Why our brains cherish humanity: Mirror neurons and colamus humanitatem

Commonsense says we are isolated. After all, our bodies are physically separate. But Seneca’s colamus humanitatem, and John Donne’s observation that “no man is an island” suggests we are neither entirely isolated nor separate. A recent discovery in neuroscience—that of mirror neurons—argues that the brain and the mind is neither built nor functions remote from what happens in other individuals. What are mirror neurons? They are brain cells that process both what happens to or is done by an individual, and, as it were, its perceived “reflection,” when that same thing happens or is done by another individual. Thus, mirror neurons are both activated when an individual does a particular action, and when that individual perceives that same action done by another. The discovery of mirror neurons suggests we need to radically revise our notions of human nature since they offer a means by which we may not be so separated as we think. Humans unlike other apes are adapted to mirror interact nonverbally when together. Notably, our faces have been evolved to display agile and nimble movements. While this is usually explained as enabling nonverbal communication, a better description would be nonverbal commune based upon mirror neurons. I argue we cherish humanity, colamus humanitatem, because mirror neurons and our adapted mirror interpersonal interface blur the physical boundaries that separate us.

Asociación de desórdenes músculo esqueléticos en región cervical, dorsal y lumbar y factores de riesgo psicosocial en conductores de vehículos de carga en una empresa de transporte terrestre en Bogotá, Colombia.

Este estudio buscó evaluar la asociación de desórdenes músculo esqueléticos en región cervical, dorsal y lumbar identificados mediante el Cuestionario Nórdico en su versión validada al español y los factores de riesgo psicosocial con el Cuestionario del contenido del trabajo (JCQ), en conductores de vehículos de carga de una empresa de transporte terrestre en Bogotá, Colombia; fue un estudio de corte transversal con la participación voluntaria de 125 conductores. Los resultados demostraron mayor prevalencia de trastornos músculo esqueléticos en región lumbar en los últimos 12 meses en el 36% de los participantes y en los últimos tres meses en región cervical con el 17.6%; la prevalencia de factores psicosociales arrojó trabajo de baja tensión en el 29.6%, trabajo activo 26.4%, trabajo con alta tensión 23.2% y trabajo pasivo con el 20.8%. El valor p fue mayor de 0,005 no hallándose asociaciones significativas de desórdenes músculo esqueléticos en región cervical, dorsal y lumbar con factores de riesgo psicosocial.

Anestesia regional y periférica guiada por ultrasonido en el paciente critico

El presente trabajo es un capítulo de libro titulado “Anestesia Regional y Periférica Guiada por Ultrasonido en el Paciente Crítico” que será incluido en la última edición del libro “Manual de Ultrasonido en Terapia Intensiva y Emergencias” cuyo editor es el Doctor José de Jesús Rincón Salas y que será publicado por la Editorial Prado de México para distribución latinoamericana desde dicho país. Por solicitud del editor y teniendo en cuenta el enfoque del libro, el presente trabajo está dirigido a estudiantes de formación, médicos graduados y especialistas en las áreas de cuidado intensivo, anestesiología, dolor, medicina interna y medicina de urgencias. Tiene como propósito empapar de conocimientos necesarios y prácticos en anestesia regional a personas que usualmente no han tenido contacto con la anestesia regional, pues desafortunadamente sólo en los últimos años ha sido posible que la anestesia regional haya comenzado a salir de las salas de cirugía, ámbito donde ha estado confinada tradicionalmente. El lenguaje utilizado es sencillo y el capítulo ha sido escrito para que sea fácil de leer y consultar, dejando así mensajes muy claros sobre la utilidad, viabilidad e implicaciones que tiene el uso de anestesia regional guiada por ultrasonido en cuidado intensivo. Los autores esperamos que de esta manera, el presente capítulo permita continuar superando los obstáculos que se interponen entre los invaluables beneficios de la anestesia regional y los pacientes de cuidado intensivo que necesitan de ella.

Symptoms of imbalance associated with cervical spine pathology

The goals of the present study are: to determine the prevalence of dizziness or imbalance in a population of patients with cervical-spine pathology as compared to that in the general population; to determine correlations between cervical spinal pathology and symptoms of dizziness or imbalance.

Expression of AmphiCoe, an amphioxus COE/EBF gene, in the developing central nervous system and epidermal sensory neurons

The COE/EBF gene family marks a subset of prospective neurons in the vertebrate central and peripheral. nervous system; including neurons deriving from some ectodermal placodes. Since placodes are often considered unique to vertebrates, we have characterised an amphioxus COE/EBF gene with the aim of using it as a marker to examine the timing and location of peripheral neuron differentiation. A single COE/EBF family member, AmphiCoe, was isolated from the amphioxus Branchiostoma floridae: AmphiCoe lies basal to the vertebrate COE/EBF genes in molecular phylogenetic analysis, suggesting that the duplications that formed the vertebrate COE/EBF family were specific to the vertebrate lineage. AmphiCoe is expressed in the central nervous system and in a small number of scattered ectodermal cells on the flanks of neurulae stage embryos. These cells become at least largely recessed beneath the ectoderm. Scanning electron microscopy was used to examine embryos in which the ectoderm had been partially peeled away. This revealed that these cells have neuronal morphology, and we infer that they are the precursors of epidermal primary sensory neurons. These characters lead us to suggest that differentiation of some ectodermal cells into sensory neurons with a tendency to sink beneath the embryonic surface represents a primitive feature that has become incorporated into placodes during vertebrate evolution. (C) 2004 Wiley-Liss, Inc.

Zinc-histidine complex protects cultured cortical neurons against oxidative stress-induced damage

The levels of zinc in the brain are directly affected by dietary zinc and deficiency has been associated with alcohol withdrawal seizures, excitotoxicity, impaired learning and memory and an accelerated rate of dysfunction in aged brain. Although zinc is essential for a healthy nervous system, high concentrations of zinc are neurotoxic, thus it is important to identify the most effective forms of zinc for treatment of conditions of the central nervous system. Accumulating evidence suggests that zinc-histidine complex (Zn(HiS)(2)) has greater biological potency and enhanced bioavailability compared with other zinc salts and also has antioxidant potential. Therefore, in this study we investigated the ability of zinc-histidine to protect cultured cortical neurons against hydrogen peroxide-induced damage. Pre-treating neurons for 18h with subtoxic concentrations of zinc-histidine (5-25 muM) improved neuronal viability and strongly inhibited hydrogen peroxide-induced (75 muM, 30 min) cell damage as assessed by MTT turnover and morphological analysis 24 It later. Low concentrations of zinc-histidine were more neuroprotective than zinc chloride. There was evidence of an anti-apoptotic mechanism of action as zinc-histidine inhibited hydrogen peroxide-induced caspase-3 activation and c-jun-N-terminal kinase phosphorylation. In summary, zinc supplementation with zinc-histidine protects cultured neurons against oxidative insults and inhibits apoptosis which suggests that zinc-histidine may be beneficial in the treatment of diseases of the CNS associated with zinc deficiency. (C) 2004 Elsevier Ireland Ltd. All rights reserved.

Activation of pro-survival Akt and ERK1/2 signalling pathways underlie the anti-apoptotic effects of flavanones in cortical neurons

There is growing interest in the potential beneficial effects of flavonoids in the aging and diseased brain. We have investigated the potential of the flavanone hesperetin and two of its metabolites, hesperetin-7-O-beta-D-glucuronide and 5-nitro-hesperetin, to inhibit oxidative stress-induced neuronal apoptosis. Exposure of cortical neurons to hydrogen peroxide led to the activation of apoptosis signal-regulating kinase 1 via its de-phosphorylation at Ser963, the phosphorylation of c-jun N-terminal kinase and c-Jun (Ser73) and the activation of caspase 3 and caspase 9. Whilst hesperetin glucuronide failed to exert protection, both hesperetin and 5-nitro-hesperetin were effective at preventing neuronal apoptosis via a mechanism involving the activation/phosphorylation of both Akt/protein kinase B and extracellular signal-regulated kinase 1 and 2 (ERK1/2). Protection against oxidative injury and the activation of Akt and ERK1/2 followed a bell-shaped response and was most apparent at 100 nmol/L concentrations. The activation of ERK1/2 and Akt by flavanones led to the inhibition of the pro-apoptotic proteins, apoptosis signal-regulating kinase 1, by phosphorylation at Ser83 and Bad, by phosphorylation at both Ser136 and Ser112 and to the inhibition of peroxide-induced caspase 9 and caspase 3 activation. Thus, flavanones may protect neurons against oxidative insults via the modulation of neuronal apoptotic machinery.

Champagne wine polyphenols protect primary cortical neurons against peroxynitrite-induced injury

White wines are generally low in polyphenol content as compared to red wines. However, Champagne wines have been shown to contain relatively high amounts of phenolic acids that may exert protective cellular actions in vivo. In this study, we have investigated the potential neuroprotective effects of Champagne wine extracts, and individual phenolics present in these extracts, against peroxynitrite-induced injury. Organic and aqueous Champagne wine extracts exhibited potent neuroprotective activity against peroxynitrite-induced injury at low concentrations (0.1 mu g/mL). This protection appeared to be in part due to the cellular actions of individual components found in the organic extracts, notably tyrosol, caffeic acid, and gallic acid. These phenolics were observed to exert potent neuroprotection at concentrations between 0.1 and 10 mu M. Together, these data suggest that polyphenols present in Champagne wine may induce a neuroprotective effect against oxidative neuronal injury.