bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neoliberalism, Race and the Redefining of Urban Redevelopment
Authors: Mele Christopher 
Published: June 2012

AbstractNeoliberal urban redevelopment is often represented as consensual, socially‐neutral ‘local economic development’ with a positive effect on both a city's overall economy and its level of racial and ethnic diversity. The purpose of this article is to focus specifically on the key ideological premises of color‐blind racial discourses that help facilitate and provide necessary legitimacy (and ideological cover) for neoliberal urban redevelopment in a mid‐sized US city. Color‐blind racial discourses facilitate the agenda and mandates behind tax abatements, enterprise zones, public–private partnerships and new forms of urban consumption. Despite efforts to the contrary, neoliberal urbanism does not retreat from race — rather, racial dynamics are reconstituted to accommodate processes of capital accumulation and uneven urban development in poor and minority cities. Drawing on the case of Chester, Pennsylvania, this article focuses on how color‐blind racial discourses influence exclusionary urban redevelopment policies and practices, facilitate their implementation and legitimize their outcomes.RésuméOn présente souvent le réaménagement urbain néolibéral comme un ‘développement économique local’ consensuel et socialement neutre, dont bénéficient à la fois l'économie générale et le degré de diversité raciale et ethnique de la ville. Cet article s'intéresse en particulier aux grands principes idéologiques des discours racialisés de type color‐blind (littéralement, aveugle aux couleurs) qui contribuent au réaménagement urbain néolibéral d'une ville américaine moyenne et fournissent la légitimité (et la caution idéologique) au projet. Ces discours facilitent les objectifs et missions que soutiennent crédits d'impôt, aides à l'installation dans certaines zones d'activité, partenariats public‐privé et nouvelles formes de consommation urbaine. En dépit d'efforts contraires, l'urbanisme néolibéral ne renonce pas à la dimension raciale. Plus précisément, les dynamiques raciales sont reconstituées pour s'adapter aux processus d'accumulation du capital et d'aménagement urbain inégal des villes aux populations pauvres ou minoritaires. À partir du cas de Chester (Pennsylvanie), ce travail montre comment les discours raciaux color‐blind influencent des politiques et pratiques d'exclusion au sein du réaménagement urbain, facilitant leur mise en place et légitimant leurs résultats.
The effects of low to moderate prenatal alcohol exposure in early pregnancy on IQ in 5‐year‐old children
Authors: Falgreen Eriksen H‐L , Mortensen EL , Kilburn T , Underbjerg M , Bertrand J , Støvring H , Wimberley T , Grove J , Kesmodel US 
Published: June 2012

Please cite this paper as: Falgreen Eriksen H, Mortensen E, Kilburn T, Underbjerg M, Bertrand J, Støvring H, Wimberley T, Grove J, Kesmodel U. The effects of low to moderate prenatal alcohol exposure in early pregnancy on IQ in 5‐year‐old children. BJOG 2012;119:1191–1200.Objective  To examine the effects of low to moderate maternal alcohol consumption during early pregnancy on children’s intelligence (IQ) at age 5 years.Design  Prospective follow‐up study.Setting  Neuropsychological testing in four Danish cities 2003–2008.Population  A cohort of 1628 women and their children sampled from the Danish National Birth Cohort.Methods  Participants were sampled based on maternal alcohol consumption during pregnancy. At 5 years of age, children were tested with the Wechsler Preschool and Primary Scale of Intelligence—Revised (WPPSI‐R). Parental education, maternal IQ, maternal smoking in pregnancy, the child’s age at testing, gender, and tester were considered core confounding factors, whereas the full model also controlled for maternal binge drinking, age, BMI, parity, home environment, postnatal smoking in the home, health status, and indicators for hearing and vision impairments.Main outcome measures  The WPPSI‐R.Results  No differences in test performance were observed between children whose mothers reported consuming between one and four or between five and eight drinks per week at some point during pregnancy, compared with children of mothers who abstained. For women who reported consuming nine or more drinks per week no differences were observed for mean differences; however, the risks of low full‐scale IQ (OR 4.6; 95% CI 1.2–18.2) and low verbal IQ (OR 5.9; 95% CI 1.4–24.9) scores, but not low performance IQ score, were increased.Conclusions  Maternal consumption of low to moderate quantities of alcohol during pregnancy was not associated with the mean IQ score of preschool children. Despite these findings, acceptable levels of alcohol use during pregnancy have not yet been established, and conservative advice for women continues to be to avoid alcohol use during pregnancy.
β‐Amyloid 1‐42 induces physiological transcriptional regulation of BACE1
Authors: Piccini Alessandra , Borghi Roberta , Guglielmotto Michela , Tamagno Elena , Cirmena Gabriella , Garuti Anna , Pollero Valeria , Cammarata Sergio , Fornaro Michele , Messa Massimo , Colombo Laura , Salmona Mario , Perry George , Tabaton Massimo 
Published: June 2012

J. Neurochem. (2012) 122, 1023–1031.AbstractThe pathogenesis of Alzheimer’s disease (AD) is only partially understood. β‐amyloid (Aβ) is physiologically generated by sequential cleavage of its precursor protein by the β‐ and the γ‐secretase and it is normally disposed of. In Alzheimer’s disease, Aβ is excessively produced or less dismissed, but the hypothesis on its physiological and pathological role are heterogeneous and often discordant. It has been described a positive feedback loop from the γ‐ to the β‐secretase cleavages of Aβ precursor protein, which is activated by mutations of Presenilin 1 (PS1), the catalytic core of the γ‐secretase. These findings show that Aβ precursor protein as well the activity of the γ‐secretase are required to obtain the up‐regulation of β‐secretase which is induced by Presenilin 1 mutations. Then, Aβ 1‐42 is the Aβ precursor protein derivative that up‐regulates the expression of β‐secretase, and c‐jun N‐terminal kinase (JNK)/c‐Jun and ERK1/2 are involved. Here, we describe the activation of β‐secretase and c‐jun N‐terminal kinase related proteins by monomeric Aβ 1‐42, defining the conditions that most efficiently strike the described signaling without producing toxicity. Taken together these data imply that monomeric Aβ 1‐42, at non‐toxic concentrations and time frames, are able to induce a signaling pathway that leads to transcriptional activation of β‐secretase.
Endoplasmic reticulum stress occurs downstream of GluN2B subunit of N‐methyl‐D‐aspartate receptor in mature hippocampal cultures treated with amyloid‐β oligomers
Authors: Costa Rui O. , Lacor Pascale N. , Ferreira Ildete L. , Resende Rosa , Auberson Yves P. , Klein William L. , Oliveira Catarina R. , Rego Ana C. , Pereira Cláudia M. F. 
Published: June 2012

SummaryAlzheimer’s disease (AD) is a progressive neurodegenerative disorder affecting both the hippocampus and the cerebral cortex. Reduced synaptic density that occurs early in the disease process seems to be partially due to the overactivation of N‐methyl‐d‐aspartate receptors (NMDARs) leading to excitotoxicity. Recently, we demonstrated that amyloid‐beta oligomers (AβO), the species implicated in synaptic loss during the initial disease stages, induce endoplasmic reticulum (ER) stress in cultured neurons. Here, we investigated whether AβO trigger ER stress by an NMDAR‐dependent mechanism leading to neuronal dysfunction and analyzed the contribution of GluN2A and GluN2B subunits of this glutamate receptor. Our data revealed that AβO induce ER stress in mature hippocampal cultures, activating ER stress‐associated sensors and increasing the levels of the ER chaperone GRP78. We also showed that AβO induce NADPH oxidase (NOX)‐mediated superoxide production downstream of GluN2B and impairs ER and cytosolic Ca2+ homeostasis. These events precede changes in cell viability and activation of the ER stress‐mediated apoptotic pathway, which was associated with translocation of the transcription factor GADD153 / CHOP to the nucleus and occurred by a caspase‐12‐independent mechanism. Significantly, ER stress took place after AβO interaction with GluN2B subunits. In addition, AβO‐induced ER stress and hippocampal dysfunction were prevented by ifenprodil, an antagonist of GluN2B subunits, while the GluN2A antagonist NVP‐AAM077 only slightly attenuated AβO‐induced neurotoxicity. Taken together, our results highlight the role of GluN2B subunit of NMDARs on ER stress‐mediated hippocampal dysfunction caused by AβO suggesting that it might be a potential therapeutic target during the early stages of AD.
Aging is associated with chronic innate immune activation and dysregulation of monocyte phenotype and function
Authors: Hearps Anna C. , Martin Genevieve E. , Angelovich Thomas A. , Cheng Wan‐Jung , Maisa Anna , Landay Alan L. , Jaworowski Anthony , Crowe Suzanne M. 
Published: June 2012

SummaryChronic inflammation in older individuals is thought to contribute to inflammatory, age‐related diseases. Human monocytes are comprised of three subsets (classical, intermediate and nonclassical subsets), and despite being critical regulators of inflammation, the effect of age on the functionality of monocyte subsets remains to be fully defined. In a cross‐sectional study involving 91 healthy male (aged 20–84 years, median 52.4) and 55 female (aged 20–82 years, median 48.3) individuals, we found age was associated with an increased proportion of intermediate and nonclassical monocytes (P = 0.002 and 0.04, respectively) and altered phenotype of specific monocyte subsets (e.g. increased expression of CD11b and decreased expression of CD38, CD62L and CD115). Plasma levels of the innate immune activation markers CXCL10, neopterin (P < 0.001 for both) and sCD163 (P = 0.003) were significantly increased with age. Whilst similar age‐related changes were observed in both sexes, monocytes from women were phenotypically different to men [e.g. lower proportion of nonclassical monocytes (P = 0.002) and higher CD115 and CD62L but lower CD38 expression] and women exhibited higher levels of CXCL10 (P = 0.012) and sCD163 (P < 0.001) but lower sCD14 levels (P < 0.001). Monocytes from older individuals exhibit impaired phagocytosis (P < 0.05) but contain shortened telomeres (P < 0.001) and significantly higher intracellular levels of TNF both at baseline and following TLR4 stimulation (P < 0.05 for both), suggesting a dysregulation of monocyte function in the aged. These data show that aging is associated with chronic innate immune activation and significant changes in monocyte function, which may have implications for the development of age‐related diseases.
Microstructural white matter abnormality and frontal cognitive dysfunctions in juvenile myoclonic epilepsy
Authors: Kim Ji Hyun , Suh Sang‐il , Park So‐Yeon , Seo Woo‐Keun , Koh InSong , Koh Seong‐Beom , Seol Hae Young 
Published: June 2012

SummaryPurpose:  Previous neuroimaging studies provide growing evidence that patients with juvenile myoclonic epilepsy (JME) have both structural and functional abnormalities of the thalamus and frontal lobe gray matter. However, limited data are available regarding the issue of white matter (WM) involvement, making the microstructural WM changes in JME largely unknown. In the present study we investigated changes of WM integrity in patients with JME, and their relationships with cognitive functions and epilepsy‐specific clinical factors.Methods:  We performed diffusion tensor imaging (DTI) and neuropsychological assessment in 25 patients with JME and 30 control subjects matched for age, gender, and education level. Between‐group comparisons of fractional anisotropy (FA) and mean diffusivity (MD) were carried out in a whole‐brain voxel‐wise manner by using tract‐based spatial statistics (TBSS). In addition, both FA and MD were correlated with cognitive performance and epilepsy‐specific clinical variables to investigate the influence of these clinical and cognitive factors on WM integrity changes.Key Findings:  Neuropsychological evaluation revealed that patients with JME had poorer performance than control subjects on most of the frontal function tests. TBSS demonstrated that, compared to controls, patients with JME had significantly reduced FA and increased MD in bilateral anterior and superior corona radiata, genu and body of corpus callosum, and multiple frontal WM tracts. Disease severity, as assessed by the number of generalized tonic–clonic seizures in given years, was negatively correlated with FA and positively correlated with MD extracted from regions of significant differences between patients and controls in TBSS.Significance:  Our findings of widespread disturbance of microstructural WM integrity in the frontal lobe and corpus callosum that interconnects frontal cortices could further support the pathophysiologic hypothesis of thalamofrontal network abnormality in JME. These WM abnormalities may implicate frontal cognitive dysfunctions and disease progression in JME.
Seizure generation: The role of nodes and networks
Authors: Terry John R. , Benjamin Oscar , Richardson Mark P. 
Published: June 2012

SummaryThe longstanding dichotomy between the concepts of “focal” and “primary generalized” epilepsy has become increasingly blurred, raising fundamental questions about the nature of ictal onset in localized brain regions versus large‐scale brain networks. We hypothesize that whether an EEG discharge appears focal or generalized is driven by the pattern of connections in brain networks, irrespective of the presence of focal brain abnormality. Using a computational model of a simple “brain” consisting of four regions and the connections between them, we explored the effects of altering connectivity structure versus the effects of introducing an “abnormal” brain region, and the interactions between these factors. Computer simulations demonstrated that electroencephalography (EEG) discharges representing either generalized or focal seizures arose purely as a consequence of subtle changes in network structure, without the requirement for any localized pathologic brain region. Furthermore we found that introducing a pathologic region gave rise to focal, secondary generalized, or primary generalized seizures depending on the network structure. Counterintuitively, we found that decreasing connectivity between regions of the brain increased the frequency of seizure‐like activity. Our findings may enlighten current controversies surrounding the concepts of focal and generalized epilepsy, and help to explain recent observations in genetic animal models and human epilepsies, where loss of white matter pathways was associated with the occurrence of seizures.
Impact of Experimental Conditions on Noncontact Laser Recordings in Microvascular Studies
Authors: MAHÉ GUILLAUME , DURAND SYLVAIN , HUMEAU‐HEURTIER ANNE , LEFTHERIOTIS GEORGES , ABRAHAM PIERRE 
Published: June 2012

Please cite this paper as: Mahé G, Durand S, Humeau‐Heurtier A, Leftheriotis G, Abraham P. Impact of experimental conditions on noncontact laser recordings in microvascular studies. Microcirculation 19: 669–675, 2012.AbstractMicrocirculation, especially skin microcirculation, is a window toward systemic vascular function in magnitude and underlying mechanisms. Different techniques have been developed to assess the microcirculation. Among these techniques, laser technology is used to perform noninvasive microvascular assessments. In the 1970s, the laser Doppler flowmetry (LDF) technique was proposed to monitor microvascular blood flow. More recently, noncontact technologies including laser Doppler perfusion imaging (LDI) and laser speckle contrast imaging (LSCI) have improved the reproducibility of the microcirculation measurements and facilitated some clinical evaluations such as on wounds and ulcers. However, due to the absence of contact between tissue and sensors, it is likely that different technical and environmental conditions may interfere with microvascular recordings. This review presents major technical and environmental conditions, which may interfere with noncontact laser recordings in microvascular studies.
The Low‐Temperature Sintering Mechanism of Sr Hexaferrite Using the Addition of CuO
Authors: Lisjak Darja , Lebourgeois Richard 
Published: June 2012

We have investigated the sintering behavior of
Sr
hexaferrite (
SrFe

12

O

19) and the effects of adding
CuO
, which partly substituted for the
Fe

2

O

3 and the
Fe
deficiency during the sintering. For the experiments, samples with nominal compositions of
SrCu

x

Fe

y−x

O

19−δ (x = 0–1.0, y = 11–12) were prepared with a solid‐state reaction at 1000°C. The overall shrinkages and the shrinkage rates were followed using dilatometry during the sintering. The addition of
CuO
was found to enhance the sintering rate of the
Sr
hexaferrite significantly at temperatures below 1100°C, whereas the
Fe
deficiency had only a moderate effect on the sintering above 1100°C. The relative densities of the
Sr
hexaferrite ceramics containing
Cu
sintered at 1000°C for 3 h were above 90%, whereas the
Cu
‐free
Sr
hexaferrite ceramics only started to sinter at 1000°C. We have shown that the addition of
CuO
enabled the reactive liquid‐phase sintering of
Sr
hexaferrite at 1000°C.
How much skin protection cream is actually applied in the workplace? Determination of dose per skin surface area in nurses
Authors: Schliemann Sibylle , Petri Maximilian , Elsner Peter 
Published: June 2012

Background. Skin protection creams (PCs) are used in the occupational setting to prevent irritant hand dermatitis. However, so far, the actual amounts of PC applied and the resulting dose per area unit on hands at work have not been a matter of systematic investigation. The quantities used in experimental studies investigating the efficacy of PCs range between 4 and 25 mg/cm2.Objectives. To develop a practical and accurate method to analyse the actual consumed quantities of PCs at workplaces in relation to hand surface area.Methods. Thirty‐one hospital nurses without hand eczema were provided with a sample PC in special monitoring tubes with Medication Event Monitoring Systems (MEMS TrackCaps®; Aardex Ltd, Zug, Switzerland), and used the product over 5 working days as usual. The consumption was calculated by weighing of the tubes and analysis of the application frequency, and related to the individual calculated hand surface area.Results. The mean PC dose applied was 0.97 ± 0.6 mg/cm2.Conclusions. The amounts of PC applied by hospital nurses were significantly lower than the amounts that have been used in experimental studies. The method appears to be suitable for use in different in occupational settings. Further investigations are needed to gain realistic insights into consumers' attitudes regarding PCs.
MiR‐21 Modulates hTERT Through a STAT3‐Dependent Manner on Glioblastoma Cell Growth
Authors: Wang Ying‐Yi , Sun Guan , Luo Hui , Wang Xie‐Feng , Lan Feng‐Ming , Yue Xiao , Fu Lin‐Shan , Pu Pei‐Yu , Kang Chun‐Sheng , Liu Ning , You Yong‐Ping 
Published: June 2012

SummaryBackground and purposeAs an important oncogenic miRNA, miR‐21 has been reported to play crucial roles in glioblastoma (GBM) carcinogenesis. However, the precise biological function and molecular mechanism of miR‐21 in GBM remain elusive. This study is designed to explore the mechanism of miR‐21 involved in the control of GBM cell growth.Methods and results
MTT assay, cell cycle analysis, and apoptosis analysis showed that reduction of miR‐21 inhibited cell growth in U87 and LN229 GBM cells. Further, reduction of miR‐21 decreased the expression of human telomerase reverse transcriptase (hTERT) and repressed STAT3 expression and STAT3 phosphorylation. STAT3 inhibition led to a remarkable depletion of hTERT at both mRNA and protein levels by binding to the hTERT gene promoter by performing luciferase reporter assay and chromatin Immunoprecipitation PCR. Finally, knockdown of miR‐21 considerably inhibited tumor growth and diminished the expression of STAT3 and hTERT in xenograft model.ConclusionOur findings indicate that miR‐21 regulates hTERT expression mediated by STAT3, therefore controlling GBM cell growth.
Computational Modeling in Cognitive Science: A Manifesto for Change
Authors: Addyman Caspar , French Robert M. 
Published: June 2012

AbstractComputational modeling has long been one of the traditional pillars of cognitive science. Unfortunately, the computer models of cognition being developed today have not kept up with the enormous changes that have taken place in computer technology and, especially, in human‐computer interfaces.  For all intents and purposes, modeling is still done today as it was 25, or even 35, years ago. Everyone still programs in his or her own favorite programming language, source code is rarely made available, accessibility of models to non‐programming researchers is essentially non‐existent, and even for other modelers, the profusion of source code in a multitude of programming languages, written without programming guidelines, makes it almost impossible to access, check, explore, re‐use, or continue to develop. It is high time to change this situation, especially since the tools are now readily available to do so. We propose that the modeling community adopt three simple guidelines that would ensure that computational models would be accessible to the broad range of researchers in cognitive science. We further emphasize the pivotal role that journal editors must play in making computational models accessible to readers of their journals.
WAGNER'S LAW REVISITED: A NOTE FROM SOUTH AFRICA
Authors: MENYAH KOJO , WOLDE‐RUFAEL YEMANE 
Published: June 2012

AbstractThe aim of this note is to reassess the validity of Wagner's law for South Africa for the period 1950‐2007 using cointegration and causality tests. The evidence shows causality running from income to government expenditure, thus supporting the Wagnerian proposition of an expanding public sector. Using five different long‐run estimators, we found that the size of South Africa's public sector was positively and significantly related to South Africa's national income. The elasticity ranges from 1.12 to 1.57, implying that a 1% increase in income leads to a 1.12‐1.57% increase in government expenditure.
Trilostane Dose versus Body Weight in the Treatment of Naturally Occurring Pituitary‐Dependent Hyperadrenocorticism in Dogs
Authors: Feldman E.C. , Kass P.H. 
Published: June 2012

BackgroundTrilostane is commonly used in the treatment of dogs with naturally occurring pituitary‐dependent hyperadrenocorticism (PDH). Dose recommendations have varied from the manufacturer and the literature.HypothesisAs body weight increases, dose/kg or dosage/day of trilostane required to control the clinical signs of PDH decreases.Animals70 dogs with naturally occurring hyperadrenocorticism.MethodsRetrospective study. Each dog must have been treated for at least 6 months and should have shown a “good response” to trilostane, as determined by owners. Statistical comparisons of dose and dosage were made after the dogs were separated into groups weighing <15 or >15 kg; groups weighing ≤10, 10.1–20, 20.1–30, and ≥30 kg; and then groups based on body surface area versus dose/kg and total amount of trilostane required to control the condition.ResultsThere was no significant difference in trilostane dose in mg/kg of body weight or in the total amount of trilostane required daily to control clinical signs, except when the dose for dogs weighing >30 kg was compared with that for the other groups. However, despite lack of statistical significance when comparing groups, there was a significant trend using polynomial regression analysis, suggesting that as body weight increases, the amount of trilostane (mg/kg/dose as well as mg/kg/daily dosage) required to control clinical signs decreases.Conclusions and Clinical ImportanceDogs weighing >30 kg, and possibly those weighing >15 kg, might require smaller amounts of trilostane per dose or per day than those weighing less, to control PDH‐associated clinical signs.