Progenitors in the Ependyma of the Spinal Cord: A Potential Resource for Self-Repair After Injury.

Traumatic injury of the spinal cord leads to devastating conditions that affect ~2.5 million people worldwide. This is because the mammalian spinal cord reacts to injury with only limited endogenous repair. Functional restoration requires the replacement of lost cells, the growth and navigation of regenerating axons on a permissive scaffold and axon re-myelination. The manipulation of endogenous spinal stem cells is regarded as a potential strategy to restore function. For this type of therapy it is necessary to determine the molecular and functional mechanisms regulating the proliferation, migration and differentiation of adult spinal progenitors. The spinal cord of animal models in which self-repair normally occurs may provide some clues. Salamanders, some fish and turtles regenerate their spinal cord after massive injury, achieving substantial functional recovery. This regeneration is orchestrated by progenitors that line the central canal (CC). Although mammals have lost the ability for self-repair, some cells in the CC react to injury by proliferating and migrating toward the lesion, where most become astrocytes in the core of the scar. Thus, CC-contacting progenitors in mammals have "latent" programs for endogenous repair of the spinal cord. Progenitor-like cells in the CC are functionally organized in lateral and midline domains, with heterogeneous molecular and membrane properties that represent targets for modulation. Understanding the mechanisms by which CC-can be manipulated will give valuable clues for endogenous spinal cord repair leading to successful functional recovery.

Early ciliary and prominin-1 dysfunctions precede neurogenesis impairment in a mouse model of type 2 diabetes.

Diabetes mellitus (DM) is reaching epidemic conditions worldwide and increases the risk for cognition impairment and dementia. Here, we postulated that progenitors in adult neurogenic niches might be particularly vulnerable. Therefore, we evaluated the different components of the mouse subventricular zone (SVZ) during the first week after chemical induction of type 1 and type 2 diabetes-like (T1DM and T2DM) conditions. Surprisingly, only T2DM mice showed SVZ damage. The initial lesions were localized to ependymal cilia, which appeared disorientated and clumped together. In addition, they showed delocalization of the ciliary membrane protein prominin-1. Impairment of neuroprogenitor proliferation, neurogenic marker abnormalities and ectopic migration of neuroblasts were found at a later stage. To our knowledge, our data describe for the first time such an early impact of T2DM on the SVZ. This is consistent with clinical data indicating that brain damage in T2DM patients differs from that in T1DM patients.

Tecido cerebral ectópico na órbita: relato de dois casos / Ectopic brain tissue in the orbit: two case report

Tecido cerebral na órbita, tendo continuidade com o conteúdo intracraniano, é relativamente incomum. Tecido cerebral isolado na órbita, entretanto, é muito mais raro. No presente trabalho säo apresentados dois casos de tecido cerebral ectópico na órbita, com cisto ependimal. Säo analisadas as similaridades e diferenças com outros casos da literatura, bem como as dificuldades no diagnóstico desta malformaçäo. Näo conhecemos nenhum caso descrito na literatura nacional.

Estudio comparativo de dosis baja de indometacina profiláctica para hemorragia subependimaria/intraventricular en neonatos pretérmino con ventilación mecánica / Low doses indomethacin for prevention of intraventricular hemorrhage in the preterm newborn baby with mechanical ventilation: final report of a randomized

Se reportan los resultados finales de un estudio prospectivo doble ciego, aplicado para evaluar la utilidad de indometacina endovenosa profiláctica versus placebo (solución fisiológica) en la prevención de la hemorragia subependimaria/intraventricular (HSE/IV) realizado en neonatos pretérmino, de 28 a 36 semanas de gestación, que requirieron ventilación mecánica convencional y que a su ingreso a la Unidad de Cuidados Intensivos Neonatales no presentaban HSE/IV evaluada por ultrasonido. De un total de 12,028 recién nacidos, se estudiaron 80 casos, 40 para el grupo control y 40 para el grupo problema. Ambos grupos fueron homogéneos para: peso, sexo, edad gestacional, vía de nacimiento, apgar y tiempo de ruptura de membranas. En morbilidad y mortalidad neonatal se presentó con mayor frecuencia el síndrome de dificultad respiratoria, sepsis e hiperbilirrubinemia multifactorial. El grupo placebo tuvo mayor presentación de persistencia de conducto arterioso (PCA) (P<0.01) y mayor mortalidad (P<0.01). No se observaron diferencias en las variables ventilatorias, hemodinámicas ni de gases arteriales. El grupo con indometacina presentó diferencias en las cifras de glucosa, plaquetas y densidad urinaria; sin embargo, los resultados nunca excedieron las variantes normales. No se encontró diferencia en la frecuencia de la HSE/IV pero se observó mayor grado de severidad para el grupo placebo (P<0.01). Se concluye que la administración de indometacina en las primeras 12 horas de vida y con las dosis empleadas no proviene la HSE/IV, pero disminuye la severidad de la misma. Por otro lado, también se asoció menor mortalidad y menor frecuencia de PCA