The N-methyl-d-aspartate receptor antagonist CPP alters synapse and spine structure and impairs long-term potentiation and long-term depression induced morphological plasticity in dentate gyrus of the awake rat

Long-term morphological synaptic changes associated with homosynaptic long-term potentiation (LTP) and heterosynaptic long-term depression (LTD) in vivo, in awake adult rats were analyzed using three-dimensional (3-D) reconstructions of electron microscope images of ultrathin serial sections from the molecular layer of the dentate gyrus. For the first time in morphological studies, the specificity of the effects of LTP and LTD on both spine and synapse ultrastructure was determined using an N-methyl-d-aspartate (NMDA) receptor antagonist CPP (3-[(R)-2-carboxypiperazin-4-yl]-propyl-1-phosphonic acid). There were no differences in synaptic density 24 h after LTP or LTD induction, and CPP alone had no effect on synaptic density. LTP increased significantly the proportion of mushroom spines, whereas LTD increased the proportion of thin spines, and both LTP and LTD decreased stubby spine number. Both LTP and LTD increased significantly spine head evaginations (spinules) into synaptic boutons and CPP blocked these changes. Synaptic boutons were smaller after LTD, indicating a pre-synaptic effect. Interestingly, CPP alone decreased bouton and mushroom spine volumes, as well as post-synaptic density (PSD) volume of mushroom spines.These data show similarities, but also some clear differences, between the effects of LTP and LTD on spine and synaptic morphology. Although CPP blocks both LTP and LTD, and impairs most morphological changes in spines and synapses, CPP alone was shown to exert effects on aspects of spine and synaptic structure

Evaluación del impacto de la ingesta de arándano sobre los niveles de colesterol, glucosa y triglicéridos en ratas wistar alimentadas con dietas ricas en lípidos.

En México, una de las principales causas de muerte en personas de edad adulta son enfermedades coronarias. Según estudios realizados en los últimos años, el 26% de los mexicanos de la tercera edad presentan niveles altos de colesterol HDL (+200 mg/dl). Estos datos son muy similares a nivel mundial. Se estima que en México prevalecían índices elevados de desnutrición, aumentando las manifestaciones de mala nutrición por exceso (ENSANUT, 2012). El arándano o “blueberry” es un frutal menor perteneciente al género Vaccinium, de la familia Ericaceae (Sudzuki, 1983). El fruto del arándano es una baya casi esférica, que dependiendo de la especie y cultivar, su tamaño puede variar entre 0,7 a 1,5 cm de diámetro, con un color azul claro hasta oscuro, conteniendo en su interior hasta 100 semillas pequeñas (Buzeta, 1997). Numerosas investigaciones relacionan al arándano con el aumento de colesterol HDL, lo que estaría asociado a una disminución en la probabilidad de sufrir afecciones cardíacas; esto debido a su gran poder antioxidante. El objetivo de este trabajo es la medición de los efectos del consumo de arándano macerado sobre la reducción y control de los niveles de colesterol (LDL, HDL), glucosa y triglicéridos en ratas Wistar en edad reproductiva

Forest hydrology in Chile: Past, present, and future

This paper reviews the current knowledge of hydrological processes in Chilean temperate forests which extend along western South America from latitude 29° S to 56 ° S. This geographic region includes a diverse range of natural and planted forests and a broad sweep of vegetation, edaphic, topographic, geologic, and climatic settings which create a unique natural laboratory. Many local communities, endangered freshwater ecosystems, and downstream economic activities in Chile rely on water flows from forested catchments. This review aims to (i) provide a comprehensive overview of Chilean forest hydrology, to (ii) review prior research in forest hydrology in Chile, and to (iii) identify knowledge gaps and provide a vision for future research on forest hydrology in Chile. We reviewed the relation between native forests, commercial plantations, and other land uses on water yield and water quality from the plot to the catchment scale. Much of the global understanding of forests and their relationship with the water cycle is in line with the findings of the studies reviewed here. Streamflow from forested catchments increases after timber harvesting, native forests appear to use less water than plantations, and streams draining native forest yield less sediment than streams draining plantations or grassland/shrublands. We identified 20 key knowledge gaps such as forest groundwater systems, soil–plant-atmosphere interactions, native forest hydrology, and the effect of forest management and restoration on hydrology. Also, we found a paucity of research in the northern geographic areas and forest types (35-36 ° S); most forest hydrology studies in Chile (56 %) have been conducted in the southern area (Los Rios Region around 39-40 ° S). There is limited knowledge of the geology and soils in many forested areas and how surface and groundwater are affected by changes in land cover. There is an opportunity to advance our understanding using process-based investigations linking field studies and modeling. Through the establishment of a forest hydrology science “society” to coordinate efforts, regional and national-scale land use planning might be supported. Our review ends with a vision to advance a cross-scale collaborative effort to use new nation-wide catchment-scale networks Long-term Ecosystem Research (LTER) sites, to promote common and complementary techniques in these studies, and to conduct transdisciplinary research to advance sound and integrated planning of forest lands in Chile

Rethinking Research Ethics for Latinos: The Policy Paradox of Health Reform and the Role of Social Justice

http://dx.doi.org/10.1080/10508422.2012.72999

Computational geometry analysis of dendritic spines by structured illumination microscopy

We are currently short of methods that can extract objective parameters of dendritic spines useful for their categorization. Authors present in this study an automatic analytical pipeline for spine geometry using 3D-structured illumination microscopy, which can effectively extract many geometrical parameters of dendritic spines without bias and automatically categorize spine population based on their morphological feature

Thioredoxin 80-Activated-Monocytes (TAMs) Inhibit the Replication of Intracellular Pathogens

BACKGROUND: Thioredoxin 80 (Trx80) is an 80 amino acid natural cleavage product of Trx, produced primarily by monocytes. Trx80 induces differentiation of human monocytes into a novel cell type, named Trx80-activated-monocytes (TAMs). PRINCIPAL FINDINGS: In this investigation we present evidence for a role of TAMs in the control of intracellular bacterial infections. As model pathogens we have chosen Listeria monocytogenes and Brucella abortus which replicate in the cytosol and the endoplasmic reticulum respectively. Our data indicate that TAMs efficiently inhibit intracellular growth of both L. monocytogenes and B. abortus. Further analysis shows that Trx80 activation prevents the escape of GFP-tagged L. monocytogenes into the cytosol, and induces accumulation of the bacteria within the lysosomes. Inhibition of the lysosomal activity by chloroquine treatment resulted in higher replication of bacteria in TAMs compared to that observed in control cells 24 h post-infection, indicating that TAMs kill bacteria by preventing their escape from the endosomal compartments, which progress into a highly degradative phagolysosome. SIGNIFICANCE: Our results show that Trx80 potentiates the bactericidal activities of professional phagocytes, and contributes to the first line of defense against intracellular bacteria

Heme oxygenase-1 derived carbon monoxide suppresses Aβ1-42 toxicity in astrocytes

Neurodegeneration in Alzheimer’s disease (AD) is extensively studied, and the involvement of astrocytes and other cell types in this process has been described. However, the responses of astrocytes themselves to amyloid β peptides ((Aβ; the widely accepted major toxic factor in AD) is less well understood. Here, we show that Aβ(1-42) is toxic to primary cultures of astrocytes. Toxicity does not involve disruption of astrocyte Ca2+ homeostasis, but instead occurs via formation of the toxic reactive species, peroxynitrite. Thus, Aβ(1-42) raises peroxynitrite levels in astrocytes, and Aβ(1-42) toxicity can be inhibited by antioxidants, or by inhibition of nitric oxide (NO) formation (reactive oxygen species (ROS) and NO combine to form peroxynitrite), or by a scavenger of peroxynitrite. Increased ROS levels observed following Aβ(1-42) application were derived from NADPH oxidase. Induction of heme oxygenase-1 (HO-1) protected astrocytes from Aβ(1-42) toxicity, and this protective effect was mimicked by application of the carbon monoxide (CO) releasing molecule CORM-2, suggesting HO-1 protection was attributable to its formation of CO. CO suppressed the rise of NADPH oxidase-derived ROS caused by Aβ(1-42). Under hypoxic conditions (0.5% O2, 48h) HO-1 was induced in astrocytes and Aβ(1-42) toxicity was significantly reduced, an effect which was reversed by the specific HO-1 inhibitor, QC-15. Our data suggest that Aβ(1-42) is toxic to astrocytes, but that induction of HO-1 affords protection against this toxicity due to formation of CO. HO-1 induction, or CO donors, would appear to present attractive possible approaches to provide protection of both neuronal and non-neuronal cell types from the degenerative effects of AD in the central nervous system

Heme oxygenase-1 derived carbon monoxide suppresses Aβ1-42 toxicity in astrocytes

Neurodegeneration in Alzheimer’s disease (AD) is extensively studied, and the involvement of astrocytes and other cell types in this process has been described. However, the responses of astrocytes themselves to amyloid peptides ((A; the widely accepted major toxic factor in AD) is less well understood. Here, we show that A(1-42) is toxic to primary cultures of astrocytes. Toxicity does not involve disruption of astrocyte Ca2+ homeostasis, but instead occurs via formation of the toxic reactive species, peroxynitrite. Thus, A(1-42) raises peroxynitrite levels in astrocytes, and A(1-42) toxicity can be inhibited by antioxidants, or by inhibition of nitric oxide (NO) formation (reactive oxygen species (ROS) and NO combine to form peroxynitrite), or by a scavenger of peroxynitrite. Increased ROS levels observed following A(1-42) application were derived from NADPH oxidase. Induction of heme oxygenase-1 (HO-1) protected astrocytes from A(1-42) toxicity, and this protective effect was mimicked by application of the carbon monoxide (CO) releasing molecule CORM-2, suggesting HO-1 protection was attributable to its formation of CO. CO suppressed the rise of NADPH oxidase-derived ROS caused by A(1-42). Under hypoxic conditions (0.5% O2, 48h) HO-1 was induced in astrocytes and A(1-42) toxicity was significantly reduced, an effect which was reversed by the specific HO-1 inhibitor, QC-15. Our data suggest that A(1-42) is toxic to astrocytes, but that induction of HO-1 affords protection against this toxicity due to formation of CO. HO-1 induction, or CO donors, would appear to present attractive possible approaches to provide protection of both neuronal and non-neuronal cell types from the degenerative effects of AD in the central nervous system