15 research outputs found

    PROCESSING SPEED DIFFERENCES BETWEEN SCHIZOPHRENIA AND SCHIZOAFFECTIVE DISORDER: A PILOT STUDY

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    We aimed to compare processing speed (PS) and its subcomponents in schizophrenia (SC) and schizoaffective disorder (SA). Thirty-five patients were divided into two groups (SC=18; SA=17). PS tasks from the MATRICS Consensus Cognitive Battery Central/South America version were used. Additional PS subcomponents were analyzed (i.e., behavioral execution, response processing, and accuracy). SA obtained significant higher scores than SC in response processing, verbal fluency and the PS general domain. Our results indicate that PS is a potential cognitive marker to differentiate between SC and SA. Further research with larger samples must be conducted

    Clinical Study Mammographic Breast Density Patterns in Asymptomatic Mexican Women

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    Breast density (BD) is a risk factor for breast cancer. Aims. To describe BD patterns in asymptomatic Mexican women and the pathological mammographic findings. Methods and Material. Prospective, descriptive, and comparative study. Women answered a questionnaire and their mammograms were analyzed according to BI-RADS. Univariate (χ 2 ) and conditional logistic regression analyses were performed. Results. In 300 women studied the BD patterns were fat 56.7% (170), fibroglandular 29% (87), heterogeneously dense 5.7% (17), and dense pattern 8.6% (26). Prevalence of fat pattern was significantly different in women under 50 years (37.6%, 44/117) and older than 50 (68.8%, 126/183). Patterns of high breast density (BD) (dense + heterogeneously dense) were observed in 25.6% (30/117) of women ≤50 years and 7.1% (13/183) of women >50. Asymmetry in BD was observed in 22% (66/300). Compression cone ruled out underlying disease in 56 cases. In the remaining 10, biopsy revealed one fibroadenoma, one complex cyst, and 6 invasive and 2 intraductal carcinomas. 2.6% (8/300) of patients had non-palpable carcinomas. Benign lesions were observed in 63.3% (190/300) of cases, vascular calcification in 150 cases (78.9%), and fat necrosis in 38 cases (20%). Conclusions. Mexican women have a low percentage of high-density patterns

    Epstein-Barr Virus Association with Peptic Ulcer Disease

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    Background. Helicobacter pylori (HP) infection and nonsteroidal anti-inflammatory drugs (NSAID) use are considered the main risk to develop peptic ulcer disease (PUD). However, PUD also occurs in the absence of HP infection and/or NSAID use. Recently, we have found evidence that Epstein-Barr virus (EBV) reactivation increases the risk to develop premalignant and malignant gastric lesions. Objective. To study a possible association between EBV and PUD. Methods. Antibodies against an EBV reactivation antigen, HP, and the HP virulence factor CagA were measured in sera from 207 Mexican subjects, controls (healthy individuals, n = 129), and PUD patients (n = 78, 58 duodenal and 20 gastric ulcers). Statistical associations were estimated. Results. Duodenal PUD was significantly associated with high anti-EBV IgG titers (p = 0.022, OR = 2.5), while anti-EBV IgA was positively associated with gastric PUD (p = 0.002, OR = 10.1). Conclusions. Our study suggests that EBV reactivation in gastric and duodenal epithelium increases the risk to develop PUD

    Osteopontin expression and localization of Ca2+ deposits in early stages of osteoarthritis in a rat model

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    Calcium deposits have been related to articular cartilage (AC) degeneration and have been observed in late stages of osteoarthritis (OA). However, the role of those deposits, whether they induce the OA pathogenesis or they appear as a consequence of such process, is still unknown. In this work, we present the kinetics of expression and tissue localisation of osteopontin (OPN), a mineralisation biomarker, and calcium deposits in samples from (normal, sham) and osteoarthritic cartilage (in a rat model). Immunohisto-chemical and Western blot assays for OPN, as well as Alizarin red staining for calcium deposits were performed; superficial, middle, and deep zones of AC were analysed. An increased expression of OPN and calcium deposits was found in the osteoarthritic cartilage compared with that of control groups, particularly in the superficial zone of AC in early stages of OA. In addition, the expression and localisation of OPN and calcium deposits during the OA pathogenesis suggest that the pathological AC mineralisation starts in the superficial zone during OA pathogenesis

    Rescue of Mitochondrial Function in Hutchinson-Gilford Progeria Syndrome by the Pharmacological Modulation of Exportin CRM1

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    Hutchinson-Gilford progeria syndrome (HGPS) is a rare premature aging disorder caused by the expression of progerin, a mutant variant of Lamin A. Recently, HGPS studies have gained relevance because unraveling its underlying mechanism would help to understand physiological aging. We previously reported that the CRM1-mediated nuclear protein export pathway is exacerbated in HGPS cells, provoking the mislocalization of numerous protein targets of CRM1. We showed that normalization of this mechanism by pharmacologically inhibiting CRM1 with LMB (specific CRM1 inhibitor), mitigates the senescent phenotype of HGPS cells. Since mitochondrial dysfunction is a hallmark of HGPS, in this study we analyze the effect of LMB on mitochondrial function. Remarkably, LMB treatment induced the recovery of mitochondrial function in HGPS cells, as shown by the improvement in mitochondrial morphology, mitochondrial membrane potential, and ATP levels, which consequently impeded the accumulation of ROS but not mitochondrial superoxide. We provide evidence that the beneficial effect of LMB is mechanistically based on a combinatory effect on mitochondrial biogenesis via upregulation of PGC-1α expression (master transcription cofactor of mitochondrial genes), and mitophagy through the recovery of lysosomal content. The use of exportin CRM1 inhibitors constitutes a promising strategy to treat HGPS and other diseases characterized by mitochondrial impairment

    The Arp2/3 Inhibitory Protein Arpin Is Required for Intestinal Epithelial Barrier Integrity

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    International audienceThe intestinal epithelial barrier (IEB) depends on stable interepithelial protein complexes such as tight junctions (TJ), adherens junctions (AJ), and the actin cytoskeleton. During inflammation, the IEB is compromised due to TJ protein internalization and actin remodeling. An important actin regulator is the actin-related protein 2/3 (Arp2/3) complex, which induces actin branching. Activation of Arp2/3 by nucleation-promoting factors is required for the formation of epithelial monolayers, but little is known about the relevance of Arp2/3 inhibition and endogenous Arp2/3 inhibitory proteins for IEB regulation. We found that the recently identified Arp2/3 inhibitory protein arpin was strongly expressed in intestinal epithelial cells. Arpin expression decreased in response to tumor necrosis factor (TNF)α and interferon (IFN)γ treatment, whereas the expression of gadkin and protein interacting with protein C-kinase α-subunit 1 (PICK1), other Arp2/3 inhibitors, remained unchanged. Of note, arpin coprecipitated with the TJ proteins occludin and claudin-1 and the AJ protein E-cadherin. Arpin depletion altered the architecture of both AJ and TJ, increased actin filament content and actomyosin contractility, and significantly increased epithelial permeability, demonstrating that arpin is indeed required for maintaining IEB integrity. During experimental colitis in mice, arpin expression was also decreased. Analyzing colon tissues from ulcerative colitis patients by Western blot, we found different arpin levels with overall no significant changes. However, in acutely inflamed areas, arpin was significantly reduced compared to non-inflamed areas. Importantly, patients receiving mesalazine had significantly higher arpin levels than untreated patients. As arpin depletion (theoretically meaning more active Arp2/3) increased permeability, we wanted to know whether Arp2/3 inhibition would show the opposite. Indeed, the specific Arp2/3 inhibitor CK666 ameliorated TNFα/IFNγ-induced permeability in established Caco-2 monolayers by preventing TJ disruption. CK666 treatment also attenuated colitis development, colon tissue damage, TJ disruption, and permeability in dextran sulphate sodium (DSS)-treated mice. Our results demonstrate that loss of arpin triggers IEB dysfunction during inflammation and that low arpin levels can be considered a novel hallmark of acute inflammation

    Changes in the Proliferation of the Neural Progenitor Cells of Adult Mice Chronically Infected with <i>Toxoplasma gondii</i>

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    During Toxoplasma gondii chronic infection, certain internal factors that trigger the proliferation of neural progenitor cells (NPCs), such as brain inflammation, cell death, and changes in cytokine levels, are observed. NPCs give rise to neuronal cell types in the adult brain of some mammals. NPCs are capable of dividing and differentiating into a restricted repertoire of neuronal and glial cell types. In this study, the proliferation of NPCs was evaluated in CD-1 adult male mice chronically infected with the T. gondii ME49 strain. Histological brain sections from the infected mice were evaluated in order to observe T. gondii tissue cysts. Sagittal and coronal sections from the subventricular zone of the lateral ventricles and from the subgranular zone of the hippocampal dentate gyrus, as well as sagittal sections from the rostral migratory stream, were obtained from infected and non-infected mice previously injected with bromodeoxyuridine (BrdU). A flotation immunofluorescence technique was used to identify BrdU+ NPC. The scanning of BrdU+ cells was conducted using a confocal microscope, and the counting was performed with ImageJ® software (version 1.48q). In all the evaluated zones from the infected mice, a significant proliferation of the NPCs was observed when compared with that of the control group. We concluded that chronic infection with T. gondii increased the proliferation of NPCs in the three evaluated zones. Regardless of the role these cells are playing, our results could be useful to better understand the pathogenesis of chronic toxoplasmosis

    Activity of Chloroformic Extract from <i>Salvia connivens</i> (Lamiales: Lamiaceae) and Its Principal Compounds against <i>Spodoptera frugiperda</i> (Lepidoptera: Noctuidae)

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    Spodoptera frugiperda (Smith) (Lepidoptera: Noctuidae) is one of the most damaging pests in maize crops. In order to manage it, synthetic insecticides such as diamides, neonicotinoids, and pyrethroids are used, but they present a risk for humans and the environment. Investigations of safer alternatives include the use of natural extracts. Thus, this research evaluated the effects of chloroform extract (CHCl3Sc) (5000, 4000, 2000, 1000, and 500 ppm) on aerial parts of Salvia connivens and of nonanal and pyrocatechol (1000, 600, 400, and 80 ppm) on S. frugiperda mortality, duration of the larva and pupae phases, and pupae weight after 24 h. The second instars of S. frugiperda larvae were fed an artificial diet incorporating the extract and compounds. The CHCl3Sc had insecticidal activity against S. frugiperda, showing an LC50 of 1504 ppm. Insectistatic activity began at 1000 ppm, increasing pupal and larval duration in 7.6 and 1.4 days, respectively. Pyrocatechol and nonanal were found in this extract. The first did not have any significant difference in larval or pupal mortalities. On the other hand, insectistatic activity was shown at 500 ppm, increasing the larval duration by 1.7 days compared with the control. In the case of nonanal, the insecticide activity was LC50 of 200 ppm, and insectistatic activity started at 80 ppm, increasing larval duration by 3.2 days compared with the control and reducing pupal weight by 3.4%. The results show that chloroformic extract had insecticidal and insectistatic activities against S. frugiperda; nonanal was an aldehyde compound present in this extract, which confers insecticidal and insectistatic activities against this pest

    TIX - Taller de Ejercicio Profesional - AR302 - 202102

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    Descripción: El curso desarrolla propuestas arquitectónicas hasta alcanzar un nivel de desarrollo que involucre las decisiones que se toman al completar un proyecto profesional (selección de materiales especificaciones, detalles constructivos) hasta acercarse al ¿expediente técnico¿. Incentivar al estudiante a la reflexión luego de investigar sobre el usuario a servir, el tema y el lugar del proyecto, el proceso constructivo le permitirá llevar a cabo, el propio desempeño de la profesión con responsabilidad y sentido crítico para la innovación. 1Propósito: El propósito del curso es enfrentar al estudiante con la resolución de un proyecto alta complejidad que le permita entender el sentido de éste en la realidad, buscando que potencie y desarrolle las competencias de un proyectista de arquitectura. La asignatura contribuye al desarrollo de las competencias específicas de la carrera: Diseño Fundamentado (que corresponde a los criterios NAAB PC2, PC3, PC8, PC5, SC3, SC5) y Técnica y Construcción (que corresponde a los criterios NAAB SC1, SC4, SC6); ambas competencias en el nivel de logro 03. Tiene como requisitos las asignaturas de Investigación Arquitectónica y Taller VIII - Arquitectura y Ciudad
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