bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Causal Attributions of Teaching Staff Towards Children with Intellectual Disabilities: A Comparison of ‘Vignettes’ Depicting Challenging Behaviour with ‘Real’ Incidents of Challenging Behaviour
Authors: Lucas Victoria L. , Collins Suzanne , Langdon Peter E. 
Published: May 2008

Background We examined whether staff attributions, emotions and helping behaviours in reaction to ‘real’ incidents of challenging behaviour (CB) exhibited by children with intellectual disabilities were different from reactions to ‘vignettes’. We also examined whether these reactions are congruent with that predicted by attribution theory.Methods Using a repeated measures design, 60 staff working with children who have severe intellectual disabilities completed measures of cognition, emotion and helping behaviour in reaction to a ‘real’ incident of CB, and then completed the same measures in reaction to reading a ‘vignette’, that was matched to the ‘real’ incident of CB. There was a 2‐week interval between the completion of measures in response to the ‘real’ incident of CB and the ‘vignette’.Results Correlational support was found forWeiner’s (1980)cognitive–emotional–action model of helping behaviour for measures completed in reaction to the ‘real’ incident of CB, regarding attributions of control only, but not for the ‘vignette’. There were significant differences between the correlations detected using ‘real’ incidents of CB in comparison to ‘vignettes’. Little evidence was found using both methods to supportWeiner’s (1979)model of achievement motivation.Conclusions The results suggest that the relationships between constructs investigated using ‘vignettes’ is different from that detected when using ‘real’ incidents of CB, which has implications for psychological research that has used ‘vignettes’.
Correlation Analyses Reveal a Substantial Influence of Allelic Gaps on the Investigation of Genetic Diversity of Modern Human Populations with Microsatellites
Authors: Guha S. , Chakraborty R. 
Published: May 2008

SummaryHigh intra‐population genetic diversity and multiple measures of genetic variability at STR loci are useful in inferring past evolutionary history. However, STRs, categorized by their repeat motif size, differ in a number of aspects, requiring separate analyses. We analyzed 783 STRs in 36 worldwide populations to examine marker suitability as well as correlations between various measurements, to evaluate the extent of genomic diversity present in modern human populations. The loci were grouped by type and analyzed separately for each population group. Genetic variation defined by gene diversity and allele size variance, shows different trends of variation across four types of STRs. Additionally, there is little variation of genetic diversity, but there is decreased allelic size variance with increasing repeat motifs. A poor correlation between genetic diversity and allelic size variance across loci in all groups for Di‐STRs is probably caused by the presence of allelic size gaps. In contrast, allelic size variance, genetic diversity, and number of alleles are strongly correlated with both tri‐ and tetra‐STRs. The positive correlation of allelic size variance and presence of gaps within the range of allelic sizes in Di‐STRs alone explains these observations. An unexpected high imbalance index (β) at Di‐STRs due to high allelic size variance also supports this assertion.
Genetic Epidemiology of Subclinical Cardiovascular Disease in the Diabetes Heart Study
Authors: Bowden D. W. , Lehtinen A. B. , Ziegler J. T. , Rudock M. E. , Xu J. , Wagenknecht L. E. , Herrington D. M. , Rich S. S. , Freedman B. I. , Carr J. J. , Langefeld C. D. 
Published: May 2008

SummaryA genome‐wide linkage scan of 357 European American (EA) and 72 African American (AA) pedigrees multiplex for type 2 diabetes mellitus (T2DM) was performed with multipoint nonparametric QTL linkage analysis. Four subclinical measures of cardiovascular disease (CVD): coronary artery (CCP), carotid artery (CarCP), and abdominal aortic calcified plaque (AACP) and carotid artery intima‐media thickness (IMT) were mapped. Analyses were adjusted for age, gender, body mass index, and (if appropriate) ethnicity and diabetes status.Evidence for linkage was observed in EA T2DM subjects to CarCP near 16p13 (LOD=4.39 at 8.4 cM; P = 0.00001). When all EA subjects were included, the LOD score was 2.52, suggesting an amplification of the linkage by diabetes. Linkage analysis of a principal components measure of vascular calcium (LOD = 3.85 at 9.3 cM on 16p in EA T2DM subjects) and bivariate analysis of CarCP X IMT (LOD = 3.77 at 9.3 cM on 16p in EA T2DM subjects) were consistent with this linkage. In addition, evidence for linkage was observed with CCP near D15S1515 (LOD = 2.34) in EAs. Additional loci on chromosomes 1, 2, 7, 10, 13, and 21 had LODs > 2.0. The identification of trait‐determining polymorphisms underlying these linkages will help delineate risk factors for CVD in T2DM and the general population.
Distribution of zinedin in the rat brain
Authors: Benoist Marion , Baude Agnès , Tasmadjian Armand , Dargent Bénédicte , Kessler Jean‐Pierre , Castets Francis 
Published: May 2008

AbstractMembers of the striatin family are scaffolding proteins involved in numerous signaling pathways principally in neurons. Zinedin is the only member of this protein family for which the brain distribution has not been determined so far. Here, we have validated a specific antibody against zinedin and used this tool to study the localization of zinedin at cellular and sub‐cellular levels in the rat brain. Zinedin is primarily expressed in neurons of the hippocampus, cerebral cortex, olfactory bulb and caudate putamen nucleus. Like other members of the striatin family, zinedin displays a polarized distribution in the somato‐dendritic compartment of neurons and is enriched in dendritic spines. The rostral expression of zinedin as well as its compartmented distribution in dendritic spines may have important implications not only for zinedin function but also in the physiology of dendritic spines of a particular subset of neurons.
Extracellular signal‐regulated kinases (ERK) and protein kinase C (PKC) activities are involved in the modulation of Nur77 and Nor‐1 expression by dopaminergic drugs
Authors: Bourhis Emmanuelle , Maheux Jérôme , Rouillard Claude , Lévesque Daniel 
Published: May 2008

AbstractThe dopamine system is the main target of antipsychotic and psychostimulant drugs. These drugs induce intracellular events that culminate in the transcription of immediate early genes, such as c‐fos. Another class of transcription factors, namely, the nuclear receptor subgroup called Nurs (Nur77, Nurr1 and Nor‐1), has recently been associated with behavioral and biochemical effects mediated by dopamine. However, the signaling cascade leading to modulation of Nur mRNA levels in the brain has never been investigated. In the present study, we explore in vivo using specific kinase inhibitors the role of mitogen‐associated and extracellular signal‐regulated kinases (MEK) and protein kinase C (PKC) in the modulation of Nur expression induced by dopamine receptor drugs. Modulation of Nur77 expression by a dopamine D2 receptor antagonist is associated with MEK and PKC activities, whereas only the PKC activity participates in the modulation of Nor‐1 expression. Both MEK and PKC activities also participate in the modulation of Nur77 mRNA levels induced by dopamine receptor agonists, whereas a selective MEK activity is associated with the modulation of Nor‐1 mRNA levels. Interestingly, modulation of dopamine drug‐induced locomotor activities by kinase inhibitors is in accordance with the effects on Nur77, but not Nor‐1, expression. Taken together, the results indicate that signaling events leading to modulation of Nur77 and Nor‐1 expression following dopamine receptor interacting drugs are distinct. Considering that orphan nuclear receptors of the Nur subgroup display an important ligand‐independent constitutive activity, characterization of the signaling cascades involved in the regulation of their expression represents an important step for understanding their role in dopamine system physiology and pathophysiology.
Adaptation to chronic MG132 reduces oxidative toxicity by a CuZnSOD‐dependent mechanism
Authors: Leak Rehana K. , Zigmond Michael J. , Liou Anthony K. F. 
Published: May 2008

AbstractTo study whether and how cells adapt to chronic cellular stress, we exposed PC12 cells to the proteasome inhibitor MG132 (0.1 μM) for 2 weeks and longer. This treatment reduced chymotrypsin‐like proteasome activity by 47% and was associated with protection against both 6‐hydroxydopamine (6‐OHDA; 100 μM) and higher dose MG132 (40 μM). Protection developed slowly over the course of the first 2 weeks of exposure and was chronic thereafter. There was no change in total GSH levels after MG132. Buthionine sulfoximine (100 μM) reduced GSH levels by 60%, but exacerbated 6‐OHDA toxicity to the same extent in both MG132‐treated and control cells and failed to reduce MG132‐induced protection. Chronic MG132 resulted in elevated antioxidant proteins CuZn superoxide dismutase (SOD; +55%), MnSOD (+21%), and catalase (+15%), as well as chaperone heat‐shock protein 70 (+42%). Examination of SOD enzyme activity revealed higher levels of CuZnSOD (+40%), with no change in MnSOD. We further assessed the mechanism of protection by reducing CuZnSOD levels with two independent siRNA sequences, both of which successfully attenuated protection against 6‐OHDA. Previous reports suggested that artificial over‐expression of CuZnSOD in dopaminergic cells is protective. Our data complement such observations, revealing that dopaminergic cells are also able to use endogenous CuZnSOD in self‐defensive adaptations to chronic stress, and that they can even do so in the face of extensive GSH loss.
Megalin is a receptor for albumin in astrocytes and is required for the synthesis of the neurotrophic factor oleic acid
Authors: Bento‐Abreu André , Velasco Ana , Polo‐Hernández Erica , Pérez‐Reyes Pedro Luis , Tabernero Arantxa , Medina José M. 
Published: May 2008

AbstractWe have previously shown that the uptake and transcytosis of albumin in astrocytes promote the synthesis of the neurotrophic factor oleic acid. Although the mechanism by which albumin induces oleic acid synthesis is well known, the mechanism of albumin uptake in astrocytes remains unknown. In this work, we found that astrocytes express megalin, an endocytic receptor for multiple ligands including albumin. In addition, when the activity of megalin is blocked by specific antibodies or by silencing megalin with specific siRNA, albumin binding and internalization is strongly reduced indicating that megalin is required for albumin binding and internalization in the astrocyte. Since the uptake of albumin in astrocytes aims at synthesizing the neurotrophic factor oleic acid, we tested the ability of megalin‐silenced astrocytes to synthesize and release oleic acid in the presence of albumin. Our results showed that the amount of oleic acid found in the extracellular medium of megalin‐silenced astrocytes was strongly reduced as compared with their controls. Together, the results of this work indicate that megalin is a receptor for albumin in astrocytes and is required for the synthesis of the neurotrophic factor oleic acid. Consequently, the possible involvement of albumin in the holoprosencephalic syndrome observed in megalin‐deficient mice is suggested.
Stem Cell Review Series: Aging of the skeletal muscle stem cell niche
Authors: Gopinath Suchitra D. , Rando Thomas A. 
Published: May 2008

SummaryDeclining stem cell function during aging contributes to impaired tissue function. Muscle‐specific stem cells (‘satellite cells’) are responsible for generating new muscle in response to injury in the adult. However, aged muscle displays a significant reduction in regenerative abilities and an increased susceptibility to age‐related pathologies. This review describes components of the satellite cell niche and addresses how age‐related changes in these components impinge on satellite cell function. In particular, we review changes in the key niche elements, the myofiber and the basal lamina that are in intimate contact with satellite cells. We address how these elements are influenced by factors secreted by interstitial cells, cells of the immune system, and cells associated with the vasculature, all of which change with age. In addition, we consider more distant sources of influence on the satellite cell niche that change with age, such as neural‐mediated trophic factors and electrical activity and systemic factors present in the circulation. A better understanding of the niche elements and their influence on the satellite cell will facilitate the development of therapeutic interventions aimed at improving satellite cell activity and ultimately tissue response to injury in aged individuals.
Hemolytic transfusion reactions after administration of intravenous immune (gamma) globulin: a case series analysis
Authors: Daw Zohra , Padmore Ruth , Neurath Doris , Cober Nancy , Tokessy Melanie , Desjardins Diane , Olberg Bernhard , Tinmouth Alan , Giulivi Antonio 
Published: May 2008

BACKGROUND: This case series summarizes our observations of hemolytic reactions after the administration of large amounts of intravenous immune (gamma) globulin (IVIG).STUDY DESIGN AND METHODS: Cases of hemolysis were identified by a decrease in hemoglobin not otherwise explained following IVIG administration.RESULTS: Sixteen cases were identified over a 2½‐year period at the Ottawa Hospital of approximately 1000 patients receiving IVIG (1.6%). Characteristics of these patients include a large dose of IVIG, female sex, non‐O blood group, and underlying inflammatory state.CONCLUSIONS: Significant hemolysis may occur after the administration of large doses of IVIG. A two‐step mechanism of hemolysis is proposed, sensitization by ABO isohemagglutinins followed by phagocytosis by activated macrophages. A simple protocol to facilitate the early detection of such cases is presented.
Can a Coherent Risk Measure Be Too Subadditive?
Authors: Dhaene J. , Laeven R. J. A. , Vanduffel S. , Darkiewicz G. , Goovaerts M. J. 
Published: May 2008

AbstractWe consider the problem of determining appropriate solvency capital requirements for an insurance company or a financial institution. We demonstrate that the subadditivity condition that is often imposed on solvency capital principles can lead to the undesirable situation where the shortfall risk increases by a merger. We propose to complement the subadditivity condition by a regulator's condition. We find that for an explicitly specified confidence level, the Value‐at‐Risk satisfies the regulator's condition and is the “most efficient” capital requirement in the sense that it minimizes some reasonable cost function. Within the class of concave distortion risk measures, of which the elements, in contrast to the Value‐at‐Risk, exhibit the subadditivity property, we find that, again for an explicitly specified confidence level, the Tail‐Value‐at‐Risk is the optimal capital requirement satisfying the regulator's condition.
The Role of Internal Capital Markets in Financial Intermediaries: Evidence From Insurer Groups
Authors: Powell Lawrence S. , Sommer David W. , Eckles David L. 
Published: May 2008

AbstractWe exploit the transparency of internal capital markets (ICMs) within insurance groups to investigate the activity and efficiency of ICMs within insurance groups. Specifically, we compare the relationship between internal capital transfers and investment to that between capital from other sources and investment. The ability to track the actual ICM transactions allows for more direct analysis of ICM activity than most previous studies. Consistent with theory, we find evidence that ICMs play a significant role in the investment behavior of affiliated insurers. We then use these detailed data to execute a more direct test of ICM efficiency than currently exists in the literature. Consistent with ICM efficiency, results suggest that capital is allocated to subsidiaries with the best expected performance.
Complex Electrograms Within the Coronary Sinus: Time‐ and Frequency‐Domain Characteristics, Effects of Antral Pulmonary Vein Isolation, and Relationship to Clinical Outcome in Patients with Paroxysmal and Persistent Atrial Fibrillation
Authors: YOSHIDA KENTARO , ULFARSSON MAGNUS , TADA HIROSHI , CHUGH AMAN , GOOD ERIC , KUHNE MICHAEL , CRAWFORD THOMAS , SARRAZIN JEAN F. , CHALFOUN NAGIB , WELLS DARRYL , JONGNARANGSIN KRIT , PELOSI FRANK , BOGUN FRANK , MORADY FRED , ORAL HAKAN 
Published: May 2008

Background:
The mechanistic and clinical significance of complex fractionated atrial electrograms (CFAE) in the coronary sinus (CS) has been unclear.
Methods and Results:
Antral pulmonary vein isolation (APVI) was performed in 77 patients with paroxysmal (32) or persistent AF (45). CS electrograms recorded for 60 seconds before and after APVI were analyzed in the time‐ and frequency‐domains. Dominant frequency (DF), complexity index (CI: change in polarity of depolarization), and fractionation index (FI: change in direction of depolarization slope) were determined. Before APVI, there was no difference in DF, CI, or FI between paroxysmal and persistent AF. APVI resulted in a significant decrease in DF, CI, and FI in all patients. Baseline CI (43 ± 13/s vs 54 ± 14/s, P = 0.03) and FI (64 ± 23/s vs 87 ± 30/s, P = 0.02) were lower in patients with paroxysmal AF who had AF terminated by ablation than who did not. At 10 ± 2 months, 69% of patients with paroxysmal AF and 49% of patients with persistent AF were free from AF after single ablation. Baseline CI was higher among patients with paroxysmal AF who had AF after APVI (56 ± 20/s vs 44 ± 10/s, P = 0.03). In patients with persistent AF, there was a larger decrease in DF after APVI among patients who remained free from AF (13 ± 11% vs 7 ± 9%, P < 0.05).
Conclusions:
Complexity of CS electrograms may reflect drivers of AF that perpetuate paroxysmal AF after APVI. In persistent AF, the extent to which APVI decreases DF in the CS correlates with efficacy, suggesting that DF identifies patients who may require additional ablation beyond APVI.
Apoptosis‐related mitochondrial dysfunction defines human monocyte‐derived dendritic cells with impaired immuno‐stimulatory capacities
Authors: Castera Laurent , Hatzfeld‐Charbonnier Anne Sophie , Ballot Caroline , Charbonnel Florence , Dhuiege Edith , Velu Thierry , Formstecher Pierre , Mortier Laurent , Marchetti Philippe 
Published: May 2008

AbstractThe death of dendritic cells (DCs) can potentially influence immune responses by affecting the duration of DC stimulation of lymphocytes. Here, we report that cultured mature monocyte‐derived DCs manifest early mitochondrial damage (i.e. within 24 hrs), characterized by mitochondrial membrane potential (ψΔm) disruption and mitochondrial release of pro‐apoptotic factors, followed by reactive oxygen species (ROS) production and activation of caspases. Afterwards, DCs with mitochondrial alterations are condemned to undergo apoptosis and necrosis. Macroarray analysis results (validated by real time quantitative‐PCR (QRT‐PCR) and immunoblotting), showed up‐regulation of the pro‐apoptotic member of the Bcl‐2 family, Bim, while expression of several anti‐apoptotic molecules was down‐regulated. Importantly, pre‐apoptotic DCs (characterized by a low Δψm) showed a modified phenotype, with down‐regulation.of HLA‐DR and of the co‐stimulatory molecules CD80 and CD86. Moreover, sorted viable low ψΔm DCs were unable to activate allogeneic T cells, indicating that pre‐apoptotic DCs have already lost some of their immuno‐stimulatory capabilities long before any detectable signs of death occur. Perturbations to mitochondrial respiration with rotenone identified the same modifications to DC immune functions. These data indicate a strong requirement for mitochondrial integrity for the immuno‐stimulatory capacities of DC. Determining ΔΨm could be a useful parameter to select ‘fully’ functional DCs for anti‐tumour vaccines.
Neonatal resuscitation after severe asphyxia – a critical evaluation of 177 Swedish cases
Authors: Berglund Sophie , Norman Mikael , Grunewald Charlotta , Pettersson Hans , Cnattingius Sven 
Published: May 2008

AbstractAim: To evaluate neonatal resuscitation of infants born with severe asphyxia.Method: All case records of the 472 claims for financial compensation due to suspected medical malpractice in conjunction with childbirth in Sweden between 1990 and 2005 were scrutinized. Inclusion criteria were: gestational age ≥33 completed weeks, planned vaginal onset of delivery, a reactive CTG at onset of labour, neonatal asphyxia (defined as metabolic acidosis {pH of < 7.05 and/or a base excess of < –12}), or an Apgar score <7 at 5 min. It was assessed that 177 infants suffered from cerebral palsy or early death due to severe asphyxia presumably caused by malpractice around labour.Results: Median Apgar score at 5 min was 3, indicating that all infants needed immediate and extensive resuscitation. There was insufficient adherence to guidelines concerning neonatal resuscitation, including delayed initiation of excessive resuscitation in 19 infants, lack of satisfactory ventilation in 79 infants, and untimely interruption of resuscitation in 38 infants.Conclusions: Compliance with guidelines for resuscitation of severely asphyctic newborn may be improved, especially concerning ventilation and prompt paging for skilled personnel in cases of imminent asphyxia. Documentation of neonatal resuscitation must be improved to enable reliable evaluation.
Visual screening versus transcutaneous bilirubinometry for predischarge jaundice assessment
Authors: Kaplan Michael , Shchors Irena , Algur Nurit , Bromiker Ruben , Schimmel Michael S , Hammerman Cathy 
Published: May 2008

AbstractObjective: Comparison of visual screening with transcutaneous bilirubinometry (TcB) in identifying neonates with plasma total bilirubin (PTB) ≥75th percentile.Design: In 100 paired readings PTB was 34 ± 24 μmol/L higher than the TcB counterpart. A TcB reading of 154 μmol/L was therefore regarded as equivalent to a PTB of 188 μmol/L, corresponding to the 75th percentile at 48 h. Predischarge, all newborns were evaluated for jaundice, first by visual inspection and then transcutaneously. PTB was ordered as indicated by visual assessment or if the TcB reading was ≥154 μmol/L.Results: Of 346 newborns tested, 25 (7.2%) had a PTB concentration ≥75th percentile. Forty‐nine had PTB determinations based on TcB compared with 83 by visual assessment. However, a similar number of affected newborns was identified by each method (21/25 (84%) by visual screening vs. 18/25 (72%) by TcB). PTB concentrations of those who had been chosen by TcB were higher than those selected visually (202 ± 24 μmol/L vs. 186 ± 31 μmol/L).Conclusions: A practical method for predischarge detection of neonates with plasma total bilirubin concentration ≥ 75th percentile, implementing transcutaneous bilirubinometry, is described. The transcutaneous technique required fewer blood tests than visual assessment for similar yield.