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Contextualización: los modelos neuronales artificiales son modelos diseñados a partir de métodos numéricos denominados Redes Neuronales Artificiales. El uso de estos, como herramienta de predicción de la Demanda Bioquímica de Oxígeno (DBO), ha demostrado diversas ventajas, entre otras, la reducción del tiempo y los costos económicos asociados a este parámetro. La DBO generalmente requiere de 5 a 7 días, así como múltiples reactivos químicos, para poder establecer los niveles de materiales orgánicos en las aguas. Vacío de investigación: los modelos neuronales artificiales permiten calcular la DBO en tiempo real, a partir de variables fisicoquímicas registradas in situ. A pesar de ello, las redes neuronales artificiales no han sido utilizadas hasta ahora como método de estimación de la DBO en aguas marinas de Colombia. Propósito del estudio: teniendo en cuenta este aspecto, en la presente investigación se elaboró un modelo neuronal artificial que permite estimar la DBPO en aguas del Mar Caribe Colombiano. Metodología: para elaborar el modelo fue necesario realizar cinco simulaciones (constituidas por un número de 2 a 3 capas ocultas, y de 5 a 20 neuronas por capa). El desempeño predictivo de cada una de estas se evaluó a través del coeficiente de correlación. Resultados y conclusiones: los valores más altos de este indicador estadístico (0,937, 0,951, 0,953, y 0,941), se obtuvieron para el modelo que utilizó 3 capas, de 20 neuronas cada una, en sus cuatro etapas de aprendizaje (entrenamiento, validación, prueba, y todos los datos). Estas cifras indican un cercano ajuste entre los datos observados y las estimaciones hechas por la red. Estos resultados demuestran además que la Demanda Bioquímica de Oxígeno puede ser estimada numéricamente, en aguas marinas, a través de modelos neuronales artificiales.

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As shown in our previous paper ('Regression I. Experimental approaches to regression', JAP, 65, 2, 345-65), the common mechanism of regression can be described as reversible dedifferentiation, which is understood as a relative increase of the proportion of low-differentiated (older) systems in actualized experience. Experimental data show that regression following disease (chronic tension headache) is followed by adaptation and an increase in system differentiation in that experience domain which contains systems responsible for that adaptation. The results of mathematical modelling support the idea that reversible dedifferentiation can be one of the mechanisms for increasing the effectiveness of adaptation through learning. Reversible dedifferentiation, which is phenomenologically described as regression, is a general mechanism for restructuring the organism-environment interactions in situations where behaviours that were effective in the past become ineffective. Reversible dedifferentiation has evolved as a component of adaptation when new behaviours are formed and large-scale modifications in the existing behaviours are required in the face of changes in the external and/or internal environment. Thus, the authors believe that this article provides evidence for Jung's view that regression is not only a 'return' to past forms of thinking, affects and behaviour, but that regressive processes provide a significant impetus for psychological growth and development. [ABSTRACT FROM AUTHOR]

Contextualization: Artificial Neural Networks are models designed from numerical methods called Artificial Neural Networks. The use of these, as a Biochemical Oxygen Demand (BOD) prediction tool, has shown various advantages, among others, the reduction of time and the economic costs associated with this parameter. BOD usually requires 5 to 7 days, as well as multiple chemical reagents, to obtain the levels of organic materials in the waters. knowledge gap: Artificial Neural Networks models allow calculating BOD in real time from physicochemical variables recorded in situ. Despite this, artificial neural networks have not been used until now as a method of estimating BOD in Colombian seawaters. Purpose: Taking this aspect into account, an artificial neural network model that allows estimating the BOD in waters of the Colombian Caribbean Sea was developed in this research. Methodology: For the elaboration of the model it was necessary to carry out five simulations (consisting of a number of 2 to 3 hidden layers, and 5 to 20 neurons per layer). The predictive performance of each of these simulations was evaluated through the correlation coefficient. Results and conclusions: The highest values of this statistical indicator (0.937, 0.951, 0.953, and 0.941), were obtained for the model that used 3 layers, of 20 neurons each, in its four learning sets (training, validation, testing, and all data). These values indicate a close fit between the observed data and estimations made by the network. These results also demonstrate that Biochemical Oxygen Demand can be estimated numerically, in seawaters, through artificial neural networks models. [ABSTRACT FROM AUTHOR]

The concept of regression is considered with an emphasis on the differences between the positions of Freud and Jung regarding its significance. The paper discusses the results of experimental analyses of individual experience dynamics (from gene expression changes and impulse neuronal activity in animals to prosocial behaviour in healthy humans at different ages, and humans in chronic pain) in those situations where regression occurs: stress, disease, learning, highly emotional states and alcohol intoxication. Common mechanisms of regression in all these situations are proposed. The mechanisms of regression can be described as reversible dedifferentiation, which is understood as a relative increase of the representation of low-differentiated (older) systems in the actualized experience. In all of the cases of dedifferentiation mentioned above, the complexity of the systemic organization of behaviour significantly decreases. [ABSTRACT FROM AUTHOR]

Entre 1887 y 1897 Santiago Ramón y Cajal realizó una serie de estudios micrográficos que jalonarían el debate acerca de la estructura y la fisiología del sistema nervioso al suministrar substrato empírico y guía heurística al marco teórico dentro del cual serían las mismas investigadas en lo sucesivo. El significado del trabajo realizado por Cajal en ese decenio no puede ponderarse sin un serio intento de establecer los pertinentes vínculos entre el mismo, sus antecedentes y su contexto contemporáneo. A tal fin, los apartados primero y segundo abordan el contexto científico en que Cajal elaborara en el periodo indicado la teoría neuronal y la ley de la polarización dinámica, prestando atención a planteamientos convergentes y divergentes de contemporáneos y antecesores. El tercero, por su parte, se dedica a la discusión del marco metodológico de la formulación de las señaladas aportaciones, soslayando recientes conatos de polémica historiográfica en torno a la paternidad de las mismas e incidiendo en que el núcleo del legado de Cajal no ha de buscarse en discusiones de esta naturaleza, sino en el amplio cuerpo de observaciones que recogiera y, muy particularmente, en la profusión de hipótesis mediante las cuales tratara de incardinarlo cabalmente en los marcos teóricos sancionados en ciencias biológicas.

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El modelo neurobiológico de la conciencia está implantado y arraigado en la ciencia actual. En esta contribución se pretende probar que posee unos débiles cimientos que deben ser reforzados. Para mostrarlo se reflexiona críticamente sobre tres de sus dimensiones que se pueden considerar esenciales: (i) la identificación de conciencia y cerebro; (ii) la negación del libre albedrío; y (iii) las escasas aplicaciones clínicas del modelo. Estas reflexiones nos indican la necesidad de construir un modelo más robusto. Se necesita un modelo predictivo cuyos resultados no solamente se puedan validar sino que además tengan aplicaciones prácticas que sirvan para mejorar el bienestar y la calidad de vida de las personas.

En la transición a la vida extrauterina, el recién nacido sufre un período de ayuno (prelactancia) que transcurre entre el cese de la nutrición placentaria y la instauración de la lactancia. El gasto de energía por las neuronas es tan alto en estas circunstancias, que la glucogenólisis es incapaz de restablecer los niveles de glucosa en la sangre. En consecuencia, durante la prelactancia debe haber otros sustratos energéticos y lipogénicos, que adicionalmente ayuden a mantener la síntesis de neurotransmisores.Este trabajo establece la importancia de acetato en el metabolismo oxidativo y del lipogénico en neuronas durante la prelactancia. Se determinaron las velocidades de oxidación y lipogénesis en cultivos quiescentes de neuronas fetales de rata incubadas con acetato (5 mM), [1- 14C]-acetato, [2- 14C]-acetato y [U- 14C]-acetato(200-300dpm/nmol Adicionalmente, se utilizaron inhibidores enzimáticos como el dicloroacetato(1 mM) y el aminooxiacetato (5 mM), e inhibidores del transporte como el α-ciano-4-hidroxicinnamato(2 mM), butilmalonato (5 mM) y 1,2,3-bencenotricarboxilato (5 mM).Los resultados en su conjunto indican que las neuronas pueden metabolizar acetato más como sustrato energético que lipogénico, lo que nos permite pensar que este sustrato puede llegar a ser más importante para ayudar a mantener el metabolismo oxidativo, favoreciendo el reciclaje de carbonos en la prelactancia.Adicionalmente, se evidenció con el uso de [1-14C]-acetato una alta actividad anaplerótica sobre todo cuando las neuronas requieren mantener los reservorios de oxalacetato y acetil-CoA para mantener la respiración. Estos resultados señalan a la acetil-CoA sintetasa (AceCS2) y la enzima málica (mME) mitocondriales, como enzimas claves para mantener el funcionamiento de las neuronas en la prelactancia.Con el uso de [2-14C]-acetato, los resultados sugieren que las neuronas tienen un alto requerimiento de carbonos, principalmente para la síntesis de neurotransmisores. Adicionalmente, la lipogénesis está soportada por la vía del citrato y la vía de la acetil-CoA sintetasa citosólica (AceCS1).

Gestational diabetes mellitus (GDM) defined as impaired glucose tolerance affects approximately 6 % of all pregnant women who have never before had diabetes, but who do have high blood glucose levels during pregnancy. This study was done to evaluate the apoptosis in the neuronal cells in the CA1, CA2 and CA3 subfields of hippocampus and dentate gyrus in offspring of gestational diabetes at the 7, 21 and 28 d in postnatal rats. Thirty Wistar rat dams were randomly allocated in control and diabetic group. Dams in diabetic group were received 40 mg/kg/BW of streptozotocin at the first day of gestation and control groups received an equivalent volume normal saline injection intraperitoneally (IP). Six offspring of GDM and control dams, at the 7, 21, 28 postnatal day were randomly were sacrificed quickly with anesthesia. The coronal sections of brain serially collected. The apoptosis neurons were evaluated with TUNEL Assay. In the CA1, the number of apoptotic cells in 7, 21 and 28 d of postnatal life were significantly increased in GDM compared to controls (P<0.001). In the CA2, CA3 the number of apoptotic cells in 7, 21 and 28 d age-old offspring were significantly increased in GDM compared to controls (P<0.001). In the dentate gyrus, the number of apoptotic cells in 7, 21 and 28 d of postnatal life were significantly increased in GDM compared to controls (P<0.01). This study showed that the uncontrolled gestational diabetes significantly increases neuronal apoptosis in hippocampal and dentate gyrus in rat offspring. [ABSTRACT FROM AUTHOR]

Durante el período perinatal el cerebro utiliza sustratos alternativos a la glucosa para mantener su desarrollo, pues en este momento sus niveles están disminuidos. El acetato es metabolizado por las neuronas y los astrocitos durante la prelactancia. La utilización del acetato por estas células puede verse mejorada por lasreacciones fijadoras de CO2, algunas de las cuales participan en el mantenimiento de los intermediarios del TCA, que son reducidos por la producción y liberación de aminoácidos, suministrando los recursos para la producción de energía y sustratos que son compartimentados intercelularmente.Se estudió el efecto de la fijación de CO2 en procesos metabólicos intercelulares donde está involucrado el acetato. En incubaciones con neuronas y astrocitos de 7 y 14 días de cultivo, utilizando acetato (5 mM) y [14C]-bicarbonato de sodio (10 µ Ci) (500-1000 dpm/nmol), se determinó la incorporación en metabolitos marcados en células y en sustratos estables liberados al medio. Adicionalmente, se realizaron experimentos similares utilizando inhibidores como el aminooxiacetato (AOA), dicloroacetato (DCA), α-ciano-4-hidroxicinnamato (α-CN), butilmalonato (BM) y bencenotricarboxílato (BT), cuantificando porcromatografía de capa delgada la concentración en el medio de incubación de alanina, aspartato, glutamato y glutamina.Los resultados indican que las neuronas tienen una menor capacidad para fijar carbonos en estructuras celulares, durante la prelactancia, pero utilizan mejor el acetato vía acetil-CoA mitocondrial (AceCS2) para la producción de energía y aminoácidos. En los astrocitos, estas reacciones favorecen la utilización del acetato vía citrato liasa y Acetil-CoA citosólica (AceCS1) para la producción de estructuras y sustratos utilizados por las neuronas, que para la producción de aminoácidos.

El mecanismo de intercambio de sustratos entre neuronas y astrocitos, no es claro y menos claro es, si los efectos metabólicos en las células receptoras, son resultado de señalización por calcio. Se plantea la posibilidad de que existan señales entre neuronas y astrocitos que relacionen su funcionamiento metabólico a través de las concentraciones de calcio. La concentración de calcio se midió por absorción atómica en el medio intra y extracelular de cultivos primarios de neuronas y astrocitos y posteriormente en el medio intra y extracelular después de una hora de incubación con lactato, glutamato, glutamina y acetato a concentraciones fisiológicas. Las comparaciones estadísticas se efectuaron con ANOVA y Duncan (p < 0.05). Se hicieron 3 replicaciones de cada experimento con 5 repeticiones. Los resultados permiten afirmar que al hacer incubaciones in vitro con los sustratos, se producen variaciones en las concentraciones de calcio extra é intracelular. El estrés metabólico puede estar influyendo en estas variaciones. Adicionalmente, se demuestra que los astrocitos son menos dependientes del calcio extracelular que las neuronas. Las variaciones del calcio intracelular pueden incrementar el metabolismo de estas células y acelerar el metabolismo mitocondrial. Se postula que cambios en la concentración de calcio afectan el metabolis-mo de células excitables en incubaciones in vitro usando diferentes sustratos.

In 1992 A. Sabin joined Scientifics from different countries to unify the criteria in nonpolio paralytic syndromes. Manuel Ramos Alvarez from the Hospital Infantil de Mexico, Federico Gomez1 and G.M. Mckhann from the school of Medicine of the Johns Hopkins University (studies of flaccid paralysis in china), accepted to work together with interchange of material from their reported cases. In the process of interchange, Manuel Ramos Alvarez found that one of the cases from China was indeed, paralytic rabies based on the lesions of the ventral horns neurons of the spinal cord, furtherly confirmed by immunohistochemistry and electronic, microscopy. This case was published as paralytic rabies, mimicking Guillian-Barre Syndrome by K. A. Sheikh and Manuel Ramos Alvarez. In our post mortem studies with normal controls, we found six cases of paralytic rabies from which two are reported, to show the typical lesions not described before, 5 and 9 days after onset; these lesions consist in clumping or conglutination of the granules of Nissl that you can easily see in H&E or Nissl stain with toluidin blue in the ventral neurons of spinal cord. These cases do not show' Negri or Lyssa bodies in all CNS, except mild perivascular inflammatory infiltration. In the figure 1, the first column shows Nissl granules from a nonrabic normal control, in different specified stains. In the second and third columns, the typical clumping or coagglutinated Nissl granules in the mentioned cases in the same indicated stains. Silver impregnation is not good for these lesions. However is ideal for Negri bodies. [ABSTRACT FROM AUTHOR]

The neurobiological model of consciousness is implanted and currently enrooted in modern science. This contribution tries to prove that this model has a weak foundation that has to be reinforced. In order to support this statement we critically reflect on three of its essential dimensions: (i) identifying brain with consciousness, (ii) the denial of free will and (iii) the limited clinical applications of the model. These reflections indicate the necessity to build a stronger model. It is required a predictive model in which the results may not just validate the model, but also configure the specific applications to improve the health and quality of people's life. [ABSTRACT FROM AUTHOR]

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Introduction: In humans and animal models, Alzheimer disease (AD) is characterised by accumulation of amyloid-β peptide (Aβ) and hyperphosphorylated tau protein, neuronal degeneration, and astrocytic gliosis, especially in vulnerable brain regions (hippocampus and cortex). These alterations are associated with cognitive impairment (loss of memory) and non-cognitive impairment (motor impairment). The purpose of this study was to identify cell changes (neurons and glial cells) and aggregation of Aβ and hyperphosphorylated tau protein in the primary motor cortex (M1) in 3xTg-AD mouse models at an intermediate stage of AD., Methods: We used female 3xTg-AD mice aged 11 months and compared them to non-transgenic mice of the same age. In both groups, we assessed motor performance (open field test) and neuronal damage in M1 using specific markers: BAM10 (extracellular Aβ aggregates), tau 499 (hyperphosphorylated tau protein), GFAP (astrocytes), and Klüver-Barrera staining (neurons)., Results: Female 3xTg-AD mice in intermediate stages of the disease displayed motor and cellular alterations associated with Aβ and hyperphosphorylated tau protein deposition in M1., Conclusions: Patients with AD display signs and symptoms of functional impairment from early stages. According to our results, M1 cell damage in intermediate-stage AD affects motor function, which is linked to progression of the disease., (Copyright © 2017 Sociedad Española de Neurología. Publicado por Elsevier España, S.L.U. All rights reserved.)

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., (Copyright © 2013 Sociedad Española de Neurología. Published by Elsevier Espana. All rights reserved.)