The nerves of government: electronic networking and social control in the information society

Informatisation was introduced as a functional parameter in social and political research in 1978 (Nora & Minc 1978). Today, nearly a quarter of a century later, popular and academic political debates in the West appear to be growing increasingly aware of the intense interaction between information technology and social development. This project follows in the footsteps of this increased awareness and explores the meaning of digitisation for the socio- political concept of citizens' privacy.This project seeks to contribute to a wider body of literature that desires to provide meaningful answers to the following questions: (1) what sociotechnical trends are evident today in information privacy policies in the United Kingdom (UK) and the United States (US)? (2) What particular political visions do these trends seem to favour and what do these visions appear to suggest for the future of citizens' privacy in the West? (3) What is the potential importance of digital networking for practices of social management and control, both by governmental decision centres and commercial bodies?As case study for the above issues, the eventful appearance of two recent legislative works has been selected: the Regulation of Investigatory Powers Act (RIPA), enacted by the UK parliament in July 2000; and the Communications Assistance for Law Enforcement Act (CALEA), enacted in the US in 1994. Both Acts, which have yet to be fully implemented, in effect make it mandatory for all telecommunications operators and service providers to, among other things, ensure that their customers' communications can be intercepted by law enforcement and intelligence organisations, whose interception capabilities have been seriously hampered by the digitisation of telecommunications during the past few years.The project combines quantitative and qualitative data on RIPA and CALEA, which have been acquired through open- source, restricted or leaked government and industry reports on the subject, as well as through a number of interviews with informed individuals representing different sides of the communications interception (CI) debate. The development of communications interception is thus placed into the context of complex relationships between political actors, such as national policy experts and government advisors, state and corporate decision -makers and members of regulatory bodies

Inorganic lead (Pb)- and mercury (Hg)-induced neuronal cell death involves cytoskeletal reorganization

Inorganic lead and mercury are widely spread xenobiotic neurotoxicants threatening public health. The exposure to inorganic lead and mercury results in adverse effects of poisoning including IQ deficit and peripheral neuropathy. Additionally, inorganic neurotoxicants have even more serious impact on earlier stages of embryonic development. This study was therefore initiated in order to determine the cytotoxic effects of lead and mercury in earlier developmental stages of chick embryo. Administration of inorganic lead and mercury into the chick embryo resulted in the prolonged accumulation of inorganics in the neonatal brain, with detrimental cytotoxicity on neuronal cells. Subsequent studies demonstrated that exposure of chick embryo to inorganic lead and mercury resulted in the reorganization of cytoskeletal proteins in the neonatal brain. These results therefore suggest that inorganics-mediated cytoskeletal reorganization of the structural proteins, resulting in neurocytotoxicity, is one of the underlying mechanisms by which inorganics transfer deleterious effects on central nervous system

Iron-Responsive Olfactory Uptake of Manganese Improves Motor Function Deficits Associated with Iron Deficiency

Iron-responsive manganese uptake is increased in iron-deficient rats, suggesting that toxicity related to manganese exposure could be modified by iron status. To explore possible interactions, the distribution of intranasally-instilled manganese in control and iron-deficient rat brain was characterized by quantitative image analysis using T1-weighted magnetic resonance imaging (MRI). Manganese accumulation in the brain of iron-deficient rats was doubled after intranasal administration of MnCl2 for 1- or 3-week. Enhanced manganese level was observed in specific brain regions of iron-deficient rats, including the striatum, hippocampus, and prefrontal cortex. Iron-deficient rats spent reduced time on a standard accelerating rotarod bar before falling and with lower peak speed compared to controls; unexpectedly, these measures of motor function significantly improved in iron-deficient rats intranasally-instilled with MnCl2. Although tissue dopamine concentrations were similar in the striatum, dopamine transporter (DAT) and dopamine receptor D1 (D1R) levels were reduced and dopamine receptor D2 (D2R) levels were increased in manganese-instilled rats, suggesting that manganese-induced changes in post-synaptic dopaminergic signaling contribute to the compensatory effect. Enhanced olfactory manganese uptake during iron deficiency appears to be a programmed “rescue response” with beneficial influence on motor impairment due to low iron status

Occupational Neurologic Disorders in Korea

This article presents a schematic review of the clinical manifestations of occupational neurologic disorders in Korea and discusses the toxicologic implications of these conditions. Vascular encephalopathy, parkinsonism, chronic toxic encephalopathy, cerebellar dysfunction, peripheral neuropathy, and neurodegenerative diseases are common presentations of occupational neurotoxic syndromes in Korea. Few neurotoxins cause patients to present with pathognomic neurologic syndrome. Detailed neurologic examinations and categorization of the clinical manifestations of neurologic disorders will improve the clinical management of occupational neurologic diseases. Physicians must be aware of the typical signs and symptoms of possible exposure to neurotoxins, and they should also pay attention to less-typical, rather-vague symptoms and signs in workers because the toxicologic characteristics of occupational neurologic diseases in Korea have changed from typical patterns to less-typical or equivocal patterns. This shift is likely to be due to several years of low-dose exposure, perhaps combined with the effects of aging, and new types of possibly toxicant-related neurodegenerative diseases. Close collaboration between neurologists and occupational physicians is needed to determine whether neurologic disorders are work-related

Administration of Thimerosal to Infant Rats Increases Overflow of Glutamate and Aspartate in the Prefrontal Cortex: Protective Role of Dehydroepiandrosterone Sulfate

Thimerosal, a mercury-containing vaccine preservative, is a suspected factor in the etiology of neurodevelopmental disorders. We previously showed that its administration to infant rats causes behavioral, neurochemical and neuropathological abnormalities similar to those present in autism. Here we examined, using microdialysis, the effect of thimerosal on extracellular levels of neuroactive amino acids in the rat prefrontal cortex (PFC). Thimerosal administration (4 injections, i.m., 240 μg Hg/kg on postnatal days 7, 9, 11, 15) induced lasting changes in amino acid overflow: an increase of glutamate and aspartate accompanied by a decrease of glycine and alanine; measured 10–14 weeks after the injections. Four injections of thimerosal at a dose of 12.5 μg Hg/kg did not alter glutamate and aspartate concentrations at microdialysis time (but based on thimerosal pharmacokinetics, could have been effective soon after its injection). Application of thimerosal to the PFC in perfusion fluid evoked a rapid increase of glutamate overflow. Coadministration of the neurosteroid, dehydroepiandrosterone sulfate (DHEAS; 80 mg/kg; i.p.) prevented the thimerosal effect on glutamate and aspartate; the steroid alone had no influence on these amino acids. Coapplication of DHEAS with thimerosal in perfusion fluid also blocked the acute action of thimerosal on glutamate. In contrast, DHEAS alone reduced overflow of glycine and alanine, somewhat potentiating the thimerosal effect on these amino acids. Since excessive accumulation of extracellular glutamate is linked with excitotoxicity, our data imply that neonatal exposure to thimerosal-containing vaccines might induce excitotoxic brain injuries, leading to neurodevelopmental disorders. DHEAS may partially protect against mercurials-induced neurotoxicity

SMF-1, SMF-2 and SMF-3 DMT1 Orthologues Regulate and Are Regulated Differentially by Manganese Levels in C. elegans

Manganese (Mn) is an essential metal that can exert toxic effects at high concentrations, eventually leading to Parkinsonism. A major transporter of Mn in mammals is the divalent-metal transporter (DMT1). We characterize here DMT1-like proteins in the nematode C. elegans, which regulate and are regulated by Mn and iron (Fe) content. We identified three new DMT1-like genes in C. elegans: smf-1, smf-2 and smf-3. All three can functionally substitute for loss of their yeast orthologues in S. cerevisiae. In the worm, deletion of smf-1 or smf-3 led to an increased Mn tolerance, while loss of smf-2 led to increased Mn sensitivity. smf mRNA levels measured by QRT-PCR were up-regulated upon low Mn and down-regulated upon high Mn exposures. Translational GFP-fusions revealed that SMF-1 and SMF-3 strongly localize to partially overlapping apical regions of the gut epithelium, suggesting a differential role for SMF-1 and SMF-3 in Mn nutritional intake. Conversely, SMF-2 was detected in the marginal pharyngeal epithelium, possibly involved in metal-sensing. Analysis of metal content upon Mn exposure in smf mutants revealed that SMF-3 is required for normal Mn uptake, while smf-1 was dispensable. Higher smf-2 mRNA levels correlated with higher Fe content, supporting a role for SMF-2 in Fe uptake. In smf-1 and smf-3 but not in smf-2 mutants, increased Mn exposure led to decreased Fe levels, suggesting that both metals compete for transport by SMF-2. Finally, SMF-3 was post-translationally and reversibly down-regulated following Mn-exposure. In sum, we unraveled a complex interplay of transcriptional and post-translational regulations of 3 DMT1-like transporters in two adjacent tissues, which regulate metal-content in C. elegans