Neocortical Sox9+ radial glia generate glutamatergic neurons for all layers, but lack discernible evidence of early laminar fate restriction.

Glutamatergic neurons in the cerebral cortex are derived from embryonic neural stem cells known as radial glial progenitors (RGPs). Early RGPs, present at the onset of cortical neurogenesis, are classically thought to produce columnar clones of glutamatergic neurons spanning the cortical layers. Recently, however, it has been reported that a subset of early RGPs may undergo early commitment to upper layer neuron fates, thus bypassing genesis of deep layer neurons. However, the latter mode of early RGP differentiation was not confirmed in some other studies, and remains controversial. To further investigate the clonal output from early RGPs, we employed genetic lineage tracing driven by Sox9, a transcription factor gene that is expressed in all early RGPs. We found that early RGPs produced columnar clones spanning all cortical layers, with no evidence of significant laminar fate restriction. These data support the classic progressive restriction model of cortical neurogenesis, and suggest that early RGPs do not undergo early commitment to only upper or lower layer fates.

AGEP sistémico, un diagnóstico oculto en una falsa psoriasis paradójica por anti-TNF / Systemic AGEP, a hidden diagnosis in a false psoriasis paradoxical by anti-TNF

La pustulosis exantemática generalizada aguda (AGEP, en inglés) es una enfermedad poco frecuente, causada por drogas, caracterizada por aparición aguda de numerosas pústulas estériles en una base eritematosa, asociada en ocasiones a fiebre y leucocitosis, en algunos casos puede causar un compromiso de piel severo pero que resuelve rápidamente con la suspensión del fármaco sin tratamiento especial requerido. Puede confundirse con otras entidades como la psoriasis pustular e inusualmente produce compromiso sistémico. Presentamos un caso de AGEP secundario a terapia anti-TNF con compromiso sistémico.

The acute generalized exanthematous pustulosis (AGEP, in english)is a rare disease caused by drugs, characterized by acute onsetof numerous sterile pustules on an erythematous base, sometimesassociated with fever and leukocytosis, in some cases may causea severe skin involvement reaction but solved quickly with the drugsuspension without special treatment required. It can be confusedwith other entities such as pustular psoriasis and unusually producesystemic involvement. We present a case of secondary to anti-TNFtherapy AGEP systemic involvement.

Postnatal shifts of interneuron position in the neocortex of normal and reeler mice: evidence for inward radial migration.

During development, interneurons migrate to precise positions in the cortex by tangential and radial migration. The objectives of this study were to characterize the net radial migrations of interneurons during the first postnatal week, and to investigate the role of reelin signaling in regulating those migrations. To observe radial migrations, we compared the laminar positions of interneurons (immunoreactive for GABA or Dlx) in mouse neocortex on postnatal days (P) 0.5 and P7.5. In addition, we used bromodeoxyuridine birthdating to reveal the migrations of different interneuron cohorts. To study the effects of reelin deficiency, experiments were performed in reeler mutant mice. In normal P0.5 cortex, interneurons were most abundant in the marginal zone and layer 5. By P7.5, interneurons were least abundant in the marginal zone, and were distributed more evenly in the cortical plate. This change was attributed mainly to inward migration of middle- to late-born interneurons (produced on embryonic days (E) 13.5 to E16.5) from the marginal zone to layers 2-5. During the same interval, late-born projection neurons (non-immunoreactive for GABA or Dlx) migrated mainly outward, from the intermediate zone to upper cortical layers. In reeler cortex, middle- and late-born interneurons migrated from the superplate on P0.5, to the deep cortical plate on P7.5. Late-born projection neurons in reeler migrated in the opposite direction, from the intermediate zone to the deep cortical plate. We conclude that many middle- and late-born interneurons migrate radially inward, from the marginal zone (or superplate) to the cortical plate, during the first postnatal week in normal and reeler mice. We propose that within the cortical plate, interneuron laminar positions may be determined in part by interactions with projection neurons born on the same day in neurogenesis.