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Direct Regulation (direct + regulation)
Selected AbstractsPolitics, industry and the regulation of industrial greenhouse-gas emissions in the UK and GermanyENVIRONMENTAL POLICY AND GOVERNANCE, Issue 4 2004Ian Bailey This paper assesses the impact of ,new' environmental policy instruments (NEPIs), such as eco-taxes, tradable permits and environmental agreements, on the politics of regulating industrial greenhouse-gas emissions. Intense academic debate surrounds the extent to which environmental policy is driven by the public interest, public choices between actor and stakeholder interests, or embedded institutional traditions. However, the effects on environmental politics of the recent shift from direct regulation to NEPIs remain seriously under-researched. Surveys and interviews with industry and policy-makers on the implementation of United Kingdom and German climate policy indicate that, although economic pressures do influence the design of policy instruments, public choice is far from dominant; nor are industry reactions to particular NEPIs uniform between countries. This suggests that national institutional traditions are far more influential in informing policy choices and industry reactions to policy innovations than is often acknowledged. Copyright © 2004 John Wiley &,Sons, Ltd and ERP,Environment. [source] Pituitary Transcription Factors: From Congenital Deficiencies to Gene TherapyJOURNAL OF NEUROENDOCRINOLOGY, Issue 9 2006M. H. Quentien Despite the existence of interspecies phenotypic variability, animal models have yielded valuable insights into human pituitary diseases. Studies on Snell and Jackson mice known to have growth hormone, prolactin and thyroid-stimulating hormone deficiencies involving the hypoplastic pituitary gland have led to identifying alterations of the pituitary specific POU homeodomain Pit-1 transcription factor gene. The human phenotype associated with rare mutations in this gene was found to be similar to that of these mice mutants. Terminal differentiation of lactotroph cells and direct regulation of the prolactin gene both require interactions between Pit-1 and cell type specific partners, including panpituitary transcriptional regulators such as Pitx1 and Pitx2. Synergistic activation of the prolactin promoter by Pitx factors and Pit-1 is involved not only in basal condition, but also in responsiveness to forskolin, thyrotrophin-releasing-hormone and epidermal growth factor. In corticotroph cells, Pitx1 interacts with Tpit. Tpit mutations have turned out to be the main molecular cause of neonatal isolated adrenocorticotrophin deficiency. This finding supports the idea that Tpit plays an essential role in the differentiation of the pro-opiomelanocortin pituitary lineage. The effects of Pit-1 are not restricted to hormone gene regulation because this factor also contributes to cell division and protects the cell from programmed cell death. Lentiviral vectors expressing a Pit-1 dominant negative mutant induced time- and dose-dependent cell death in somatotroph and lactotroph adenomas in vitro. Gene transfer by lentiviral vectors should provide a promising step towards developing an efficient specific therapeutic approach by which a gene therapy programme for treating human pituitary adenomas could be based. [source] Incentives for pollution abatement: Regulation, regulatory threats, and non-governmental pressuresJOURNAL OF POLICY ANALYSIS AND MANAGEMENT, Issue 3 2003Kathryn Harrison In the last decade, voluntary efforts by firms to reduce their environmental impacts have received increasing attention from both policymakers and scholars. This article discusses polluters' incentives to reduce their releases. In particular, using data from Canada's National Pollutant Release Inventory, it examines the impacts of conventional regulation, threats of regulation, and non-governmental pressures facilitated by public dissemination of information about pollutant releases. The vast majority of reductions reported to the inventory to date were found not to be voluntary, as has often been assumed, but are, rather, the result of direct regulation of a relatively small number of polluters. Strong effects of federal regulation were found among other sources, as well, with much weaker responses to the mere threat of regulation. However, of concern are the growth of less visible waste streams,such as land disposal and underground injection,as well as transfers of wastes to other communities. Finally, evidence is reported that some waste streams are increasing in toxicity, an effect that may outweigh the benefits of reductions in releases. © 2003 by the Association for Public Policy Analysis and Management. [source] MicroRNA-29, a key regulator of collagen expression in systemic sclerosisARTHRITIS & RHEUMATISM, Issue 6 2010Britta Maurer Objective To investigate the role of microRNA (miRNA) as posttranscriptional regulators of profibrotic genes in systemic sclerosis (SSc). Methods MicroRNA, which target collagens, were identified by in silico analysis. Expression of miRNA-29 (miR-29) was determined by TaqMan real-time polymerase chain reaction analysis of skin biopsy and fibroblast samples from SSc patients and healthy controls as well as in the mouse model of bleomycin-induced skin fibrosis. Cells were transfected with precursor miRNA (pre-miRNA)/anti-miRNA of miR-29 using Lipofectamine. Collagen gene expression was also studied in luciferase reporter gene assays. For stimulation, recombinant transforming growth factor , (TGF,), platelet-derived growth factor B (PDGF-B), or interleukin-4 (IL-4) was used. The effects of inhibiting PDGF-B and TGF, signaling on the levels of miR-29 were studied in vitro and in the bleomycin model. Results We found that miR-29a was strongly down-regulated in SSc fibroblasts and skin sections as compared with the healthy controls. Overexpression in SSc fibroblasts significantly decreased, and accordingly, knockdown in normal fibroblasts increased, the levels of messenger RNA and protein for type I and type III collagen. In the reporter gene assay, cotransfection with pre-miR-29a significantly decreased the relative luciferase activity, which suggests a direct regulation of collagen by miR-29a. TGF,, PDGF-B, or IL-4 reduced the levels of miR-29a in normal fibroblasts to those seen in SSc fibroblasts. Similar to human SSc, the expression of miR-29a was reduced in the bleomycin model of skin fibrosis. Inhibition of PDGF-B and TGF, pathways by treatment with imatinib restored the levels of miR-29a in vitro and in the bleomycin model in vivo. Conclusion These data add the posttranscriptional regulation of collagens by miR-29a as a novel aspect to the fibrogenesis of SSc and suggest miR-29a as a potential therapeutic target. [source] Claudin-5a in developing zebrafish brain barriers: another brick in the wallBIOESSAYS, Issue 9 2010Salim Abdelilah-Seyfried Abstract Claudins serve essential roles in regulating paracellular permeability properties within occluding junctions. Recent studies have begun to elucidate developmental roles of claudins within immature tissues. This work has uncovered an involvement of several claudins in determining tight junction properties that have an effect on embryonic morphogenesis and physiology. During zebrafish brain morphogenesis, Claudin-5a determines the paracellular permeability of tight junctions within a transient neuroepithelial-ventricular barrier that maintains the hydrostatic fluid pressure required for brain ventricular lumen expansion. However, the roles of Claudins in development may well extend beyond being mere junctional components. Several post-translational modifications of Claudins have been characterized that indicate a direct regulation by developmental signals. This review focuses on the involvement of Claudin-5a in cerebral barrier formation in the zebrafish embryo and includes some speculations about possible modes of regulation. [source] Excitation,Contraction Coupling In Skeletal Muscle: Comparisons With Cardiac MuscleCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2000Gd Lamb SUMMARY 1. The present review describes the mechanisms involved in controlling Ca2+ release from the sarcoplasmic reticulum (SR) of skeletal muscle, which ultimately regulates contraction. 2. Comparisons are made between cardiac and skeletal muscle with respect to: (i) the role of the dihydropyridine receptors (DHPR) as Ca2+ channels and voltage-sensors; (ii) the regulation of the ryanodine receptor (RyR)/Ca2+ -release channels in the SR; and (iii) the importance of Ca2+ -induced Ca2+ release. 3. It is shown that the key differences of the skeletal muscle Ca2+ -release channel (RyR1), namely the increase in its stimulation by ATP and its inhibition by Mg2+, are critical for its direct regulation by the associated DHPR and, consequently, for the fast, accurate control of skeletal muscle contraction. [source] | ||||||||||