bluuebunny/crossref_metadata_2025_split huggingface dataset:
A novel mechanism for evoked responses in the human brain
Authors: Nikulin Vadim V. , Linkenkaer‐Hansen Klaus , Nolte Guido , Lemm Steven , Müller Klaus R. , Ilmoniemi Risto J. , Curio Gabriel 
Published: June 2007

AbstractMagnetoencephalographic and electroencephalographic evoked responses are primary real‐time objective measures of cognitive and perceptual processes in the human brain. Two mechanisms (additive activity and phase reset) have been debated and considered as the only possible explanations for evoked responses. Here we present theoretical and empirical evidence of a third mechanism contributing to the generation of evoked responses. Interestingly, this mechanism can be deduced entirely from the characteristics of spontaneous oscillations in the absence of stimuli. We show that the amplitude fluctuations of neuronal α oscillations at rest are associated with changes in the mean value of ongoing activity in magnetoencephalography, a phenomenon that we term baseline shifts associated with α oscillations. When stimuli modulate the amplitude of α oscillations, baseline shifts become the basis of a novel mechanism for the generation of evoked responses; the averaging of several trials leads to a cancellation of the oscillatory component but the baseline shift remains, which gives rise to an evoked response. We propose that the presence of baseline shifts associated with α oscillations can be explained by the asymmetric flow of inward and outward neuronal currents related to the generation of α oscillations. Our findings are relevant to the vast majority of electroencephalographic and magnetoencephalographic studies involving perceptual, cognitive and motor activity.
Assembly of two distinct dimers and higher‐order oligomers from full‐length tau
Authors: Sahara Naruhiko , Maeda Sumihiro , Murayama Miyuki , Suzuki Takehiro , Dohmae Naoshi , Yen Shu‐Hui , Takashima Akihiko 
Published: June 2007

AbstractAbnormal accumulation of tau as filamentous structures is a neuropathological hallmark of neurodegenerative diseases referred to as tauopathies. Little is known about the role of native cysteine residues in tau assembly because their substitution with other amino acids has no effect on tau filament morphology. To understand the process involved in tau oligomerization, we analysed both heparin‐induced assembly of different forms of recombinant human tau and assembly of tau from COS‐7 cells transiently expressing different human tau constructs. Here, we demonstrated that tau assembly involves two distinct dimers (cysteine‐dependent and cysteine‐independent) that differ in resistance to reduction. During assembly, an increase of cysteine‐dependent tau oligomer was observed prior to detection of increased thioflavin T fluorescence signals. The latter event was accompanied by an increase of cysteine‐independent dimer. Fewer higher‐order oligomers and aggregates were assembled from four‐repeat tau containing two amino‐terminus inserts that have either the C291A/C322A mutation (cysless‐4R2N) or a hexapeptide deletion at residues 306–311 (ΔPHF6–4R2N) compared with those assembled from wild‐type tau. Assembly of distinct types of dimers was also observed in lysates from COS‐7 cells expressing wild‐type 4R2N and brain extracts from mice expressing P301L mutant tau. In contrast, COS‐7 cells expressing cysless‐ or ΔPHF6–4R2N tau contained very little cysteine‐dependent dimer. Together, the results indicate that intermolecular disulfide crosslinking along with PHF6 hexapeptide facilitates tau oligomerization and that this event is accompanied by cysteine‐independent intermolecular bridging of microtubule‐binding domain, leading to assembly of higher‐order oligomers. The levels of these dimers may be used to gauge the potential for tau assembly.
5‐HT2Creceptor activation inhibits appetitive and consummatory components of feeding and increases brain c‐fosimmunoreactivity in mice
Authors: Somerville Elizabeth M. , Horwood Julia M. , Lee Michelle D. , Kennett Guy A. , Clifton Peter G. 
Published: June 2007

Abstract5‐Hydroxytryptamine (5‐HT)2Cand 5‐HT1Breceptors are implicated in the inhibitory modulation of feeding behaviour. However, their respective, and possibly different, roles have not been clearly identified because of a lack of selective 5‐HT2Creceptor agonists. Here, using the putative, selective 5‐HT2Creceptor agonist VER23779, we show that its effects on feeding are fully reversed by pretreatment with a selective 5‐HT2Creceptor antagonist, but unaffected by pretreatment with either a 5‐HT1Bor a 5‐HT2Areceptor antagonist. In mice eating a palatable mash, feeding ends earlier, inactivity is increased but the behavioural satiety sequence is preserved. In a second‐order schedule of reinforcement with an initial, non‐food‐reinforced appetitive phase, VER23779 produces a much greater relative reduction in appetitive responding than the 5‐HT1Breceptor agonist CP‐94,253. Increased c‐fosimmunoreactivity patterns following VER23779 also differ from those described for CP‐94,253, in particular showing strong activation of the basolateral amygdala. The different behavioural consequences of 5‐HT2Cand 5‐HT1Breceptor activation may relate to the patterns of c‐fosimmunoreactivity. In particular, the basolateral amygdala may have a role in maintaining response in the appetitive phase of the second‐order schedule and also be susceptible to serotonergic modulation through activation of 5‐HT2Creceptors.
Synaptic plasticity of the CA3 commissural projection in epileptic rats: an in vivo electrophysiological study
Authors: Queiroz Claudio M. T. , Mello Luiz Eugênio 
Published: June 2007

AbstractThe hippocampal commissural system has recently been found to participate in the generation of mirror foci after kainate‐induced epileptiform discharges. In the present study we have evaluated the electrophysiological alterations in the ventral commissural hippocampal system that originates in the pyramidal CA3 cells and connects to the contralateral CA3 pyramidal cells. The recordings were performed in epileptic rats 24 h after an early behavioural spontaneous seizure between 5 and 21 days after pilocarpine‐induced status epilepticus. Epileptic animals presented a marked increase in neuronal excitability after contralateral CA3 stimulation, characterized by a shift to the left in the input–output curve and the clear appearance of a population spike. Input–output curves showed that maximum population excitatory postsynaptic potential (pEPSP) amplitude was decreased by 30%, which could be related to cell death in these regions. Using paired‐pulse protocols to evaluate a fast form of synaptic plasticity (i.e. paired‐pulse facilitation) we observed that, despite the similar pEPSP amplitude between control and experimental groups, only epileptic animals showed strong paired‐pulse population spike facilitation up to 500 ms interstimulus intervals. Despite increased excitability and pyramidal cell death, epileptic animals presented a more robust potentiation after high‐frequency stimulation than controls, a protocol used to evaluate a slow form of synaptic plasticity (i.e. long‐term potentiation). The increased excitability in CA3 pyramidal neurons enhanced the probability of burst activity in these neurons; this could lead to greater CA1 synchronization. The present results might have relevance for the understanding of epileptogenesis and of learning and memory deficits seen in temporal lobe epilepsy.
Proteasome‐dependent and ‐independent mechanisms for FosB destabilization: identification of FosB degron domains and implications for ΔFosB stability
Authors: Carle Tiffany L. , Ohnishi Yoshinori N. , Ohnishi Yoko H. , Alibhai Imran N. , Wilkinson Matthew B. , Kumar Arvind , Nestler Eric J. 
Published: June 2007

AbstractThe transcription factor ΔFosB (Delta FosB) accumulates in a region‐specific manner in the brain during chronic exposure to stress, drugs of abuse or other chronic stimuli. Once induced, ΔFosB persists in the brain for at least several weeks following cessation of the chronic stimulus. The biochemical basis of the persistent expression of ΔFosB has remained unknown. Here, we show that the FosB C‐terminus, absent in ΔFosB as a result of alternative splicing, contains two degron domains. Pulse‐chase experiments of C‐terminal truncation mutants of full‐length FosB indicate that removal of its most C‐terminal degron increases its half‐life ∼ fourfold, and prevents its proteasome‐mediated degradation and ubiquitylation, properties similar to ΔFosB. In addition, removal of a second degron domain, which generates ΔFosB, further stabilizes FosB ∼ twofold, but in a proteasome‐independent manner. These data indicate that alternative splicing specifically removes two destabilizing elements from FosB in order to generate a longer‐lived transcription factor, ΔFosB, in response to chronic perturbations to the brain.
Testing the impact of climate variability on European plant diversity: 320 000 years of water–energy dynamics and its long‐term influence on plant taxonomic richness
Authors: Willis Katherine J. , Kleczkowski Adam , New Mark , Whittaker Robert J. 
Published: June 2007

AbstractModels examining the present‐day relationship between macro‐scale patterns in terrestrial species richness and variables of water and energy demonstrate that a combined water–energy model is a good predictor of richness in mid‐to‐high latitude regions. However, the power of the individual water and energy variables to explain this richness through time has never been explored. Here, we assess how well energy and water can predict long‐term variations in plant richness using a 320 000‐year fossil pollen data set from Hungary. Results demonstrate that a combined water–energy model best explains the variation in plant diversity through time. However, this long temporal record also demonstrates that amplitude of energy variation appears to be a strong determinant of richness. Decreased richness correlates with increased climate variability and certain species appear to be more susceptible according to their ecological traits. These findings have important implications for predicting richness at times of increasing climate variability.
Landscape heterogeneity shapes predation in a newly restored predator–prey system
Authors: Kauffman Matthew J. , Varley Nathan , Smith Douglas W. , Stahler Daniel R. , MacNulty Daniel R. , Boyce Mark S. 
Published: June 2007

AbstractBecause some native ungulates have lived without top predators for generations, it has been uncertain whether runaway predation would occur when predators are newly restored to these systems. We show that landscape features and vegetation, which influence predator detection and capture of prey, shape large‐scale patterns of predation in a newly restored predator–prey system. We analysed the spatial distribution of wolf (Canis lupus) predation on elk (Cervus elaphus) on the Northern Range of Yellowstone National Park over 10 consecutive winters. The influence of wolf distribution on kill sites diminished over the course of this study, a result that was likely caused by territorial constraints on wolf distribution. In contrast, landscape factors strongly influenced kill sites, creating distinct hunting grounds and prey refugia. Elk in this newly restored predator–prey system should be able to mediate their risk of predation by movement and habitat selection across a heterogeneous risk landscape.
ARE MOVERS STILL THE SAME? CHARACTERISTICS OF INTERREGIONAL MIGRANTS IN SWEDEN 1970–2001
Authors: LUNDHOLM EMMA 
Published: June 2007

ABSTRACTThe purpose of this study is to investigate interregional migration in Sweden during the last three decades and to discuss the effects that changes on the labour market and in household structures have had on migration patterns. The empirical data consists of all interregional migrants in Sweden from 1970 to 2001. The results indicate that the pattern of labour market‐related migration has changed as more migrants today migrate at an age prior to having become established on the labour market. The increase in interregional migration is to a large extent an effect of increased student migration. The study further shows that changed household structures have also had an impact on migration patterns during the studied period. Interregional migration among families has become rarer as dual income households have become the norm.
PORT COMPETITION BETWEEN LOS ANGELES and LONG BEACH: AN INSTITUTIONAL ANALYSIS
Authors: JACOBS WOUTER 
Published: June 2007

ABSTRACTThis paper focuses on the process of institutional change at the leading ports of the United States: Los Angeles and Long Beach. In order to do so, it makes use of the structure of provision‐approach and the concept of regime politics which allows for a systematic analysis and comparison. Key questions are: how are both ports institutionally structured? How do they evolve in relation to each other? And what is the role of agency in this process? The paper reveals how both ports remain institutionally different in spite of competition. This persistent institutional diversity can be explained by that fact that institutions represent territorially rooted structures of power in which competitive performance will not always be the decisive interest.
GEOPOLITICS OF THE SATELLITE INDUSTRY
Authors: WARF BARNEY 
Published: June 2007

ABSTRACTThis paper situates the international satellite industry within three lines of contemporary geographic thought. Second, it reviews the industry's Cold War origins. Third, it explains changing international regulatory structures of satellites, particularly Intelsat, which control access to and use of the technology. Fourth, it summarises the changing role of satellites in the post‐Cold War era, including the impacts of deregulation, rising competition between Intelsat and national and commercial providers, and the heated rivalry between satellites and fibre optic carriers. Throughout, it emphasises the ways in which terrestrial power relations alter access and applications to this sector.
A EUROPEAN CULTURAL IDENTITY? HERITAGE and SHARED HISTORIES IN THE EUROPEAN UNION
Authors: VAN GORP BOUKE , RENES HANS 
Published: June 2007

ABSTRACTDo the people in the European Union share a cultural identity? One important aspect of cultural identity is shared histories or common memories. Such histories can be presented by heritage. Heritage is those traces of the past a society chooses to preserve. Heritage is therefore also a way of defining oneself. To this day, the European Union has not yet compiled its own list of heritage. This paper analyses the World Heritage Sites of EU member states: sites that are considered to be of universal value. When taken together, what image of European history do these sites represent?
Lotteries, Group Size, and Public Good Provision
Authors: PECORINO PAUL , TEMIMI AKRAM 
Published: June 2007

AbstractWe analyze the effect of group size on public good provision under theMorgan (2000)lottery mechanism. For a pure public good, the lottery performs quite well as public good provision is found to increase in group size, even when the lottery prize is held constant. By contrast, for fully rival public goods, per capita provision is found to decrease in group size, even when the lottery prize is proportional to group size. Further, the per capita level of provision will approach zero when group size is sufficiently large.
Help the Low Skilled or Let the Hardworking Thrive? A Study of Fairness in Optimal Income Taxation
Authors: FLEURBAEY MARC , MANIQUET FRANÇOIS 
Published: June 2007

AbstractIn a model where agents have unequal wages and heterogeneous preferences, we study the optimal redistribution via an income tax, when the social objective is based on a combination of efficiency and fairness principles, and when incentive issues are taken into account. We show how some fairness principles entail specific features for the optimal taxes, such as progressivity or tax exemption for incomes below the minimum wage.
Longitudinal changes in serum lipids among HIV‐infected men on highly active antiretroviral therapy
Authors: Riddler SA , Li X , Chu H , Kingsley LA , Dobs A , Evans R , Palella F , Visscher B , Chmiel JS , Sharrett AR 
Published: June 2007

ObjectiveThe aim of the study was to describe longitudinal changes in serum lipids among HIV‐infected men receiving highly active antiretroviral therapy (HAART) with long‐term follow‐up.MethodsA total of 304 HIV‐infected men who initiated HAART and who had serum lipid measurements prior to and for up to 7 years after HAART initiation were identified from the Multicenter AIDS Cohort Study (MACS). Mean levels of total cholesterol (TC), high‐density lipoprotein cholesterol (HDL‐C) and low‐density lipoprotein cholesterol (LDL‐C) were examined at biannual time‐points.ResultsSignificant lipid changes were seen within 0.5 years of HAART initiation but increases in TC (+1.09 mmol/L), LDL‐C (+0.57 mmol/L), HDL‐C (+0.16 mmol/L) and non‐HDL‐C (+0.91 mmol/L) reached peak levels 2–3 years after HAART initiation. Declines in serum TC, LDL‐C and non‐HDL‐C in subsequent years occurred concurrently with a substantial increase in use of lipid‐lowering medications (from 1% usage pre‐HAART to 43% 6–7 years after HAART initiation) but the proportion of men who either were treated with cholesterol‐lowering medication or had elevated cholesterol levels (>5.18 mmol/L) did not change during the 2–7‐year interval after HAART. Mean HDL‐C also decreased after 2–3 years and was low (<1.04 mmol/L) in 55% of HIV‐infected men 6–7 years after HAART initiation.ConclusionsAtherogenic serum lipids increased early after the initiation of HAART, peaked at 2–3 years and remained high or required treatment thereafter. Low HDL‐C levels persisted in the majority of men. The long‐term effects of lipid abnormalities on cardiovascular risk and the effectiveness and toxicity of prolonged use of lipid‐lowering medications in combination with HAART are not known.
The significance of Epstein–Barr virus detected in the cerebrospinal fluid of people with HIV infection
Authors: Wang J , Ozzard A , Nathan M , Atkins M , Nelson M , Gazzard B , Bower M 
Published: June 2007

IntroductionEpstein–Barr virus (EBV) is detected in the cerebrospinal fluid (CSF) in people with HIV infection who develop primary cerebral lymphoma (PCL). However, EBV may also be detected in the CSF of patients without PCL, and here the significance is uncertain.MethodsNinety‐eight HIV‐positive patients had lumbar punctures performed and polymerase chain reaction (PCR) for EBV was undertaken on the CSF. Thirty‐eight patients had non‐Hodgkin's lymphoma (NHL), including four with PCL. Sixty patients had a CSF examination for other indications. The clinicopathological details, symptoms, diagnosis, CSF and neuroimaging findings and therapy at time of CSF were recorded and correlated with CSF EBV PCR results.ResultsEBV was detected in the CSF in three of four patients (75%) with PCL, one of three (33%) with systemic lymphoma and meningeal involvement, and four of 31 (13%) with systemic lymphoma and no meningeal disease. Seven of 60 patients (12%) without lymphoma were CSF EBV‐positive. There were no differences in immunological, clinical, biochemical or radiological parameters between patients with and without EBV in the CSF. After a median follow‐up time of 30 weeks (maximum 102 weeks), none of the seven CSF EBV‐positive patients has developed PCL.ConclusionEBV was detected in up to 12% of patients with neurological symptoms but without lymphoma. A positive result did not correlate with more advanced immunosuppression or a particular neurological diagnosis. Patients with EBV in their CSF did not appear to be at increased risk of developing PCL in the short term.
Enhancement of α‐secretase cleavage of amyloid precursor protein by a metalloendopeptidase nardilysin
Authors: Hiraoka Yoshinori , Ohno Mikiko , Yoshida Kazuhiro , Okawa Katsuya , Tomimoto Hidekazu , Kita Toru , Nishi Eiichiro 
Published: June 2007

AbstractAmyloid‐β (Aβ) peptide, the principal component of senile plaques in the brains of patients with Alzheimer’s disease, is derived from proteolytic cleavage of amyloid precursor protein (APP) by β‐ and γ‐secretases. Alternative cleavage of APP by α‐secretase occurs within the Aβ domain and precludes generation of Aβ peptide. Three members of the ADAM (a disintegrin and metalloprotease) family of proteases, ADAM9, 10 and 17, are the main candidates for α‐secretases. However, the mechanism that regulates α‐secretase activity remains unclear. We have recently demonstrated that nardilysin (EC 3.4.24.61, N‐arginine dibasic convertase; NRDc) enhances ectodomain shedding of heparin‐binding epidermal growth factor‐like growth factor through activation of ADAM17. In this study, we show that NRDc enhances the α‐secretase activity of ADAMs, which results in a decrease in the amount of Aβ generated. When expressed with ADAMs in cells, NRDc dramatically increased the secretion of α‐secretase‐cleaved soluble APP and reduced the amount of Aβ peptide generated. A peptide cleavage assay in vitro also showed that recombinant NRDc enhances ADAM17‐induced cleavage of the peptide substrate corresponding to the α‐secretase cleavage site of APP. A reduction of endogenous NRDc by RNA interference was accompanied by a decrease in the cleavage by α‐secretase of APP and increase in the amount of Aβ generated. Notably, NRDc is clearly expressed in cortical neurons in human brain. Our results indicate that NRDc is involved in the metabolism of APP through regulation of the α‐secretase activity of ADAMs, which may be a novel target for the treatment of Alzheimer’s disease.
Rapid down‐regulation of Ret following exposure of dopaminergic neurons to neurotoxins
Authors: Hirata Yoko , Kiuchi Kazutoshi 
Published: June 2007

AbstractThe survival and functional maintenance of vertebrate neurons depends on the availability of specific neurotrophic factors. We studied the influence of neurotrophic support on responses of dopaminergic neurons to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine, a neurotoxin known to damage the nigrostriatal dopaminergic pathway in humans and other mammals. Treatment of mice with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine caused decreases in levels of Ret, a tyrosine kinase receptor for glial cell line‐derived neurotrophic factor (GDNF) in the striatum, under the condition in which tyrosine hydroxylase was moderately decreased and the GDNF family receptor α1, another receptor of GDNF that is the ligand‐binding subunit, were unaffected. Down‐regulation of Ret was also observed in dopamine‐producing PC12 cells undergoing apoptosis induced by rotenone, another toxic substance for dopaminergic neurons, while other cellular components were not affected. Ret was also extremely vulnerable to other apoptotic inducing conditions. Taken together, these results indicate that Ret, an important signal molecule in dopaminergic neurons, may be down‐regulated in the early stages of neuronal degeneration caused by various neurotoxic substances, and may lead to reduced neurotrophic influences.