bluuebunny/crossref_metadata_2025_split huggingface dataset:
LIBERALIZATION AND PRIVATIZATION OF PUBLIC UTILITIES: ORIGINS OF THE DEBATE, CURRENT ISSUES AND CHALLENGES FOR THE FUTURE
Authors: Bognetti Giuseppe , Obermann Gabriel 
Published: September 2008

ABSTRACT*:  Public utilities, public enterprises, privatizations, liberalizations and related topics have been the object of far reaching and intense debate among economists, politicians and practitioners for more than a century. Ideas have frequently changed, and practical solutions chosen to manage public utilities have also undergone significant changes over time. Presently we are witnessing a renewed debate on the relative opportunity of public and private enterprise. In the last twenty years privatization and liberalization have dominated the field. The outcome of this process has produced mixed results. Merits and demerits of privatization, liberalization and regulation are reviewed and discussed in the first part of the paper. The second part of the paper provides an overview of the scientific work of CIRIEC related to issues of public enterprises and services of general interest. It refers primarily to relevant research activities done in the International Scientific Commission ‘Public services/Public enterprises’. Over the past two decades CIRIEC contributed some recognized theoretical and empirical studies dealing with the functioning, governance and reform of public enterprises, based on an international perspective. Theoretical arguments and empirical findings put forward in this paper leads to the conclusion, that the often stated dominant position against public enterprises is not at all convincing. In order to arrive at a fair and valid evaluation of public utilities, it is indispensable to look more closely to the particular circumstances of the technological, economic and social environment and the goals of the provision of a concrete service of public interest.
Involvement of nuclear factor‐kappa B in bcl‐xL‐induced interleukin 8 expression in glioblastoma
Authors: Gabellini Chiara , Castellini Laura , Trisciuoglio Daniela , Kracht Michael , Zupi Gabriella , Del Bufalo Donatella 
Published: September 2008

AbstractWe recently reported that bcl‐xL regulates interleukin 8 (CXCL8) protein expression and promoter activity in glioblastoma cells. In this paper we demonstrate that CXCL8 induction by bcl‐xL is mediated through a nuclear factor‐kappa B (NF‐kB)‐dependent mechanism. Mutational studies on the CXCL8 promoter showed that NF‐kB binding site was required for bcl‐xL‐induced promoter activity and an enhanced nuclear expression of NF‐kB subunits p65 and p50 was observed after bcl‐xL over‐expression. Electrophoretic mobility shift assay showed an increased DNA‐binding activity of NF‐kB in bcl‐xL over‐expressing cells and the use of specific antibodies confirmed the involvement of p65 and p50 in NF‐kB activity on CXCL8 promoter sequence. NF‐kB activity regulation by bcl‐xL involved IkBα and IKK complex signaling pathway. In fact, bcl‐xL over‐expression induced a decrease of cytoplasmic expression of the IkBα protein, paralleled by an increase in the phosphorylation of the same IkBα and IKKα/β. Moreover, the down‐regulation of the ectopic or endogenous bcl‐xL expression through RNA interference confirmed the ability of bcl‐xL to modulate NF‐kB pathway, and the transient expression of a degradation‐resistant form of the cytoplasmic NF‐kB inhibitor IkBα in bcl‐xL transfectants confirmed the involvement of that inhibitor in bcl‐xL‐induced CXCL8 expression and promoter activity. In conclusion, our results demonstrate the role of NF‐kB as the mediator of bcl‐xL‐induced CXCL8 up‐regulation in glioblastoma cells.
Phosphorus magnetic resonance spectroscopy 2 h after perinatal cerebral hypoxia‐ischemia prognosticates outcome in the newborn piglet
Authors: Cady Ernest B. , Iwata Osuke , Bainbridge Alan , Wyatt John S. , Robertson Nicola J. 
Published: September 2008

AbstractPhosphorus magnetic resonance spectroscopy (31P MRS) often reveals apparently normal brain metabolism in the first hours after intrapartum hypoxia‐ischemia (HI) at a time when conventional clinical assessment of injury severity is problematic. We aimed to elucidate very‐early, injury‐severity biomarkers. Twenty‐seven newborn piglets underwent cerebral HI: 31P‐MRS measures ∼2 h after HI were compared between injury groups defined by secondary‐energy‐failure severity as quantified by the minimum nucleotide triphosphate (NTP) observed after 6 h. For severe and moderate injury versus baseline, [Pi]/[total exchangeable high‐energy phosphate pool (EPP)] was increased (p < 0.001 and < 0.02, respectively), and [NTP]/[EPP] decreased (p < 0.03 and < 0.006, respectively): severe‐injury [Pi]/[EPP] was also increased versus mild injury (p < 0.04). Mild‐injury [phosphocreatine]/[EPP] was increased (p < 0.004). Severe‐injury intracellular pH was alkaline versus baseline (p < 0.002). For severe and moderate injury [total Mg]/[ATP] (p < 0.0002 and < 0.02, respectively) and [free Mg] (p < 0.0001 and < 0.02, respectively) were increased versus baseline. [Pi]/[EPP], [phosphocreatine]/[Pi] and [NTP]/[EPP] correlated linearly with injury severity (p < 0.005, < 0.005 and < 0.02, respectively). Increased [Pi]/[EPP], intracellular pH and intracellular Mg ∼2 h after intrapartum HI may prognosticate severe injury, whereas increased [phosphocreatine]/[EPP] may suggest mild damage. In vivo31P MRS may have potential to provide very‐early prognosis in neonatal encephalopathy.
Normobaric hyperoxia inhibits NADPH oxidase‐mediated matrix metalloproteinase‐9 induction in cerebral microvessels in experimental stroke
Authors: Liu Wenlan , Sood Rohit , Chen Qingchuan , Sakoglu Unal , Hendren Jill , Çetin Özdemir , Miyake Minoru , Liu Ke Jian 
Published: September 2008

AbstractMatrix metalloproteinase‐9 (MMP‐9) and NADPH oxidase contribute to blood–brain barrier (BBB) disruption after ischemic stroke. We have previously shown that normobaric hyperoxia (NBO) treatment reduces MMP‐9 and oxygen free radical generation in ischemic brain. In this study, we tested the hypothesis that NBO protects the BBB through inhibiting NADPH oxidase‐mediated MMP‐9 induction in transient focal cerebral ischemia. Male Sprague–Dawley rats (n = 69) were given NBO (95% O2) or normoxia (21% O2) during 90‐min filament occlusion of the middle cerebral artery. Cerebral microvessels were isolated for analyzing MMP‐9 and NADPH oxidase. BBB damage was non‐invasively quantified with magnetic resonance imaging. In normoxic rats, both NADPH oxidase catalytic subunit gp91phox and MMP‐9 expression were up‐regulated in ischemic hemispheric microvessels after 90‐min middle cerebral artery occlusion with 22.5 h reperfusion. Inhibition of NADPH oxidase with apocynin reduced the MMP‐9 increase, indicating a causal link between NADPH oxidase‐derived superoxide and MMP‐9 induction. NBO treatment inhibited gp91phox expression, NADPH oxidase activity, and MMP‐9 induction, which led to significantly less BBB damage and brain edema in the ischemic brain. These results suggest that gp91phox containing NADPH oxidase plays an important role in MMP‐9 induction in ischemic BBB microvasculature, and that NBO treatment may attenuate MMP‐9 induction and brain edema through inhibiting NADPH oxidase after transient cerebral ischemia.
Cystamine prevents haloperidol‐induced decrease of BDNF/TrkB signaling in mouse frontal cortex
Authors: Pillai Anilkumar , Veeranan‐Karmegam Rajalakshmi , Dhandapani Krishnan M. , Mahadik Sahebarao P. 
Published: September 2008

AbstractThe role of brain‐derived neurotrophic factor (BDNF) has been implicated in the pathophysiology as well as treatment outcome of schizophrenia. Rodent studies indicate that several antipsychotic drugs have time‐dependent (and differential) effects on BDNF levels in the brain. Earlier studies from our laboratory have indicated that long‐term treatment with haloperidol (HAL) decreases BDNF, reduced GSH and anti‐apoptotic marker, Bcl‐xl protein levels and increases the expression of pro‐apoptotic proteins in rat frontal cortex. Furthermore, findings from human as well as rodent studies suggest that treatment of schizophrenia must involve the neuroprotective strategies to improve the neuropathology and thereby clinical outcome. In the present study, we investigated the potential of cystamine (CYS), an anti‐oxidant and anti‐apoptotic compound, to prevent HAL‐induced reduction in BDNF, GSH, and Bcl‐xl protein levels in mice and the signaling mechanism(s) involved in the beneficial effects of CYS. The results indicated that CYS as well as cysteamine (the FDA‐approved precursor of CYS) increased BDNF protein levels in mouse frontal cortex 7 days after treatment. CYS co‐treatment prevented chronic HAL treatment‐induced reduction in BDNF, GSH, and Bcl‐xl protein levels. CYS treatment enhanced TrkB‐tyrosine phosphorylation and activated Akt and extracellular signal‐regulated kinase (ERK)1/2, downstream molecules of TrkB signaling. In addition, in vitro experiments with mouse cortical neurons showed that CYS prevented the HAL‐induced reduction in neuronal cell viability and BDNF protein levels, and increase in apoptosis. BDNF‐neutralizing antibody as well as K252a, a selective inhibitor of neurotrophin signaling blocked the CYS‐mediated neuroprotection. Moreover, CYS‐mediated neuroprotection is also blocked by LY294002, a phosphatidylinositol 3‐kinase inhibitor or PD98059, a mitogen‐activated protein kinase kinase (MEK) inhibitor. Thus, CYS protects cortical neurons through a mechanism involving TrkB receptor activation, and a signaling pathway involving phosphatidylinositol 3‐kinase and MAPK. The findings from the present study may be helpful for the development of novel neuroprotective strategies to improve the treatment outcome of schizophrenia.
Neuroprotective effect of sonic hedgehog up‐regulated in Schwann cells following sciatic nerve injury
Authors: Hashimoto Manabu , Ishii Kunihiro , Nakamura Yasuko , Watabe Kazuhiko , Kohsaka Shinichi , Akazawa Chihiro 
Published: September 2008

AbstractThe physiological roles of sonic hedgehog (Shh) have been intensively characterized in development of various organs. However, their functions in adult tissues have not been fully elucidated. We investigated the expression and the potential function of Shh in crush‐injured adult rat sciatic nerves. The Shh expression was up‐regulated in Schwann cells adjacent to the injured site. The time‐course analyses of various neurotrophic factors revealed the up‐regulation of Shh mRNA followed by that of brain‐derived neurotrophic factor (BDNF) mRNA. The continuous administration of cyclopamine, a hedgehog signal inhibitor, to the injured site suppressed the increase of BDNF expression and deteriorated the survival of motor neurons in lumbar spinal cord. Treatment of exogenous Shh in cultured Schwann cells enhanced the BDNF expression. The BDNF promoter activity (exon I and II) was increased in IMS32 cells co‐transfected with Shh and its receptor Smoothened. These findings imply that the up‐regulated expression of Shh in Schwann cells may play an important role in injured motor neurons through the induction of BDNF.
Up‐regulation of the SOX3 gene expression by retinoic acid: characterization of the novel promoter‐response element and the retinoid receptors involved
Authors: Nikčević Gordana , Savić Tijana , Kovačević‐Grujičić Nataša , Stevanović Milena 
Published: September 2008

Abstract Sox3/SOX3 gene is considered to be one of the earliest neural markers in vertebrates and it is implicated in the genetic cascades that direct brain formation. We have previously shown that early phases of differentiation and neural induction of NT2/D1 embryonal carcinoma cells by retinoic acid (RA) involve up‐regulation of the SOX3 gene expression. Here, we present identification of a novel positive regulatory promoter element involved in RA‐dependent activation of the SOX3 gene expression in NT2/D1 cells. This element represents a direct repeat 3‐like motif that directly interacts with retinoid X receptor (RXR) α in a sequence‐specific manner. It is capable of independently mediating the RA effect in a heterologous promoter context and its disruption caused significant reduction of RA/RXR transactivation of the SOX3 promoter. Furthermore, by using synthetic antagonists of retinoid receptors, we have shown for the first time, that RA‐induced SOX3 gene expression could be significantly down‐regulated by the synthetic antagonist of RXR. Also, this data showed that RXRs, but not RA receptors, are mediators of RA effect on the SOX3 gene up‐regulation in NT2/D1 cells. Presented data will be valuable for future investigation of SOX3 gene expression, not only in NT2/D1 model system, but also in diverse developmental, physiological and pathological settings.
Regulatory role of C‐terminus in the G‐protein coupling of the metabotropic glutamate receptor 1
Authors: Tateyama Michihiro , Kubo Yoshihiro 
Published: September 2008

AbstractThe signaling property of metabotropic glutamate receptor 1α (mGlu1α) is different from that of short‐form splice variants. This could be caused by the exposure of a cluster of positively charged amino acid residues, RRKK, in the proximal C‐tail which is thought to be masked by the long C‐tail of mGlu1α. We found that the RRKK residues, when exposed, attenuate Gq coupling and decrease the basal activity and the surface expression of mGlu1, in agreement with previous results. Moreover, these residues abolish the Gi/o coupling of mGlu1, but do not affect glutamate‐induced dimeric rearrangement and protein kinase A‐dependent modulation of mGlu1. These results suggest that the RRKK residues do not inhibit the conformational change upon glutamate binding and protein accessibility to the intracellular loops where G‐protein coupling occurs, but rather act as an inhibitory domain against G‐protein coupling in a different manner depending on the type of G protein.
Role of histamine in short‐ and long‐term effects of methamphetamine on the developing mouse brain
Authors: Acevedo Summer F. , Pfankuch Timothy , Van Meer Peter , Raber Jacob 
Published: September 2008

AbstractWith the rise in methamphetamine (MA) use among women of childbearing age, the potential consequences of MA exposure to the developing brain for cognition in adulthood is a major concern. Histamine might mediate these MA effects. Following MA administration in neonatal mice, histamine levels in brain were elevated and the hypothalamic‐pituitary‐adrenal axis was activated. Co‐administration of MA with the H3 receptor agonist immepip antagonized these effects. The effects of MA on histamine levels and on hypothalamic‐pituitary‐adrenal axis activation at P20 were more pronounced in female than male mice. These sex differences could have contributed to the increased susceptibility of female mice to the detrimental long‐term cognitive effects of MA and the H3/H4 antagonist thioperamide. Following behavioral testing, mice neonatally treated with MA or thioperamide showed reduced levels of the dendritic marker microtubule‐associated protein 2 in the CA3 region of the hippocampus and the enthorhinal cortex. This was not seen in mice neonatally treated with immepip and MA who did not show cognitive impairments, suggesting that these brain areas might be particularly important for the long‐term effects of MA on cognitive function. These data support a role for histamine in the effects of MA on the developing brain.
Oligodendrogenesis of adult neural progenitors: differential effects of ciliary neurotrophic factor and mesenchymal stem cell derived factors
Authors: Rivera Francisco J. , Kandasamy Mahesh , Couillard‐Despres Sebastien , Caioni Massimiliano , Sanchez Rosario , Huber Christophe , Weidner Norbert , Bogdahn Ulrich , Aigner Ludwig 
Published: September 2008

AbstractThe oligodendrogenic program of progenitor cells in the adult CNS follows a sequential process of progenitor proliferation, fate choice, determination, differentiation, maturation and survival. Previously, we described a soluble activity derived from mesenchymal stem cells that induces oligodendrogenesis in adult neural progenitor cells. Here, we hypothesized that ciliary neurotrophic factor might be a candidate for this activity, since (i) it is expressed by mesenchymal stem cells and (ii) it can promote oligodendrogenesis during development. Along the course of the study, we found differential effects by ciliary neurotrophic factor and by the mesenchymal stem cells‐derived activity on neural progenitors. While the mesenchymal stem cells‐derived activity induced oligodendrogenesis at the expense of astrogenesis and promoted oligodendroglial differentiation/maturation, the effect of ciliary neurotrophic factor was restricted to the latter one. This was reflected at the levels of the cell fate determinants Olig1, Olig2, Id2, and the oligodendroglia‐maturation transcription factor GTX/Nkx6.2. Finally, experiments using blocking antibodies excluded ciliary neurotrophic factor to be the mesenchymal stem cell‐derived oligodendroglial activity. In summary, this work provides evidence for differential effects of ciliary neurotrophic factor and mesenchymal stem cells‐derived activity on oligodendrogenesis of adult neural progenitor cells.
The antipsychotic spiperone attenuates inflammatory response in cultured microglia via the reduction of proinflammatory cytokine expression and nitric oxide production
Authors: Zheng Long Tai , Hwang Jaegyu , Ock Jiyeon , Lee Maan Gee , Lee Won‐Ha , Suk Kyoungho 
Published: September 2008

AbstractGlial activation and neuroinflammatory processes play an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and HIV dementia. Activated glia cells can secrete various proinflammatory cytokines and neurotoxic mediators, which may influence neuronal cell survival. Recent studies have demonstrated that glia cell‐mediated neuroinflammation is also related to the pathophysiology of schizophrenia. In the present study, anti‐inflammatory and neuroprotective effects of antipsychotics were investigated using cultured brain cells as a model. The results showed that spiperone significantly decreased the production of nitric oxide in lipopolysaccharide‐stimulated BV‐2 microglia cells, primary microglia and primary astrocyte cultures. Spiperone also significantly inhibited nitric oxide production in adenosine 5′‐triphosphate (ATP)‐stimulated primary microglia cultures. Spiperone markedly decreased the production of tumor necrosis factor‐alpha in BV‐2 microglia cells. Spiperone attenuated the expression of inducible nitric oxide synthase and proinflammatory cytokines such as interleukin‐1β and tumor necrosis factor‐alpha at mRNA levels in BV‐2 microglia cells. Spiperone inhibited nuclear translocation and DNA binding of the p65 subunit of nuclear factor kappa B (NF‐κB), inhibitor of kappa B (IκB) degradation, and phosphorylation of p38 mitogen‐activated protein kinase in the lipopolysaccharide‐stimulated BV‐2 microglia cells. Moreover, spiperone was neuroprotective, as the drug reduced microglia‐mediated neuroblastoma cell death in the microglia/neuron co‐culture. These results imply that the antipsychotic spiperone has anti‐inflammatory and neuroprotective effects in the central nervous system by modulating glial activation.
Adult diet affects lifespan and reproduction of the fruit‐feeding butterflyCharaxes fulvescens
Authors: Molleman Freerk , Ding Jimin , Wang Jane‐Ling , Zwaan Bas J. , Carey James R. , Brakefield Paul M. 
Published: September 2008

AbstractFruit‐feeding butterflies are among the longest lived Lepidoptera. While the use of pollen‐derived amino acids byHeliconiusbutterflies has been interpreted as important for the evolution of extended lifespans, very little is known about the life‐history consequences of frugivory. This issue is addressed by investigating effects of four adult diets (sugar, sugar with amino acids, banana, and moistened banana) on lifespan and reproduction in the fruit‐feeding butterflyCharaxes fulvescensAurivillius (Lepidoptera: Nymphalidae). Female butterflies were collected from Kibale National Park, Uganda, and kept individually in cages near their natural habitat and data were collected on lifespan, oviposition, and hatching of eggs. Lifespan in captivity was longer for the sugar and the amino acid cohort, than for the banana cohorts. The longitudinal pattern of oviposition was erratic, with many days without oviposition and few periods with high numbers of eggs laid. Butterflies typically did not lay eggs during their 1st week in captivity and the length of the period between capture and first reproduction was significantly shorter for butterflies fed moistened banana. The length of the reproduction period (first reproduction–last reproduction in captivity) and the reproduction rate (total number of eggs/length of the reproduction period) did not differ significantly between the diet treatments. Those fed with amino acid and moistened banana had significantly higher egg hatchability than those fed with sugar and banana. We found no evidence for a lifespan cost of reproduction. Our results show that (1) femaleC. fulvescenscan use amino acids in their diet for laying fertile eggs, (2) more wing‐wear does correlate with lower survival in captivity (indicating aging in the wild), but not with intensity of reproduction (providing no evidence for reproductive aging), and (3) fruit‐feeding butterflies may be dietary restricted in the field.
Mortality of Rhagoletis indifferens exposed to hydrolyzed protein baits and spinosad in the absence and presence of yeast extract
Authors: Yee Wee L. 
Published: September 2008

AbstractWestern cherry fruit fly, Rhagoletis indifferens Curran (Diptera: Tephritidae), is the major quarantine pest of sweet cherry, Prunus avium (L.) L. (Rosaceae), in the Pacific northwest of the USA and in British Columbia in Canada. Although spinosad bait (GF‐120 NF Naturalyte® Fruit Fly Bait) is used for the control of R. indifferens in this region, the effects of alternate food sources on fly responses to this bait have not been studied. In this study, experiments were conducted to determine mortalities of flies exposed to hydrolyzed protein baits in the presence of sugar only and sugar + yeast extract food. All baits contained Entrust® (termed ‘spinosad alone’). When flies were exposed to GF‐120 with or without added ammonia compounds (uric acid, ammonium acetate, and ammonium carbonate) for 48 h, mortalities were higher in the presence of sugar only than in the presence of sugar + yeast extract, but when flies were exposed to spinosad alone, mortalities were similar in presence of either of the two foods. In another experiment comparing GF‐120, Nu‐Lure, Mazoferm, Baker's yeast extract, and spinosad alone, mortalities in the GF‐120, Mazoferm, and Baker's yeast extract treatments were higher in the presence of sugar only than in the presence of sugar + yeast extract, but in the Nu‐Lure and spinosad alone treatments, mortalities were similar in the presence of either of the two foods. Overall results suggest that the indirect effects of yeast extract food on mortality are dependent on bait type and that mortalities caused by spinosad alone and baits are similar. Nu‐Lure and spinosad alone may have an advantage over other treatments for fly control, because their effects do not appear to be affected by the presence of nitrogenous food.