bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hyperbranched Poly(amidoamine)-modified Multi-walled Carbon Nanotubes via Grafting-from Method
Authors: Cao Liang , Yang Wuli , Yang Junwei , Wang Changchun , Fu Shoukuan 
Published: March 2004

Abstract
Hyperbranched poly(amidoamine) (h-PAMAM)-grafted multi-walled carbon nanotubes (MWNTs) were successfully synthesized by grafting-from method. The modified MWNTs, which gave stable dispersion in organic solvents, were reacted with the fluorescein isothiocyanate (FITC) and then showed strong photoluminescent property.
Head and neck cancer in patients with human immunodeficiency virus-1 infection: incidence, outcome and association with Epstein-Barr virus
Authors: Powles T. , Powles J. , Nelson M. , Sandison A. , Peston D. , Buchannan J. , Mandalia S. , Gazzard B. , Bower M. 
Published: March 2004

Head and neck cancers have been described in patients with human immunodeficiency virus-1 (HIV-1) infection. However the incidence, aetiology and clinical features of the disease remain unclear.Patients with head and neck cancer and HIV were identified from a large HIV centre. The incidence and clinical features were recorded, and the tumours were stained for Epstein-Barr virus (EBV).Head and neckcancer occurred more frequently than in an age-matched control group (1.66 vs 0.55/10,000 patient years respectively p < 0.05). Highly active anti-retroviral therapy has not significantly altered the incidence of the disease. All of the tumours tested were positive for EBV. Patients were moderately immunosuppressed at diagnosis and had aggressive tumours. All but one of the patients died of cancer with a median survival of 28 months.Head and neck cancer occurs more frequently in HIV. It is an aggressive disease and EBV may play a role in its pathogenesis.
Anticonvulsant and Antiepileptogenic Effects Mediated by Adeno-Associated Virus Vector Neuropeptide Y Expression in the Rat Hippocampus
Authors: Richichi Cristina , Lin En-Ju D. , Stefanin Daniela , Colella Daniele , Ravizza Teresa , Grignaschi Giuliano , Veglianese Pietro , Sperk Günther , During Matthew J. , Vezzani Annamaria 
Published: March 2004

Neuropeptide Y (NPY) inhibits seizures in experimental models and reduces excitability in human epileptic tissue. We studied the effect of long-lasting NPY overexpression in the rat hippocampus with local application of recombinant adeno-associated viral (AAV) vectors on acute kainate seizures and kindling epileptogenesis.Transgene expression was significantly increased by 7 d, reached maximal expression by 2 weeks, and persisted for at least 3 months. Serotype 2 AAV vector increased NPY expression in hilar interneurons, whereas the chimeric serotype 1/2 vector caused far more widespread expression, also including mossy fibers, pyramidal cells, and the subiculum. EEG seizures induced by intrahippocampal kainate were reduced by 50–75%, depending on the vector serotype, and seizure onset was markedly delayed.In rats injected with the chimeric serotype 1/2 vector, status epilepticus was abolished, and kindling acquisition was significantly delayed. Thus, targeted NPY gene transfer provides a potential therapeutic principle for the treatment of drug-resistant partial epilepsies.
Activation of Adenosine A2AReceptor Facilitates Brain-Derived Neurotrophic Factor Modulation of Synaptic Transmission in Hippocampal Slices
Authors: Diógenes Maria José , Fernandes Catarina Cunha , Sebastião Ana Maria , Ribeiro Joaquim Alexandre 
Published: March 2004

Both brain-derived neurotrophic factor (BDNF) and adenosine influence neuronal plasticity. We now investigated how adenosine influences the action of BDNF on synaptic transmission in the CA1 area of the rat hippocampal slices. Alone, BDNF (20–100 ng/ml) did not significantly affect field EPSPs (fEPSPs). However, a 2 min pulse of high-K+(10 mm) 46 min before the application of BDNF (20 ng/ml) triggered an excitatory action, an effect blocked by the TrkB receptor inhibitor K252a (200 nm), by the adenosine A2Areceptor antagonist ZM 241385 (50 nm), and by the protein kinase A inhibitor H-89 (1 μm). Presynaptic, rather than postsynaptic depolarization was required to trigger the BDNF action because after K+depolarization BDNF also increased EPSCs recorded from pyramidal neurons voltage-clamped at –60 mV, and transient postsynaptic depolarization was unable to unmask the BDNF action. A weak theta burst stimulation of the afferents could elicit potentiation of synaptic transmission only when applied in the presence of BDNF. Activation of adenosine A2Areceptors with CGS 21680 (10 nm), or the increase in extracellular adenosine levels induced by 5-iodotubercidin (100 nm) triggered the excitatory action of BDNF, a process prevented by ZM 241385 and by H-89. In the presence of dibutyryl-cAMP (0.5 mm), BDNF also increased fEPSPs but postsynaptic cAMP (0.5 mm) was unable to trigger the BDNF action.It is concluded that presynaptic activity-dependent release of adenosine, through activation of A2Areceptors, facilitates BDNF modulation of synaptic transmission at hippocampal synapses.
Electrical conductivity of carbon filled nylon 6,6
Authors: Heiser Jessica A. , King Julia A. , Konell Jeremiah P. , Sutter Lawrence L. 
Published: March 2004

AbstractThe electrical conductivity of resins can be increased by adding electrically conductive carbon fillers. A significant amount of work has been conducted varying the amount of single conductive fillers in a composite material. Limited work has been conducted concerning the effect of combinations of different conductive fillers. In this study, three different carbon fillers were used in nylon 6,6: carbon black, synthetic graphite particles, and a surface treated polyacrylonitrile (PAN) based carbon fiber. The goal of this project was to determine the effect of each filler and combinations of different fillers on the electrical conductivity of conductive resins. A 23 factorial design was analyzed to determine the effects of the three different carbon fillers in nylon 6,6. The results showed that carbon fiber caused the largest increase in composite electrical conductivity and that all the combinations of different fillers do have a statistically significant effect on composite electrical conductivity. © 2004 Wiley Periodicals, Inc. Adv Polym Techn 23: 135–146, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/adv.20004
Altered expression of the glutamate transporter EAAT2b in neurological disease
Authors: Maragakis Nicholas J. , Dykes‐Hoberg Margaret , Rothstein Jeffrey D. 
Published: March 2004

AbstractFunctional studies suggest that up to 95% of all glutamate transport is handled by the glutamate transporter EAAT2. Amino and C‐terminal antibodies demonstrate that under normal conditions EAAT2 is specific to astrocytes. A truncated splice variant of EAAT2, known as EAAT2b, also has been identified in astrocytes and some neurons. In vitro studies suggest EAAT2b transports glutamate similar to EAAT2, although the contribution of EAAT2b to normal clearance of extracellular glutamate is unknown. To investigate EAAT2b biology in pathological conditions, we examined the cellular and regional distribution of EAAT2b in amyotrophic lateral sclerosis. Using epitope‐specific, affinity purified antibodies, we found that EAAT2b tissue levels were increased by more than twofold in amyotrophic lateral sclerosis motor cortex, whereas EAAT2 levels were decreased by up to 95%. EAAT2b distribution in normal human cortex was largely confined to the neuropil‐like EAAT2, with occasional faint neuronal expression. In contrast, amyotrophic lateral sclerosis motor cortex had an obvious qualitative increase in neuropil EAAT2b staining and a drastic increase in neuronal soma and dendritic EAAT2b immunostaining. Despite these increases in EAAT2b immunostaining, functional transporter studies demonstrated a large loss of EAAT2 function. These studies clearly document altered regulation and splicing of the dominant glutamate transporter EAAT2 under conditions of neurological stress. Ann Neurol 2004;55:000–000
UCHL1 is a Parkinson's disease susceptibility gene
Authors: Maraganore Demetrius M. , Lesnick Timothy G. , Elbaz Alexis , Chartier‐Harlin Marie‐Christine , Gasser Thomas , Krüger Rejko , Hattori Nobutaka , Mellick George D. , Quattrone Aldo , Satoh Jun‐Ichi , Toda Taksushi , Wang Jian , Ioannidis John P.A. , de Andrade Mariza , Rocca Walter A. ,   the UCHL1 Global Genetics Consortium
Published: March 2004

AbstractAn Erratum has been published for this article in Ann Neurol 2004;55:899.The reported inverse association between the S18Y variant of the ubiquitin carboxy‐terminal hydrolase L1 (UCHL1) gene and Parkinson's disease (PD) has strong biological plausibility. If confirmed, genetic association of this variant with PD may support molecular targeting of the UCHL1 gene and its product as a therapeutic strategy for PD. In this light, we performed a collaborative pooled analysis of individual‐level data from all 11 published studies of the UCHL1 S18Y gene variant and PD. There were 1,970 cases and 2,224 unrelated controls. We found a statistically significant inverse association of S18Y with PD. Carriers of the variant allele (Y/Y plus Y/S vs S/S) had an odds ratio (OR) of 0.84 (95% confidence interval [CI], 0.73–0.95) and homozygotes for the variant allele (Y/Y vs S/S plus Y/S) had an OR of 0.71 (95% CI, 0.57–0.88). There was a linear trend in the log OR consistent with a gene dose effect (p = 0.01). The inverse association was most apparent for young cases compared with young controls. There was no evidence for publication bias and the associations remained significant after excluding the first published, hypothesis‐generating study. These findings confirm that UCHL1 is a susceptibility gene for PD and a potential target for disease‐modifying therapies. Ann Neurol 2004
Delayed myelopathy induced by chronic compression in the rat spinal cord
Authors: Kim Phyo , Haisa Toshihiko , Kawamoto Toshiki , Kirino Takaaki , Wakai Susumu 
Published: March 2004

AbstractCervical myelopathy is a common cause of neurological disability among the elderly; however, the exact mechanism for the insidious and progressive deterioration remains to be elucidated. To study the pathophysiology, we developed a simple experimental model reproducing the course. In rats, a thin sheet of expanding polymer was implanted microsurgically underneath the C5‐C6 laminae. In the control group, the polymer sheet was removed immediately. Changes in motor functions were monitored for 25 weeks after the operation, with voluntary exercise activity measured by odometer attached to revolving cages, and forced running capability measured by duration of exercise on a rotating treadmill. Motor neurons were counted stereologically in continuous sections. In the compression group, the forced running capability deteriorated after a latent period of 17 weeks and progressively thereafter. In the control group, it stayed unchanged throughout 25 weeks. Course of the voluntary exercise was comparable between the groups. Motor neuron density in the compression group decreased significantly in 9 weeks (−20.3%) and 25 weeks (−35.5%), but not in 1 or 3 weeks. This practical model properly reproduces characteristic features of the clinical cervical myelopathy, with progressive motor disturbance after a latency and insidious neuronal loss preceding the symptoms. Ann Neurol 2004
Benign familial neonatal‐infantile seizures: Characterization of a new sodium channelopathy
Authors: Berkovic Samuel F. , Heron Sarah E. , Giordano Lucio , Marini Carla , Guerrini Renzo , Kaplan Robert E. , Gambardella Antonio , Steinlein Ortrud K. , Grinton Bronwyn E. , Dean Joanne T. , Bordo Laura , Hodgson Bree L. , Yamamoto Toshiyuki , Mulley John C. , Zara Federico , Scheffer Ingrid E. 
Published: March 2004

AbstractWe recently reported mutations in the sodium channel geneSCN2Ain two families with benign familial neonatal‐infantile seizures (BFNISs). Here, we aimed to refine the molecular‐clinical correlation ofSCN2Amutations in early childhood epilepsies.SCN2Awas analyzed in 2 families with probable BFNIS, 9 with possible BFNIS, 10 with benign familial infantile seizures, and in 93 additional families with various early childhood epilepsies. Mutations effecting changes in conserved amino acids were found in two of two probable BFNIS families, in four of nine possible BFNIS families, and in none of the others. Our eight families had six differentSCN2Amutations; one mutation (R1319Q) occurred in three families. BFNIS is an autosomal dominant disorder presenting between day 2 and 7 months (mean, 11.2 ± 9.2 weeks) with afebrile secondarily generalized partial seizures; neonatal seizures were not seen in all families. The frequency of seizures varied; some individuals had only a few attacks without treatment and others had clusters of many per day. Febrile seizures were rare. All cases remitted by 12 months. Ictal recordings in four subjects showed onset in the posterior quadrants.SCN2Amutations appear specific for BFNIS; the disorder can now be strongly suspected clinically and the families can be given an excellent prognosis. Ann Neurol 2004
Abnormal imitation‐related cortical activation sequences in Asperger's syndrome
Authors: Nishitani Nobuyuki , Avikainen Sari , Hari Riitta 
Published: March 2004

AbstractSubjects with Asperger's syndrome (AS) are impaired in social interaction and imitation, but the underlying brain mechanisms are poorly understood. Because the mirror‐neuron system (MNS) that matches observed and executed actions has been suggested to play an important role in imitation and in reading of other people's intentions, we assessed MNS functions in 8 adult AS subjects and in 10 healthy control subjects during imitation of still pictures of lip forms. In the control subjects, cortical activation progressed in 30 to 80‐millisecond steps from the occipital cortex to the superior temporal sulcus, to the inferior parietal lobe, and to the inferior frontal lobe, and finally, 75 to 90 milliseconds later, to the primary motor cortex of both hemispheres. Similar activation sites were found in AS subjects but with slightly larger scatter. Activation of the inferior frontal lobe was delayed by 45 to 60 milliseconds and activations in the inferior frontal lobe and in the primary motor cortex were weaker than in control subjects. The observed abnormal premotor and motor processing could account for a part of imitation and social impairments in subjects with AS. Ann Neurol 2004
Plasma amyloid β, apolipoprotein E, lacunar infarcts, and white matter lesions
Authors: Van Dijk Ewoud J. , Prins Niels D. , Vermeer Sarah E. , Hofman Albert , Van Duijn Cornelia M. , Koudstaal Peter J. , Breteler Monique M.B. 
Published: March 2004

AbstractLacunar brain infarcts and cerebral white matter lesions are frequently observed on magnetic resonance imaging scans in elderly subjects. These lesions are also frequent in patient with cerebral amyloid angiopathy. We examined whether plasma amyloid β peptide (Aβ) levels are associated with lacunar infarcts and white matter lesions in the general population, and whether the apolipoprotein E (APOE) genotype modifies these associations. We studied 1,077 participants within the population‐based Rotterdam Scan Study, who were 60 to 90 years of age and free of dementia. Cross‐sectional associations were analyzed by regression models with adjustments for age, sex, creatinine levels, and hypertension. In APOE ε4 carriers, plasma Aβ levels were positively associated with lacunar infarcts and white matter lesions, whereas in noncarriers no associations were observed. Per standard deviation increase in Aβ1‐40 and Aβ1‐42 levels the odds ratios for lacunar infarcts were 1.72 (95% confidence interval [CI] = 1.22–2.43) and 1.93 (95% CI = 1.31–2.85), the periventricular white matter lesion grade increased by 0.32 (95% CI = 0.08–0.57) and 0.29 (95% CI = 0.00–0.57), and the subcortical white matter lesion volume increased by 0.48ml (95% CI = 0.04–0.91) and 0.24ml (95% CI = −0.27–0.75). Higher Aβ levels are associated with more lacunar infarcts and white matter lesions in elderly subjects who carry an APOE ε4 allele. Ann Neurol 2004
Ataxia after pontine stroke: Insights from pontocerebellar fibers in monkey
Authors: Schmahmann Jeremy D. , Rosene Douglas L. , Pandya Deepak N. 
Published: March 2004

AbstractBasis pontis lacunes cause contralateral but rarely ipsilateral ataxia. We explored this phenomenon with isotope tract tracing in the rhesus monkey. Labeled pontocerebellar fibers cross midline and disperse widely in the opposite hemipons before coalescing in the brachium pontis. This anatomical arrangement suggests that small pontine strokes spare sufficient decussating pontocerebellar fibers to prevent ipsilateral dysmetria, and that ipsilateral dysmetria after large pontine stroke represents a disconnection syndrome.
Detection and characterization of MuSK antibodies in seronegative myasthenia gravis
Authors: McConville John , Farrugia Maria Elena , Beeson David , Kishore Uday , Metcalfe Richard , Newsom‐Davis John , Vincent Angela 
Published: March 2004

AbstractAntibodies to rat muscle specific kinase, MuSK, have recently been identified in some generalized “seronegative” myasthenia gravis (SNMG) patients, who are often females with marked bulbar symptoms. Using immunoprecipitation of 125I‐labelled‐human MuSK, 27 of 66 (41%) seronegative patients were positive, but 18 ocular SNMG patients, 105 AChR antibody positive MG patients, and 108 controls were negative. The antibodies are of high affinity (Kds around 100 pM) with titers between 1 and 200 nM. They bind to the extracellular Ig‐like domains of soluble or native MuSK. Surprisingly they are predominantly in the IgG4 subclass. MuSK‐antibody associated MG may be differnet in etiological and pathological mechanisms.
The ketogenic diet increases mitochondrial uncoupling protein levels and activity
Authors: Sullivan Patrick G. , Rippy Nancy A. , Dorenbos Kristina , Concepcion Rachele C. , Agarwal Aakash K. , Rho Jong M. 
Published: March 2004

AbstractFatty acids are known to enhance mitochondrial uncoupling protein (UCP) activity. We asked whether a high‐fat ketogenic diet (KD) increases UCP levels and activity in hippocampi of juvenile mice. Maximum mitochondrial respiration rates were significantly (p < 0.001) higher in KD‐ versus standard diet (SD)–treated animals, indicating increased UCP‐mediated proton conductance that can reduce reactive oxygen species (ROS) production. Western blots showed significant (p < 0.05) or borderline significant increases in UCP2, UCP4, and UCP5 protein levels, and increased immunoreactivity to these three UCP isoforms was most prominently seen in the dentate gyrus of KD‐fed mice. Finally, we found that oligomycin‐induced ROS production was significantly (p < 0.05) lower in KD‐fed mice than in SD controls. Collectively, our data suggest that a KD may exert neuroprotective effects by diminishing ROS production through activation of mitochondrial UCPs.
Die Eintopfkondensation von Pyrrolen mit Aldehyden als vielseitiger Selbstorganisationsprozess
Authors: Ghosh Abhik 
Published: March 2004

AbstractDie Pyrrol‐Aldehyd‐Cyclokondensation gilt seit über einem halben Jahrhundert als die klassische Eintopfsynthese symmetrischer Porphyrine, lieferte aber auch viele nichtporphyrinartige Makrocyclen wie “N‐invertierte” Porphyrine, Corrole, Sapphyrine und expandierte Porphyrine. Sie erwies sich somit als vielseitiger Selbstorganisationsprozess. Ein herausragendes Beispiel ist die Corrol‐Eintopfsynthese. Die mannigfaltigen Zwischenprodukte der anaeroben Phase einer Synthese vom Lindsey‐Typ wurden als ein dynamisches kovalentes Selbstorganisationssystem interpretiert. Dies eröffnet die Möglichkeit, durch Zugabe eines Wirts die Gleichgewichtskonzentrationen der Zwischenprodukte zu ändern und damit zu beeinflussen, welches Hauptprodukt nach dem oxidativen Quenchen isoliert wird.
A formal knowledge management ontology: Conduct, activities, resources, and influences
Authors: Holsapple C.W. , Joshi K.D. 
Published: March 2004

AbstractThis article describes a collaboratively engineered general‐purpose knowledge management (KM) ontology that can be used by practitioners, researchers, and educators. The ontology is formally characterized in terms of nearly one hundred definitions and axioms that evolved from a Delphi‐like process involving a diverse panel of over 30 KM practitioners and researchers. The ontology identifies and relates knowledge manipulation activities that an entity (e.g., an organization) can perform to operate on knowledge resources. It introduces a taxonomy for these resources, which indicates classes of knowledge that may be stored, embedded, and/or represented in an entity. It recognizes factors that influence the conduct of KM both within and across KM episodes. The Delphi panelists judge the ontology favorably overall: its ability to unify KM concepts, its comprehensiveness, and utility. Moreover, various implications of the ontology for the KM field are examined as indicators of its utility for practitioners, educators, and researchers.
Effect of wave frequency of clinical electric shock: pain sensation and startle response
Authors: Duker P. C. , Hendriks C. , Schroen J. 
Published: March 2004

AbstractContingent shock has been used in a number of studies to suppress health‐threatening self‐injurious behavior of individuals with mental retardation and autism. As sustained suppression is an issue of clinical concern, research into procedural variables of contingent shock is needed. As research on subjects who have mental retardation and who show self‐injurious behavior is ethically impossible, we conducted research on healthy volunteers. In this study, we compared the effect of wave frequency (i.e. Hz) of electric shock on subjects' pain sensation and startle response. It was found that 60 Hz revealed a significantly stronger pain sensation rating than 30 Hz and that 90 Hz revealed a significantly stronger rating than 60 Hz. Also, the magnitude of subjects' startle response significantly increased as wave frequency increased from 30 Hz to 60 Hz and from 60 to 90 Hz. Copyright © 2004 John Wiley & Sons, Ltd.
Opinion formation in evaluating sanity at the time of the offense: an examination of 5175 pre‐trial evaluations
Authors: Warren Janet I. , Murrie Daniel C. , Chauhan Preeti , Dietz Park E. , Morris James 
Published: March 2004

AbstractSanity evaluations are high‐stake undertakings that explicitly examine the defendant's culpability for a crime and implicitly explore clinical information that might inform a plea agreement. Despite the gravity of such evaluations, relatively little research has investigated the process by which evaluators form their psycholegal opinions. In the current study, we explore this process by examining 5175 sanity evaluations conducted by a cohort of forensic evaluators in Virginia over a ten‐year period. Our analyses focus on (i) the clinical, criminal, and demographic attributes of the defendant correlated with opinions indicative of insanity; (ii) the clinical content of the evaluations and the legal criteria referenced as the basis for the psycholegal opinion; (iii) the process and outcome differences in the sanity evaluations conducted by psychologists versus psychiatrists; and (iv) the consistency in these opinions over a ten year period. Analyses predicting an opinion of insanity indicate a positive relationship with psychotic, organic, and affective diagnoses and previous psychiatric treatment. Analyses also indicate a negative relationship with prior criminal history, drug charges, personality disorder diagnosis, and intoxication at the time of the offense. Modest racial disparities were observed with evaluators offering opinions that the defendant was insane more often for white than for minority defendants despite comparable psychiatric and criminal characteristics. Copyright © 2003 John Wiley & Sons, Ltd.