bluuebunny/crossref_metadata_2025_split huggingface dataset:
Major histocompatibility complex class II polymorphisms in Macaca mulatta: factors influencing comprehensive genotyping of Macaca mulatta (Mamu)‐DQA1 alleles by PCR‐RFLP in archival samples
Authors: Rolfs Becky K. , Wu Ching Ching , Lerche Nicholas W. , Smith David G. 
Published: August 2002

AbstractIn the last 5 years, HLA class II genotyping methods have been adapted for genotyping of class II loci in rhesus macaques. Since previously published typing protocols were used on samples that were collected and stored under ideal conditions, it was of interest to determine if these methods were adequate for genotyping a large collection of archival samples from which DNA had been isolated and stored under various conditions. Established macaque DQA1 typing protocols were modified to optimize the typing procedure and enhance the ability to successfully genotype DNA from samples that were of poor quality and/or quantity. Long‐term storage of whole‐blood buffy coats or stored DNA extracted from whole‐blood buffy coats did not affect typing success; however, amplification and typing of DNA extracted from archival samples of plasma were difficult and resulted in a low success rate. This suggests that amplification and DQA1‐genotyping of archival samples is possible with a modified protocol, but is influenced by the age and source of the sample, and to a lesser extent, the method used to extract DNA from sample substrates. Am J Phys Anthropol 116:296–301, 2001. © 2001 Wiley‐Liss, Inc.
Cigarette smoking and the incidence of Parkinson's disease in two prospective studies
Authors: Hernán Miguel A. , Zhang Shumin M. , Rueda‐DeCastro Ana M. , Colditz Graham A. , Speizer Frank E. , Ascherio Alberto 
Published: August 2002

AbstractAn inverse association between cigarette smoking and idiopathic Parkinson's disease has been reported in several retrospective studies, but prospective evidence is available only for men. We assessed the association between the incidence of Parkinson's disease and smoking in two large prospective cohort studies comprising men and women. New cases of Parkinson's disease were identified in the Nurses' Health Study for 1976–1996, and in the Health Professionals Follow‐up Study for 1986–1996. Smoking history was assessed at baseline and updated on subsequent biennial questionnaires. In women, the age‐adjusted rate ratios (95% confidence intervals) for Parkinson's disease relative to never‐smokers were 0.7 (0.5, 1.0) for past smokers, and 0.4 (0.2, 0.7) for current smokers. In men, the age‐adjusted rate ratios for Parkinson's disease relative to never‐smokers were 0.5 (0.4, 0.7) for past smokers, and 0.3 (0.1, 0.8) for current smokers. In both cohorts, the strength of the association decreased with time since quitting (among past smokers), increased with number of cigarettes per day (among current smokers), and increased with pack‐years of smoking. These prospective findings confirm that an inverse association between smoking and the incidence of Parkinson's disease exists in both men and women.
Diffusion‐ and perfusion‐weighted MRI response to thrombolysis in stroke
Authors: Parsons Mark W. , Barber P. Alan , Chalk Jonathon , Darby David G. , Rose Stephen , Desmond Patricia M. , Gerraty Richard P. , Tress Brian M. , Wright Peter M. , Donnan Geoffrey A. , Davis Stephen M. 
Published: August 2002

AbstractDiffusion‐ and perfusion‐weighted magnetic resonance imaging provides important pathophysiological information in acute brain ischemia. We performed a prospective study in 19 sub‐6‐hour stroke patients using serial diffusion‐ and perfusion‐weighted imaging before intravenous thrombolysis, with repeat studies, both subacutely and at outcome. For comparison of ischemic lesion evolution and clinical outcome, we used a historical control group of 21 sub‐6‐hour ischemic stroke patients studied serially with diffusion‐ and perfusion‐weighted imaging. The two groups were well matched for the baseline National Institutes of Health Stroke Scale and magnetic resonance parameters. Perfusion‐weighted imaging–diffusion‐weighted imaging mismatch was present in 16 of 19 patients treated with tissue plasminogen activator, and 16 of 21 controls. Perfusion‐weighted imaging–diffusion‐weighted imaging mismatch patients treated with tissue plaminogen activator had higher recanalization rates and enhanced reperfusion at day 3 (81% vs 47% in controls), and a greater proportion of severely hypoperfused acute mismatch tissue not progressing to infarction (82% vs −25% in controls). Despite similar baseline diffusion‐weighted imaging lesions, infarct expansion was less in the recombinant tissue plaminogen activator group (14cm3 vs 56cm3 in controls). The positive effect of thrombolysis on lesion growth in mismatch patients translated into a greater improvement in baseline to outcome National Institutes of Health Stroke Scale in the group treated with recombinant tissue plaminogen activator, and a significantly larger proportion of patients treated with recombinant tissue plaminogen activator having a clinically meaningful improvement in National Institutes of Health Stroke Scale of ≥7 points. The natural evolution of acute perfusion‐weighted imaging–diffusion‐weighted imaging mismatch tissue may be altered by thrombolysis, with improved stroke outcome. This has implications for the use of diffusion‐ and perfusion‐weighted imaging in selecting and monitoring patients for thrombolytic therapy.
Dopaminergic modulation of cortical function in patients with Parkinson's disease
Authors: Mattay Venkata S. , Tessitore Alessandro , Callicott Joseph H. , Bertolino Alessandro , Goldberg Terry E. , Chase Thomas N. , Hyde Thomas M. , Weinberger Daniel R. 
Published: August 2002

AbstractPatients with idiopathic Parkinson's disease suffer not only from classic motor symptoms, but from deficits in cognitive function, primarily those subserved by the prefrontal cortex as well. The aim of the current study was to investigate the modulatory effects of dopaminergic therapy on neural systems subserving working memory and motor function in patients with Parkinson's disease. Ten patients with stage I and II Parkinson's disease were studied with functional magnetic resonance imaging, during a relatively hypodopaminergic state (ie, 12 hours after a last dose of dopamimetic treatment), and again during a dopamine‐replete state. Functional magnetic resonance imaging was performed under three conditions: a working memory task, a cued sensorimotor task and rest. Consistent with prior data, the cortical motor regions activated during the motor task showed greater activation during the dopamine‐replete state; however, the cortical regions subserving working memory displayed greater activation during the hypodopaminergic state. Interestingly, the increase in cortical activation during the working memory task in the hypodopaminergic state positively correlated with errors in task performance, and the increased activation in the cortical motor regions during the dopamine‐replete state was positively correlated with improvement in motor function. These results support evidence from basic research that dopamine modulates cortical networks subserving working memory and motor function via two distinct mechanisms: nigrostriatal projections facilitate motor function indirectly via thalamic projections to motor cortices, whereas the mesocortical dopaminergic system facilitates working memory function via direct inputs to prefrontal cortex. The results are also consistent with evidence that the hypodopaminergic state is associated with decreased efficiency of prefrontal cortical information processing and that dopaminergic therapy improves the physiological efficiency of this region.
A functional polymorphism in the prodynorphin gene promotor is associated with temporal lobe epilepsy
Authors: Stögmann Elisabeth , Zimprich Alexander , Baumgartner Christoph , Aull‐Watschinger Susanne , Höllt Volker , Zimprich Fritz 
Published: August 2002

AbstractThe prodynorphin gene (PDYN) encoding the anticonvulsant peptide dynorphin is a strong candidate for a seizure suppressor gene and thus a possible modulator of susceptibility to temporal lobe epilepsy. We performed a case control association study in 155 patients with nonlesional temporal lobe epilepsy and 202 controls and found that PDYN promotor low‐expression L‐alleles confer an increased risk for temporal lobe epilepsy in patients with a family history for seizures. Irrespective of the familial background, L‐homozygotes display a higher risk for secondarily generalized seizures and status epilepticus.
Human brain mapping in dystonia reveals both endophenotypic traits and adaptive reorganization
Authors: Meunier Sabine , Garnero Line , Ducorps Antoine , Mazières Leonor , Lehéricy Stéphane , Tézenas Du Montcel Sophie , Renault Bernard , Vidailhet Marie 
Published: August 2002

AbstractDystonia has a wide clinical spectrum from early‐onset generalized to late‐onset sporadic, task‐specific forms. The genetic origin of the former has been clearly established. A critical role of repetitive skilled motor tasks has been put forward for the latter, while underlying vulnerability traits are still being searched for. Using magnetoencephalography, we looked for structural abnormalities reflecting a preexisting dysfunction. We studied finger representations of both hands in the primary sensory cortex, as compared in 23 patients with unilateral task‐specific dystonia and 20 control subjects. A dramatic disorganization of the nondystonic hand representation was found in all patients, and its amount paralleled the severity of the dystonic limb motor impairment. Abnormalities were also observed in the cortex coding the dystonic limb representation, but they were important only in the most severely affected patients. The abnormal cortical finger representations from the nondystonic limb appear to be endophenotypic traits of dystonia. That finger representations from the dystonic limb were almost normal for the less severely affected patients may be due to intrinsic beneficial remapping in reaction against the primary disorder.
Disease mechanisms revealed by transcription profiling in SOD1‐G93A transgenic mouse spinal cord
Authors: Olsen Mary K. , Roberds Steven L. , Ellerbrock Brenda R. , Fleck Timothy J. , McKinley Denise K. , Gurney Mark E. 
Published: August 2002

AbstractMutations of copper,zinc‐superoxide dismutase (cu,zn SOD) are found in patients with a familial form of amyotrophic lateral sclerosis. When expressed in transgenic mice, mutant human cu,zn SOD causes progressive loss of motor neurons with consequent paralysis and death. Expression profiling of gene expression in SOD1‐G93A transgenic mouse spinal cords indicates extensive glial activation coincident with the onset of paralysis at 3 months of age. This is followed by activation of genes involved in metal ion regulation (metallothionein‐I, metallothionein‐III, ferritin‐H, and ferritin‐L) at 4 months of age just prior to end‐stage disease, perhaps as an adaptive response to the mitochondrial destruction caused by the mutant protein. Induction of ferritin–H and –L gene expression may also limit iron catalyzed hydroxyl radical formation and consequent oxidative damage to lipids, proteins, and nucleic acids. Thus, glial activation and adaptive responses to metal ion dysregulation are features of disease in this transgenic model of familial amyotrophic lateral sclerosis.
Depletion of corticotrophin‐releasing factor neurons in the pontine micturition area in multiple system atrophy
Authors: Benarroch Eduardo E. , Schmeichel Ann M. 
Published: August 2002

AbstractWe sought to determine whether the putative pontine micturition center in the human dorsal pons contains corticotrophin‐releasing factor (CRF) neurons, and whether these neurons are depleted in patients with multiple system atrophy and bladder dysfunction. Brains were obtained at autopsy from 4 control subjects and 4 patients with clinical diagnosis of multiple system atrophy, confirmed neuropathologically. Serial 50μm cryostat sections were obtained throughout the rostral half of the pons, and every eighth section was processed for CRF immunocytochemistry (rabbit polyclonal antibody). Consecutive sections were stained for nicotinamide adenine dinucleotide phosphate diaphorase (NADPH‐d) to identify neurons of the laterodorsal tegmental nucleus or for both CRF and NADPH. Locus ceruleus neurons were identified by their neuromelanin content. Abundant CRF immunoreactive neurons were identified in the dorsal pontine tegmentum just ventral to the locus ceruleus. CRF neurons were intermingled with, but distinct from, the NADPH‐d‐reactive neurons of the laterodorsal tegmental nucleus. In all multiple system atrophy cases, there was a severe depletion of these CRF‐immunoreactive neurons (26.6 ± 3 neurons/section in patients; 73.7 ± 4 neurons/section in controls). Our results suggest that depletion of CRF neurons in the putative pontine micturition center may contribute to the severe bladder dysfunction that characterizes multiple system atrophy.
A disorder similar to Huntington's disease is associated with a novel CAG repeat expansion
Authors: Margolis Russell L. , O'Hearn Elizabeth , Rosenblatt Adam , Willour Virginia , Holmes Susan E. , Franz Mary L. , Callahan Colleen , Hwang Hyon S. , Troncoso Juan C. , Ross Christopher A. 
Published: August 2002

AbstractHuntington's disease (HD) is an autosomal dominant disorder characterized by abnormalities of movement, cognition, and emotion and selective atrophy of the striatum and cerebral cortex. While the etiology of HD is known to be a CAG trinucleotide repeat expansion, the pathways by which this mutation causes HD pathology remain unclear. We now report a large pedigree with an autosomal dominant disorder that is clinically similar to HD and that arises from a different CAG expansion mutation. The disorder is characterized by onset in the fourth decade, involuntary movements and abnormalities of voluntary movement, psychiatric symptoms, weight loss, dementia, and a relentless course with death about 20 years after disease onset. Brain magnetic resonance imaging scans and an autopsy revealed marked striatal atrophy and moderate cortical atrophy, with striatal neurodegeneration in a dorsal to ventral gradient and occasional intranuclear inclusions. All tested affected individuals, and no tested unaffecteds, have a CAG trinucleotide repeat expansion of 50 to 60 triplets, as determined by the repeat expansion detection assay. Tests for the HD expansion, for all other known CAG expansion mutations, and for linkage to chromosomes 20p and 4p were negative, indicating that this mutation is novel. Cloning the causative CAG expansion mutation for this new disease, which we have termed Huntington's disease‐like 2 (HDL2), may yield valuable insight into the pathogenesis of HD and related disorders.
Cytotoxic evaluation of arsenic compounds in alveolar macrophages in hamsters
Authors: Okada Mitsushi , Inoue Yoko , Karube Hitomi , Niitsuya Masato , Tohnori Hideki , Aizawa Yoshiharu , Okayasu Isao , Kotani Makoto 
Published: August 2002

AbstractGallium arsenide (GaAs) causes various toxic effects in animals, including pulmonary diseases. Although their toxicity is not completely investigated, GaAs is used in workplaces in various semiconductor products. The present report was designed to clarify the toxicity of GaAs suspension and arsenic chloride (AsCl3) solution as additives to the alveolar macrophages in hamsters using magnetometry, enzyme release assays and morphological examinations. Alveolar macrophages obtained from hamsters by tracheobronchial lavage and adhered to disks in the bottom of wells were exposed to ferrosoferric oxide and additives. Ferrosoferric oxide particles were magnetized externally and the remanent magnetic field was measured. Relaxation, a fast decline of remanent magnetic fields radiated from alveolar macrophages, was delayed and decay constants decreased dose‐dependently due to exposure to GaAs suspensions. Relaxation was much delayed and decay constants decreased considerably due to exposure to AsCl3 solutions. Because the relaxation is thought to be associated with the cytoskeleton, exposure to GaAs impairs their motor function. Enzyme release assay and morphological findings indicated damage to macrophages. Thus the cytotoxicity caused cytostructural changes and cell death. According to DNA electrophoresis and TUNEL methods, necrotic changes occur more frequently than apoptotic changes. In conclusion, exposure to GaAs suspension and AsCl3 solution induced cytotoxicity of alveolar macrophages. Copyright © 2001 John Wiley & Sons, Ltd.
Toward new biosilicones: hydrosilylation of fish oil unsaturated fatty acid esters
Authors: Delpech Fabien , Asgatay Saadia , Castel Annie , Rivière Pierre , Rivière‐Baudet Monique , Amin‐Alami Amal , Manriquez Juan 
Published: August 2002

AbstractHydrosilylation of fatty acid methyl esters (FAMEs) were efficiently catalyzed by Speier's and Wilkinson's catalysts in the case of vinylic acid esters, but less efficiently in the case of ­non‐vinylic ones, which gave non‐regiospecific additions. In the latter case, initiation by radicals led to regiospecific reactions for oleic esters (C10‐silylation). This regiospecificity can be attributed to the higher stability of the C10‐silylated adduct and of the corresponding radical intermediate. Only regioselective addition was observed for linoleic esters (C13‐silylation ≈ 70%, C10 ≈ 20%, C9 ≈ 10%). Molecular modeling was used to examine the stability of the isomeric products and radicals. The new concept of radical initiation sequence has been successfully applied to FAMEs and then was extended to crude fish oil. Copyright © 2001 John Wiley & Sons, Ltd.
Organotin mefenamic complexes—preparations, spectroscopic studies and crystal structure of a triphenyltin ester of mefenamic acid: novel anti‐tuberculosis agents
Authors: Kovala‐Demertzi Dimitra , Dokorou Vaso , Ciunik Zbigniew , Kourkoumelis Nikolaos , Demertzis Mavroudis A. 
Published: August 2002

AbstractThe triphenyltin adduct of mefenamic acid, [SnPh3L] (1), the monophenyltin complex [PhSnOL]
n (2), and the dibutyltin complex [SnBu2L2] (3), where HL is 2‐[bis(2,3‐dimethylphenyl)amino]benzoic acid (mefenamic acid), have been prepared and structurally characterized by means of vibrational, 1H and 13C NMR spectroscopies. The crystal structure of 1 has been determined by X‐ray crystallography. X‐ray analysis revealed a pseudo‐pentacoordinated structure containing Ph3Sn coordinated to the carboxylato group. The structural distortion is a displacement from the tetrahedron toward the trigonal bipyramid. Significant CH–π interactions and intramolecular hydrogen bonds stabilize the structure 1. The polar imino hydrogen atom participates in intramolecular hydrogen bonds. Complex 1 is self‐assembled via CH–π and stacking interactions. Vibrational and NMR data are discussed in terms of the crystal structure and the proposed structures for 1–3. Compounds 1 and 3 were tested for antimycobacterial activity against Mycobacterium tuberculosis H37Rv. Copyright © 2002 John Wiley & Sons, Ltd.
Evaluation of electrical conductivity models for conductive polymer composites
Authors: Clingerman Matthew L. , King Julia A. , Schulz Kirk H. , Meyers Jeffrey D. 
Published: August 2002

AbstractThe electrical conductivity of polymeric materials can be increased by the addition of carbon fillers, such as carbon fibers and graphite. The resulting composites could be used in applications such as interference shielding and electrostatic dissipation. Electrical conductivity models are often proposed to predict the conductivity behavior of these materials in order to achieve more efficient material design that could reduce costly experimental work. The electrical conductivity of carbon‐filled polymers was studied by adding four single fillers to nylon 6,6 and polycarbonate in increasing concentrations. The fillers used in this project include chopped and milled forms of polyacrylonitrile (PAN) carbon fiber, ThermocarbTM Specialty Graphite, and Ni‐coated PAN carbon fiber. Material was extruded and injection‐molded into test specimens, and then the electrical conductivity was measured. Data analysis included a comparison of the results to existing conductivity models. The results show that the model proposed by Mamunya, which takes into account the filler aspect ratio and the surface energy of the filler and polymer, most closely matched the conductivity data. This information will then be used in the development of improved conductivity models. © 2002 Wiley Periodicals, Inc. J Appl Polym Sci 83: 1341–1356, 2002
New conducting thermoplastic elastomers. I. Synthesis and chemical characterization
Authors: Carone E. , D'Ilario L. , Martinelli A. 
Published: August 2002

AbstractIn the last 20 years, much interest has been focused on conducting polymers to find new materials to transfer from research to industry. However, in many cases, as for elastomers for which intrinsically conducting materials are unavailable, it is necessary to use conducting particles that are physically mixed with the polymeric matrix to give loaded rubbers. In this work we report the synthesis and the chemical characterization of an intrinsically conducting material with good mechanical and electrical conduction properties. To achieve such a global goal, we covalently linked, by an amidation reaction, the terminal NH2 of Emeraldine (EB) and sulfonated Emeraldine (SPAN) to a free carboxylic group belonging to the repetitive unit of a functionalized segmented polyurethane. The reaction was carried out by activating such a carboxylic group with N,N′‐dicyclohexylcarbodiimide and N‐hydroxysuccinimide. The reaction yields and the chemical properties of the polymers were studied by proton and carbon‐13 nuclear magnetic resonance, ultraviolet, and Fourier transform infrared spectroscopy. The average numbers of EB or SPAN aromatic rings per polyether urethane acid (PEUA) repetitive unit, which cannot be assumed to be amidation degree because at this moment the molecular weights of the inserted EB and SPAN chains are unavailable, were 6 in case of the polymer obtained from the pristine Emeraldine and 1 for that obtained from the sulfonated Emeraldine. This result could be because SPAN was used in the acidic form, which depresses the nucleophilicity of the NH2 group because of the presence of the sulfonic protons. © 2002 Wiley Periodicals, Inc. J Appl Polym Sci 83: 857–867, 2002
UV exposure and temperature effects on curing mechanisms in thin linseed oil films: Spectroscopic and chromatographic studies
Authors: Boyatzis S. , Ioakimoglou E. , Argitis P. 
Published: August 2002

AbstractThe influence of thermal and photochemical treatment in the curing mechanisms of thin linseed oil films is studied. The role of copper acetate pigments is also investigated under the above conditions. UV and FTIR absorption spectroscopy and chromatographic product analysis are used as the main analytical techniques, which allowed the identification of significant changes in the curing mechanism in each case. Yellowing, crosslinking, and fragmentation inside the film material proceed to a different extent according to the conditions. Peroxide destruction is induced by UV exposure at early curing stages and affects the course of the yellowing process. Yellow product formation is also favored by curing at elevated temperatures, which is accompanied in this case by decreased crosslinking in the cured film. © 2002 Wiley Periodicals, Inc. J Appl Polym Sci 84: 936–949, 2002; DOI 10.1002/app.10117