3,676 research outputs found

    Can economic rationality explain the feminization of shareholding? Evidence from female shareholders in Spain (1918-1948)

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    Our results reinforce the thesis that the presence of women investors was not only pioneering by developed economies but was rather a reflection of a deeper phenomenon associated with institutions and modernization. We examine the feminization of shareholding employing data from Spanish commercial banks (1918-1948). We build a unique dataset of more than 30.000 women shareholders who took the opportunity to invest in stocks in well-established banks, drawn by the potential economic profitability. Family ties played a crucial role in explaining the presence of women and – specially – men shareholders. The profile of women differs from that of men in terms of their portfolio size, and volatility. Evidence indicates that the feminization of shareholding was a sing of modernization, not a cycle derived from a sternal shock. This paper aims to contribute to the current debate on gender financial gap, tracing women investors in assets and their rational behavior

    Evaluation of neuroinflammation as modulator of tau aggregation in response to repetitive mild traumatic brain injury

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    The pathological misfolding and aggregation of hyper-phosphorylated tau (ptau) protein in neurofibrillary tangles (NFTs) is the main hallmark of a group of neurodegenerative diseases called tauopathies. These include important disorders such as Alzheimer’s Disease (AD) and chronic traumatic encephalopathy (CTE). Mounting evidence supports that the aggregation and deposition of misfolded proteins is an early event in the development of AD and CTE. Several studies uphold traumatic brain injury (TBI) as an important risk factor for both disorders, since there is a relationship between TBI severity and frequency, and the vulnerability to develop dementia. Importantly, individuals affected by TBI show elevated levels of ptau in cerebrospinal fluid and NFTs in specific brain areas. Although previous studies on tau mice subjected to TBI show increased ptau burden, the mechanisms underlying this phenomenon have not been explored. Besides, previous research neither recapitulate the effects of repetitive mild TBI (rmTBI), reported to lead to long-lasting neurological consequences. Acute and chronic inflammation are intimately associated to TBI events, but its role on tau aggregation over time remains unknown. Here, we analyze the neuroinflammatory response, at both short- and long-term, in transgenic tau mice after rmTBI. Our data suggest that rmTBI triggers microglia and astroglia activation and that they may be involved in the increase observed on tau pathology in concussed mice. This could indicate that neuroinflammation could have an active role in the increased risk to develop tauopathies after brain concussion.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

    Late-life depression is able to accelerate learning and memory impairment in a mouse model of Alzheimer´s disease

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    Clinical studies suggest that depression could be considered an important risk factor for the future development of cognitive impairment and Alzheimer's disease (AD). In fact, there is a strong association between late-life depression and AD. The age of AD onset has been shown to be accelerated in patients with mild cognitive impairment (MCI) with a history of depression, and women appear to be particularly more vulnerable to this condition. In addition, individuals with MCI who present depressive symptoms have an elevated burden of amyloid-beta (Aβ), the main toxic protein associated with Alzheimer's pathology, and a higher risk of developing AD compared to non-depressed MCI patients. Although it has been described that some transgenic models of AD can develop signs similar to depression in advanced stages, the induction of Alzheimer's pathology due to a depressive process has not been studied under experimental conditions to emulate late-life depression as a risk factor for AD. The objective of this study is to determine, by inducing unpredictable mild chronic stress (CUMS) in tau transgenic P301S mice, whether depression is a cause, rather than a consequence, of AD development. The results of our study indicate that the induction of CUMS in transgenic animals induces phenotypic changes related to a depressive state. Behavioral and histological studies suggest that depression-like induction can worse AD pathology. The findings generated in this project could provide evidence of depression as a risk factor for AD

    SARS-CoV-2 infection in children with cystic fibrosis: A cross-sectional multicenter study in Spain. New waves, new knowledge

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    COVID-19; Pediatria; VacunacióCOVID-19; Pediatría; VacunaciónCOVID-19; Pediatrics; VaccinationIntroduction The association between viral infections and pulmonary exacerbations in children with cystic fibrosis (cwCF) is well established. However, the question of whether cwCF are at a higher risk of COVID-19 or its adverse consequences remains controversial. Methods We conducted an observational, multicenter, cross-sectional study of cwCF infected by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) between March 2020 and June 2022, (first to sixth COVID-19 pandemic waves) in Spain. The study aimed to describe patients' basal characteristics, SARS-CoV-2 clinical manifestations and outcomes, and whether there were differences across the pandemic waves. Results During study time, 351 SARS-CoV2 infections were reported among 341 cwCF. Median age was 8.5 years (range 0–17) and 51% were female. Cases were unevenly distributed across the pandemic, with most cases (82%) clustered between November 2021 and June 2022 (sixth wave, also known as Omicron Wave due to the higher prevalence of this strain in that period in Spain). Most cwCF were asymptomatic (24.8%) or presented with mild Covid-19 symptoms (72.9%). Among symptomatic, most prevalent symptoms were fever (62%) and increased cough (53%). Infection occurring along the sixth wave was the only independent risk factor for being symptomatic. Just eight cwCF needed hospital admission. No multisystem inflammatory syndrome, persisting symptoms, long-term sequelae, or deaths were reported. Conclusions Spanish current data indicate that cwCF do not experience higher risks of SARS-CoV-2 infection nor worse health outcomes or sequelae. Changes in patients' basal characteristics, clinical courses, and outcomes were detected across waves. While the pandemic continues, a worldwide monitoring of COVID-19 in pediatric CF patients is needed

    Crosslinked electrospun zein-based food packaging coatings containing bioactive chilto fruit extracts

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    peer-reviewedIn this work, zein fibers loaded with phenolic-enriched extracts from pulp, seed and skin of orange chilto were collected on polyhydroxyalkanoate (PHA) films through the electrospinning technique, for their potential use as bioactive internal coatings for food packaging applications. The zein fibers were characterized by scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy and thermogravimetric analysis (TGA). The water stability of the zein fibers was improved by crosslinking with glutaraldehyde vapors. The encapsulation efficiency of all bioactive phenolic-enriched extracts was greater than 90%. Encapsulation in the zein fibers improved the thermostability of the extracts. Two food simulants (50% ethanol and 3% acetic acid) were used to evaluate the release of the extracts from the crosslinked zein fibers. It was observed that crosslinking delayed the release of phenolic compounds (rosmarinic acid, caffeic acid and its derivates) in both solvents (80% released after 7 days of contact in 50% ethanol and 23 days in 3% acetic acid) and their antioxidant properties were kept. Therefore, this work demonstrates the potential of the developed zein-based encapsulation structures containing chilto extracts to be applied as antioxidant coatings in food packaging structures to contribute to the preservation of both hydrophilic and lipophilic food products

    Susceptibility patterns and molecular identification of Trichosporon species

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    The physiological patterns, the sequence polymorphisms of the internal transcriber spacer (ITS), and intergenic spacer regions (IGS) of the rRNA genes and the antifungal susceptibility profile were evaluated for their ability to identify Trichosporon spp. and their specificity for the identification of 49 clinical isolates of Trichosporon spp. Morphological and biochemical methodologies were unable to differentiate among the Trichosporon species. ITS sequencing was also unable to differentiate several species. However, IGS1 sequencing unambiguously identified all Trichosporon isolates. Following the results of DNA-based identification, Trichosporon asahii was the species most frequently isolated from deep sites (15 of 25 strains; 60%). In the main, other Trichosporon species were recovered from cutaneous samples. The majority of T. asahii, T. faecale, and T. coremiiforme clinical isolates exhibited resistance in vitro to amphotericin B, with geometric mean (GM) MICs >4 mug/ml. The other species of Trichosporon did not show high MICs of amphotericin B, and GM MICs were <1 mug/ml. Azole agents were active in vitro against the majority of clinical strains. The most potent compound in vitro was voriconazole, with a GM MIC </=0.14 mug/ml. The sequencing of IGS correctly identified Trichosporon isolates; however, this technique is not available in many clinical laboratories, and strains should be dispatched to reference centers where these complex methods are available. Therefore, it seems to be more practical to perform antifungal susceptibility testing of all isolates belonging to Trichosporon spp., since correct identification could take several weeks, delaying the indication of an antifungal agent which exhibits activity against the infectious strain.S

    Lung ultrasound as a translational approach for non-invasive assessment of heart failure with reduced or preserved ejection fraction in mice

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    Aims: Heart failure (HF) has become an epidemic and constitutes a major medical, social, and economic problem worldwide. Despite advances in medical treatment, HF prognosis remains poor. The development of efficient therapies is hampered by the lack of appropriate animal models in which HF can be reliably determined, particularly in mice. The development of HF in mice is often assumed based on the presence of cardiac dysfunction, but HF itself is seldom proved. Lung ultrasound (LUS) has become a helpful tool for lung congestion assessment in patients at all stages of HF. We aimed to apply this non-invasive imaging tool to evaluate HF in mouse models of both systolic and diastolic dysfunction. Methods and results: We used LUS to study HF in a mouse model of systolic dysfunction, dilated cardiomyopathy, and in a mouse model of diastolic dysfunction, diabetic cardiomyopathy. LUS proved to be a reliable and reproducible tool to detect pulmonary congestion in mice. The combination of LUS and echocardiography allowed discriminating those mice that develop HF from those that do not, even in the presence of evident cardiac dysfunction. The study showed that LUS can be used to identify the onset of HF decompensation and to evaluate the efficacy of therapies for this syndrome. Conclusions: This novel approach in mouse models of cardiac disease enables for the first time to adequately diagnose HF non-invasively in mice with preserved or reduced ejection fraction, and will pave the way to a better understanding of HF and to the development of new therapeutic approaches.This study was supported by grants from the Spanish Ministerio de Economia y Competitividad (SAF2015-65722-R), Comunidad Autonoma de Madrid (2010-BMD2321, FIBROTEAM Consortium), European Union's FP7 (CardioNeT-ITN-289600, CardioNext-ITN-608027) and the Spanish Instituto de Salud Carlos III (CPII14/00027 to E.L-P, RD12/0042/0054 to B.I. and RD12/0042/066 to P.G.-P. and E.L-P). This work was also supported by the Plan Estatal de I+D+I 2013-2016 - European Regional Development Fund (FEDER) "A way of making Europe", Spain. The CNIC is supported by the Ministry of Economy, Industry and Competitiveness (MINECO) and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (MINECO award SEV-2015-0505).S

    Nrf2 Activation Provides Atheroprotection in Diabetic Mice Through Concerted Upregulation of Antioxidant, Anti-inflammatory, and Autophagy Mechanisms

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    Interactive relationships between metabolism, inflammation, oxidative stress, and autophagy in the vascular system play a key role in the pathogenesis of diabetic cardiovascular disease. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a stress-sensitive guarantor of cellular homeostasis, which cytoprotective contributions extend beyond the antioxidant defense. We investigated the beneficial effects and underlying mechanisms of the Nrf2 inducer tert-butyl hydroquinone (tBHQ) on diabetes-driven atherosclerosis. In the experimental model of streptozotocin-induced diabetes in apolipoprotein E-deficient mice, treatment with tBHQ increased Nrf2 activity in macrophages and vascular smooth muscle cells within atherosclerotic lesions. Moreover, tBHQ significantly decreased the size, extension and lipid content of atheroma plaques, and attenuated inflammation by reducing lesional macrophages (total number and M1/M2 phenotype balance), foam cell size and chemokine expression. Atheroprotection was accompanied by both systemic and local antioxidant effects, characterized by lower levels of superoxide anion and oxidative DNA marker 8-hydroxy-2′-deoxyguanosine, reduced expression of NADPH oxidase subunits, and increased antioxidant capacity. Interestingly, tBHQ treatment upregulated the gene and protein expression of autophagy-related molecules and also enhanced autophagic flux in diabetic mouse aorta. In vitro, Nrf2 activation by tBHQ suppressed cytokine-induced expression of pro-inflammatory and oxidative stress genes, altered macrophage phenotypes, and promoted autophagic activity. Our results reinforce pharmacological Nrf2 activation as a promising atheroprotective approach in diabetes, according to the plethora of cytoprotective mechanisms involved in the resolution of inflammation and oxidative stress, and restoring autophagy

    Targeting nf-κb by the cell-permeable nemo-binding domain peptide improves albuminuria and renal lesions in an experimental model of type 2 diabetic nephropathy

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    Diabetic nephropathy (DN) is a multifactorial disease characterized by hyperglycemia and close interaction of hemodynamic, metabolic and inflammatory factors. Nuclear factor-κB (NF-κB) is a principal matchmaker linking hyperglycemia and inflammation. The present work investigates the cell-permeable peptide containing the inhibitor of kappa B kinase γ (IKKγ)/NF-κB essential modulator (NEMO)-binding domain (NBD) as therapeutic option to modulate inflammation in a preclinical model of type 2 diabetes (T2D) with DN. Black and tan, brachyuric obese/obese mice were randomized into 4 interventions groups: Active NBD peptide (10 and 6 µg/g body weight); Inactive mutant peptide (10 µg/g); and vehicle control. In vivo/ex vivo fluorescence imaging revealed efficient delivery of NBD peptide, systemic biodistribution and selective renal metabolization. In vivo administration of active NBD peptide improved albuminuria (&gt;40% reduction on average) and kidney damage, decreased podocyte loss and basement membrane thickness, and modulated the expression of proinflammatory and oxidative stress markers. In vitro, NBD blocked IKK-mediated NF-κB induction and target gene expression in mesangial cells exposed to diabetic-like milieu. These results constitute the first nephroprotective effect of NBD peptide in a T2D mouse model that recapitulates the kidney lesions observed in DN patients. Targeting IKK-dependent NF-κB activation could be a therapeutic strategy to combat kidney inflammation in DN.This work was supported by grants from: Fondecyt Project No 1160465 to S.M. and PhD CONICYT Grant No 21150768 to L.O-R.; Spanish Ministry of Economy and Competitiveness (MINECO/FEDER; SAF2015-63696-R to C.G-G.), Ministry of Science and Innovation (MICINN/FEDER; RTI2018-098788-B-1I00 to C.G-G.) and Instituto de Salud Carlos III (FIS/FEDER; PI17/01495 and DTS-2017/00203 to J.E.

    Growth response of Saccharomyces cerevisiae strains to stressors associated to the vine cycle

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    Saccharomyces cerevisiae isolates from grapes, soil, vine bark and buds collected at seven phenological stages of an annual growth cycle, were molecular typed by Microsatellite Multiplex PCR. Subsequently 30 S. cerevisiae genotypes were selected and the effect of vineyard environmental stressors, in both sublethal upper and lower levels, on their growth parameters was evaluated. The effect of low and high temperature (7–40 ◦C), pH (2.5–8.0), glucose concentration (3.0–300.0 g/L), nitrogen concentration (0.008–8.0 g/L), and copper presence (24 mg/L) were modelled individually using the reparametrized Gompertz equation. Multivariate ANOVA and Generalized Procrustes Analysis were used to determine the environmental stressor’s influence over the lag phase (λ) and the maximum specific growth rate (μmax). Both parameters were significantly affected by the S. cerevisiae genotype, the treatments, and the interaction between them. Despite a generalized reduction in μmax and a variable answer in λ, the 30 S. cerevisiae genotypes were able to overcome all the treatments. Extreme glucose limitation, copper presence and low temperature had the highest impact over the growth parameters. Interestingly, ten genotypes mostly distributed in the vineyard were the least affected, suggesting a greater acclimatization fitness and the possibility to persist in the changing conditions of the vine annual cycle.EEA MendozaFil: Gonzalez, Magali Lucia Rosa. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Gonzalez, Magali Lucia Rosa. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Mendoza; ArgentinaFil: Valero, Eva. Universidad Pablo de Olavide. Departamento de Biología Molecular e Ingeniería Bioquímica; EspañaFil: Chimeno, Selva Valeria. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Mendoza; ArgentinaFil: Garrido Fernandez, Antonio. Universidad Pablo de Olavide. Departamento de Biotecnología de Alimentos, Instituto de la Grasa (IG); España. Consejo Superior de Investigaciones Científicas (CSIC); EspañaFil: Rodriguez Gomez, Francisco. Universidad Pablo de Olavide. Departamento de Biotecnología de Alimentos, Instituto de la Grasa (IG); España. Consejo Superior de Investigaciones Científicas (CSIC); EspañaFil: Rojo, Cecilia. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Mendoza; ArgentinaFil: Rojo, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Paolinelli, Marcos. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Mendoza; ArgentinaFil: Arroyo Lopez, Francisco Noe. Universidad Pablo de Olavide. Departamento de Biotecnología de Alimentos, Instituto de la Grasa (IG); España. Consejo Superior de Investigaciones Científicas (CSIC); EspañaFil: Combina, Mariana. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Mendoza; ArgentinaFil: Mercado, Laura Analia. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Mendoza; Argentin
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