bluuebunny/crossref_metadata_2025_split huggingface dataset:
Laser‐Assisted etching and metallisation of via‐holes in polyethylene terephthalate
Authors: Lyalin A. A. , Nunuparov M. S. , Simakin A. V. , Shafeev G. A. 
Published: May 2005

AbstractExperimental results are presented on via‐hole etching in a thick (100 μm) film of polyethylene terephthalate (PET) with the help of a copper vapour laser (wavelength γ=510 nm, pulse duration 10 ns, repetition rate 8 kHz). The rate of via‐hole formation is as high as 100 μms−1. The effective coupling of the polymer film to the laser radiation is due to the formation of highly absorbing graphitised regions in the bulk of the film, which is initially transparent at the laser wavelength. The side walls of the hole can be metallised by simultaneous decomposition of a Pd(acac)2 spun‐on layer as a precursor for subsequent electroless Ni deposition. The activation of the inner surface of the hole is achieved as a result of the precursor vapour entering the hole during laser etching. The metallised via‐hole provides a good electrical interconnection of the two sides of the PET film.
Organic molecular rectifiers
Authors: Geddes N. J. , Sambles J. R. , Martin A. S. 
Published: May 2005

AbstractIn the field of molecular scale electronics the drive is towards the fabrication of self‐assembled, organic, nanoscale architectures which will have an active role to play in novel electronic devices. As a formative step towards this goal the creation of an organic analogue to the p–n junction was proposed by Aviram and Ratner in the 1970s. In their proposal a monomolecular layer of a charge transfer species controls current flow between a pair of metal electrodes, allowing easy flow for only one polarity of the applied voltage. Such metal/molecular layer/metal structures have now been fabricated, utilising the self‐ordering properties of Langmuir–Blodgett films to form the organic layer, with one dimension of the device being reduced to the molecular scale. The fabrication techniques involved in the generation of these M/LB/M junctions are now described along with the present understanding of conduction mechanisms through such nanoscale thickness junctions. These structures clearly show that the organic molecular layers can control current passage in electronic devices emulating some of the characteristics of an inorganic semiconducting p–n junction.
Photoreflectance characterisation of GaAs and GaAs/GaAIAs structures grown by MOCVD
Authors: Misiewicz J. , Jezierski K. , Sitarek P. , Markiewicz P. , Korbutowicz R. , Panek M. , Ściana B. , Tłaczała M. 
Published: May 2005

AbstractEpitaxial undoped and doped (Si and Zn) GaAs and GaAIAs layers as well as heterostructures of GaAs/GaAIAs have been grown in an atmospheric pressure, vertical MOCVD system. Room temperature photoreflectance (PR) has been applied to characterise the layers and heterostructures as well as multiple quantum wells. The surface‐ and interface‐related PR has been studied by application of Kramers–Kronig analysis. A decomposition of the PR spectrum into spectra connected with the surface region and with the interface has been proposed.
Gene transfer of glutamic acid decarboxylase reduces neuropathic pain
Authors: Hao Shuanglin , Mata Marina , Wolfe Darren , Glorioso Joseph C. , Fink David J. 
Published: May 2005

AbstractWe tested whether transfer of the gene coding for glutamic acid decarboxylase to dorsal root ganglion using a herpes simplex virus vector to achieve release of GABA in dorsal horn would attenuate nociception in this condition. Subcutaneous inoculation of a replication‐defective herpes simplex virus vector expressing glutamic acid decarboxylase (vector QHGAD67) 7 days after selective L5 spinal nerve ligation reversed mechanical allodynia and thermal hyperalgesia; the antiallodynic effect lasted 6 weeks and was reestablished by reinoculation. QHGAD67 inoculation also suppressed induction of c‐Fos and phosphorylated extracellular signal–regulated kinase 1 and 2 in the spinal cord. Ann Neurol 2005;57:914–918
The nervous system as ectopic germinal center: CXCL13 and IgG in lyme neuroborreliosis
Authors: Narayan Kavitha , Dail Donna , Li Libin , Cadavid Diego , Amrute Sheela , Fitzgerald‐Bocarsly Patricia , Pachner Andrew R. 
Published: May 2005

AbstractLyme neuroborreliosis (LNB) is a chronic infection in which B‐cell activation, plasma cell infiltration, and enhanced Ig production in infected tissue are prominent feature. However, little is known about how B cells and plasma cells invade and persist in target organs. To assess this issue, we developed real‐time PCR measurements of IgG and CXCL13 production. We used these RNA assays and specific enzyme‐linked immunosorbent assays for protein and demonstrated that human peripheral blood mononuclear cells (PBMCs), stimulated by Borrelia burgdorferi sonicate, produced CXCL13 and IgG. Magnetic separation of PBMC populations and flow cytometry showed that CXCL13 is produced by dendritic cells. We then measure the expression of CXCL13 and IgG in tissues and correlated the expression of these host genes with spirochetal load. We also measured expression of dbpA and BBK32, two spirochetal genes important in chronic infection. There was a strong correlation between host immune response gene expression (CXCL13 and IgG) and spirochetal load. Immunohistochemistry of infected nonhuman primates tissue confirmed that CXCL13 is expressed in the nervous system. We conclude that persistent production of CXCL13 and IgG within infected tissue, two characteristics of ectopic germinal centers, are definitive features of LNB. Ann Neurol 2005;57:813–823
Cerebrospinal fluid neprilysin is reduced in prodromal Alzheimer's disease
Authors: Maruyama Masahiro , Higuchi Makoto , Takaki Yoshie , Matsuba Yukio , Tanji Haruko , Nemoto Miyako , Tomita Naoki , Matsui Toshifumi , Iwata Nobuhisa , Mizukami Hiroaki , Muramatsu Shin‐Ichi , Ozawa Keiya , Saido Takaomi C. , Arai Hiroyuki , Sasaki Hidetada 
Published: May 2005

AbstractAmyloid β peptide (Aβ) has been implicated in Alzheimer's disease (AD) as an initiator of the pathological cascades. Several lines of compelling evidence have supported major roles of Aβ‐degrading enzyme neprilysin in the pathogenesis of sporadic AD. Here, we have shown a substantial reduction of cerebrospinal fluid (CSF) neprilysin activity (CSF‐NEP) in patients with AD‐converted mild cognitive impairment and early AD as compared with age‐matched control subjects. The altered CSF‐NEP likely reflects changes in neuronal neprilysin, since transfer of neprilysin from brain tissue into CSF was demonstrated by injecting neprilysin‐carrying viral vector into the brains of neprilysin‐deficient mice. Interestingly, CSF‐NEP showed an elevation with the progression of AD. Along with a close association of CSF‐NEP with CSF tau proteins, this finding suggests that presynaptically located neprilysin can be released into CSF as a consequence of synaptic disruption. The impact of neuronal damages on CSF‐NEP was further demonstrated by a prominent increase of CSF‐NEP in rats exhibiting kainate‐induced neurodegeneration. Our results unequivocally indicate significance of CSF‐NEP as a biochemical indicator to pursue a pathological process that involves decreased neprilysin activity and Aβ‐induced synaptic toxicity, and the support the potential benefits of neprilysin up‐regulation in ameliorating neuropathology in prodromal and early AD. Ann Neurol 2005;57:832–842
NOA‐03 trial of high‐dose methotrexate in primary central nervous system lymphoma: Final report
Authors: Herrlinger Ulrich , Küker Wilhelm , Uhl Martin , Blaicher Hans‐Peter , Karnath Hans‐Otto , Kanz Lothar , Bamberg Michael , Weller Michael 
Published: May 2005

AbstractThe NOA‐03 trial explored high‐dose methotrexate alone in 37 patients with primary central nervous system lymphoma. The overall median survival was 25 months. After 4 years, the rate of leukoencephalopathy in patients surviving more than 12 months was 58% with and 10% without whole‐brain radiotherapy given at relapse (p = 0.11). Attention deficits were found in all six tested patients, and memory deficits in four patients. Two patients had normal, three had moderately restricted, and one had markedly restricted quality of life. Thus, high‐dose methotrexate with deferred radiotherapy had only moderate efficacy and was associated with significant neurotoxicity in long‐term surviving patients. Ann Neurol 2005;57:843–847
Molecular pathology and clinical characteristics of oligodendroglial neoplasms
Authors: Walker Carol , Du Plessis Daniel G. , Joyce Kathy A. , Fildes Diane , Gee Abigail , Haylock Brian , Husband David , Smith Trevor , Broome John , Warnke Peter C. 
Published: May 2005

AbstractTo evaluate the role of molecular genetics in the routine clinic, we investigated allelic imbalance at 1p36, 19q13, 17p13, 10p12‐15, and 10q22‐26 and p53 mutation in 100 oligodendroglial neoplasms diagnosed at a single treatment center between 2000 and 2003. The ‐1p/‐19q genotype, seen in 64, 34, 77, and 30% of OII, OAII, OIII, and OAIII respectively, was inversely related to p53 mutation and 17p13 loss. Genotype was unrelated to tumor location and could not distinguish high‐grade tumors that presented de novo from those that progressed from a previous lower grade malignancy. Presentation with seizures was more common in cases with the ‐1p/‐19q genotype, and these remained stable for longer before treatment. In longitudinal samples, 74% retained their initial histological differentiation, whereas 29% showed new genetic alterations, the ‐1p/‐19q genotype being acquired in three cases. Loss of 1p36 and 19q13, 17p13, chromosome 10, and p53 mutation were significantly associated with survival from presentation in Kaplan–Meier analysis (p < 0.01), and loss of 1p36 and 19q13 and loss of 17p13 retained significance in multivariate analysis. In this recently diagnosed unselected series, clinical differences in tumors with and without the ‐1p/‐19q genotype support a genetic approach to aid diagnosis and prognostication for oligodendroglial neoplasms. Ann Neurol 2005;57:855–865
Triaging transient ischemic attack and minor stroke patients using acute magnetic resonance imaging
Authors: Coutts Shelagh B. , Simon Jessica E. , Eliasziw Michael , Sohn Chul‐Ho , Hill Michael D. , Barber Philip A. , Palumbo Vanessa , Kennedy James , Roy Jayanta , Gagnon Alexis , Scott James N. , Buchan Alastair M. , Demchuk Andrew M. 
Published: May 2005

AbstractWe examined whether the presence of diffusion‐weighted imaging (DWI) lesions and vessel occlusion on acute brain magnetic resonance images of minor stroke and transient ischemic attack patients predicted the occurrence of subsequent stroke and functional outcome. 120 transient ischemic attack or minor stroke (National Institutes of Health Stroke Scale ≤ 3) patients were prospectively enrolled. All were examined within 12 hours and had a magnetic resonance scan within 24 hours. Overall, the 90‐day risk for recurrent stroke was 11.7%. Patients with a DWI lesion were at greater risk for having a subsequent stroke than patients without and risk was greatest in the presence of vessel occlusion and a DWI lesion. The 90‐day risk rates, adjusted for baseline characteristics, were 4.3% (no DWI lesion), 10.8% (DWI lesion but no vessel occlusion), and 32.6% (DWI lesion and vessel occlusion) (p = 0.02). The percentages of patients who were functionally dependent at 90 days in the three groups were 1.9%, 6.2%, and 21.0%, respectively (p = 0.04). The presence of a DWI lesion and a vessel occlusion on a magnetic resonance image among patients presenting acutely with a transient ischemic attack or minor stroke is predictive of an increased risk for future stroke and functional dependence. Ann Neurol 2005;57:848–854
POLG mutations and Alpers syndrome
Authors: Davidzon Guido , Mancuso Michelangelo , Ferraris Silvio , Quinzii Catarina , Hirano Michio , Peters Heidi L. , Kirby Denise , Thorburn David R. , DiMauro Salvatore 
Published: May 2005

AbstractAlpers–Huttenlocher syndrome (AHS) an autosomal recessive hepatocerebral syndrome of early onset, has been associated with mitochondrial DNA (mtDNA) depletion and mutations in polymerase gamma gene (POLG). We have identified POLG mutations in four patients with hepatocerebral syndrome and mtDNA depletion in liver, who fulfilled criteria for AHS. All were compound heterozygous for the G848S and W748S mutations, previously reported in patients with progressive external ophtalmoplegia or ataxia. We conclude that AHS should be included in the clinical spectrum of mtDNA depletion and is often associated with POLG mutations, which can cause either multiple mtDNA deletions or mtDNA depletion. Ann Neurol 2005;57:921–924
Genetic dissection of photosensitivity and its relation to idiopathic generalized epilepsy
Authors: Tauer Ulrike , Lorenz Susanne , Lenzen Kirsten P. , Heils Armin , Muhle Hiltrud , Gresch Meike , Neubauer Bernd A. , Waltz Stephan , Rudolf Gabrielle , Mattheisen Manuel , Strauch Konstantin , Nürnberg Peter , Schmitz Bettina , Stephani Ulrich , Sander Thomas 
Published: May 2005

AbstractPhotosensitivity or photoparoxysmal response (PPR) is a common and highly heritable electroencephalographic trait characterized by an abnormal visual sensitivity of the brain in reaction to intermittent photic stimulation. PPR occurs frequently associated with idiopathic generalized epilepsies (IGEs). The present genomewide linkage scan was designed to map susceptibility loci for PPR and to explore their genetic relationship with IGE. The study included 60 families with at least two siblings displaying PPR. To dissect PPR‐specific and IGE‐related susceptibility loci, we defined two distinct family subgroups, comprising 19 families with predominantly pure PPR and photosensitive seizures (PPR‐families) and 25 families, in which PPR was strongly associated with IGE (PPR/IGE‐families). MOD score analyses provided significant evidence for linkage to the region 6p21.2 in the PPR‐families (empirical p = 0.00004) and suggestive evidence for linkage to the region 13q31.3 in the PPR/IGE families (p = 0.00015), both with a best‐fitting recessive mode of inheritance. In the PPR/IGE‐families, linkage evidence was even stronger (p = 0.00003) when the trait definition was broadened by IGE traits. Our study shows two PPR‐related susceptibility loci, depending on the familial background of IGE. The locus on 6p21.2 seems to predispose to PPR itself, whereas the locus on 13q31.3 also confers susceptibility to IGE. Ann Neurol 2005;57:866–873
Autologous mesenchymal stem cell transplantation in stroke patients
Authors: Bang Oh Young , Lee Jin Soo , Lee Phil Hyu , Lee Gwang 
Published: May 2005

AbstractMesenchymal stem cell (MSC) transplantation improves recovery from ischemic stroke in animals. We examined the feasibility, efficacy, and safety of cell therapy using culture‐expanded autologous MSCs in patients with ischemic stroke. We prospectively and randomly allocated 30 patients with cerebral infarcts within the middle cerebral arterial territory and with severe neurological deficits into one of two treatment groups: the MSC group (n = 5) received intravenous infusion of 1 × 108 autologous MSCs, whereas the control group (n = 25) did not receive MSCs. Changes in neurological deficits and improvements in function were compared between the groups for 1 year after symptom onset. Neuroimaging was performed serially in five patients from each group. Outcomes improved in MSC‐treated patients compared with the control patients: the Barthel index (p = 0.011, 0.017, and 0.115 at 3, 6, and 12 months, respectively) and modified Rankin score (p = 0.076, 0.171, and 0.286 at 3, 6, and 12 months, respectively) of the MSC group improved consistently during the follow‐up period. Serial evaluations showed no adverse cell‐related, serological, or imaging‐defined effects. In patients with severe cerebral infarcts, the intravenous infusion of autologous MSCs appears to be a feasible and safe therapy that may improve functional recovery. Ann Neurol 2005;57:874–882
RON‐regulated innate immunity is protective in an animal model of multiple sclerosis
Authors: Tsutsui Shigeki , Noorbakhsh Farshid , Sullivan Andrea , Henderson Andrew J. , Warren Kenneth , Toney‐Earley Kenya , Waltz Susan E. , Power Christopher 
Published: May 2005

AbstractThe tyrosine kinase receptor RON and its ligand, macrophage stimulating protein (MSP), exert inhibitory effects on systemic innate immunity, but their CNS expression and impact on human neuroinflammatory diseases are unknown were RON and MSP present in human brain perivascular macrophages and microglia, but RON mRNA and protein abundance in the CNS were diminished in both MS patients and the MS animal model, experimental autoimmune encephalomyelitis (EAE). Treatment of differentiated human monocytoid cells with MSP resulted in significant reduction of interleukin (IL)–1β, tumor necrosis factor (TNF)–α and MMP‐9 mRNA levels, whereas minimal effects were observed in human astrocytes. After induction of EAE, RON knockout and heterozygote animals exhibited significantly increased CNS proinflammatory gene (TNF‐α, MMP‐12) expression compared with wild‐type littermate controls, although IL‐4 levels were suppressed in both RON‐deficient groups. Neurological disease in RON‐deficient animals showed a more rapid onset with overall worsened severity, together with exacerbated demyelination, axonal injury, and neuroinflammation after EAE induction. The proto‐oncogene, c‐Cbl, which modulates ubiquitylation of RON, was increased in glia in both MS brains and EAE spinal cords. Thus, the MSP‐RON pathway represents a novel regulatory mechanism within the CNS by which innate immunity and its pathogenic effects could be targeted for future therapeutic interventions. Ann Neurol 2005;57:883–895
Correlates of hippocampal neuron number in Alzheimer's disease and ischemic vascular dementia
Authors: Zarow Chris , Vinters Harry V. , Ellis William G. , Weiner Michael W. , Mungas Dan , White Lon , Chui Helena C. 
Published: May 2005

AbstractThe cornu ammonis 1 region of the hippocampus (CA1) sector of hippocampus is vulnerable to both Alzheimer's disease (AD)‐type neurofibrillary degeneration and anoxia–ischemia. The objective of this article is to compare number and size of neurons in CA1 in AD versus ischemic vascular dementia. Unbiased stereological methods were used to estimate the number and volume of neurons in 28 autopsy‐derived brain samples. For each case, the entire hippocampus from one cerebral hemisphere was sliced into 5mm slabs (5–7 slabs/case), cut into 50μm sections, and stained with gallocyanine. Using the optical dissector, we systematically sampled the number and size of neurons throughout the extent of CA1 and CA2. The total number of neurons was significantly less in AD compared with ischemic vascular dementia (p < 0.02), but there was no significant difference in neuron size. The greatest loss of neurons was observed in two cases with combined AD and hippocampal sclerosis. Regardless of causative diagnosis, the number of CA1 neurons correlates with magnetic resonance imaging–derived hippocampal volume (r = 0.72; p < 0.001) and memory score (r = 0.62; p < 0.01). We conclude that although CA1 neuron loss is more consistently observed in AD than ischemic vascular dementia, severity of loss shows the expected correlation with structure and function across causative subtype. Reductions in magnetic resonance imaging–derived hippocampal volume reflect loss, rather than shrinkage, of CA1 neurons. Ann Neurol 2005;57:896–903
Sparse multifocal stimuli for the detection of multiple sclerosis
Authors: Ruseckaite Rasa , Maddess Teddy , Danta Gytis , Lueck Christian J. , James Andrew C. 
Published: May 2005

AbstractWe compared the diagnostic capabilities of contrast reversal and sparse pattern pulse stimulation for dichoptic multifocal visual evoked potentials (mfVEPs) measured in normal subjects and multiple sclerosis (MS) patients. Multifocal responses were obtained from 27 normal subjects and 50 relapsing‐remitting patients, 26 of whom had experienced optic neuritis (ON+). The patient groups were matched for length of disease and number of clinical attacks. Compared with the responses of normal subjects those of MS patients had significantly smaller response amplitudes, lower signal‐to‐noise ratios, more complex response waveforms, and longer response delays. The effects were larger for sparser stimuli. Sensitivities and specificities for the different stimulus types were estimated from receiver operator characteristic (ROC) plots. Bootstrap estimates of the accuracies of the ROCs for the most promising measure, the template delays, indicated the sparsest stimulus would deliver 92% sensitivity at a false‐positive rate of 0%. In contrast, at 92% sensitivity the conventional mfVEP stimulus misdiagnosed more than 20% of the normal population. The results were similar for patients with no history of ON (ON−). In performing well in patients with no history of ON, the sparse mfVEPs seem to measure progressive damage associated with axon and gray matter losses rather than damage associated with a history of serious inflammation. Ann Neurol 2005;57:904–913
Deep brain stimulation to relieve drug‐resistant SUNCT
Authors: Leone Massimo , Franzini Angelo , D'Andrea Giovanni , Broggi Giovanni , Casucci Gerardo , Bussone Gennaro 
Published: May 2005

AbstractThe rare primary headache short‐lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) is characterized by 3 to 200 attacks per day of severe unilateral orbital pain. Functional magnetic resonance imaging shows increased blood flow in the ipsilateral posterior inferior hypothalamus during attacks, indicating activation. We report the first patient with SUNCT in whom severe intractable pain (70 per day) was well controlled by electrode implant to and continuous stimulation of the posterior inferior hypothalamus. Ann Neurol 2005;57:925–927
Methylenetetrahydrofolate reductase C677T genotype and PD
Authors: de Lau Lonneke M. L. , Koudstaal Peter J. , van Meurs Joyce B. J. , Uitterlinden André G. , Hofman Albert , Breteler Monique M. B. 
Published: May 2005

AbstractIn a prospective, population‐based cohort study among 5,920 participants aged 55 years or older, we observed that the TT variant of the methylenetetrahydrofolate reductase C677T polymorphism is associated with an increased risk for Parkinson's disease in smokers. Both smoking and the TT genotype are known to induce hyperhomocystinemia, and synergistic effects on homocysteine levels have been reported. Increased plasma levels of homocysteine through direct neurotoxic effects might accelerate the selective dopaminergic cell death underlying Parkinson's disease. Our findings support the hypothesis that homocysteine plays a role in the pathogenesis of Parkinson's disease. Ann Neurol 2005;57:927–930