The Educational Gender Gap in Latin America and the Caribbean

This paper analyzes the evolution of gender differences in school attendance and attainment in Latin America and the Caribbean, for both adults who left the educational system and children in school. For individuals 21 years old and above the paper uses a cohort analysis of school attainment. The results indicate that the schooling gap has closed for the cohort born at the end of the 1960s. Since then, the gap has reversed such that within the cohort born in 1980, females have, on average, ¼ of a schooling year more than males. During the four decades of birth cohorts of our analysis (1940-1980) the gender gap in attainment has moved in favor of females at a pace of 0. 27 years of schooling per decade. A decomposition exercise suggests that the changes in the schooling gap are mainly explained by the educational attainment of females at the higher levels, rather than improvements in the early years of education. An analysis of attendance and attainment among girls and boys between 6 and 18, for Bolivia, Guatemala, Mexico and Peru (the countries that have not closed the gap in adult schooling attainment) reveals noticeable gender differences, favoring boys, only among older children of the lowest income quintiles and indigenous ethnicity.

Treatment Options for Paediatric Anaplastic Large Cell Lymphoma (ALCL): Current Standard and beyond.

Anaplastic Lymphoma Kinase (ALK)-positive Anaplastic Large Cell Lymphoma (ALCL), remains one of the most curable cancers in the paediatric setting; multi-agent chemotherapy cures approximately 65-90% of patients. Over the last two decades, major efforts have focused on improving the survival rate by intensification of combination chemotherapy regimens and employing stem cell transplantation for chemotherapy-resistant patients. More recently, several new and 'renewed' agents have offered the opportunity for a change in the paradigm for the management of both chemo-sensitive and chemo-resistant forms of ALCL. The development of ALK inhibitors following the identification of the EML4-ALK fusion gene in Non-Small Cell Lung Cancer (NSCLC) has opened new possibilities for ALK-positive ALCL. The uniform expression of CD30 on the cell surface of ALCL has given the opportunity for anti-CD30 antibody therapy. The re-evaluation of vinblastine, which has shown remarkable activity as a single agent even in the face of relapsed disease, has led to the consideration of a revised approach to frontline therapy. The advent of immune therapies such as checkpoint inhibition has provided another option for the treatment of ALCL. In fact, the number of potential new agents now presents a real challenge to the clinical community that must prioritise those thought to offer the most promise for the future. In this review, we will focus on the current status of paediatric ALCL therapy, explore how new and 'renewed' agents are re-shaping the therapeutic landscape for ALCL, and identify the strategies being employed in the next generation of clinical trials

Early recruitment of boreal forest trees in hybrid poplar plantations of different densities on mine waste rock slopes

Mine wastes create harsh recruitment conditions for forest tree seedlings, especially waste rock piles where erodible slopes are prone to drought. Plantations using fast-growing tree species can potentially accelerate the conversion of degraded mine sites into forests through facilitation of tree recruitment, while contributing to the stability of slopes. In this study, hybrid poplars were tested as a means of achieving reclamation objectives by providing shelter for forest tree seedlings on waste rock slopes (3H:1V ratio) in the Canadian southern boreal region. Density effects of young hybrid poplars were assessed on the emergence and survival of early, mid and late successional species, naturally occurring or hand-seeded, and on the understory micro-environmental parameters in plantations of different spacings (1 × 1, 2 × 2, 4 × 4 m and control without planted trees). Results were also compared in 2 × 2-m plantations with and without a hydroseeded herbaceous cover, traditionally used to control erosion in slopes. During the 2nd growing season of the plantations, seedling emergence of naturally established Salicaceae (Populus and Salix) species followed a quadratic pattern along the density gradient, as emergence values were higher under an intermediary density. Nonetheless, decrease in light transmission emerged as a limiting factor of seedling survival for these early-successional, shade-intolerant species by the next summer. Following a spring sowing experiment in the 3rd growing season of the plantations, emergence rates for later-successional Picea glauca and Abies balsamea seedlings increased with hybrid poplar density. During their peak emergence period, in early season, higher soil moisture content was found under denser cover. However, at the end of the third year of the plantations, only A. balsamea showed moderate increase in early recruitment success rates under denser tree cover. In hydroseeded plots, a competitive effect of the herbaceous cover was observed on Salicaceae emergence and A. balsamea survival. These results suggest that planting of young plantations without a hydroseeded cover may offer a more suitable solution in order to quickly provide early recruitment opportunities for later-successional seedlings in waste rock slopes. Despite this, a significant decrease in moisture content recorded during the second half of the 3rd growing season under the 1 × 1-m cover, compared to the 2 × 2-m, likely signalled an increasing competitive effect from hybrid poplars, which may compromise their nursing potential in the longer term. Therefore, further monitoring is imperative for a better understanding of longer-term facilitation and competition interactions between nurse trees and understory seedlings in waste rock slopes, where competition for limited resources, such as water, may be severe

N-terminal myristoylation is required for membrane localization of cGMP-dependent protein kinase type II

The apical membrane of intestinal epithelial cells harbors a unique isozyme of cGMP-dependent protein kinase (cGK type II) which acts as a key regulator of ion transport systems, including the cystic fibrosis transmembrane conductance regulator (CFTR)-chloride channel. To explore the mechanism of cGK II membrane-anchoring, recombinant cGK II was expressed stably in HEK 293 cells or transiently in COS-1 cells. In both cell lines, cGK II was found predominantly in the particulate fraction. Immunoprecipitation of solubilized cGK II did not reveal any other tightly associated proteins, suggesting a membrane binding motif within cGK II itself. The primary structure of cGK II is devoid of hydrophobic transmembrane domains; cGK II does, however, contain a penultimate glycine, a potential acceptor for a myristoyl moiety. Metabolic labeling showed that cGK II was indeed able to incorporate [3H]myristate. Moreover, incubation of cGK II-expressing 293 cells with the myristoylation inhibitor 2-hydroxymyristic acid (1 mM) significantly increased the proportion of cGK II in the cytosol from 10 +/- 5 to 35 +/- 4%. Furthermore, a nonmyristoylated cGK II Gly2 --> Ala mutant was localized predominantly in the cytosol after transient expression in COS-1 cells. The absence of the myristoyl group did not affect the specific enzyme activity or the Ka for cGMP and only slightly enhanced the thermal stability of cGK II. These results indicate that N-terminal myristoylation fulfills a crucial role in directing cGK II to the membrane

Red light variation an effective alternative to regulate biomass and lipid profiles in Phaeodactylum tricornutum

Abstract: Marine water diatom Phaeodactylum tricornutum is a photosynthetic organism that is known to respond to the changing light environment and adapt to different temperatures to prevent photoinhibition and maintain its metabolic functions. The objective of the present study was to test whether light shift variations in different growth phases impact the growth and lipid metabolism of P. tricornutum. Thus, we investigated R exposure in different growth phases to find the most effective light shift condition. The results showed that substituting white light (W) by red light (R) under autotrophic conditions, a condition called red shift (RS), increased biomass and lipid content compared to levels found under continuous W or R exposure alone. We observed an increase by 2-fold biomass and 2.3-fold lipid content in RS as compared to W. No significant change was observed in the morphology of lipid droplets, but the fatty acid (FA) composition was altered. Specifically, polyunsaturated FAs were increased, whereas monounsaturated FAs decreased in P. tricornutum grown in RS compared to W control. Therefore, we propose that a light shift during the beginning of the stationary phase is a low-cost cultivation strategy to boost the total biomass and lipids in P. tricornutum

Isotype-specific activation of cystic fibrosis transmembrane conductance regulator-chloride channels by cGMP-dependent protein kinase II

Type II cGMP-dependent protein kinase (cGKII) isolated from pig intestinal brush borders and type I alpha cGK (cGKI) purified from bovine lung were compared for their ability to activate the cystic fibrosis transmembrane conductance regulator (CFTR)-Cl- channel in excised, inside-out membrane patches from NIH-3T3 fibroblasts and from a rat intestinal cell line (IEC-CF7) stably expressing recombinant CFTR. In both cell models, in the presence of cGMP and ATP, cGKII was found to mimic the effect of the catalytic subunit of cAMP-dependent protein kinase (cAK) on opening CFTR-Cl-channels, albeit with different kinetics (2-3-min lag time, reduced rate of activation). By contrast, cGKI or a monomeric cGKI catalytic fragment was incapable of opening CFTR-Cl- channels and also failed to potentiate cGKII activation of the channels. The cAK activation but not the cGKII activation was blocked by a cAK inhibitor peptide. The slow activation by cGKII could not be ascribed to counteracting protein phosphatases, since neither calyculin A, a potent inhibitor of phosphatase 1 and 2A, nor ATP gamma S (adenosine 5'-O-(thiotriphosphate)), producing stable thiophosphorylation, was able to enhance the activation kinetics. Channels preactivated by cGKII closed instantaneously upon removal of ATP and kinase but reopened in the presence of ATP alone. Paradoxically, immunoprecipitated CFTR or CF-2, a cloned R domain fragment of CFTR (amino acids 645-835) could be phosphorylated to a similar extent with only minor kinetic differences by both isotypes of cGK. Phosphopeptide maps of CF-2 and CFTR, however, revealed very subtle differences in site-specificity between the cGK isoforms. These results indicate that cGKII, in contrast to cGKI alpha, is a potential activator of chloride transport in CFTR-expressing cell types

Isotype-specific activation of cystic fibrosis transmembrane conductance regulator-chloride channels by cGMP-dependent protein kinase II

Type II cGMP-dependent protein kinase (cGKII) isolated from pig intestinal brush borders and type Iα cGK (cGKI) purified from bovine lung were compared for their ability to activate the cystic fibrosis transmembrane conductance regulator (CFTR)-Cl- channel in excised, inside-out membrane patches from NIH-3T3 fibroblasts and from a rat intestinal cell line (IEC-CF7) stably expressing recombinant CFTR. In both cell models, in the presence of cGMP and ATP, cGKII was found to mimic the effect of the catalytic subunit of cAMP- dependent protein kinase (cAK) on opening CFTR-Cl-channels, albeit with different kinetics (2-3-min lag time, reduced rate of activation). By contrast, cGKI or a monomeric cGKI catalytic fragment was incapable of opening CFTR-Cl- channels and also failed to potentiate cGKII activation of the channels. The cAK activation but not the cGKII activation was blocked by a cAK inhibitor peptide. The slow activation by cGKII could not be ascribed to counteracting protein phosphatases, since neither calyculin A, a potent inhibitor of phosphatase 1 and 2A, nor ATPγS (adenosine 5'-O- (thiotriphosphate)), producing stable thiophosphorylation, was able to enhance the activation kinetics. Channels preactivated by cGKII closed instantaneously upon removal of ATP and kinase but reopened in the presence of ATP alone. Paradoxically, immunoprecipitated CFTR or CF-2, a cloned R domain fragment of CFTR (amino acids 645-835) could be phosphorylated to a similar extent with only minor kinetic differences by both isotypes of cGK. Phosphopeptide maps of CF-2 and CFTR, however, revealed very subtle differences in site-specificity between the cGK isoforms. These results indicate that cGKII, in contrast to cGKIα, is a potential activator of chloride transport in CFTR-expressing cell types.</p

M & L Jaargang 21/2

Suzanne Van Aerschot-Van Haeverbeeck Brugge Werelderfgoed. [Bruges on the World Heritage List.]Hugo Vandenborre en Anne Botte De Brugse Sint-Annakerk. Een weelderig barok interieur in een sobere parochiekerk. [The Bruges St Annes church: a sumptuous Baroque interior behind the facade of a sober parish church.]Dirk Van Eenhooge Middeleeuwse Brugse huizen: bouwhistorisch onderzoek in de Florentijnse loge en het huis Hertsberghe in de Academiestraat. [Medieval Houses in Bruges (1): the Florentijnse Loge and house Hertsberghe.]Frans Caignie Een betegelde schouw in het Osterrieth-huis te Antwerpen. [A tiled chimney in the Osterrieth-house in Antwerp.]Summar

cGMP stimulation of cystic fibrosis transmembrane conductance regulator Cl- channels co-expressed with cGMP-dependent protein kinase type II but not type Ibeta

In order to investigate the involvement of cGMP-dependent protein kinase (cGK) type II in cGMP-provoked intestinal Cl- secretion, cGMP-dependent activation and phosphorylation of cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels was analyzed after expression of cGK II or cGK Ibeta in intact cells. An intestinal cell line which stably expresses CFTR (IEC-CF7) but contains no detectable endogenous cGK II was infected with a recombinant adenoviral vector containing the cGK II coding region (Ad-cGK II) resulting in co-expression of active cGK II. In these cells, CFTR was activated by membrane-permeant analogs of cGMP or by the cGMP-elevating hormone atrial natriuretic peptide as measured by 125I- efflux assays and whole-cell patch clamp analysis. In contrast, infection with recombinant adenoviruses expressing cGK Ibeta or luciferase did not convey cGMP sensitivity to CFTR in IEC-CF7 cells. Concordant with the activation of CFTR by only cGK II, infection with Ad-cGK II but not Ad-cGK Ibeta enabled cGMP analogs to increase CFTR phosphorylation in intact cells. These and other data provide evidence that endogenous cGK II is a key mediator of cGMP-provoked activation of CFTR in cells where both proteins are co-localized, e. g. intestinal epithelial cells. Furthermore, they demonstrate that neither the soluble cGK Ibeta nor cAMP-dependent protein kinase are able to substitute for cGK II in this cGMP-regulated function