17 research outputs found

    Outcomes from elective colorectal cancer surgery during the SARS-CoV-2 pandemic

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    This study aimed to describe the change in surgical practice and the impact of SARS-CoV-2 on mortality after surgical resection of colorectal cancer during the initial phases of the SARS-CoV-2 pandemic

    [Morphological analysis of the hippocampal region associated with an innate behaviour task in the transgenic mouse model (3xTg-AD) for Alzheimer disease]

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    INTRODUCTION: Different animal models for Alzheimer disease (AD) have been designed to support the hypothesis that the neurodegeneration (loss of neurons and synapses with reactive gliosis) associated with Abeta and tau deposition in these models is similar to that in the human brain. These alterations produce functional changes beginning with decreased ability to carry out daily and social life activities, memory loss, and neuropsychiatric disorders in general. Neuronal alteration plays an important role in early stages of the disease, especially in the CA1 area of hippocampus in both human and animal models. METHODS: Two groups (WT and 3xTg-AD) of 11-month-old female mice were used in a behavioural analysis (nest building) and a morphometric analysis of the CA1 region of the dorsal hippocampus. RESULTS: The 3xTg-AD mice showed a 50% reduction in nest quality associated with a significant increase in damaged neurons in the CA1 hippocampal area (26%+/-6%, P<.05) compared to the WT group. CONCLUSIONS: The decreased ability to carry out activities of daily living (humans) or nest building (3xTg-AD mice) is related to the neuronal alterations observed in AD. These alterations are controlled by the hippocampus. Post-mortem analyses of the human hippocampus, and the CA1 region in 3xTg-AD mice, show that these areas are associated with alterations in the deposition of Abeta and tau proteins, which start accumulating in the early stages of AD.Copyright 2013 Sociedad Espanola de Neurologia. Published by Elsevier Espana. All rights reserved

    Morphological analysis of the hippocampal region associated with an innate behaviour task in the transgenic mouse model (3xTg-AD) for Alzheimer disease

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    Introduction: Different animal models for Alzheimer disease (AD) have been designed to support the hypothesis that the neurodegeneration (loss of neurons and synapses with reactive gliosis) associated with Aβ and tau deposition in these models is similar to that in the human brain. These alterations produce functional changes beginning with decreased ability to carry out daily and social life activities, memory loss, and neuropsychiatric disorders in general. Neuronal alteration plays an important role in early stages of the disease, especially in the CA1 area of hippocampus in both human and animal models. Methods: Two groups (WT and 3xTg-AD) of 11-month-old female mice were used in a behavioural analysis (nest building) and a morphometric analysis of the CA1 region of the dorsal hippocampus. Results: The 3xTg-AD mice showed a 50% reduction in nest quality associated with a significant increase in damaged neurons in the CA1 hippocampal area (26% ± 6%, P < .05) compared to the WT group. Conclusions: The decreased ability to carry out activities of daily living (humans) or nest building (3xTg-AD mice) is related to the neuronal alterations observed in AD. These alterations are controlled by the hippocampus. Post-mortem analyses of the human hippocampus, and the CA1 region in 3xTg-AD mice, show that these areas are associated with alterations in the deposition of Aβ and tau proteins, which start accumulating in the early stages of AD. Resumen: Introducción: Se han diseñado diferentes modelos animales de la enfermedad de Alzheimer (EA) para apoyar la hipótesis de que la neurodegeneración (pérdida de neuronas, sinapsis y gliosis reactiva) asociada al depósito de Aβ y tau en estos animales es similar a la del cerebro humano. Estas alteraciones producen cambios funcionales que se inician con el deterioro en la habilidad para realizar actividades de la vida cotidiana, pérdida de la memoria y, en general, trastorno neuropsiquiátrico. La alteración neuronal desempeña un papel importante en las etapas tempranas de la enfermedad, especialmente en el área CA1 del hipocampo de animales y humanos. Métodos: Se utilizaron ratones WT y 3xTg-AD hembras de 11 meses de edad, para el análisis conductual (construcción del nido) e histológico en la región CA1 del hipocampo dorsal. Resultados: Los ratones 3xTg-AD mostraron deficiencia del 50% en la calidad de construcción del nido asociado a un aumento del 26 ± 6% (p < 0,05) de neuronas dañadas en comparación con el grupo WT. Conclusiones: El deterioro de la capacidad para llevar a cabo las actividades de la vida diaria (en el hombre) y la construcción del nido (en el ratón 3xTg-AD) están relacionados con las alteraciones en los circuitos nerviosos observados en la EA. Estas alteraciones son controladas por el hipocampo que en el análisis post mortem (en el humano), así como en la región CA1 (en el modelo de ratón 3xTg-AD) se han relacionado con alteraciones en el depósito de las proteínas Aß y tau que comienzan a acumularse al inicio de la EA. Keywords: Alzheimer disease, Transgenic mouse, Hippocampus, CA1 area, Neuron, Morphology, Palabras clave: Enfermedad de Alzheimer, Ratón transgénico, Hipocampo, Área CA1, Neurona, Morfologí

    Marcaje colinérgico en la corteza cerebral y el hipocampo en algunas especies animales y su relación con la enfermedad de Alzheimer

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    Resumen: Introducción: El sistema colinérgico incluye neuronas localizadas en el cerebro basal anterior y sus axones largos proyectan a la corteza cerebral e hipocampo. Este sistema modula la función cognitiva. En la enfermedad de Alzheimer (EA) y en el proceso de envejecimiento la disfunción colinérgica hay una asociación entre el deterioro cognitivo y el daño progresivo de las fibras colinérgicas, lo que conduce al postulado de la hipótesis colinérgica. Desarrollo: En la EA se producen alteraciones en la expresión y en la actividad de la colina acetiltransferasa (ChAT) y la acetilcolinesterasa (AChE), enzimas específicas relacionadas con la función del SC. Ambas proteínas juegan un papel importante en la transmisión colinérgica mostrando variaciones en la corteza cerebral y en el hipocampo, tanto por el envejecimiento, como por la EA. En ambas estructuras, los desórdenes demenciales están asociados a la destrucción severa y desorganización de las proyecciones colinérgicas que se encuentran afectadas. Para el estudio de este sistema se han usado marcadores específicos como los anticuerpos contra ChAT y AChE que han sido empleados en las técnicas de inmuhistoquímica de luz y microscopia electrónica en algunas especies animales. Conclusiones: En este trabajo se hace una revisión de los principales estudios inmunomorfológicos de la corteza cerebral e hipocampo de varias especies animales con énfasis en el SC y su relación con la EA. Abstract: Introduction: The cholinergic system includes neurons located in the basal forebrain and their long axons that reach the cerebral cortex and the hippocampus. This system modulates cognitive function. In Alzheimer's disease (AD) and ageing, cognitive impairment is associated with progressive damage to cholinergic fibres, which leads us to the cholinergic hypothesis for AD. Development: The AD produces alterations in the expression and activity of acetyltransferase (ChAT) and acetyl cholinesterase (AChE), enzymes specifically related to cholinergic system function. Both proteins play a role in cholinergic transmission, which is altered in both the cerebral cortex and the hippocampus due to ageing and AD. Dementia disorders are associated with the severe destruction and disorganisation of the cholinergic projections extending to both structures. Specific markers, such as anti-ChAT and anti-AChE antibodies, have been used in light immunohistochemistry and electron microscopy assays to study this system in adult members of certain animal species. Conclusions: This paper reviews the main immunomorphological studies of the cerebral cortex and hippocampus in some animal species with particular emphasis on the cholinergic system and its relationship with the AD. Palabras clave: Inervación colinérgica, Colina acetiltransferasa, Acetilcolinesterasa, Corteza cerebral, Hipocampo, Enfermedad de Alzheimer, Keywords: Cholinergic innervation, Choline acetyltransferase, Acetyl cholinesterase, Cerebral cortex, Hippocampus, Alzheimer's diseas

    Análisis morfológico de la región del hipocampo asociado a una tarea conductual innata en el modelo de ratón transgénico (3xTg-AD) para la enfermedad de Alzheimer

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    Resumen: Introducción: Se han diseñado diferentes modelos animales de la enfermedad de Alzheimer (EA) para apoyar la hipótesis de que la neurodegeneración (pérdida de neuronas, sinapsis y gliosis reactiva) asociada al depósito de Aβ y tau en estos animales es similar a la del cerebro humano. Estas alteraciones producen cambios funcionales que se inician con el deterioro en la habilidad para realizar actividades de la vida cotidiana, pérdida de la memoria y, en general, trastorno neuropsiquiátrico. La alteración neuronal desempeña un papel importante en las etapas tempranas de la enfermedad, especialmente en el área CA1 del hipocampo de animales y humanos. Métodos: Se utilizaron ratones WT y 3xTg-AD hembras de 11 meses de edad, para el análisis conductual (construcción del nido) e histológico en la región CA1 del hipocampo dorsal. Resultados: Los ratones 3xTg-AD mostraron deficiencia del 50% en la calidad de construcción del nido asociado a un aumento del 26 ± 6% (p < 0,05) de neuronas dañadas en comparación con el grupo WT. Conclusiones: El deterioro de la capacidad para llevar a cabo las actividades de la vida diaria (en el hombre) y la construcción del nido (en el ratón 3xTg-AD) están relacionados con las alteraciones en los circuitos nerviosos observados en la EA. Estas alteraciones son controladas por el hipocampo que en el análisis post mortem (en el humano), así como en la región CA1 (en el modelo de ratón 3xTg-AD) se han relacionado con alteraciones en el depósito de las proteínas Aß y tau que comienzan a acumularse al inicio de la EA. Abstract: Introduction: Different animal models for Alzheimer disease (AD) have been designed to support the hypothesis that the neurodegeneration (loss of neurons and synapses with reactive gliosis) associated with Aβ and tau deposition in these models is similar to that in the human brain. These alterations produce functional changes beginning with decreased ability to carry out daily and social life activities, memory loss, and neuropsychiatric disorders in general. Neuronal alteration plays an important role in early stages of the disease, especially in the CA1 area of hippocampus in both human and animal models. Methods: Two groups (WT and 3xTg-AD) of 11-month-old female mice were used in a behavioural analysis (nest building) and a morphometric analysis of the CA1 region of the dorsal hippocampus. Results: The 3xTg-AD mice showed a 50% reduction in nest quality associated with a significant increase in damaged neurons in the CA1 hippocampal area (26% ± 6%, P < .05) compared to the WT group. Conclusions: The decreased ability to carry out activities of daily living (humans) or nest building (3xTg-AD mice) is related to the neuronal alterations observed in AD. These alterations are controlled by the hippocampus. Post-mortem analyses of the human hippocampus, and the CA1 region in 3xTg-AD mice, show that these areas are associated with alterations in the deposition of Aβ and tau proteins, which start accumulating in the early stages of AD. Palabras clave: Enfermedad de Alzheimer, Ratón transgénico, Hipocampo, Área CA1, Neurona, Morfología, Keywords: Alzheimer disease, Transgenic mouse, Hippocampus, CA1 area, Neuron, Morpholog

    Chemical treatment with different levels of acetic organic acid on Agave tequilana Weber variety blue leafes for its disappearance in situ in canulated ruminant

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    Introduction: The cholinergic system includes neurons located in the basal forebrain and their long axons that reach the cerebral cortex and the hippocampus. This system modulates cognitive function. In Alzheimer's disease (AD) and ageing, cognitive impairment is associated with progressive damage to cholinergic fibres, which leads us to the cholinergic hypothesis for AD. Development: The AD produces alterations in the expression and activity of acetyltransferase (ChAT) and acetyl cholinesterase (AChE), enzymes specifically related to cholinergic system function. Both proteins play a role in cholinergic transmission, which is altered in both the cerebral cortex and the hippocampus due to ageing and AD. Dementia disorders are associated with the severe destruction and disorganisation of the cholinergic projections extending to both structures. Specific markers, such as anti-ChAT and anti-AChE antibodies, have been used in light immunohistochemistry and electron microscopy assays to study this system in adult members of certain animal species. Conclusions: This paper reviews the main immunomorphological studies of the cerebral cortex and hippocampus in some animal species with particular emphasis on the cholinergic system and its relationship with the AD. " 2012 Sociedad Española de Neurología.",,,,,,"10.1016/j.nrl.2012.10.007",,,"http://hdl.handle.net/20.500.12104/40036","http://www.scopus.com/inward/record.url?eid=2-s2.0-84908249415&partnerID=40&md5=fbd00c875df20647a45037081784b56

    Dissecting phosphatidylinositol 4,5-bisphosphate activation and thermosensation in TRP channels

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    Gonzalez Nilo, Danilo and Gonzalez, Wendy. Centro de Bioinformatica y Simulacion Molecular, Universidad de Talca, Talca, Chile.Phosphatidylinositol 4,5-bisphosphate (PIP2) is able to regulate the activity of many ion channels, transporters and enzymes. In particular, the activation of several TRP channels has been shown to be PIP2-dependent. For the case of TRPM8, this activation is supposed to be possible through a direct the interaction between PIP2 and key positively charged residues present in the TRP Domain. Because of the high sequence similarity among Transient Receptor Potential (TRP) channels on their TRP Domain, that region has been proposed as a common PIP2 binding site. In this work, we have exchanged different segments of the C-terminal region between TRPM8 and TRPV1 trying to understand the role of PIP2 during temperature activation of the channel. A chimera dubbed TRPM8(CTV1686-752) is activated by PIP2 and is able to confer the phenotype of heat activation. PIP2 sensitivity disappears when charges R701 and K710 were neutralized. When the exchanged fragment reached a length of 11 amino acid TRPM8(CTV1741-752), temperature dependence disappears. Together, our findings suggest the existence of different activation domains for temperature, PIP2 and voltage. Here, we also provide a simple interpretation for Channel-PIP2 interaction using a refined full-atom molecular model of TRPV1, and PIP2 docking analysis. (Supported by Fondecyt Grants Nº 3060003 (GO), 1040254 (FG) and 103-0830 (RL)

    Особенности силовой подготовки студентов 1 курса БГУИР : метод. рекомендации для преподавателей и студентов

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    В данных рекомендациях в краткой форме изложены основные методические принципы силовой подготовки студентов 1 курса университета. Предложены примерные комплексы упражнений для юношей и девушек, направленные на развитие силовых качеств основных мышечных групп. Издание предназначено для преподавателей и студентов

    Dissection of the components for PIP2 activation and thermosensation in TRP channels

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    Phosphatidylinositol 4,5-bisphosphate (PIP2) plays a central role in the activation of several transient receptor potential (TRP) channels. The role of PIP2 on temperature gating of thermoTRP channels has not been explored in detail, and the process of temperature activation is largely unexplained. In this work, we have exchanged different segments of the C-terminal region between cold-sensitive (TRPM8) and heat-sensitive (TRPV1) channels, trying to understand the role of the segment in PIP2 and temperature activation. A chimera in which the proximal part of the C-terminal of TRPV1 replaces an equivalent section of TRPM8 C-terminal is activated by PIP2 and confers the phenotype of heat activation. PIP2, but not temperature sensitivity, disappears when positively charged residues contained in the exchanged region are neutralized. Shortening the exchanged segment to a length of 11 aa produces voltage-dependent and temperature-insensitive channels. Our findings suggest the existence of different activation domains for temperature, PIP2, and voltage. We provide an interpretation for channel–PIP2 interaction using a full-atom molecular model of TRPV1 and PIP2 docking analysis
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