La Universitat de Barcelona (UB) ha recuperat el privilegi de ser la institució d’educació superior de tot l’Estat espanyol més ben posicionada en els prestigiosos QS World University Ranquings 2014-2015. La UB, que ocupa el lloc 166è en el rànquing mundial, guanya dotze posicions en relació amb l’any passat (178a posició), i és una de les primeres 200 universitats del món, seguida de la UAB (173è) i la UAM (178è). Recentment, la UB va aconseguir posicionar-se entre les 200 millors universitats del món a l’Academic Ranking of World Universities 2014 (ARWU) com a únic centre a l’Estat.
En els QS World University Rankings s’avaluen la qualitat de la recerca i la docència, la contractació dels graduats i el grau d’internacionalització de cada centre universitari, entre altres indicadors.
La UB millora en gairebé tots els indicadors emprats, però molt especialment en reputació empresarial (escala 42 posicions i ocupa el lloc 151è) i en les citacions per professor (millora 20 posicions i ocupa el lloc 293è), un valor que avalua l’impacte internacional de la recerca.
En relació amb les cinc grans àrees de coneixement que estableixen els rànquings, la UB millora la puntuació en tots els àmbits i continua entre les 100 primeres universitats del món en Arts i Humanitats, Ciències de la Vida i Medicina i Ciències Naturals.
A study led at Vall d’Hebron Institute of Research (VHIR) has demonstrated that the pathological forms of alpha-Synuclein protein extracted from patients who died with Parkinson Disease have the capacity to initiate and spread the same neurodegenerative process in mice and monkeys. The finding, published in the cover of the March issue of Annals of Neurology, may have important implications for the development of disease-modifying therapies to stop Parkinson Disease aimed at targeting expression levels, pathological conversion, and cell-to-cell transmission of alpha-Synuclein.
Recent studies concluded that synthetic alpha-Synuclein forms are toxics for neurons, both in in vitro models (cell cultures) and in vivo animal models (mice), and that can be transmitted cell-to-cell. However, it was still uncertain whether the pathogenic effects of this synthetic protein may apply to the human pathological alpha-Synuclein and occur in species closer to humans.
In this study, led by Dr. Miquel Vila, head of the Neurodegenerative Diseases group at Vall d’Hebron Institute of Research (VHIR) and member of CIBERNED, and with the participation of two additional groups from CIBERNED, and a group from the Université de Bordeaux in France , researchers extracted alpha-Synuclein aggregates from patients who died with Parkinson Disease to inoculate them in the brain of mice and monkeys.
Four months after the inoculation in mice and nine months later in monkeys, the animals started the neurodegenerative process, starting at striatal dopaminergic terminals. With these results, Dr. Vila concludes that “human pathological alpha-Synuclein aggregates trigger in mice and monkeys the same neurodegeneration process than Parkinson Disease”.
The title is a play on words with the abbreviated name of a protein (DOR, Diabetes and Obesity Regulated), which sounds like “d’or”, a word that in Catalan means golden. This protein, DOR, has been identified as a therapeutic target to treat muscle wasting associated to pathological conditions such as type 1 diabetes, or cachexia in patients with cancer or infectious diseases.
This is the conclusion from a study performed by scientists at the Institute for Research in Biomedicine (IRB), in Barcelona, headed by Antonio Zorzano, professor from the Department of Biochemistry and Molecular Biology at the University of Barcelona (UB), and published in the Journal of Clinical Investigation. The study indicates that DOR is a negative regulator of skeletal muscle mass that enhances basal autophagy. Autophagy is pathway that degrades long-lived proteins and organelles from the cell to maintain a correct cellular function. Thus, autophagy is like a quality control process that ensures cells stay healthy, but an excessive autophagy may cause muscle atrophy favoring muscle loss. The results of the study showed that DOR is highly repressed in muscle from type 2 diabetic patients, and the researchers propose that this repression is part of a mechanism responsible for the preservation of muscle mass in type 2 diabetes. The researchers also found that increased DOR expression in the muscle of diabetic mice leads to enhanced autophagy, which in turn favours the loss of muscle mass in these animals.
The results of the study point to DOR as a plausible target against which to develop a drug to prevent muscle deterioration in certain diseases. The advantage of developing a DOR inhibitor is that autophagy, a process necessary to keep cells healthy, would not be completely blocked in the absence of this protein. DOR is not essential for autophagy, but acts more as an accelerator. Thus, the inhibition of DOR would only partially reduce autophagy as other molecules involved would exert their activity normally, thus maintaining the levels of autophagy in a beneficial range for cells.
Xavier Fernández-Busquets is the head of the Nanomalaria group, a sub-group of the Nanobioengineering lab (IBEC) with joint affiliation with the Centre de Recerca en Salut Internacional de Barcelona (CRESIB). This group focus his reseach on the optimization of the nanovectors being currently developed with the objective of exploring sustained drug release strategies inside Plasmodium-infected red blood cells (pRBCs), and the improvement of the targeting agents used to direct nanovectors to pRBCs.
Dr. Xavier Fernàndez-Busquets has a background training in Biochemistry and Molecular Biology. He has developed his career in several research centers, among which the Universitat Autònoma de Barcelona, Basel, USA, the Universitat de Barcelona, the Institute for Bioengineering of Catalonia and the Barcelona Center for International Health Research.
A recent published study of this group demonstrates that an antimalarial drug (chloroquine salts) encapsulated in nanoparticles is significantly more effective when delivered in vivo than free (unencapsulated) drugs and may help to curb drug resistance.
The study, which is published in the Journal of Controlled Release, indicates that the nanoparticles are capable of recognising different Plasmodium species, making their potential as carriers for malarial drugs broader than that of other options.
Current malaria therapies require strategies capable of selectively delivering drugs to the cells infected by Plasmodium. In this study, the researchers explored the usefulness of two polymeric nanosystems, AGMA1 and ISA23, as carriers for cloroquina that selectively target the pathogen.
The study showed that both polymers bind preferentially to Plasmodium-infected red blood cells, compared to uninfected cells. Moreover, they are capable of recognising widely divergent species, such as P. falciparum and P. yoelii, malaria parasites that infect humans and mice respectively. Administration of 0.8 mg/kg of the drug chloroquine as either AGMA1 or ISA23 salts cured P yoelii-infected mice, whereas control animals treated with twice as much free drug did not survive.
“These polymers have low toxicity, high biodegradability and selectively target red blood cells infected by different species of Plasmodium,” explains Xavier Fernàndez-Busquets, head of the Nanomalaria joint unit of IBEC/CRESIB, who led the study. “This all means that they’re extremely promising candidates as therapeutic antimalarials.”
The Barcelona Supercomputing Center (BSC), the Centre for Genomic Regulation (CRG), and the Institute for Research in Biomedicine (IRB Barcelona) launch a Joint BSC-CRG-IRB Programme in Computational Biology for a period of five years and renewable every three years. These three institutes are Severo Ochoa Centres of Excellence and nodes of the Spanish Bioinformatics Network. Their long-term expertise and research quality will turn Barcelona into one of the most outstanding clusters worldwide.
The programme is headed by Modesto Orozco (IRB), with Roderic Guigó (CRG) and David Torrents (BSC) as associate directors, and comprises 10 research groups from these three centres
The goals of this joint programme are to retain the critical mass of researchers, to attract talent, and to boost computational biology
IRB and CRG will offer 10 scientific platforms, including the Experimental Laboratory hosted by IRB, and will provide the link to experimental biologists. BSC offers access to computing resources, such as the MareNostrum supercomputer, one of the most powerful machines in Europe and part of the PRACE Research Infrastructure
The International Psoriasis Council (IPC) has chosen an article published by the translational research group on immunodermatology led by Luis Francisco Santamaria from the Faculty of Biology of the University of Barcelona and the Barcelona Science Park, as one of the best of 2013 about psoriasis. Psoriasis is a chronic cutaneous inflammatory disease of the skin that is highly prevalent and significantly affects the quality of life of patients. Last year a total of 1,908 papers on the disease were published, according to data obtained from the portal PubMed.
One of the main conclusions of the article, published in the Journal of Investigative Dermatology, is that Streptococcus pyogenes antigens are directly involved in the pathological mechanisms that result in the appearance of psoriasis lesions. According to Dr. Santamaria, “although many research studies have been focused on psoriasis, immunopathogenic mechanisms are essential but remain hardly known”. He adds that ” the particularity of the study is that it establishes a new ex-vivo model to elucidate how psoriasis lesions are initiated and triggered by means of the interaction among the bacterium Streptococcus pyogenes, CLA+ T lymphocytes (a group of circulating cells which play a major role in psoriasis physiopathology), and epidermal cells”.
Treatment of infections produced by Gram-negative bacteria is difficult because most of them are resistant to multiple drugs. In response to this problem, the Innovative Medicines Initiative, Europe’s largest public-private partnership aiming to improve the drug development process, has launched the ENABLE (European Gram Negative Antibacterial Engine) project. The programme works with seven lines of compounds developed across Europe. One of them has been developed by Professor Francesc Rabanal, from the Department of Organic Chemistry of the Faculty of Chemistry at the University of Barcelona. According to Professor Rabadal, “ENABLE is a really competitive project that has selected the best laboratories that have the best antibiotic candidates across Europe. Each antibiotic line will be evaluated every three months”. For the moment, the research of the University of Barcelona is in the project for two years; during this period of time, details the expert, “the chemical synthesis will be done and the action mechanism of the compound line will be studied with a maximum budget of 751,000 euros”. “In two years —he adds—, if we have provided new compounds, we will continue competing”.
The ENABLE project is a good example of collaboration between public and private sectors. Over 30 European universities and European companies, led by the multinational pharmaceutical GlaxoSmithKline and Uppsala University (Sweden), collaborate in this project. The goal of this and other projects is to mobilise expertise from universities and industry in Europe to meet global challenges and place Europe at the forefront of collaborative research between industry and academia for health challenges.
Evolutionary biology aims at studying the processes and mechanisms generating biodiversity, based on the understanding of the genetic basis of the difference among species (divergence) as well as within every species (variation, polymorphism). Recently, researchers of the Institute of Evolutionary Biology (CSIC-Universitat Pompeu Fabra) participated in two interesting studies that tell us stories about men and dogs in prehistory.
The first study, directed by Carles Lalueza-Fox and published in Nature, is a genomic study of a man who lived in León 7.000 years ago. One of the most astonishing results is that he had dark skin, darker than present Europeans, but his eyes were blue, indicative of a nord-european phenotype. It was thought that white skin was related to the latitude and less insolation of European countries compared with Africa. However, the hominid studied had dark skin, despite his ancestors had lived in Europe for thousands of years. The results of this study suggest that changes in skin pigmentation may not be related to latitude but to diet. Thus, in the Neolithic men ate less meat and therefore the intake of vitamin D was reduced. In this context, having a clear skin is an advantage because it allows vitamin D synthesis under sunlight influence.
The second study refers to the relationship between men and domestic dogs. In the study participated several research groups from USA, China and several European countries, including researchers of the Institute of Evolutionary Biology Belén Lorente-Galdós, Óscar Ramírez and Tomás Marquès-Bonet. To identify genetic changes underlying dog domestication and reconstruct their early evolutionary history, the researchers generated high-quality genome sequences from three gray wolves, one from each of the three putative centers of dog domestication, two basal dog lineages (Basenji and Dingo) and a golden jackal as an outgroup. Analysis of these sequences supports a demographic model in which dogs and wolves diverged through a dynamic process involving population bottlenecks in both lineages and post-divergence gene flow. In dogs, the domestication bottleneck involved at least a 16-fold reduction in population size, a much more severe bottleneck than estimated previously. The study narrowed the plausible range for the date of initial dog domestication to an interval spanning 11–16 thousand years ago, predating the rise of agriculture. This suggests that the earliest dogs arose alongside hunter-gathers rather than agriculturists.
|Manel Esteller, Director of Epigenetics and Cancer Biology , Institute of Biomedical Research of Bellvitge (IDIBELL), with the collaboration of the Institute of Neuropathology IDIBELL led by Isidre Ferrer, have demonstrated for the first time the existence of an epigenetic lesion in the hippocampus of the brain of patients with Alzheimer. The study has been published in the prestigious international journal “Hippocampus”.
Pathologically, Alzheimer ‘s disease is characterized by the accumulation of protein deposits in the brain of patients. These deposits are formed by plates of a protein amyloid-beta and protein tau that when phosphorylated folds as tangles. The root cause of these lesions in most cases is unknown, but specific alterations in regulating genes expression might be involved. So far very few mutations associated with the disease have been reported, and never one that was common to all patients.
“We first started studying 30,000 molecular switches that turn on and off genes in the hippocampal region in the brains of Alzheimer patients in different stages of disease and compared with that of healthy patients of the same age. We note that DUSP22 gene switches off (methylates) as the disease advances” explained Manel Esteller, director of the study.
“But more importantly” continues “was the discovery that this gene regulates tau protein. Perhaps therefore the accumulation of tau protein produced in the brain of patients with Alzheimer results from DUSP22 epigenetic inactivation”. DUSP22 is a dual-specific phosphatase that inhibits PKA and thereby determines tau phosphorylation status.
According Esteller “the finding is relevant not only to determine the causes of the disease, but also to test potential treatments in the future to act on these epigenetic molecular switches”. Currently there is no effective drug treatment for this neurodegenerative condition, existing drugs only slow the progress of the disease.
IDIBELL is a foundation created in 2004 from the merger of several research entities. The centre manages the research of the Bellvitge University Hospital, the Institut Català d’Oncologia (Catalan Institute of Oncology) and the University of Barcelona.
Researchers from Lleida University (UdL) obtained pork meat with a lower proportion of saturated fat and a higher content in monounsaturated fatty acids. This meat is healthier, but it has also better organoleptic properties. Researchers from the School of Agrifood and Forestry Science and Engineering (ETSEA) identified a genetic variant in the promoter of the stearoyl-CoA desaturase gene, responsible for the conversion of stearic acid, a saturated fatty acid, into oleic acid, a monounsaturated one. The presence of this variant in the promoter enhances the fat desaturation activity of the enzyme. This also increases the levels of palmitoleic acid in intramuscular fat.
The use of this genetic variant in commercial genetic improvement programmes is under a protection process. At present, these results have been published in the open access journal Plos One.
The Unit of Pig Genetic Improvement of ETSEA has been working for 12 years in the improvement of Duroc pork meat, which is characterized by a high degree of fat infiltration. For this reason, Duroc pork meat is very appreciated to elaborate high quality cured products. The effect of the reported genetic variant has been observed in pigs from all controlled generations since 2001, even when they were bred in different farms or fed different diets.