bluuebunny/crossref_metadata_2025_split huggingface dataset:
Levofloxacin‐associated hypoglycaemia complicated by pontine myelinolysis and quadriplegia
Authors: Vallurupalli S. , Huesmann G. , Gregory J. , Jakoby M. G. 
Published: July 2008

AbstractBackground  Central pontine myelinolysis (CPM) usually presents in chronic alcoholics and in patients in whom hyponatraemia has been corrected rapidly. However, CPM may occur in other clinical circumstances, including patients with severe hypoglycaemia. We describe the occurrence of CPM and quadriplegia in a patient who experienced fluoroquinolone‐associated severe hypoglycaemia.Case report  A 63‐year‐old man with Type 2 diabetes mellitus was admitted to hospital for resection of a large liposarcoma. Renal‐dose levofloxacin was utilized as part of an antimicrobial regimen to treat post‐operative peritonitis. On days 6–8 of levofloxacin therapy, the patient experienced recurrent hypoglycaemia despite total parenteral nutrition, 10% dextrose containing fluids and cessation of insulin therapy 3 days prior to the first hypoglycaemic episode. Hypoglycaemia resolved within 24 h of stopping levofloxacin. After a final and severe hypoglycaemic event, the patient developed quadriplegia and tonic left deviation of gaze. Magnetic resonance imaging revealed a high‐intensity lesion in the central pons consistent with CPM.Conclusions  Fluoroquinolones should be considered as a potential cause of hypoglycaemia. Severe hypoglycaemia has the potential to cause white matter lesions in the pons. Putative mechanisms include failure of membrane ion channels, oligodendrocyte apoptosis and oxidative stress of glucose reperfusion. Fluoroquinolone‐associated hypoglycaemia and hypoglycaemia‐induced quadriplegia are both rare and we believe this is the first case report linking the two events.
Increased levels of monokine induced by interferon‐γ (Mig) in the vitreous of patients with diabetic retinopathy
Authors: Wakabayashi Y. , Usui Y. , Okunuki Y. , Takeuchi M. , Kezuka T. , Iwasaki T. , Goto H. 
Published: July 2008

AbstractAim  To determine the intravitreous concentration of monokine induced by interferon‐γ (Mig) in patients with diabetic retinopathy (DR) and the relation between Mig and vascular endothelial growth factor (VEGF).Research design and methods  Vitreous samples were obtained at the time of vitrectomy from 41 eyes of 38 DR patients (30 with active DR and 11 with inactive DR) and from 15 eyes of 15 non‐diabetic patients who had macular disease (control subjects). Human Mig and VEGF were quantified using a FACS Caliber® flow cytometer.Results  The vitreous concentration of Mig was increased significantly in patients with both active and inactive DR [148.0 (31.6–997.2; median range) and 82.3 (25.7–347.7) pg/ml, respectively] compared with control subjects [21.0 (5.2–74.3) pg/ml; P < 0.0001 and P < 0.001, respectively]. In DR patients, a significant (P < 0.01) correlation was observed between vitreous concentrations of Mig and VEGF.Conclusion  Our results suggest that Mig may play an important role in the pathogenesis of DR and works in consort with VEGF in the progression of pathological angiogenesis in DR.
Gender differences in the perception and acceptance of online games
Authors: Wang Hsiu‐Yuan , Wang Yi‐Shun 
Published: July 2008

AbstractWith the proliferation of online games, understanding users' intention to play online games has become a new issue for academics and practitioners. Prior studies have investigated the factors affecting behavioural intention to play online games. However, little research has been conducted to investigate the gender differences in the acceptance of online games. Thus, this study is to investigate the effects of perceived playfulness and its potential antecedents (ie, computer self‐efficacy, computer anxiety, challenge, speed and feedback) on the behavioural intention to play online games, and to examine the gender differences in the perception and acceptance of online games. Data collected from 281 respondents in Taiwan were tested against the research model using analysis of variance and structural equation modelling approaches. The theoretical and practical implications of the results were discussed.
Deficits in early emotional reactivity in alexithymia
Authors: Pollatos Olga , Schubö Anna , Herbert Beate M. , Matthias Ellen , Schandry Rainer 
Published: July 2008

AbstractAlexithymia is characterized by a difficulty in identifying and describing one's emotions. This study addressed the question of whether alexithymic tendencies are related to limited affective reactivity to briefly presented emotional stimuli. Skin conductance responses were assessed and backward masking was used to minimize elaborated processing of emotional pictures. Results indicated that alexithymic tendencies are associated with smaller electrodermal responses to briefly presented negative pictures. These effects were driven by difficulties in identifying and communicating emotions whereas externally orientated thinking was unrelated to affective reactivity. We conclude that there is an early processing deficit in response to negative stimuli in participants with high scores in alexithymia. Differences in the early emotional reactivity to arousing material could contribute to difficulties in emotional processes related to alexithymia.
The effects of achievement motivation, task difficulty, and goal difficulty on physiological, behavioral, and subjective effort
Authors: Capa Rémi L. , Audiffren Michel , Ragot Stéphanie 
Published: July 2008

AbstractThe purpose of the study was to present experimental arguments evaluating the Humphreys and Revelle's model of effort. Two important factors were tested: achievement motivation and difficulty. Heart rate, heart rate variability, blood pressure, facial electromyographic reactivity, and reaction time were measured as an index of effort expenditure. A 2 × 2 × 2 factorial design was used with two levels of resultant achievement motivation, two levels of task difficulty, and two levels of goal difficulty. As expected, the 16 participants high in resultant achievement motivation showed a better performance and had a larger decrease of the midfrequency band than the 16 participants low in resultant achievement motivation, especially during the difficult task. Results lend some support for the impact of resultant achievement motivation, task difficulty, and goal difficulty on effort mobilization.
Neuroanatomical correlates of aging, cardiopulmonary fitness level, and education
Authors: Gordon Brian A. , Rykhlevskaia Elena I. , Brumback Carrie R. , Lee Yukyung , Elavsky Steriani , Konopack James F. , McAuley Edward , Kramer Arthur F. , Colcombe Stanley , Gratton Gabriele , Fabiani Monica 
Published: July 2008

AbstractFitness and education may protect against cognitive impairments in aging. They may also counteract age‐related structural changes within the brain. Here we analyzed volumetric differences in cerebrospinal fluid and gray and white matter, along with neuropsychological data, in adults differing in age, fitness, and education. Cognitive performance was correlated with fitness and education. Voxel‐based morphometry was used for a whole‐brain analysis of structural magnetic resonance images. We found age‐related losses in gray and white matter in medial‐temporal, parietal, and frontal areas. As in previous work, fitness within the old correlated with preserved gray matter in the same areas. In contrast, higher education predicted preserved white matter in inferior frontal areas. These data suggest that fitness and education may both be predictive of preserved cognitive function in aging through separable effects on brain structure.
Intramodal and crossmodal processing delays in the attentional blink paradigm revealed by event‐related potentials
Authors: Ptito Alexia , Arnell Karen , Jolicœur Pierre , Macleod Jeffrey 
Published: July 2008

AbstractIn the attentional blink (AB), processing of a second target (T2) is impaired if it is presented shortly after the onset of a first target (T1), leading to a decrease in accurate report of T2 if T2 is masked. Some prominent theories of the AB suggest that an amodal bottleneck in working memory consolidation underlies the AB. We investigated this by factorially manipulating T1 and T2 modalities (visual or auditory) using equivalent stimuli and tasks in both modalities to minimize task switching. T2 was not masked. In all modality combinations, the electrophysiological P3 component to T2, obtained by subtracting T1 only trials from T1+T2 trials, was delayed and reduced in amplitude when T2 was presented soon after T1 relative to when T1 and T2 were presented farther apart. Results provide support for a common amodal bottleneck that underlies the AB effects observed in all visual/auditory modality combinations.
Comparative analysis of sialic acid levels in the colostrum and milk of ruminants: possible role in the passive immunity against neonatal infections
Authors: USEH NICODEMUS M , OLANIYAN OLABODE A , NOK ANDREW J 
Published: July 2008

A study was conducted to determine the levels of free sialic acid in the colostrum and milk of apparently healthy indigenous Nigerian ruminants (Zebu cows, Yankassa sheep and Sokoto Red/Kano Brown goats). Haematological investigation indicates that the apparently healthy ruminants were also clinically healthy. The mean free sialic acid concentration in the colostrum of all the animal species examined was higher than those of milk and the difference in each case was statistically significant (P < 0.05). The significance of the high sialic acid level in colostrum for the immunity of neonates against microbial infections is discussed.
Gene transfer of PEDF attenuates ischemic brain damage in the rat middle cerebral artery occlusion model
Authors: Sanagi Tomomi , Yabe Takeshi , Yamada Haruki 
Published: July 2008

AbstractPigment epithelium‐derived factor (PEDF) is a 50‐kDa glycoprotein that protects various types of cultured neurons against neurotoxic stimuli, but its precise role in the CNS is not fully understood. In this study, we used rats whose brains were transfected to over‐express human PEDF in order to elucidate the neuroprotective effect of PEDF following transient middle cerebral artery occlusion (MCAO). A replication‐defective adenoviral vector containing the human PEDF gene (Ad.PEDF) or E. coliβ‐galactosidase (Ad.LacZ) was directly injected into the right striatum at 7 days prior to 70 min of MCAO in rats. Infarct volume and degree of edema of the Ad.PEDF‐treated group were significantly reduced compared to the Ad.LacZ‐treated group 24 h after MCAO. Degeneration of neurons, astrocytes, and oligodendrocytes caused by MCAO were attenuated by over‐expression of PEDF. The up‐regulation of pro‐inflammatory genes (TNFα, IL‐1β, IL‐6, COX‐2, and iNOS) and water channel aquaporin 4 after MCAO was significantly reduced in Ad.PEDF‐injected striatum. In conclusion, the results from this study provide the first in vivo evidence that PEDF is effective in protecting CNS neurons from ischemic insult, suggesting that PEDF may have a role as an endogenous neuroprotectant in the CNS.
c‐Abl is involved in high glucose‐induced apoptosis in embryonic E12.5 cortical neural progenitor cells from the mouse brain
Authors: Jia De‐yong , Du Zhan‐hui , Liu Shang‐ming , Liu Hui‐juan , Wang Fu‐wu , Ling Eng‐Ang , Liu Kai , Hao Ai‐jun 
Published: July 2008

AbstractHyperglycemia causes direct apoptosis of neural progenitor cells (NPCs) in diabetic‐induced neural tube defects in embryos. However, the underlying mechanisms are poorly understood. The present study is aimed to investigate the specific cellular proteins that may be involved in NPCs apoptosis as well as mechanisms by which the proteins regulate the oxidative stress‐induced NPCs apoptosis. Our present results have shown that the expression of c‐Abl was up‐regulated in NPCs exposed to high glucose in vitro. The increased c‐Abl was localized mainly in the nucleus. High glucose also induced an increase in nuclear p53 protein levels and the p53‐c‐Abl complex in NPCs. Administration of reactive oxygen species scavengers decreased the protein level of c‐Abl, p53 and NPCs apoptosis. Inhibition of c‐Abl reduced NPCs apoptosis and the nuclear protein level of p53 in response to high glucose. These results demonstrate that c‐Abl is involved in the reactive oxygen species‐activated apoptotic pathways in NPCs apoptosis. Inhibition of c‐Abl may protect NPCs against insults induced by high glucose via the modulation of NPCs apoptotic machinery.
Long‐term administration of cocaine or serotonin reuptake inhibitors results in anatomical and neurochemical changes in noradrenergic, dopaminergic, and serotonin pathways
Authors: Horne Malcolm K. , Lee Joohyung , Chen Feng , Lanning Katherine , Tomas Doris , Lawrence Andrew J. 
Published: July 2008

AbstractThe catechol and indole pathways are important components underlying plasticity in the frontal cortex and basal ganglia. This study demonstrates that administering rats either cocaine or a selective serotonin (or 5‐hydroxytryptamine; 5‐HT) reuptake inhibitor (SSRI) for 16 weeks results in reduced density of dopaminergic and noradrenergic terminals in the striatum and olfactory bulb, respectively, reflecting pruning of the terminal arbor of ventral midbrain dopaminergic and locus coeruleus noradrenergic neurones. In the striatum of cocaine‐treated animals, basal dopamine levels, as well as cocaine‐induced dopamine release, is diminished compared with controls. In contrast, serotonergic fibers, projecting from the raphe, sprout and have increased terminal density in the lateral septal nucleus and frontal cortex, following long‐term cocaine or SSRI treatment. This is associated with elevated basal 5‐HT and enhanced cocaine‐induced 5‐HT release in the frontal cortex. The anatomical and neurochemical changes in serotonergic fibers following cocaine or SSRI treatment may be explained by attenuated 5‐HT1Aautoreceptor function in the raphe. This study demonstrates extensive plasticity in the morphology and neurochemistry of the catechol and indole pathways that contribute to drug‐induced plasticity of the corticostriatal (and other) projections. Moreover, our data suggest that drug‐induced plastic adaptation is anatomically widespread and consequently, likely to have multiple and complex consequences.
Transregulation of leukemia inhibitor factor receptor expression and function by growth factors in neuroblastoma cells
Authors: Port Martha D. , Laszlo George S. , Nathanson Neil M. 
Published: July 2008

AbstractThe cytokines that signal through the leukemia inhibitory factor (LIF) receptor are members of the neuropoietic cytokine family and have varied and numerous roles in the nervous system. In this report, we have determined the effects of growth factor stimulation on LIF receptor (LIFR) expression and signal transduction in the human neuroblastoma cell line NBFL. We show here that stimulation of NBFL cells with either epidermal growth factor or fibroblast growth factor decreases the level of LIFR in an extracellular signal‐regulated kinase (Erk)1/2‐dependent manner and that this down‐regulation is due to an increase in the apparent rate of lysosomal LIFR degradation. Growth factor‐induced decreases in LIFR level inhibit both LIF‐stimulated phosphorylation of signal transducers and activators of transcription 3 and LIFR‐mediated gene induction. We also show that Ser1044 of LIFR, which we have previously shown to be phosphorylated by Erk1/2, is required for the inhibitory effects of growth factors. Neurons are exposed to varying combinations and concentrations of growth factors and cytokines that influence their growth, development, differentiation, and repair in vivo. These findings demonstrate that LIFR expression and signaling in neuroblastoma cells can be regulated by growth factors that are potent activators of the mitogen‐activated protein kinase pathway, and thus illustrate a fundamental mechanism that underlies crosstalk between receptor tyrosine kinase and neuropoietic cytokine signaling pathways.
Glutamate mobilizes [Zn2+]i through Ca2+‐dependent reactive oxygen species accumulation
Authors: Dineley Kirk E. , Devinney II Michael J. , Zeak Jennifer A. , Rintoul Gordon L. , Reynolds Ian J. 
Published: July 2008

AbstractLiberation of zinc from intracellular stores contributes to oxidant‐induced neuronal injury. However, little is known regarding how endogenous oxidant systems regulate intracellular free zinc ([Zn2+]i). Here we simultaneously imaged [Ca2+]i and [Zn2+]i to study acute [Zn2+]i changes in cultured rat forebrain neurons after glutamate receptor activation. Neurons were loaded with fura‐2FF and FluoZin‐3 to follow [Ca2+]i and [Zn2+]i, respectively. Neurons treated with glutamate (100 μM) for 10 min gave large Ca2+ responses that did not recover after termination of the glutamate stimulus. Glutamate also increased [Zn2+]i, however glutamate‐induced [Zn2+]i changes were completely dependent on Ca2+ entry, appeared to arise entirely from internal stores, and were substantially reduced by co‐application of the membrane‐permeant chelator TPEN during the glutamate treatment. Pharmacological maneuvers revealed that a number of endogenous oxidant producing systems, including nitric oxide synthase, phospholipase A2, and mitochondria all contributed to glutamate‐induced [Zn2+]i changes. We found no evidence that mitochondria buffered [Zn2+]i during acute glutamate receptor activation. We conclude that glutamate‐induced [Zn2+]i transients are caused in part by [Ca2+]i‐induced reactive oxygen species that arises from both cytosolic and mitochondrial sources.
Activation of β‐catenin signalling by GSK‐3 inhibition increases p‐glycoprotein expression in brain endothelial cells
Authors: Lim Joseph C. , Kania Katarzyna D. , Wijesuriya Hasini , Chawla Sangeeta , Sethi Jaswinder K. , Pulaski Lukasz , Romero Ignacio A. , Couraud Pierre O. , Weksler Babette B. , Hladky Stephen B. , Barrand Margery A. 
Published: July 2008

AbstractThis study investigates involvement of β‐catenin signalling in regulation of p‐glycoprotein (p‐gp) expression in endothelial cells derived from brain vasculature. Pharmacological interventions that enhance or that block β‐catenin signalling were applied to primary rat brain endothelial cells and to immortalized human brain endothelial cells, hCMEC/D3, nuclear translocation of β‐catenin being determined by immunocytochemistry and by western blot analysis to confirm effectiveness of the manipulations. Using the specific glycogen synthase kinase‐3 (GSK‐3) inhibitor 6‐bromoindirubin‐3′‐oxime enhanced β‐catenin and increased p‐gp expression including activating the MDR1 promoter. These increases were accompanied by increases in p‐gp‐mediated efflux capability as observed from alterations in intracellular fluorescent calcein accumulation detected by flow cytometry. Similar increases in p‐gp expression were noted with other GSK‐3 inhibitors, i.e. 1‐azakenpaullone or LiCl. Application of Wnt agonist [2‐amino‐4‐(3,4‐(methylenedioxy) benzylamino)‐6‐(3‐methoxyphenyl)pyrimidine] also enhanced β‐catenin and increased transcript and protein levels of p‐gp. By contrast, down‐regulating the pathway using Dickkopf‐1 or quercetin decreased p‐gp expression. Similar changes were observed with multidrug resistance protein 4 and breast cancer resistance protein, both known to be present at the blood–brain barrier. These results suggest that regulation of p‐gp and other multidrug efflux transporters in brain vasculature can be influenced by β‐catenin signalling.
Neuroactive steroids and GABAAreceptor plasticity in the brain of the WAG/Rij rat, a model of absence epilepsy
Authors: Pisu Maria Giuseppina , Mostallino Maria Cristina , Dore Riccardo , Mura Maria Luisa , Maciocco Elisabetta , Russo Emilio , De Sarro Giovambattista , Serra Mariangela 
Published: July 2008

AbstractThe role of neuroactive steroids and GABAAreceptors in the generation of spontaneous spike‐and‐wave discharges (SWDs) was investigated in the WAG/Rij rat model of absence epilepsy. The plasma, cerebrocortical, and thalamic concentrations of the progesterone metabolite 3α‐hydroxy‐5α‐pregnan‐20‐one (3α,5α‐TH PROG) were increased in the WAG/Rij rat at 2 months of age compared with those in control (Wistar) rats. In contrast, the brain and peripheral levels of 3α,5α‐tetrahydrodeoxycorticosterone (3α,5α‐TH DOC) did not differ between the two rat strains at this age. At 6 months of age, when absence epilepsy worsens in WAG/Rij rats, the plasma concentration of 3α,5α‐TH PROG remained high whereas that of 3α,5α‐TH DOC had increased, the cerebrocortical levels of both 3α,5α‐TH PROG and 3α,5α‐TH DOC had increased, and the thalamic concentrations of these metabolites had decreased. At 6 months of age the expression of the α4and δ subunits of the GABAAreceptor in relay nuclei was increased. Finally, chronic stress induced by social isolation elicited a reduction in the amount of 3α,5α‐TH PROG in the thalamus of 2‐month‐old WAG/Rij rats that was associated with a reduction in the number and overall duration of SWDs at 6 months of age. Absence epilepsy in the WAG/Rij rat is thus associated with changes in the abundance of neuroactive steroids and in the expression of specific GABAAreceptor subunits in the thalamus, a brain area key to the pathophysiology of this condition.
Neurotrophin receptor homolog‐2 regulates nerve growth factor signaling
Authors: Wong Agnes W. , Willingham Melanie , Xiao Junhua , Kilpatrick Trevor J. , Murray Simon S. 
Published: July 2008

AbstractThe neurotrophin receptor homolog (NRH2) is closely related to the p75 neurotrophin receptor (p75NTR); however, its function and role in neurotrophin signaling are unclear. NRH2 does not bind to nerve growth factor (NGF), however, is able to form a receptor complex with tropomyosin‐related kinase receptor A (TrkA) and to generate high‐affinity NGF binding sites. Despite this, the mechanisms underpinning the interaction between NRH2 and TrkA remain unknown. Here, we identify that the intracellular domain of NRH2 is required to form an association with TrkA. Our data suggest extensive intracellular interaction between NRH2 and TrkA, as either the juxtamembrane or death domain regions of NRH2 are sufficient for interaction with TrkA. In addition, we demonstrate that TrkA signaling is dramatically influenced by the co‐expression of NRH2. Importantly, NRH2 did not influence all downstream TrkA signaling pathways, but rather exerted a specific effect, enhancing src homology 2 domain‐containing transforming protein (Shc) activation. Moreover, downstream of Shc, the co‐expression of NRH2 resulted in TrkA specifically modulating mitogen‐activated protein kinase pathway activation, but not the phosphatidylinositol 3‐kinase/Akt pathway. These results indicate that NRH2 utilizes intracellular mechanisms to not only regulate NGF binding to TrkA, but also specifically modulate TrkA receptor signaling, thus adding further layers of complexity and specificity to neurotrophin signaling.