of the resistant mutants. By combining pharmacokinetic/pharmacodynamic concepts and an MPC strategy, the selection of resistant mutants can be limited. Early treatment avoiding an increase of the inoculum size as well as a regimen restricting the time within the MSW can reduce the probability of emergence of the resistant mutants. Physiological and, possibly, genetic adaptation in biofilms and a high proportion of mutator clones that may arise during chronic infections influence the emergence of resistant mutants. Moreover, a resistant population can emerge in a specific selective compartment after acquiring a resistance trait by horizontal gene transfer, but this may also be avoided to some extent when the MPC is reached. Known linkage between antimicrobial use and resistance should encourage actions for the design of antimicrobial treatment regimens that minimize the emergence of resistance. Emergence of a resistant bacterial subpopulation within a susceptible wild-type population can be restricted with a regimen using an antibiotic dose that is sufficiently high to inhibit both susceptible and resistant bacteria © 2011 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd.

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