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Legal aspects of withdrawing nourishment from an incurably ill patient.
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Right to die (second of two parts): a set of fact sheets.
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Evolving Delaware law on the termination of life-sustaining treatment.
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A unique palindromic element mediates gamma interferon induction of mig gene expression.
To define the molecular mechanisms involved in the action of gamma interferon (IFN-gamma), we have analyzed the transcriptional regulation of the mig (monokine induced by gamma interferon) gene, a member of the platelet factor 4-interleukin-8 cytokine family that is expressed in murine macrophages specifically in response to IFN-gamma. Analysis of mig/CAT chimeric constructs transiently transfected into the RAW 264.7 mouse monocytic cell line revealed a unique IFN-gamma-responsive element (gamma RE-1). The sequence of this cis regulatory element defined by deletion analysis contains an imperfect inverted repeat extending 27 bp. Examination of mig/CAT constructs with mutations in gamma RE-1 revealed that the palindromic positions in the element were essential for activity. Consistent with its function as an enhancer, a single copy of gamma RE-1 conferred IFN-gamma inducibility to a heterologous (herpes simplex virus thymidine kinase) promoter. Exonuclease III protection assays demonstrated symmetrical protection of a mig promoter fragment centered about the gamma RE-1 palindromic sequence. Using the gel electrophoretic mobility shift assay, we identified a factor (gamma RF-1) present in nuclear extracts prepared from IFN-gamma-stimulated RAW 264.7 cells which binds to gamma RE-1. The activation of gamma RF-1 occurred rapidly (within 1 min) in response to IFN-gamma and was independent of protein synthesis. Similar to the expression of mig mRNA, the formation of gamma RF-1 was selectively induced by IFN-gamma and not IFN-alpha. The regulation of gene expression through gamma RF-1 and gamma RE-1 may explain the preferential activation of a subset of interferon-inducible genes by IFN-gamma.
Evidence for declining levels of heavy-metals in the Severn Estuary and Bristol Channel, U.K. and their spatial distribution in sediments.
Levels of heavy-metals (Cd, Cu, Cr, Ni, Pb and Zn) in suspended particulate and in surface and subsurface sediments were determined at seven locations in the Severn Estuary and Bristol Channel. Sediment metal concentrations were highest at sites close to industrial centres but levels have decreased significantly over the last 30 years so that they are now close to, or meet, environmental quality guidelines. The greatest metal concentrations in deposited sediments were usually associated with the finest particulates at locations with muddy sediments, but this was not always true at sites with predominantly sandy sediments. The metals bound to suspended particulates at all sites were remarkably consistent, presumably reflecting the mixing capacity of this macro-tidal estuary. The re-exposure of older, more contaminated sediments could explain the observed differences between deposited and suspended material. Sediment redistribution due to strong seasonal currents might also explain the differences between winter and summer samples.
IFN-gamma induces a p91/Stat1 alpha-related transcription factor with distinct activation and binding properties.
The 5' flanking region of the mig gene, a member of the chemokine family of small m.w. chemoattractant and growth regulatory factors, contains an IFN-gamma-responsive enhancer, gamma RE-1, consisting of an extended imperfect palindrome. In this report we show that a novel factor, gamma RF-1, which binds to the gamma RE-1 element, is rapidly activated in a variety of primary cell types and tumor cell lines treated with IFN-gamma. Our data indicate that gamma RF-1 is present in a latent form in unstimulated cells and its DNA-binding activity is dependent upon tyrosine phosphorylation. UV cross-linking studies revealed that gamma RF-1 consists of at least two proteins of approximately 95 and 130 kDa, which interact with the gamma RE-1 element. A comparison of gamma RF-1 and GAF, an IFN-gamma-activated transcription factor containing the p91/Stat1 alpha protein (Stat, signal transducer and activator of transcription), showed that these two factors exhibited differences in electrophoretic mobility, responsiveness to IFN-alpha, and kinetics of activation. Using anti-Stat Ab, however, we found that one or more subunits of gamma RF-1 are antigenically related to p91/Stat1 alpha. Our results indicate, therefore, that gamma RF-1 and GAF are distinct IFN-gamma-responsive transcription factors and probably contain closely related members of the Stat protein family.