734 research outputs found

    Validation of the CAchexia SCOre (CASCO). Staging cancer patients: The use of miniCASCO as a simplified tool

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    The CAchexia SCOre (CASCO) was described as a tool for the staging of cachectic cancer patients. The aim of this study is to show the metric properties of CASCO in order to classify cachectic cancer patients into three different groups, which are associated with a numerical scoring. The final aim was to clinically validate CASCO for its use in the classification of cachectic cancer patients in clinical practice. We carried out a case -control study that enrolled prospectively 186 cancer patients and 95 age-matched controls. The score includes five components: (1) body weight loss and composition, (2) inflammation/metabolic disturbances/immunosuppression, (3) physical performance, (4) anorexia, and (5) quality of life. The present study provides clinical validation for the use of the score. In order to show the metric properties of CASCO, three different groups of cachectic cancer patients were established according to the results obtained with the statistical approach used: mild cachexia (15 â\u89¤ Ã\u97 â\u89¤ 28), moderate cachexia (29 â\u89¤ Ã\u97 â\u89¤ 46), and severe cachexia (47 â\u89¤ Ã\u97 â\u89¤ 100). In addition, a simplified version of CASCO, MiniCASCO (MCASCO), was also presented and it contributes as a valid and easy-to-use tool for cachexia staging. Significant statistically correlations were found between CASCO and other validated indexes such as Eastern Cooperative Oncology Group (ECOG) and the subjective diagnosis of cachexia by specialized oncologists. A very significant estimated correlation between CASCO and MCASCO was found that suggests that MCASCO might constitute an easy and valid tool for the staging of the cachectic cancer patients. CASCO and MCASCO provide a new tool for the quantitative staging of cachectic cancer patients with a clear advantage over previous classifications

    Xanthomonas prunicola sp. nov., a novel pathogen that affects nectarine (Prunus persica var. nectarina) trees

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    Three isolates obtained from symptomatic nectarine trees (Prunus persica var. nectarina) cultivated in Murcia, Spain, which showed yellow and mucoid colonies similar to Xanthomonas arboricola pv. pruni, were negative after serological and real-time PCR analyses for this pathogen. For that reason, these isolates were characterized following a polyphasic approach that included both phenotypic and genomic methods. By sequence analysis of the 16S rRNA gene, these novel strains were identified as members of the genus Xanthomonas, and by multilocus sequence analysis (MLSA) they were clustered together in a distinct group that showed similarity values below 95 % with the rest of the species of this genus. Whole-genome comparisons of the average nucleotide identity (ANI) of genomes of the strains showed less than 91 % average nucleotide identity with all other species of the genus Xanthomonas. Additionally, phenotypic characterization based on API 20 NE, API 50 CH and BIOLOG tests differentiated the strains from the species of the genus Xanthomonas described previously. Moreover, the three strains were confirmed to be pathogenic on peach (Prunus persica), causing necrotic lesions on leaves. On the basis of these results, the novel strains represent a novel species of the genus Xanthomonas, for which the name Xanthomonas prunicola is proposed. The type strain is CFBP 8353 (=CECT 9404=IVIA 3287.1)

    Nuclear Tracks Morphology Study Using Raman Methodology

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    In this work, a new methodology for rendering profiles of etched nuclear tracks is presented, using confocal micro-Raman spectrometry instrumentation. The precise profile of etched nuclear tracks with normal and/or angular incidence of the particle can be determined in few minutes, with a great visual and numerical resolution, that means a quantitative and qualitative simultaneous chemical and morphology characterization with the Raman technique. The Raman image routine is designed to acquire at each image pixel a complete Raman spectrum. This is a mapping of the functional groups that form the polymeric structure, which may be broken by the damage caused by the incident radiation and/or the etching process

    Improvement of lifetime in the power electronic drive of a BLDCM through the optimization of Fuzzy Logic Control

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    [EN] Power electronics elements lifetime in BLDCM drives can be affected due to power losses by conduction and switching during their operation. These losses normally aren´t consider in the design of controller, hence the controller lifetime is reduced or generate early failures. In this work, a fuzzy controller optimization through of PSO algorithm is proposed, this controller design considers the semiconductors temperature and the speed of BLDCM, it allows to increase power electronics lifetime at the same time that the speed desired is achieved. Finally, The Fuzzy-PSO controller results are compared with a PID conventional controller and Fuzzy conventional controller. These results are superior in comparison to conventional controllers since increase the power electronics lifetime and reach the speed set point. Additionally, the co-simulation as a methodology that allows to design, to implement and to validate prototypes in a reliable way. In this co-simulation the power electronics devices, the BLDCM and the controller proposed were designed in MultisimTM and LabVIEWTM from National Instrument (NI).[ES] El tiempo de vida útil en los elementos de electrónica de potencia en accionamientos eléctricos para motores de corriente directa sin escobillas BLDCM (por sus siglas en inglés Brushless Direct Current Motor), pueden verse afectados debido a las pérdidas por conmutación y conducción que aparecen durante su operación. Estas pérdidas normalmente no se considerarán en el diseño del controlador, por lo que su vida útil disminuye drásticamente o genera fallas prematuramente. El presente trabajo propone la optimización de un controlador difuso mediante el algoritmo PSO (por sus siglas en inglés Particle Swarm Optimization), este diseño considera la temperatura en los semiconductores y la velocidad mecánica del BLDCM, lo que permite incrementar la vida útil de los semiconductores utilizados en los módulos de electrónica de potencia, al mismo tiempo que alcanza la velocidad de referencia asignada. Finalmente, los resultados del controlador difuso optimizado (Difuso-PSO) propuesto se comparan con un controlador proporcional, derivativo e integral (PID) convencional, y un controlador difuso convencional. Estos resultados muestran ser superiores en comparación a los controladores convencionales, ya que incrementan el tiempo de vida de los semiconductores y alcanzan las velocidades de referencia establecidas. Adicionalmente, se emplea la co-simulación como una herramienta que permite diseñar, implementar y validar los resultados de manera confiable. En esta co-simulación la electrónica de potencia, el BLDCM y el controlador propuesto fueron diseñados en MultisimTM y LabVIEWTM de National Instrument (NI).Esta investigación es un producto del proyecto 266632 “Laboratorio Binacional para la Gestión Inteligente de la Sustentabilidad Energética y la Formación Tecnológica” financiado a través de Fondo CONACYT SENER de Sustentabilidad Energética (S0019201401).Garcia Lopez, M.; Ponce, P.; Soriano, LA.; Molina, A.; Rodriguez, JJ. (2018). Mejora de la Vida Útil en los Módulos de Electrónica de Potencia de un BLDCM Mediante la Optimización de un Control Difuso. Revista Iberoamericana de Automática e Informática. 16(1):66-78. https://doi.org/10.4995/riai.2018.9078SWORD667816

    Amyloid-β reduces the expression of neuronal FAIM-L, thereby shifting the inflammatory response mediated by TNFα from neuronal protection to death

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    The brains of patients with Alzheimer’s disease (AD) present elevated levels of tumor necrosis factor-α (TNFα), a cytokine that has a dual function in neuronal cells. On one hand, TNFα can activate neuronal apoptosis, and on the other hand, it can protect these cells against amyloid-β (Aβ) toxicity. Given the dual behavior of this molecule, there is some controversy regarding its contribution to the pathogenesis of AD. Here we examined the relevance of the long form of Fas apoptotic inhibitory molecule (FAIM) protein, FAIM-L, in regulating the dual function of TNFα. We detected that FAIM-L was reduced in the hippocampi of patients with AD. We also observed that the entorhinal and hippocampal cortex of a mouse model of AD (PS1M146LxAPP751sl) showed a reduction in this protein before the onset of neurodegeneration. Notably, cultured neurons treated with the cortical soluble fractions of these animals showed a decrease in endogenous FAIM-L, an effect that is mimicked by the treatment with Aβ-derived diffusible ligands (ADDLs). The reduction in the expression of FAIM-L is associated with the progression of the neurodegeneration by changing the inflammatory response mediated by TNFα in neurons. In this sense, we also demonstrate that the protection afforded by TNFα against Aβ toxicity ceases when endogenous FAIM-L is reduced by short hairpin RNA (shRNA) or by treatment with ADDLs. All together, these results support the notion that levels of FAIM-L contribute to determine the protective or deleterious effect of TNFα in neuronal cells

    A Molecular Platinum Cluster Junction: A Single-Molecule Switch

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    We present a theoretical study of the electronic transport through single-molecule junctions incorporating a Pt6 metal cluster bound within an organic framework. We show that the insertion of this molecule between a pair of electrodes leads to a fully atomically engineered nano-metallic device with high conductance at the Fermi level and two sequential high on/off switching states. The origin of this property can be traced back to the existence of a HOMO which consists of two degenerate and asymmetric orbitals, lying close in energy to the Fermi level of the metallic leads. Their degeneracy is broken when the molecule is contacted to the leads, giving rise to two resonances which become pinned close to the Fermi level and display destructive interference.Comment: 4 pages, 4 figures. Reprinted (adapted) with permission from J. Am. Chem. Soc., 2013, 135 (6), 2052. Copyright 2013 American Chemical Societ

    Adipose atrophy in cancer cachexia:morphologic and molecular analysis of adipose tissue in tumour-bearing mice

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    Extensive loss of adipose tissue is a hallmark of cancer cachexia but the cellular and molecular basis remains unclear. This study has examined morphologic and molecular characteristics of white adipose tissue in mice bearing a cachexia-inducing tumour, MAC16. Adipose tissue from tumour-bearing mice contained shrunken adipocytes that were heterogeneous in size. Increased fibrosis was evident by strong collagen-fibril staining in the tissue matrix. Ultrastructure of 'slimmed' adipocytes revealed severe delipidation and modifications in cell membrane conformation. There were major reductions in mRNA levels of adipogenic transcription factors including CCAAT/enhancer binding protein alpha (C/EBPα), CCAAT/enhancer binding protein beta, peroxisome proliferator-activated receptor gamma, and sterol regulatory element binding protein-1c (SREBP-1c) in adipose tissue, which was accompanied by reduced protein content of C/EBPα and SREBP-1. mRNA levels of SREBP-1c targets, fatty acid synthase, acetyl CoA carboxylase, stearoyl CoA desaturase 1 and glycerol-3-phosphate acyl transferase, also fell as did glucose transporter-4 and leptin. In contrast, mRNA levels of peroxisome proliferators-activated receptor gamma coactivator-1alpha and uncoupling protein-2 were increased in white fat of tumour-bearing mice. These results suggest that the tumour-induced impairment in the formation and lipid storing capacity of adipose tissue occurs in mice with cancer cachexia. © 2006 Cancer Research UK

    Dynamic fronto-amygdalar interactions underlying emotion-regulation deficits in women at higher weight

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    Objective: The regulation of negative emotions entails the modulation of subcortical regions, such as the amygdala, by prefrontal regions. There is preliminary evidence suggesting that individuals at higher weight may present with hypoactivity in prefrontal regulatory systems during emotional regulation, although the directionality of these pathways has not been tested. In this study, we compared fronto-amygdalar effective connectivity during cognitive reappraisal as a function of BMI in 48 adult women with obesity and 54 control participants. Methods: Dynamic causal modeling and parametric empirical Bayes were used to map effective connectivity between the dorsomedial prefrontal cortex, orbitofrontal cortex, dorsolateral prefrontal cortex, and the amygdala. Results: Difficulty in Emotion Regulation Scale scores were higher in the obesity group compared with control participants (p < 0.001). A top-down cortical model best explained our functional magnetic resonance imaging data (posterior probability = 86%). Participants at higher BMI were less effective at inhibiting activity in the amygdala via the orbitofrontal cortex and dorsomedial prefrontal cortex during reappraisal compared with those at lower BMI. In contrast, increased excitatory modulation of dorsolateral prefrontal cortex-to-amygdalar connectivity was found in participants at lower BMI. Conclusions: These findings support a framework involving alterations in fronto-amygdalar connectivity contributing to difficulties in regulating negative affect in individuals at higher weight
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