60 research outputs found

    Hierarchical Color Quantization with a Neural Gas Model Based on Bregman Divergences

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    In this paper, a new color quantization method based on a self-organized artificial neural network called the Growing Hierarchical Bregman Neural Gas (GHBNG) is proposed. This neural network is based on Bregman divergences, from which the squared Euclidean distance is a particular case. Thus, the best suitable Bregman divergence for color quantization can be selected according to the input data. Moreover, the GHBNG yields a tree-structured model that represents the input data so that a hierarchical color quantization can be obtained, where each layer of the hierarchy contains a different color quantization of the original image. Experimental results confirm the color quantization capabilities of this approach.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

    Prospective multicenter study of carbapenemase-producing Enterobacteriaceae from 83 hospitals in Spain reveals high in vitro susceptibility to colistin and meropenem

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    The aim of this study was to determine the impact of carbapenemase-producing Enterobacteriaceae (CPE) in Spain in 2013 by describing the prevalence, dissemination, and geographic distribution of CPE clones, and their population structure and antibi- otic susceptibility. From February 2013 to May 2013, 83 hospitals (about 40,000 hospital beds) prospectively collected nondupli- cate Enterobacteriaceae using the screening cutoff recommended by EUCAST. Carbapenemase characterization was performed by phenotypic methods and confirmed by PCR and sequencing. Multilocus sequencing types (MLST) were determined for Kleb- siella pneumoniae and Escherichia coli. A total of 702 Enterobacteriaceae isolates met the inclusion criteria; 379 (54%) were CPE. OXA-48 (71.5%) and VIM-1 (25.3%) were the most frequent carbapenemases, and K. pneumoniae (74.4%), Enterobacter cloacae (10.3%), and E. coli (8.4%) were the species most affected. Susceptibility to colistin, amikacin, and meropenem was 95.5%, 81.3%, and 74.7%, respectively. The most prevalent sequence types (STs) were ST11 and ST405 for K. pneumoniae and ST131 for E. coli. Forty-five (54.1%) of the hospitals had at least one CPE case. For K. pneumoniae, ST11/OXA-48, ST15/OXA-48, ST405/ OXA-48, and ST11/VIM-1 were detected in two or more Spanish provinces. ST11 isolates carried four carbapenemases (VIM-1, OXA-48, KPC-2, and OXA-245), but ST405 isolates carried OXA-48 only. A wide interregional spread of CPE in Spain was ob- served, mainly due to a few successful clones of OXA-48-producing K. pneumoniae (e.g., ST11 and ST405). The dissemination of OXA-48-producing E. coli is a new finding of public health concern. According to the susceptibilities determined in vitro, most of the CPE (94.5%) had three or more options for antibiotic treatment

    Prospective multicenter study of carbapenemase-producing Enterobacteriaceae from 83 hospitals in Spain reveals high in vitro susceptibility to colistin and meropenem

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    The aim of this study was to determine the impact of carbapenemase-producing Enterobacteriaceae (CPE) in Spain in 2013 by describing the prevalence, dissemination, and geographic distribution of CPE clones, and their population structure and antibiotic susceptibility. From February 2013 to May 2013, 83 hospitals (about 40,000 hospital beds) prospectively collected nonduplicate Enterobacteriaceae using the screening cutoff recommended by EUCAST. Carbapenemase characterization was performed by phenotypic methods and confirmed by PCR and sequencing. Multilocus sequencing types (MLST) were determined for Klebsiella pneumoniae and Escherichia coli. A total of 702 Enterobacteriaceae isolates met the inclusion criteria; 379 (54%) were CPE. OXA-48 (71.5%) and VIM-1 (25.3%) were the most frequent carbapenemases, and K. pneumoniae (74.4%), Enterobacter cloacae (10.3%), and E. coli (8.4%) were the species most affected. Susceptibility to colistin, amikacin, and meropenem was 95.5%, 81.3%, and 74.7%, respectively. The most prevalent sequence types (STs) were ST11 and ST405 for K. pneumoniae and ST131 for E. coli. Forty-five (54.1%) of the hospitals had at least one CPE case. For K. pneumoniae, ST11/OXA-48, ST15/OXA-48, ST405/OXA-48, and ST11/VIM-1 were detected in two or more Spanish provinces. ST11 isolates carried four carbapenemases (VIM-1, OXA-48, KPC-2, and OXA-245), but ST405 isolates carried OXA-48 only. A wide interregional spread of CPE in Spain was observed, mainly due to a few successful clones of OXA-48-producing K. pneumoniae (e.g., ST11 and ST405). The dissemination of OXA-48-producing E. coli is a new finding of public health concern. According to the susceptibilities determined in vitro, most of the CPE (94.5%) had three or more options for antibiotic treatment.This work was supported by a grant from the Fondo de Investigación Sanitaria (grant PI12/01242); the Antibiotic Resistance Surveillance Programme of the Spanish Centro Nacional de Microbiología, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad; the Plan Nacional de I+D+I 2008–2011; and the Instituto de Salud Carlos III, Subdirección General de Redes y Centros de Investigación Cooperativa, Ministerio de Economía y Competitividad, Spanish Network for Research in Infectious Diseases (REIPI RD12/0015), cofinanced by the European Development Regional Fund (ERDF) “A way to achieve Europe.”S

    A BAX/BAK and Cyclophilin D-Independent Intrinsic Apoptosis Pathway

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    Most intrinsic death signals converge into the activation of pro-apoptotic BCL-2 family members BAX and BAK at the mitochondria, resulting in the release of cytochrome c and apoptosome activation. Chronic endoplasmic reticulum (ER) stress leads to apoptosis through the upregulation of a subset of pro-apoptotic BH3-only proteins, activating BAX and BAK at the mitochondria. Here we provide evidence indicating that the full resistance of BAX and BAK double deficient (DKO) cells to ER stress is reverted by stimulation in combination with mild serum withdrawal. Cell death under these conditions was characterized by the appearance of classical apoptosis markers, caspase-9 activation, release of cytochrome c, and was inhibited by knocking down caspase-9, but insensitive to BCL-XL overexpression. Similarly, the resistance of BIM and PUMA double deficient cells to ER stress was reverted by mild serum withdrawal. Surprisingly, BAX/BAK-independent cell death did not require Cyclophilin D (CypD) expression, an important regulator of the mitochondrial permeability transition pore. Our results suggest the existence of an alternative intrinsic apoptosis pathway emerging from a cross talk between the ER and the mitochondria

    MEGARA, the new intermediate-resolution optical IFU and MOS for GTC: getting ready for the telescope

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    MEGARA (Multi-Espectrógrafo en GTC de Alta Resolución para Astronomía) is an optical Integral-Field Unit (IFU) and Multi-Object Spectrograph (MOS) designed for the GTC 10.4m telescope in La Palma that is being built by a Consortium led by UCM (Spain) that also includes INAOE (Mexico), IAA-CSIC (Spain), and UPM (Spain). The instrument is currently finishing AIV and will be sent to GTC on November 2016 for its on-sky commissioning on April 2017. The MEGARA IFU fiber bundle (LCB) covers 12.5x11.3 arcsec2 with a spaxel size of 0.62 arcsec while the MEGARA MOS mode allows observing up to 92 objects in a region of 3.5x3.5 arcmin2 around the IFU. The IFU and MOS modes of MEGARA will provide identical intermediate-to-high spectral resolutions (RFWHM~6,000, 12,000 and 18,700, respectively for the low-, mid- and high-resolution Volume Phase Holographic gratings) in the range 3700-9800ÅÅ. An x-y mechanism placed at the pseudo-slit position allows (1) exchanging between the two observing modes and (2) focusing the spectrograph for each VPH setup. The spectrograph is a collimator-camera system that has a total of 11 VPHs simultaneously available (out of the 18 VPHs designed and being built) that are placed in the pupil by means of a wheel and an insertion mechanism. The custom-made cryostat hosts a 4kx4k 15-μm CCD. The unique characteristics of MEGARA in terms of throughput and versatility and the unsurpassed collecting are of GTC make of this instrument the most efficient tool to date to analyze astrophysical objects at intermediate spectral resolutions. In these proceedings we present a summary of the instrument characteristics and the results from the AIV phase. All subsystems have been successfully integrated and the system-level AIV phase is progressing as expected

    CNS targets of adipokines

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    This is the author accepted manuscript. The final version is available from American Physiological Society via the DOI in this record.Our understanding of adipose tissue as an endocrine organ has been transformed over the last twenty years. During this time a number of adipocyte-derived factors or adipokines have been identified. This paper will review evidence for how adipokines acting via the central nervous system (CNS) regulate normal physiology and disease pathology. The reported CNS-mediated effects of adipokines are varied and include the regulation of energy homeostasis, autonomic nervous system activity, the reproductive axis, neurodevelopment, cardiovascular function, and cognition. Due to the wealth of information available and the diversity of their known functions, the archetypal adipokines leptin and adiponectin will be the focused on extensively. Other adipokines with established CNS actions will also be discussed. Due to the difficulties associated with studying CNS function on a molecular level in humans, the majority of our knowledge, and as such the studies described in this paper, comes from work in experimental animal models; however, where possible the relevant data from human studies are also highlighted

    Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

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    Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

    Identificación de biomarcadores en el ictus hemorrágico y su estudio funcional en modelos experimentales

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    La hemorragia intracerebral (HIC) se define como la extravasación de sangre al parénquima encefálico. Aunque la HIC presenta una elevada tasa de mortalidad y discapacidad, muchos de los mecanismos moleculares implicados en esta patología aún se desconocen. Su diagnóstico y pronóstico se basa en las pruebas de neuroimagen, siendo en ocasiones poco accesibles y específicas. Por ello, el objetivo principal de esta tesis se centra en la identificación de moléculas implicadas en la patología de la HIC que pudieran emplearse en mejorar las aproximaciones diagnósticas y terapéuticas de esta enfermedad. Por ello, la primera parte de la tesis se basó en encontrar biomarcadores de etiología de HIC primaria (arteriosclerosis hipertensiva y/o angiopatía amiloide cerebral (AAC), mediante el análisis transcriptómico de células sanguíneas. A pesar de que no fuimos capaces de identificar ningún biomarcador que diferenciara ambas etiologías, encontramos que la expresión del gen GOLGA8A (Golgin A8 Family, Member A), así como los niveles de la proteína en sangre, estaban incrementados en pacientes con HIC respecto a controles. En segundo lugar, nos centramos en identificar moléculas implicadas en una de las causas de HIC secundaria, como es la transformación hemorrágica (TH) en el ictus isquémico tras el tratamiento trombolítico. A pesar de la eficacia del Activador Tisular del Plasminógeno recombinante (r-tPA), el uso de esta terapia en el ictus isquémico agudo sigue limitado en parte por la estrecha ventana terapéutica y la presencia ocasional de hemorragias sintomáticas. Por ello, nuestro estudio in vitro se centró en la identificación masiva de transcritos expresados por el tratamiento con r-tPA en condiciones de privación de oxígeno y glucosa (POG) a nivel endotelial. Identificamos el factor de transcripción nuclear Nurr1 (NR4A2, del inglés Nuclear receptor subfamily 4 groupA member 2) como molécula implicada en la muerte celular y la inflamación. Además, pudimos establecer una asociación entre los niveles basales de Nurr1 séricos y la posterior aparición de TH sintomática en pacientes con ictus isquémico que habían recibido r-tPA. Por último, en un tercer estudio, evaluamos cómo las apolipoproteínas ApoJ y ApoA1 recombinantes humanas modulaban el transporte del péptido β–amiloide (1-40) a través de un modelo in vitro de barrera hematoencefálica, como posible aproximación terapéutica para la AAC. En resumen, consideramos que esta tesis doctoral contribuye a definir mejor la fisiopatología de la HIC, al desarrollo de posibles aplicaciones de diagnóstico y pronóstico de los pacientes que sufren hemorragias cerebrales, así como a proponer nuevas aproximaciones terapéuticas para diferentes subtipos de HIC.Intracerebral hemorrhage (ICH) is a focal bleeding from a blood vessel in the brain parenchyma. Despite the high ratio of ICH severity and mortality, the molecular mechanisms involved in this disease are still unknown. Therefore, the main objective of this thesis is focused on the identification of molecules involved in the pathology of the ICH that might be candidates for a better diagnosis, treatment and prognosis of the disease. Primary ICH is caused by hypertensive arteriosclerosis and/or cerebral amyloid angiopathy (CAA). The diagnosis and prognosis is based on neuroimaging criteria, but these techniques remain inaccessible and not enough specific. Therefore, our first study was based on the search of biomarkers of primary ICH etiology through the transcriptome analysis of blood cells using microarray technology. Although we were unable to identify biomarkers to differentiate between CAA associated-ICH and hypertensive associated-ICH, we found that GOLGA8A (Golgin A8 Family, Member A) gene expression and the corresponding plasma protein levels were increased in patients with ICH in comparison to controls. Secondly, we aimed to identify molecules involved in a cause of secondary ICH, such as the hemorrhagic transformation (HT) in the ischemic stroke after the thrombolytic therapy. Despite the effectiveness of recombinant tissue plasminogen activator (r-tPA), its therapeutic window remains limited, mainly by occasional vascular deleterious effects. Thus, we focused our study on the discovery of molecules altered by the combination of r-tPA and ischemic conditions in endothelial cells in vitro. We identified the nuclear transcription factor Nurr1 (NR4A2, Nuclear receptor subfamily 4 groupA member 2) as a candidate molecule involved in cell death and inflammation. In addition, we established an association between baseline serum levels of Nurr1 and the subsequent development of symptomatic HT in patients with ischemic stroke who received r-tPA. Finally, in a third study, we planned to determine the modulation of β-amyloid (Aβ) trafficking by the chaperones apolipoproteins ApoA1 and ApoJ across the BBB. In this regard, we confirmed that both recombinant human ApoA1 and ApoJ proteins influenced the Aβ(1-40) clearance through different mechanisms in a mouse in vitro BBB model. Our results suggest that the modulation of the balance of these apolipoproteins between the periphery and the brain may be a future strategy to develop an effective therapy for CAA. In summary, we consider that our studies contribute to the understanding of some mechanism involved in the ICH pathology and propose new preclinical and therapeutic approaches for different ICH subtypes
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