Hemispheric asymmetry in the maturation of the extra striate checkerboard onset evoked potential

Recently we have shown that the single positive deflection in the checkerboard onset evoked potential (EP) of young children of striate origin develops into a negative-positive complex. However, also an early positive peak becomes apparent in the checkerboard onset EP. To determine the origin and development of the activity underlying this early positive deflection we studied the checkerboard onset EPs in children of 9¿16 years of age. It was found that for the children in this age group two different dipole sources are responsible for the activity underlying the pattern onset EP. One of the dipoles corresponds to the activity generated in the striate cortex, whereas a second dipole of extrastriate origin is responsible for the appearance of the early positive deflection. This extrastriate activity shows hemispheric asymmetry, i.e. the strength of the right hemispheric extrastriate source exceeds the strength of the left hemispheric source. These results are in accordance with histological studies of Conel (1939¿1963) [The postnatal development of the human cerebral cortex (Vols 1¿8). Cambridge, Mass.: Harvard Univ. Press] which show that the maturation of the extrastriate areas of the left hemisphere is delayed with respect to the right hemisphere

The time of the Roma in times of crisis: Where has European neoliberal capitalism failed?

This paper argues that the economic and financial crisis that has ensnared Europe from the late 2000s has been instrumental in reshaping employment and social relations in a detrimental way for the majority of the European people. It argues that the crisis has exacerbated the socio-economic position of most Roma people, immigrants as well as of other vulnerable groups. This development is approached here as an outcome of the widening structural inequalities that underpin the crisis within an increasingly neoliberalised Europe. Through recent policy developments and public discourses from a number of European countries I show how rising inequalities nurture racialised social tensions. My account draws on classic and contemporary theoretical propositions that have been propounded about the nature of capitalism, its contemporary re-articulation as well as its ramification for the future of Europe

Extent and Severity of Caliciopsis Canker in New England, USA: An Emerging Disease of Eastern White Pine (Pinus strobus L.)

Caliciopsis canker is an emerging problem in Pinus growing regions of Eastern North America. The fungal disease caused by Caliciopsis pinea is associated with overstocked stands and poor sites, but few quantitative data are available. The objective of this study, therefore, was to assess the extent and severity of Caliciopsis canker and to explore environmental variables associated with disease to identify areas at risk of damage. During 2014, 58 sites across New England with \u3e75% P. strobus basal area in public lands were surveyed. Most sites (72%) had Caliciopsis canker signs or symptoms. Caliciopsis pinea was successfully identified with molecular techniques. In sites with Caliciopsis canker, 36% of the mature pines were symptomatic. Pole sized and suppressed trees were more likely to be damaged than larger trees with dominant crown positions (p \u3c 0.05). Pinus strobus density for sites with Caliciopsis canker was 311 trees/ha (mean P. strobus stand diameter = 40 cm) compared to 220 trees/ha (mean white pine stand diameter = 43 cm) for sites without Caliciopsis canker (p = 0.1). Caliciopsis canker symptoms tended to appear more frequently in stands with excessively drained, coarse textured soils derived from glacial outwash (86%) or stands with poorly drained soils and low fertility (78%) than in stands with well drained, more fertile soils (59%) (p = 0.1). The severity of symptoms varied among soil groups and was greater for excessively drained, nutrient poor soils than for well-drained, more fertile soils (p = 0.027)

Differentiated type II pneumocytes can be reprogrammed by ectopic Sox2 expression

The adult lung contains several distinct stem cells, although their properties and full potential are still being sorted out. We previously showed that ectopic Sox2 expression in the developing lung manipulated the fate of differentiating cells. Here, we addressed the question whether fully differentiated cells could be redirected towards another cell type. Therefore, we used transgenic mice to express an inducible Sox2 construct in type II pneumocytes, which are situated in the distal, respiratory areas of the lung. Within three days after the induction of the transgene, the type II cells start to proliferate and form clusters of cuboidal cells. Prolonged Sox2 expression resulted in the reversal of the type II cell towards a more embryonic, precursor-like cell, being positive for the stem cell markers Sca1 and Ssea1. Moreover, the cells started to co-express Spc and Cc10, characteristics of bronchioalveolar stem cells. We demonstrated that Sox2 directly regulates the expression of Sca1. Subsequently, these cells expressed Trp63, a marker for basal cells of the trachea. So, we show that the expression of one transcription factor in fully differentiated, distal lung cells changes their fate towards proximal cells through intermediate cell types. This may have implications for regenerative medicine, and repair of diseased and damaged lungs

Hypoxia Inducible Factor 3α Plays a Critical Role in Alveolarization and Distal Epithelial Cell Differentiation during Mouse Lung Development

Lung development occurs under relative hypoxia and the most important oxygen-sensitive response pathway is driven by Hypoxia Inducible Factors (HIF). HIFs are heterodimeric transcription factors of an oxygen-sensitive subunit, HIFα, and a constitutively expressed subunit, HIF1β. HIF1α and HIF2α, encoded by two separate genes, contribute to the activation of hypoxia inducible genes. A third HIFα gene, HIF3α, is subject to alternative promoter usage and splicing, leading to three major isoforms, HIF3α, NEPAS and IPAS. HIF3α gene products add to the complexity of the hypoxia response as they function as dominant negative inhibitors (IPAS) or weak transcriptional activators (HIF3α/NEPAS). Previously, we and others have shown the importance of the Hif1α and Hif2α factors in lung development, and here we investigated the role of Hif3α during pulmonary development. Therefore, HIF3α was conditionally expressed in airway epithelial cells during gestation and although HIF3α transgenic mice were born alive and appeared normal, their lungs showed clear abnormalities, including a post-pseudoglandular branching defect and a decreased number of alveoli. The HIF3α expressing lungs displayed reduced numbers of Clara cells, alveolar epithelial type I and type II cells. As a result of HIF3α expression, the level of Hif2α was reduced, but that of Hif1α was not affected. Two regulatory genes, Rarβ, involved in alveologenesis, and Foxp2, a transcriptional repressor of the Clara cell specific Ccsp gene, were significantly upregulated in the HIF3α expressing lungs. In addition, aberrant basal cells were observed distally as determined by the expression of Sox2 and p63. We show that Hif3α binds a conserved HRE site in the Sox2 promoter and weakly transactivated a reporter construct containing the Sox2 promoter region. Moreover, Hif3α affected the expression of genes not typically involved in the hypoxia response, providing evidence for a novel function of Hif3α beyond the hypoxia response