Síndrome hemorrágico neonatal

PROTOCOLOS TERAPÉUTICOS. SINDROME HEMORRAGICO NEONATAL. La hemorragia neonatal puede aparecer ante una gran variedad de situaciones. Es importante tener en cuenta que la volemia a esta edad es de 80 ml/Kg de lo que se deduce la importancia de cualquier pÉrdida sanguÍnea por pequeÑa que sea..

Distress respiratorio neonatal

PROTOCOLOS TERAPÉUTICOS. Distress respiratorio neonatal. El distress respiratorio neonatal puede ser una situación grave que llegue a poner en peligro la vida del recién nacido. 1) Diagnóstico. Es fundamentalmente clínico y se establece cuando el test de Silverman es superior a 2...

Cianosis neonatal

PROTOCOLOS TERAPEUTICOS. CIANOSIS NEONATAL. 1. CONCEPTO Se considera cianosis a la coloración azulada de la piel o de las mucosas secundaria a un oscurecimiento sanguíneo producido por un aumento de la hemoglobina reducida (principalmente HbFe ++) a valores superiores a los 3-5 gr/dl. Toda cianosis neonatal que persista más de 30 minutos tras el nacimiento...

Insuficiencia cardíaca neonatal

PROTOCOLOS TERAPEUTICOS. INSUFICIENCIA CARDIACA NEONATAL. 1. CONCEPTO La insuficiencia cardíaca (IC) en el recién nacido suele manifestarse de forma global salvo en contadas ocasiones (ciertas cardiopatías congénitas). Las causas pueden ser múltiples, desde problemas hidroelectrolíticos hasta infecciones, pasando por la yatrogenia de la sobrecarga hídrica debida a una mala prescripción de las perfusiones. Un intento de clasificación puede ser el siguiente...

Tuberculosis neonatal

PROTOCOLOS TERAPEUTICOS. TUBERCULOSIS NEONATAL 1. CONCEPTO La tuberculosis neonatal es la infección del recién nacido producida por el bacilo de Koch. Es una situación rara pero grave que requiere un diagnóstico precoz y un tratamiento enérgico..

Convulsión neonatal

Se define el 'estado convulsivo neonatal como una convulsión (cualquiera que sea su forma) que se mantiene de forma continuada o bien que tras desaparecer se repite en un período inferior a 20 minutos a pesar de un tratamiento correcto...

Levetiracetam versus Phenobarbital. Effects in the neurodevelopment in newborns treated for neonatal seizures: a clinical trial

Purpose: To analyze if the use of Phenobarbital compared with Levetiracetam, it’s associated with more neurodevelopmental problems in newborns treated for neonatal seizures. As a secondary objective identify which are the most affected areas of the neurodevelopment: cognition, socio-­‐emotional, motor or language skills.Design: A 5 years long clinical trial administering, with double-­‐blind and a randomized distribution of the sample, Phenobarbital or Levetiracetam for the management of neonatal seizures

Epigenetic alterations in hippocampus of SAMP8 senescent mice and modulation by voluntary physical exercise.

The senescence-accelerated SAMP8 mouse model displays features of cognitive decline and Alzheimer's disease. With the purpose of identifying potential epigenetic markers involved in aging and neurodegeneration, here we analyzed the expression of 84 mature miRNAs, the expression of histone-acetylation regulatory genes and the global histone acetylation in the hippocampus of 8-month-old SAMP8 mice, using SAMR1 mice as control. We also examined the modulation of these parameters by 8 weeks of voluntary exercise. Twenty-one miRNAs were differentially expressed between sedentary SAMP8 and SAMR1 mice and seven miRNAs were responsive to exercise in both strains. SAMP8 mice showed alterations in genes involved in protein acetylation homeostasis such as Sirt1 and Hdac6 and modulation of Hdac3 and Hdac5 gene expression by exercise. Global histone H3 acetylation levels were reduced in SAMP8 compared with SAMR1 mice and reached control levels in response to exercise. In sum, data presented here provide new candidate epigenetic markers for aging and neurodegeneration and suggest that exercise training may prevent or delay some epigenetic alterations associated with accelerated aging.

Epigenetic alterations in hippocampus of SAMP8 senescent mice and modulation by voluntary physical exercise.

The senescence-accelerated SAMP8 mouse model displays features of cognitive decline and Alzheimer's disease. With the purpose of identifying potential epigenetic markers involved in aging and neurodegeneration, here we analyzed the expression of 84 mature miRNAs, the expression of histone-acetylation regulatory genes and the global histone acetylation in the hippocampus of 8-month-old SAMP8 mice, using SAMR1 mice as control. We also examined the modulation of these parameters by 8 weeks of voluntary exercise. Twenty-one miRNAs were differentially expressed between sedentary SAMP8 and SAMR1 mice and seven miRNAs were responsive to exercise in both strains. SAMP8 mice showed alterations in genes involved in protein acetylation homeostasis such as Sirt1 and Hdac6 and modulation of Hdac3 and Hdac5 gene expression by exercise. Global histone H3 acetylation levels were reduced in SAMP8 compared with SAMR1 mice and reached control levels in response to exercise. In sum, data presented here provide new candidate epigenetic markers for aging and neurodegeneration and suggest that exercise training may prevent or delay some epigenetic alterations associated with accelerated aging.

In vivo co-ordinated interactions between inhibitory systems to control glutamate mediated hippocampal excitability.

We present an overview of the long-term adaptation of hippocampal neurotransmission to cholinergic and GABAergic deafferentation caused by excitotoxic lesion of the medial septum. Two months after septal microinjection of 2.7 nmol a -amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA), a 220% increase of GABA A receptor labelling in the hippo- campal CA3 and the hilus was shown, and also changes in hippocampal neurotransmission characterised by in vivo microdialysis and HPLC. Basal amino acid and purine extra- cellular levels were studied in control and lesioned rats. In vivo effects of 100 m M KCl perfusion and adenosine A 1 receptor blockade with 1,3-dipropyl- 8-cyclopentylxanthine (DPCPX) on their release were also investigated. In lesioned animals GABA, glutamate and glutamine basal levels were decreased and taurine, adenosine and uric acid levels increased. A similar response to KCl infusion occurred in both groups except for GABA and glutamate, which release decreased in lesioned rats. Only in lesioned rats, DPCPX increased GABA basal level and KCl-induced glutamate release, and decreased glutamate turnover. Our results evidence that an excitotoxic septal lesion leads to increased hippocampal GABA A receptors and decreased glutamate neurotransmis- sion. In this situation, a co-ordinated response of hippocampal retaliatory systems takes place to control neuron excitability.

Functional connectivity of reward processing in the brain

Controversial results have been reported concerning the neural mechanisms involved in the processing of rewards and punishments. On the one hand, there is evidence suggesting that monetary gains and losses activate a similar fronto-subcortical network. On the other hand, results of recent studies imply that reward and punishment may engage distinct neural mechanisms. Using functional magnetic resonance imaging (fMRI) we investigated both regional and interregional functional connectivity patterns while participants performed a gambling task featuring unexpectedly high monetary gains and losses. Classical univariate statistical analysis showed that monetary gains and losses activated a similar fronto-striatallimbic network, in which main activation peaks were observed bilaterally in the ventral striatum. Functional connectivity analysis showed similar responses for gain and loss conditions in the insular cortex, the amygdala, and the hippocampus that correlated with the activity observed in the seed region ventral striatum, with the connectivity to the amygdala appearing more pronounced after losses. Larger functional connectivity was found to the medial orbitofrontal cortex for negative outcomes. The fact that different functional patterns were obtained with both analyses suggests that the brain activations observed in the classical univariate approach identifi es the involvement of different functional networks in the current task. These results stress the importance of studying functional connectivity in addition to standard fMRI analysis in reward-related studies.

Pleiotrophin as a central nervous system neuromodulator, evidences from the hippocampus

Pleiotrophin (PTN) is a secreted growth factor, and also a cytokine, associated with the extracellular matrix, which has recently starting to attract attention as a significant neuromodulator with multiple neuronal functions during development. PTN is expressed in several tissues, where its signals are generally related with cell proliferation, growth, and differentiation by acting through different receptors. In Central Nervous System (CNS), PTN exerts post-developmental neurotrophic and -protective effects, and additionally has been involved in neurodegenerative diseases and neural disorders. Studies in Drosophila shed light on some aspects of the different levels of regulatory control of PTN invertebrate homologs. Specifically in hippocampus, recent evidence from PTN Knock-out (KO) mice involves PTN functioning in learning and memory. In this paper, we summarize, discuss, and contrast the most recent advances and results that lead to proposing a PTN as a neuromodulatory molecule in the CNS, particularly in hippocampus.

Pleiotrophin as a central nervous system neuromodulator, evidences from the hippocampus

Pleiotrophin (PTN) is a secreted growth factor, and also a cytokine, associated with the extracellular matrix, which has recently starting to attract attention as a significant neuromodulator with multiple neuronal functions during development. PTN is expressed in several tissues, where its signals are generally related with cell proliferation, growth, and differentiation by acting through different receptors. In Central Nervous System (CNS), PTN exerts post-developmental neurotrophic and -protective effects, and additionally has been involved in neurodegenerative diseases and neural disorders. Studies in Drosophila shed light on some aspects of the different levels of regulatory control of PTN invertebrate homologs. Specifically in hippocampus, recent evidence from PTN Knock-out (KO) mice involves PTN functioning in learning and memory. In this paper, we summarize, discuss, and contrast the most recent advances and results that lead to proposing a PTN as a neuromodulatory molecule in the CNS, particularly in hippocampus.

Prevención de la infección neonatal precoz por estreptococo del grupo B

El estreptococo del grupo B (EGB) constituye la principal causa de morbimortalidad neonatal y de morbilidad materna durante el embarazo y el posparto. Coloniza el aparato digestivo y el genitourinario en un 10-30% de las gestantes, con una tasa de transmisión vertical del 50%. De entre los recién nacidos colonizados, un 1-2% desarrollará una sepsis grave precoz. Se ha realizado una revisión bibliográfica con el objetivo de conocer las estrategias de prevención de la infección neonatal por EGB. Los resultados ponen de manifiesto que las recomendaciones para su prevención consisten en el cribado universal prenatal de colonización por EGB mediante cultivo vaginorrectal a las 35-37 semanas, y la administración de profilaxis antibiótica intraparto a todas las embarazadas portadoras.

Prevención de la infección neonatal precoz por estreptococo del grupo B

El estreptococo del grupo B (EGB) constituye la principal causa de morbimortalidad neonatal y de morbilidad materna durante el embarazo y el posparto. Coloniza el aparato digestivo y el genitourinario en un 10-30% de las gestantes, con una tasa de transmisión vertical del 50%. De entre los recién nacidos colonizados, un 1-2% desarrollará una sepsis grave precoz. Se ha realizado una revisión bibliográfica con el objetivo de conocer las estrategias de prevención de la infección neonatal por EGB. Los resultados ponen de manifiesto que las recomendaciones para su prevención consisten en el cribado universal prenatal de colonización por EGB mediante cultivo vaginorrectal a las 35-37 semanas, y la administración de profilaxis antibiótica intraparto a todas las embarazadas portadoras.