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Lezers, boeken en lectuur van een humanistenkring in de zestiende eeuw: Boekbestellingen door Arias Montano en zijn Sevilliaanse vrienden

  • Dávila Pérez, Antonio
Después de su salida de Amberes, Benito Arias Montano (ca. 1525/27-1598) mantuvo una frecuente correspondencia con la oficina tipográfica de Cristóbal Plantino. Las cartas no se limitaron a intercambiar noticias públicas y privadas; el teólogo español envió muy a menudo listas de títulos de libros que él o su cenáculo de humanistas sevillanos estaban interesados en comprar. Este artículo se centra en quince listas enviadas entre 1585 y 1596 y conservadas en el Museo Plantin-Moretus de Amberes. El autor no se limita a publicar una transcripción de los documentos, sino que también trata de identificar los títulos de los listados. En varios casos logra también encontrar información extra sobre el envío de los libros que realmente fueron comprados. Un análisis de estos listados arroja luz sobre los amplios intereses culturales y científicos de este grupo, así como sobre su situación socio-económica.

Evidence for a relationship between mitochondrial Complex I activity and mitochondrial aldehyde dehydrogenase during nitroglycerin tolerance: Effects of mitochondrial antioxidants

The medical use of nitroglycerin (GTN) is limited by patient tolerance. The present study evaluated the role of mitochondrial Complex I in GIN biotransformation and the therapeutic effect of mitochondrial antioxidants. The development of GIN tolerance (in rat and human vessels) produced a decrease in mitochondrial 02 consumption. Co-incubation with the mitochondria-targeted antioxidant mitoquinone (MQ 10(-6) mol/L) or with glutathione ester (GEE, 10(-4) mol/L) blocked GTN tolerance and the effects of GTN on mitochondrial respiration and aldehyde dehydrogenase 2 (ALDH-2) activity. Biotransformation of GTN depended on the mitochondria being functionally active, particularly mitochondrial Complex I. Tolerance induced mitochondrial ROS production and oxidative stress, though these effects were not detected in HUVEC rho(0) cells or Complex I mutant cells. Experiments performed to evaluate Complex I-dependent respiration demonstrated that its inhibition by GIN was prevented by the antioxidants in control samples. These results point to a key role for mitochondrial Complex I in the adequate functioning of ALDH-2. In addition, we have identified mitochondrial Complex I as one of the targets at which the initial oxidative stress responsible for GIN tolerance takes place. Our data also suggest a role for mitochondrial-antioxidants as therapeutic tools in the control of the tolerance that accompanies chronic nitrate use. (C) 2012 Elsevier B.V. All rights reserved.

The C-terminal region of the Hot1 transcription factor binds GGGACAAA-related sequences in the promoter of its target genes.

Response to hyperosmotic stress in the yeast Saccharomyces cerevisiae involves the participation of the general stress response mediated by Msn2/4 transcription factors and the HOG pathway. One of the transcription factors activated through this pathway is Hot1, which contributes to the control of the expression of several genes involved in glycerol synthesis and flux, or in other functions related to adaptation to adverse conditions. This work provides new data about the interaction mechanism of this transcription factor with DNA. By means of one-hybrid and electrophoretic mobility assays, we demonstrate that the C-terminal region, which corresponds to amino acids 610-719, is the DNA-binding domain of Hot1. We also describe how this domain recognizes sequence 5'-GGGACAAA-3' located in the promoter of gene STL1. The bioinformatics analysis carried out in this work allowed the identification of identical or similar sequences (with up to two mismatches) in the promoter of other Hot1 targets, where central element GGACA was quite conserved among them. Finally, we found that small variations in the sequence recognized by Hot1 may influence its ability to recognize its targets in vivo.

La localització de Facebook al sard

  • Beccu, Alessandro
  • Martín Mor, Adrià
Aquest article descriu l'experiència de localització de la plataforma Facebook a la llengua sarda. Atès que es tracta d'una llengua en procés d'estandardització, la localització de la xarxa social més gran del món representa una oportunitat per a la presència digital del sard, alhora que implica un repte en els plans organitzatiu i terminològic, com també pel que fa al procés d'estandardització., Custu artìculu contat s'esperièntzia de localizatzione de sa prataforma Facebook in limba sarda. Sigomente si tratat de una limba in fase de istandardizatzione, sa localizatzione de sa rete sotziale chi tenet prus membros in su mundu rapresentat un'oportunidade pro sa presèntzia digitale de su sardu, ma est fintzas unu disafiu pro su chi pertocat sa terminologia e su pranu organizativu e gasi etotu pro su protzessu de normalizatzione., This article describes the experience of localising the Facebook platform into Sardinian. Since this is a language in the process of being standardised, the localisation of the biggest social network in the world into Sardinian represents an opportunity to promote this minoritised language digitally. At the same time, this project also posed challenges from the perspectives of organisation, terminology not to mention the process of standardisation this language is undergoing., Este artículo describe la experiencia de localización de la plataforma Facebook a la lengua sarda. Dado que esta es una lengua en proceso de estandarización, la localización de la red social más grande del mundo representa una oportunidad para la presencia digital del sardo, a la vez que implica un reto en el plano organizativo y terminológico, así como en cuanto al proceso de estandarización.

Small heterodimer partner (SHP) contributes to insulin resistance in cardiomyocytes.

Small heterodimer partner (SHP) is an atypical nuclear receptor expressed in heart that has been shown to inhibit the hypertrophic response. Here, we assessed the role of SHP in cardiac metabolism and inflammation. Mice fed a high-fat diet (HFD) displayed glucose intolerance accompanied by increased cardiac mRNA levels of Shp. In HL-1 cardiomyocytes, SHP overexpression inhibited both basal and insulin-stimulated glucose uptake and impaired the insulin signalling pathway (evidenced by reduced AKT and AS160 phosphorylation), similar to insulin resistant cells generated by high palmitate/high insulin treatment (HP/HI; 500µM/100nM). In addition, SHP overexpression increased Socs3 mRNA and reduced IRS-1 protein levels. SHP overexpression also induced Cd36 expression (~6.2 fold; p0.001) linking to the observed intramyocellular lipid accumulation. SHP overexpressing cells further showed altered expression of genes involved in lipid metabolism, i.e., Acaca, Acadvl or Ucp3, augmented NF-?B DNA-binding activity and induced transcripts of inflammatory genes, i.e., Il6 and Tnf mRNA (~4-fold induction, p0.01). Alterations in metabolism and inflammation found in SHP overexpressing cells were associated with changes in the mRNA levels of Ppara (79% reduction, p0.001) and Pparg (~58-fold induction, p0.001). Finally, co-immunoprecipitation studies showed that SHP overexpression strongly reduced the physical interaction between PPARa and the p65 subunit of NF-?B, suggesting that dissociation of these two proteins is one of the mechanisms by which SHP initiates the inflammatory response in cardiac cells. Overall, our results suggest that SHP upregulation upon high-fat feeding leads to lipid accumulation, insulin resistance and inflammation in cardiomyocytes.

High-fat diet-induced deregulation of hippocampal insulin signaling and mitochondrial homeostasis deficiences contribute to Alzheimer disease pathology in rodents.

Global obesity is a pandemic status, estimated to affect over 2 billion people, that has resulted in an enormous strain on healthcare systems worldwide. The situation is compounded by the fact that apart from the direct costs associated with overweight pathology, obesity presents itself with a number of comorbidities, including an increased risk for the development of neurodegenerative disorders. Alzheimer disease (AD), the main cause of senile dementia, is no exception. Spectacular failure of the pharmaceutical industry to come up with effective AD treatment strategies is forcing the broader scientific community to rethink the underlying molecular mechanisms leading to cognitive decline. To this end, the emphasis is once again placed on the experimental animal models of the disease. In the current study, we have focused on the effects of a high-fat diet (HFD) on hippocampal-dependent memory in C57/Bl6 Wild-type (WT) and APPswe/PS1dE9 (APP/PS1) mice, a well-established mouse model of familial AD. Our results indicate that the continuous HFD administration starting at the time of weaning is sufficient to produce ß-amyloid-independent, hippocampal-dependent memory deficits measured by a 2-object novel-object recognition test (NOR) in mice as early as 6months of age. Furthermore, the resulting metabolic syndrome appears to have direct effects on brain insulin regulation and mitochondrial function. We have observed pathological changes related to both the proximal and distal insulin signaling pathway in the brains of HFD-fed WT and APP/PS1 mice. These changes are accompanied by a significantly reduced OXPHOS metabolism, suggesting that mitochondria play an important role in hippocampus-dependent memory formation and retention in both the HFD-treated and AD-like rodents at a relatively young age.

PPARß/d ameliorates fructose-induced insulin resistance in adipocytes by preventing Nrf2 activation.

We studied whether PPARß/d deficiency modifies the effects of high fructose intake (30% fructose in drinking water) on glucose tolerance and adipose tissue dysfunction, focusing on the CD36-dependent pathway that enhances adipose tissue inflammation and impairs insulin signaling. Fructose intake for 8 weeks significantly increased body and liver weight, and hepatic triglyceride accumulation in PPARß/d-deficient mice but not in wild-type mice. Feeding PPARß/d-deficient mice with fructose exacerbated glucose intolerance and led to macrophage infiltration, inflammation, enhanced mRNA and protein levels of CD36, and activation of the JNK pathway in white adipose tissue compared to those of water-fed PPARß/d-deficient mice. Cultured adipocytes exposed to fructose also exhibited increased CD36 protein levels and this increase was prevented by the PPARß/d activator GW501516. Interestingly, the levels of the nuclear factor E2-related factor 2 (Nrf2), a transcription factor reported to up-regulate Cd36 expression and to impair insulin signaling, were increased in fructose-exposed adipocytes whereas co-incubation with GW501516 abolished this increase. In agreement with Nrf2 playing a role in the fructose-induced CD36 protein level increases, the Nrf2 inhibitor trigonelline prevented the increase and the reduction in insulin-stimulated AKT phosphorylation caused by fructose in adipocytes. Protein levels of the well-known Nrf2 target gene

Interrelation of attention and prediction in visual processing: Effects of task-relevance and stimulus probability.

The potentially interactive influence of attention and prediction was investigated by measuring event-related potentials (ERPs) in a spatial cueing task with attention (task-relevant) and prediction (probabilistic) cues. We identified distinct processing stages of this interactive influence. Firstly, in line with the attentional gain hypothesis, a larger amplitude response of the contralateral N1, and Nd1 for attended gratings was observed. Secondly, conforming to the attenuation-by-prediction hypothesis, a smaller negativity in the time window directly following the peak of the N1 component for predicted compared to unpredicted gratings was observed. In line with the hypothesis that attention and prediction interface, unpredicted/unattended stimuli elicited a larger negativity at central-parietal sites, presumably reflecting an increased prediction error signal. Thirdly, larger P3 responses to unpredicted stimuli pointed to the updating of an internal model. Attention and prediction can be considered as differentiated mechanisms that may interact at different processing stages to optimise perception.

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