Fluid reasoning and the developing brain.

Fluid reasoning is the cornerstone of human cognition, both during development and in adulthood. Despite this, the neural mechanisms underlying the development of fluid reasoning are largely unknown. In this review, we provide an overview of this important cognitive ability, the method of measurement, its changes over the childhood and adolescence of an individual, and its underlying neurobiological underpinnings. We review important findings from psychometric, cognitive, and neuroscientific literatures, and outline important future directions for this interdisciplinary research

Brain drain in developing countries

Relying on an original data set on international migration by educational attainment for 1990 and 2000, we analyze the determinants of the brain drain from developing countries. We start from a simple decomposition of the brain drain in two multiplicative components, the degree of openess of sending countries (as measured by their average emigration rate) and the schooling gap (as measured by the relative education level of emigrants compared to natives). Using various regression models, we put forward the determinants of the components and explain cross-country differences in skilled migration. unsurprisingly, the brain drain is strong in small countries which are not too distant from the major OECD regions, which share colonial links with OECD countries and which send most of their migrants to host countries where quality-selective immigration programs exist. More interestingly, the brain drain increases with political instability and the degree of fractionalization at origin; it globally decreases with natives’human capital.International migration, Brain drain, Human capital, Developping countries

Effect of lithium on acetylcholine esterase activity, and isozyme pattern in developing chick brain

Acetylcholine Esterase is an enzyme, which hydrolyses acetylcholine and is used as a marker for cholinergic neural function. It is known to be involved in synaptogenesis. While on one hand it is known to be a marker for the developing chick brain it is also implicated in neurodegenerative diseases. In vertebrates the protein is synthesized by a single gene and undergoes alternative splicing to give 6-8 isoforms. Isozyme patterns of acetylcholine esterase have been suggested to be useful prognostic markers of neuronal degeneration. Lithium a well-known teratogen is known to induce apoptosis in the developing chick brain. Understanding the dynamics of acetylcholine esterase isoform pattern in lithium induced neural tissue damage would help elucidating the role of these isoforms in frank neurodegenerative diseases. We have therefore studied activity and isozyme pattern of acetylcholine esterase in lithium treated and control 7 day old developing chick brain and report the same

Skilled migration: the perspective of developing countries

This chapter focuses on the effects of skilled migration on developing countries. We first present new evidence on the magnitude of the "brain drain" at the international level. Using a stylized model of education investment in a context of migration, we then survey the theoretical and empirical brain drain literature in a unified framework. Finally we use a particular specification of the model to discuss a number of policy issues from the perspective of developing countries.Migration; Brain Drain;

Involvement of the JNK/FOXO3a/Bim Pathway in Neuronal Apoptosis after Hypoxic-Ischemic Brain Damage in Neonatal Rats.

c-Jun N-terminal kinase (JNK) plays a key role in the regulation of neuronal apoptosis. Previous studies have revealed that forkhead transcription factor (FOXO3a) is a critical effector of JNK-mediated tumor suppression. However, it is not clear whether the JNK/FOXO3a pathway is involved in neuronal apoptosis in the developing rat brain after hypoxia-ischemia (HI). In this study, we generated an HI model using postnatal day 7 rats. Fluorescence immunolabeling and Western blot assays were used to detect the distribution and expression of total and phosphorylated JNK and FOXO3a and the pro-apoptotic proteins Bim and CC3. We found that JNK phosphorylation was accompanied by FOXO3a dephosphorylation, which induced FOXO3a translocation into the nucleus, resulting in the upregulation of levels of Bim and CC3 proteins. Furthermore, we found that JNK inhibition by AS601245, a specific JNK inhibitor, significantly increased FOXO3a phosphorylation, which attenuated FOXO3a translocation into the nucleus after HI. Moreover, JNK inhibition downregulated levels of Bim and CC3 proteins, attenuated neuronal apoptosis and reduced brain infarct volume in the developing rat brain. Our findings suggest that the JNK/FOXO3a/Bim pathway is involved in neuronal apoptosis in the developing rat brain after HI. Agents targeting JNK may offer promise for rescuing neurons from HI-induced damage