bluuebunny/crossref_metadata_2025_split huggingface dataset:
Can mood‐inducing videos affect problem‐solving activities in a web‐based environment?
Authors: Verleur Ria , Verhagen Pløn W. , Heuvelman Ard 
Published: March 2007

AbstractThe purpose of this study was to examine whether a video‐induced positive and negative mood has a differential effect on subsequent problem‐solving activities in a web‐based environment. The study also examined whether task conditions (task demands) moderated the mood effect. As in traditional experimental mood‐effect studies, the affective video materials were not related to the tasks. The results show that affective video clips did impact performance on an insight task but not on a divergent‐thinking task. This provides evidence that in some cases affective video has an effect on the performance of unrelated tasks in a web‐based environment.
The use of Meta‐Analysis Risk Estimates for Candidate Genes in Combination to Predict Coronary Heart Disease Risk
Authors: Drenos F. , Whittaker J. C. , Humphries S. E. 
Published: March 2007

SummaryAlthough the risk for coronary heart disease (CHD) associated with single SNPs is modest it has been suggested that, in combination, several common risk‐associated alleles could lead to a substantially better heart disease risk prediction. We have modelled this using 10 SNPs in ten candidate genes (APOB, NOS3, APOE, ACE, SERPINE1, MTHFR, ITGA2B, PON 1, LPL, and CETP) and their predicted summary risk estimates from meta‐analysis. Based on published allele frequencies, ∼29% of the general population would be expected to carry less than three risk alleles, approximately 55% would carry 3 or 4 risk alleles, 4% would have 6 and 1% 7 or more risk alleles. Compared to the mean of those with 3 or 4 risk associated genotypes, those with 6 and 7‐or‐more alleles have a significantly higher risk odds ratio (OR) of CHD (mean OR (95% Confidence Intervals), 1.70 (1.14 to 2.55); and 4.51 (2.89 to 7.04) respectively), while compared to those in the lowest decile of risk, those in the highest decile have a CHD odds ratio in the range of 3.05 (2.24 to 4.14). Taking into account age and the risk alleles carried, the mean 10 year probability for developing CHD for a 55 year old man was calculated to be 15% (8.6% to 24.8%), with nearly 1 in 5 having more than 20% risk. Whether this particular group of 10 SNPs will improve the accuracy of CHD predictions over the combination of classical risk factors in clinical use requires further experimental evidence.
Delay of photoreceptor degeneration in tubby mouse by sulforaphane
Authors: Kong Li , Tanito Masaki , Huang Zhong , Li Feng , Zhou Xiaohong , Zaharia Alexander , Yodoi Junkie , McGinnis James F. , Cao Wei 
Published: March 2007

AbstractIn this study, the homozygous tubby (tub/tub) mutant mouse, with an early progressive hearing loss and photoreceptor degeneration, was used as a model system to examine the effects of systemic administration of a naturally occurring isothiocyanate, sulforaphane (SF), on photoreceptor degeneration. Several novel observations have been made: (i) the mRNA and protein expression of thioredoxin (Trx), thioredoxin reductase (TrxR) and NF‐E2‐related factor‐2 (Nrf2) were significantly reduced even prior to photoreceptor cell degeneration in the retinas of tub/tub mice, suggesting that retinal expression of the Trx system is impaired and that Trx regulation is involved in the pathogenesis of retinal degeneration in this model, (ii) intraperitoneal injection with SF significantly up‐regulated retinal levels of Trx, TrxR, and Nrf2, and effectively protected photoreceptor cells in tub/tub mice as evaluated functionally by electroretinography and morphologically by quantitative histology, and (iii) treatment with PD98059, an inhibitor of extracellular signal‐regulated kinases (ERKs), blocked SF‐mediated ERKs activation and up‐regulation of Trx/TrxR/Nrf2 in the retinas of tub/tub mice. This suggests that ERKs and Nrf2 are involved in the mechanism of SF‐mediated up‐regulation of the Trx system to protect photoreceptor cells in this model. These novel findings are significant and could provide important information for the development of a unique strategy to prevent sensorineural deafness/retinal dystrophic syndromes and also other forms of inherited neurological disorders.
Ketone bodies are protective against oxidative stress in neocortical neurons
Authors: Kim Do Young , Davis Laurie M. , Sullivan Patrick G. , Maalouf Marwan , Simeone Timothy A. , Brederode Johannes van , Rho Jong M. 
Published: March 2007

AbstractKetone bodies (KB) have been shown to prevent neurodegeneration in models of Parkinson’s and Alzheimer’s diseases, but the mechanisms underlying these effects remain unclear. One possibility is that KB may exert antioxidant activity. In the current study, we explored the effects of KB on rat neocortical neurons exposed to hydrogen peroxide (H2O2) or diamide – a thiol oxidant and activator of mitochondrial permeability transition (mPT). We found that: (i) KB completely blocked large inward currents induced by either H2O2 or diamide; (ii) KB significantly decreased the number of propidium iodide‐labeled cells in neocortical slices after exposure to H2O2 or diamide; (iii) KB significantly decreased reactive oxygen species (ROS) levels in dissociated neurons and in isolated neocortical mitochondria; (iv) the electrophysiological effects of KB in neurons exposed to H2O2 or diamide were mimicked by bongkrekic acid and cyclosporin A, known inhibitors of mPT, as well as by catalase and DL – dithiothreitol, known antioxidants; (v) diamide alone did not significantly alter basal ROS levels in neurons, supporting previous studies indicating that diamide‐induced neuronal injury may be mediated by mPT opening; and (vi) KB significantly increased the threshold for calcium‐induced mPT in isolated mitochondria. Taken together, our data suggest that KB may prevent mPT and oxidative injury in neocortical neurons, most likely by decreasing mitochondrial ROS production.
Hyaluronan‐CD44 interaction stimulates Rac1 signaling and PKNγ kinase activation leading to cytoskeleton function and cell migration in astrocytes
Authors: Bourguignon Lilly Y. W. , Gilad Eli , Peyrollier Karine , Brightman Amy , Swanson Raymond A. 
Published: March 2007

AbstractBoth hyaluronan [HA, the major glycosaminoglycans in the extracellular matrix (ECM)] and CD44 (a primary HA receptor) are associated with astrocyte activation and tissue repair following central nervous system (CNS) injury. In this study we investigated the question of whether HA‐CD44 interaction influences astrocyte signaling and migration. Our data indicated that HA binding to the cultured astrocytes stimulated Rac1 signaling and cytoskeleton‐mediated migration. To determine the cellular and molecular basis of these events, we focused on PKNγ, a Rac1‐activated serine/threonine kinase in astrocytes. We determined that HA binding to astrocytes stimulated Rac1‐dependent PKNγ kinase activity which, in turn, up‐regulated the phosphorylation of the cytoskeletal protein, cortactin, and attenuated the ability of cortactin to cross‐link F‐actin. Further analyses indicated that the N‐terminal antiparallel coiled‐coil (ACC) domains of PKNγ interacted with Rac1, and transfection of astrocytes with PKNγ‐ACCcDNA inhibited PKNγ activity. Over‐expression of the PKNγ‐ACC domain also functions as a dominant‐negative mutant to block HA/CD44‐mediated PKNγ activation of cortactin and astrocyte migration. Taken together, these findings strongly suggest that hyaluronan/CD44 interaction with Rac1‐PKNγ plays a pivotal role in cytoskeleton activation and astrocyte migration. These newly discovered HA/CD44‐induced astrocyte function may provide important insight into novel therapeutic treatments for tissue repair following CNS injury.
Glutamate release from activated microglia requires the oxidative burst and lipid peroxidation
Authors: Barger Steven W. , Goodwin Mary E. , Porter Mandy M. , Beggs Marjorie L. 
Published: March 2007

AbstractWhen activated by proinflammatory stimuli, microglia release substantial levels of glutamate, and mounting evidence suggests this contributes to neuronal damage during neuroinflammation. Prior studies indicated a role for the Xc exchange system, an amino acid transporter that antiports glutamate for cystine. Because cystine is used for synthesis of glutathione (GSH) synthesis, we hypothesized that glutamate release is an indirect consequence of GSH depletion by the respiratory burst, which produces superoxide from NADPH oxidase. Microglial glutamate release triggered by lipopolysaccharide was blocked by diphenylene iodonium chloride and apocynin, inhibitors of NADPH oxidase. This glutamate release was also blocked by vitamin E and elicited by lipid peroxidation products 4‐hydroxynonenal and acrolein, suggesting that lipid peroxidation makes crucial demands on GSH. Although NADPH oxidase inhibitors also suppressed nitrite accumulation, vitamin E did not; moreover, glutamate release was largely unaffected by nitric oxide donors, inhibitors of nitric oxide synthase, or changes in gene expression. These findings indicate that a considerable degree of the neurodegenerative consequences of neuroinflammation may result from conversion of oxidative stress to excitotoxic stress. This phenomenon entails a biochemical chain of events initiated by a programmed oxidative stress and resultant mass‐action amino acid transport. Indeed, some of the neuroprotective effects of antioxidants may be due to interference with these events rather than direct protection against neuronal oxidation.
Two isoforms of the cold‐inducible mRNA‐binding protein RBM3 localize to dendrites and promote translation
Authors: Smart Fiona , Aschrafi Armaz , Atkins Annette , Owens Geoffrey C. , Pilotte Julie , Cunningham Bruce A. , Vanderklish Peter W. 
Published: March 2007

AbstractA diverse set of mRNA‐binding proteins (BPs) regulate local translation in neurons. However, little is known about the role(s) played by a family of cold‐inducible, glycine‐rich mRNA‐BPs. Unlike neuronal mRNA‐BPs characterized thus far, these proteins are induced by hypothermia and are comprised of one RNA recognition motif and an adjacent arginine‐ and glycine‐rich domain. We studied the expression and function of the RNA‐binding motif protein 3 (RBM3), a member of this family, in neurons. RBM3 was expressed in multiple brain regions, with the highest levels in cerebellum and olfactory bulb. In dissociated neurons, RBM3 was observed in nuclei and in a heterogeneous population of granules within dendrites. In sucrose gradient assays, RBM3 cofractionated with heavy mRNA granules and multiple components of the translation machinery. Two alternatively spliced RBM3 isoforms that differed by a single arginine residue were identified in neurons; both were post‐translationally modified. The variant lacking the spliced arginine exhibited a higher dendritic localization and was the only isoform present in astrocytes. When overexpressed in neuronal cell lines, RBM3 isoforms‐enhanced global translation, the formation of active polysomes, and the activation of initiation factors. These data suggest that RBM3 plays a distinctive role in enhancing translation in neurons.
Baicalin protects mouse from Concanavalin A‐induced liver injury through inhibition of cytokine production and hepatocyte apoptosis
Authors: Liu Lin‐lin , Gong Li‐kun , Wang Hui , Xiao Ying , Wu Xiong‐fei , Zhang Yun‐hai , Xue Xiang , Qi Xin‐ming , Ren Jin 
Published: March 2007

AbstractBackground: Baicalin (BA) exhibits an anti‐inflammatory effect in vivo and in vitro and is used to treat chronic hepatitis. However, the mechanism by which BA exerts the liver‐protective effect remains largely unknown.Aims: The present study reports that BA inhibits cytokine production and hepatocyte apoptosis to protect mice from liver injury induced by concanavalin A (Con A), a T‐cell‐dependent liver injury model.Results: Con A injection of mice induced severe immune responses and extensive hepatocellular apoptosis within 24 h. Pretreatment of 200 or 100 mg/kg BA markedly reduced serum aminotransferase activities, protected hepatoycte apoptosis and reduced the increase of plasma cytokine levels, including tumor necrosis factor‐α (TNF‐α), interferon‐γ (IFN‐γ) and interleukin‐6 (IL‐6). Furthermore, BA pretreatment decreased tissue myeloperoxidase activity and lipid peroxidation, but increased the superoxide dismutase level. In vitro studies indicated that the beneficial effect of BA was associated with reduced cytokine production from lymphocytes and reduced TNF‐α‐induced hepatocyte apoptosis.Conclusion: These results suggest that BA has therapeutic potential for T‐cell‐mediated liver injury.
Current concepts in the pathogenesis of nonalcoholic fatty liver disease
Authors: Méndez‐Sánchez Nahum , Arrese Marco , Zamora‐Valdés Daniel , Uribe Misael 
Published: March 2007

AbstractNonalcoholic fatty liver disease (NAFLD) is an increasingly recognized cause of chronic liver disease, representing the leading cause of hepatology referral in some centres. However, its pathophysiology is not completely understood. Insulin resistance is one of the major mechanisms involved in disease prevalence and progression. Owing to the lack of an effective pharmacological therapy, recommendations on treatment are scarce and are based mainly on lifestyle changes, including diet and exercise. A review of the current literature on pathogenesis of NAFLD is presented in this article.
Too Close to Call? Uncertainty and Bias in Election‐Night Reporting*
Authors: Uscinski Joseph E. 
Published: March 2007

Objective. Previous research has found that early election‐night projections can have a depressing effect on turnout in presidential elections. Although this effect has been found to be small in the past, it may be enough to sway state outcomes and, potentially, the final outcomes of close presidential and other elections. Therefore, this article analyzes the election‐night presidential projections of the three major cable news networks in 2000 and 2004 to examine the forces that lead to the timing of election‐night calls.Method. I collect the on‐air projection times of the cable news networks from videotapes, transcripts, and network documents. I apply duration analysis, specifically Cox models, to examine the forces that lead networks to make projections when they do.Results. Results of duration analysis indicate that while the cable networks timed their state‐by‐state projections primarily on the competitiveness of the state presidential races, network competition appears to drive projections at the beginning of election night. Furthermore, I find that early in the night in 2000, the cable networks appeared to call states sooner for Al Gore than for George W. Bush when controlling for the competitiveness of the state presidential races.Conclusions. This article provides support for Republican allegations of biased election‐night projections in 2000. However, it appears that because the networks amended their election‐night procedures, there were no miscalls or differences in how cable networks called states for the two presidential candidates in 2004.
Nonprofit Advocacy Organizations: Their Characteristics and Activities*
Authors: Child Curtis D. , Grønbjerg Kirsten A. 
Published: March 2007

Objectives. In this article we examine political advocacy by nonprofit organizations. Relatively little is known about the types of organizations that participate in advocacy, their characteristics, the issues for which they advocate, and the resources they devote to it. This is especially the case for nonprofits that operate at the state or local level.Methods. Using data from a large survey of Indiana nonprofit organizations, we use logistic and multinomial regression to determine which organizational characteristics relate to participation in varying levels of advocacy.Results. We find that the size of the organization, its access to information and communication technology, its charitable status, and, in some cases, the field of activity in which it operates all help predict nonprofit advocacy. The age of the organization, its reliance on government funding (except when substantial), and its proximity to the state's major economic and political center do not generally help differentiate nonprofits that advocate from those that do not.Conclusions. Our findings suggest that most nonprofits are ambivalent about advocacy. Some do no advocacy at all; many participate in some form of it although it does not constitute their primary purpose or mission; and only a small minority devotes considerable resources to it. However, these patterns differ systematically by type of nonprofit.
Invariant natural killer T cells from rhesus macaque spleen and peripheral blood are phenotypically and functionally distinct populations
Authors: Gansuvd Balgansuren , Goodwin Jeanine , Asiedu Clement K. , Jiang Xiao Ling , Jargal Uuganbayar , Andrades Patricio , Exley Mark A. , Thomas Judith M. 
Published: March 2007

AbstractBackground  Natural killer T cells (NKT) possess dual functions of innate and adaptive immune systems, controlling viral infections and regulating autoimmune diseases. Non‐human primates (NHP) are penultimate models for advancing therapeutic immunoregulatory strategies for translational application in humans, though, little is known about NHP NKT cells. Here we characterized rhesus macaque NKT cells ex vivo.Methods  The frequency, phenotype and intracellular cytokine production of Vα24+6B11+ invariant NKT (iNKT) cells were analyzed by multi‐color flow cytometry. Vα24JαQ mRNA expression was analyzed by real‐time RT‐PCR.Results  The frequencies of peripheral blood (PB) and spleen Vα24+6B11+ iNKT cells were not significantly different. The iNKT cell subset in spleen was significantly increased for CD4+CD8+ and CD3+CD56+ co‐expression as well as intracellular interleukin‐4 production, which was rarely observed in circulating PB.Conclusion  Spleen iNKT cells in rhesus macaques are Th2 biased and display phenotypically and functionally distinct profiles from their PB counterpart.
Periodontitis and premature death: a 16‐year longitudinal study in a Swedish urban population
Authors: Söder B. , Jin L. J. , Klinge B. , Söder P.‐Ö. 
Published: March 2007

Background and Objective:  Growing experimental evidence implicates chronic inflammation/infection due to periodontal diseases as a risk factor for death. The objective was to evaluate the role of periodontitis in premature death in a prospective study.Methods:  The causes of death in 3273 randomly‐selected subjects, aged 30–40 years, from 1985 to 2001 were registered. At baseline, 1676 individuals underwent a clinical oral examination (Group A) and 1597 did not (Group B). Mortality and causes of death from 1985 to 2001 were recorded according to ICD‐9‐10.Results:  In Groups A (clinically examined group) and B, a total of 110 subjects had died: 40 subjects in Group A, and 70 in Group B. In Group A significant differences were present at baseline between survivors and persons who later died, with respect to dental plaque, calculus, gingival inflammation and number of missing molars in subjects with periodontitis (p < 0.001). The multiple logistic regression analysis results of the relationship between being dead (dependent variable) and several independent variables identified periodontitis with any missing molars as a principal independent predictor of death.Conclusions:  Young individuals with periodontitis and missing molars seem to be at increased risk for premature death by life‐threatening diseases, such as neoplasms, and diseases of the circulatory and digestive systems.
Overexpression of interleukin‐1β and interleukin‐6 may play an important role in periodontal breakdown in type 2 diabetic patients
Authors: Duarte P. M. , De Oliveira M. C. G. , Tambeli C. H. , Parada C. A. , Casati M. Z. , Nociti F. H. 
Published: March 2007

Background and Objective:  This study evaluated whether the biochemical changes associated with type 2 diabetes modulate the expression of interleukin‐1β, interleukin‐6, interleukin‐8, and interferon‐γ in sites with chronic periodontitis.Material and Methods:  Biopsies were harvested and divided into three groups: group 1, systemically and periodontally healthy subjects (n = 10); group 2, systemically healthy subjects with moderate‐to‐severe chronic periodontitis (probing depth > 6 mm) (n = 20); and group 3, type 2 diabetic subjects with periodontitis (n = 20). Cytokine levels were assessed in the gingival tissues by enzyme‐linked immunosorbent assay analysis.Results:  Data analysis demonstrated that the interleukin‐1β, interleukin‐6, interleukin‐8, and interferon‐γ levels were higher in the presence of periodontal inflammation than in the absence of inflammation, regardless of systemic status. The interleukin‐1β and interleukin‐6 levels were higher in diabetic subjects (group 3) than in systemically healthy patients with comparable types of periodontitis (group 2). No difference was observed for the interleukin‐8 and interferon‐γ levels between groups 2 and 3.Conclusion:  Within the limits of this study, it was concluded that type 2 diabetes was associated with increased expression of interleukin‐1β and interleukin‐6 in periodontally inflamed tissues of diabetic patients, relative to nondiabetic subjects, and that such overexpression may be involved in the mechanisms by which type 2 diabetes enhances periodontal destruction.
Susceptibility of various oral bacteria to antimicrobial peptides and to phagocytosis by neutrophils
Authors: Ji S. , Hyun J. , Park E. , Lee B.‐L. , Kim K.‐K. , Choi Y. 
Published: March 2007

Background and Objective:  The aim of this study was to compare the susceptibility of nonperiodontopathic and periodontopathic bacteria to major defense mechanisms for bacterial clearance in gingival sulcus.Material and Methods:  Twenty strains of 13 oral bacterial species were studied for their susceptibility to phagocytosis by human neutrophils and to the antimicrobial peptides LL‐37 and human beta defensin‐3. The minimum inhibitory concentrations of LL‐37 and human beta defensin‐3 were determined by a liquid dilution assay, and susceptibility to phagocytosis was examined by a flow cytometric phagocytosis assay.Results:  The minimum inhibitory concentrations of LL‐37 and human beta defensin‐3 varied greatly, depending on the strain and species. Although a significant difference between the non‐ and periodontopathic groups was not observed, the red‐complex bacteria were more resistant to LL‐37 than the others (p = 0.004). The susceptibility of oral bacteria to phagocytosis was quite variable, depending on the species but not on the strains. The periodontopathic bacteria, especially Actinobacillus actinomycetemcomitans and the red‐complex triad, were more resistant to phagocytosis than were the nonperiodontopathic bacteria (p = 0.0003). In addition, bacteria resistant both to antimicrobial peptides and to phagocytosis were more common in the periodontopathic group.Conclusion:  Our results indicate that immune evasion may contribute to the pathogenicity of some periodontopathic bacteria.