SAFE Professor Michalis Haliassos was a member of the Council for Research and Technology (ESET) established by the Government of Greece for the period 2010-2013. The council, consisting of eleven scientists from a range of disciplines, has now published their communique National Strategic Framework for Research and Innovation 2014-2020. To promote the advancement of research, technology and innovation in Greece, the strategic plan proposed by the authors seeks to identify areas of existing research strength and excellence that can be further advanced to become engines for progress and growth in Greece, as well as flaws inherent to the present system. The authors stress the need to address current constraints to growth, which include the declining education system; the confusion and weaknesses of RD the discontinuities and inefficiencies of resource allocation and investment; the lack of adaptation to clearly-defined national priorities; and the inadequate opportunities and funding for high-quality research and development to flourish. They stress the need for prioritisation and efficient allocation; stability of the policy frame; predictability of planning; provision of opportunity; recognition of excellence; and responsiveness to current and future needs.
Adrenal corticosteroids, i.e. glucocorticoids and mineralocorticoids, play important physiological roles in humans. Their actions are mediated by intracellular receptor molecules, the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR), which function as hormone-dependent transcription factors. Ligand-activated receptors modulate the transcription rates of responsive genes by interacting with responsive elements in the promoters of these genes or by influencing the activities of other transcription factors, via protein-protein interactions. Natural inactivating mutations of the GR or MR genes have been reported in humans with significant clinical phenotypes. The former causes sporadic or familial glucocorticoid resistance characterized by generalized partial insensitivity of tissues to glucocorticoids and subsequent activation of the hypothalamic/pituitary/adrenal axis with resultant hyperandrogenism in children and women and/or mineralocorticoid excess symptoms in both sexes. The latter develop pseudohypoaldosteronism type 1, i.e. hypotension and hyperkalaemic acidosis, as a result of reduced aldosterone actions in the kidney. An activating mutation in the MR gene causing early-onset, periodic hypertension was reported recently. The biological relevance of the GR and MR receptors was also addressed in mice whose GR or MR genes were inactivated or modified by gene targeting. The results were generally confirmatory of the concepts obtained by the human studies. Similarly, natural, compensated glucocorticoid and/or mineralocorticoid 'resistance' were described in several mammalian species, including non-human primates and rodents. Here we discuss the actions of GR and MR and the molecular defects of naturally occuring mutations in these receptors with associated pathophysiological changes.
No abstract is provided for this article.
No abstract is provided for this article.
Glucocorticoids, the major effector hormones of the stress system, influence almost all aspects of mammalian physiology. These steroids exert their effects on a large network of primary, secondary, and tertiary target genes, encompassing up to 20% of the expressed genome in a tissue. New evidence shows quantitative and qualitative gender-specific differences in the actions of glucocorticoids on the rat liver transcriptome, suggesting that the pervasive actions of these hormones are modulated by gender, both as an inherent property of the target tissues and as a result of exposure of these tissues to estrogens and possibly also androgens. Generally, albeit not always, female mammals have more robust behavioral and somatic responses to stress and more potent immune and inflammatory reactions than males--differences that are inherent, sex steroid-mediated, or both and possibly the evolutionary products of natural selection of female and male roles.
