bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential modulation in human primary and secondary somatosensory cortices during the preparatory period of self‐initiated finger movement
Authors: Wasaka Toshiaki , Nakata Hiroki , Akatsuka Kosuke , Kida Tetsuo , Inui Koji , Kakigi Ryusuke 
Published: September 2005

AbstractTo elucidate the mechanisms underlying sensorimotor integration, we investigated modulation in the primary (SI) and secondary (SII) somatosensory cortices during the preparatory period of a self‐initiated finger extension. Electrical stimulation of the right median nerve was applied continuously, while the subjects performed a self‐initiated finger extension and were instructed not to pay attention to the stimulation. The preparatory period was divided into five sub‐periods from the onset of the electromyogram to 3000 ms before movement and the magnetoencephalogram signals following stimulation in each sub‐period were averaged. Multiple source analysis indicated that the equivalent current dipoles (ECDs) were located in SI and bilateral SII. Although the ECD moment for N20m (the upward deflection peaking at around 20 ms) was not significantly changed, that for P30m (the downward deflection peaking at around 30 m) was significantly smaller in the 0‐ to −500‐ms sub‐period than the −2000‐ to −3000‐ms sub‐period. As for SII, the ECD moment for the SII ipsilateral to movement showed no significant change, while that for the contralateral SII was significantly larger in the 0‐ to −500‐ms sub‐period than the −1500‐ to −2000‐ms or −2000‐ to −3000‐ms sub‐period. The opposite effects of movement on SI and SII cortices indicated that these cortical areas play a different role in the function of the sensorimotor integration and are affected differently by the centrifugal process.
Brain‐derived neurotrophic factor induces a rapid dephosphorylation of tau protein through a PI‐3Kinase signalling mechanism
Authors: Elliott Evan , Atlas Roee , Lange Aya , Ginzburg Irith 
Published: September 2005

AbstractThe microtubule‐associated protein tau is essential for microtubule stabilization in neuronal axons. Hyperphosphorylation and intracellular fibrillar formation of tau protein is a pathology found in Alzheimer's disease (AD) brains, and in a variety of neurodegenerative disorders referred to as ‘taupathies’. In the present study, we investigated how brain‐derived neurotrophic factor (BDNF), an extracellular factor that is down‐regulated in AD brains, affects tau phosphorylation. BDNF stimulation of neuronally differentiated P19 mouse embryonic carcinoma cells resulted in a rapid decrease in tau phosphorylation, at phosphorylation sites recognized by Tau1, AT8, AT180 and p262‐Tau antibodies. K252a, a tyrosine receptor kinase (Trk) inhibitor, attenuated this dephosphorylation event, suggesting that BNDF activation of TrkB is responsible for the tau dephosphorylation. In addition, BDNF had no affect on tau phosphorylation in the presence of wortmannin, a PI‐3Kinase inhibitor, or lithium, a GSK3β inhibitor, suggesting that these two kinases are part of the signaling transduction cascade leading from TrkB receptor activation to tau dephosphorylation. These results suggest a link between a correlate of AD, decrease in BDNF levels and an AD pathology, tau hyperphosphorylation.
An fMRI study of causal judgments
Authors: Satpute Ajay B. , Fenker Daniela B. , Waldmann Michael R. , Tabibnia Golnaz , Holyoak Keith J. , Lieberman Matthew D. 
Published: September 2005

AbstractThe capacity to evaluate causal relations is fundamental to human cognition, and yet little is known of its neurocognitive underpinnings. A functional magnetic resonance imaging study was performed to investigate an hypothesized dissociation between the use of semantic knowledge to evaluate specifically causal relations in contrast to general associative relations. Identical pairs of words were judged for causal or associative relations in different blocks of trials. Causal judgments, beyond associative judgments, generated distinct activation in left dorsolateral prefrontal cortex and right precuneus. These findings indicate that the evaluation of causal relations in semantic memory involves additional neural mechanisms relative to those required to evaluate associative relations.
Hyperthermic reactions induced by orexin A: role of the ventromedial hypothalamus
Authors: Monda M. , Viggiano An. , Viggiano Al. , Viggiano E. , Lanza A. , De Luca V. 
Published: September 2005

AbstractThis experiment tested the involvement of the ventromedial hypothalamus (VMH) in the sympathetic and hyperthermic reactions induced by an intracerebroventricular (i.c.v.) injection of orexin A (1.5 nmol). In the first part of the experiment, the firing rate and cytochrome oxidase activity of the VMH neurons, and the colonic temperature were monitored in 12 urethane‐anaesthetized rats before an i.c.v. injection of orexin and over a period of 2 h after the injection. Orexin induced an increase in the firing rate, colonic temperature and cytochrome oxidase activity. A group of 12 rats was used as a control: saline, but not orexin, was injected. No modifications in the firing rate, cytochrome oxidase reactivity and colonic temperature were noted. In the second part of the experiment, 12 rats were anaesthetized and lesioned bilaterally in the VMH with an injection of ibotenic acid. Sham lesions were carried out in 12 control rats. After 48 h, all animals were anaesthetized with ethyl‐urethane. The firing rates of the sympathetic nerves to interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures and heart rate were monitored before and over a period of 2 h after an i.c.v. injection of orexin or saline in the lesioned and sham‐lesioned rats. Orexin increased the sympathetic firing rate, IBAT and colonic temperatures and heart rate in the sham‐lesioned rats. These increases were reduced by lesion of VMH. Saline did not induce any modification. These findings indicate that the VMH is involved in the control of the orexin‐induced hyperthermia.
Selective rather than inductive mechanisms favour specific replacement of Purkinje cells by embryonic cerebellar cells transplanted to the cerebellum of adult Purkinje cell degeneration (pcd) mutant mice
Authors: Carletti Barbara , Rossi Ferdinando 
Published: September 2005

AbstractCell replacement after neuronal degeneration in the adult CNS depends on the availability of specific cues to direct specification, differentiation and integration of newly born neurons into mature circuits. Following recent reports indicating that neurogenic signals may be reactivated in the adult injured CNS, here we asked whether such signals are expressed in the cerebellum after Purkinje cell degeneration. Thus, we compared the fate of embryonic cerebellar cells transplanted to the cerebella of adult wild‐type and Purkinje cell degeneration (pcd) mutant mice. Donor cells were dissected from β‐actin‐enhanced green fluorescent protein (EGFP) transgenic mice and transplanted as a single cell suspension. In both hosts, grafted cells generated all major cerebellar phenotypes, with a precise localization in the recipient cortex or white matter. Nevertheless, the phenotypic distributions showed striking quantitative differences. Most notably, in the pcd cerebellum there was a higher amount of Purkinje cells, while other phenotypes were less frequent. Analysis of cell proliferation by 5‐bromo‐2′‐deoxyuridine (BrDU) incorporation revealed that in both hosts mitotic activity was strongly reduced shortly after transplantation, and virtually all donor Purkinje cells were actually generated before grafting. Together, these results indicate that some compensatory mechanisms operate in the pcd environment. However, the very low mitotic rate of transplanted cells suggests that the adult cerebellum, either wild‐type or mutant, does not provide instructive neurogenic cues to direct the specification of uncommitted progenitors. Rather, specific replacement in mutant hosts is achieved through selective mechanisms that favour the survival and integration of donor Purkinje cells at the expense of other phenotypes.
The role of phenotypic variation in rhizosphere Pseudomonas bacteria
Authors: Van Den Broek Daan , Bloemberg Guido V. , Lugtenberg Ben 
Published: September 2005

SummaryColony phase variation is a regulatory mechanism at the DNA level which usually results in high frequency, reversible switches between colonies with a different phenotype. A number of molecular mechanisms underlying phase variation are known: slipped‐strand mispairing, genomic rearrangements, spontaneous mutations and epigenetic mechanisms such as differential methylation. Most examples of phenotypic variation or phase variation have been described in the context of host–pathogen interactions as mechanisms allowing pathogens to evade host immune responses. Recent reports indicate that phase variation is also relevant in competitive root colonization and biological control of phytopathogens. Many rhizospere Pseudomonas species show phenotypic variation, based on spontaneous mutation of the gacA and gacS genes. These morphological variants do not express secondary metabolites and have improved growth characteristics. The latter could contribute to efficient root colonization and success in competition, especially since (as shown for one strain) these variants were observed to revert to their wild‐type form. The observation that these variants are present in rhizosphere‐competent Pseudomonas bacteria suggests the existence of a conserved strategy to increase their success in the rhizosphere.
Novel hydrolase diversity retrieved from a metagenome library of bovine rumen microflora
Authors: Ferrer Manuel , Golyshina Olga V. , Chernikova Tatyana N. , Khachane Amit N. , Reyes‐Duarte Dolores , Santos Vitor A. P. Martins Dos , Strompl Carsten , Elborough Kieran , Jarvis Graeme , Neef Alexander , Yakimov Michail M. , Timmis Kenneth N. , Golyshin Peter N. 
Published: September 2005

SummaryA metagenome expression library of bulk DNA extracted from the rumen content of a dairy cow was established in a phage lambda vector and activity‐based screening employed to explore the functional diversity of the microbial flora. Twenty‐two clones specifying distinct hydrolytic activities (12 esterases, nine endo‐β‐1,4‐glucanases and one cyclodextrinase) were identified in the library and characterized. Sequence analysis of the retrieved enzymes revealed that eight (36%) were entirely new and formed deep‐branched phylogenetic lineages with no close relatives among known ester‐ and glycosyl‐hydrolases. Bioinformatic analyses of the hydrolase gene sequences, and the sequences and contexts of neighbouring genes, suggested tentative phylogenetic assignments of the rumen organisms producing the retrieved enzymes. The phylogenetic novelty of the hydrolases suggests that some of them may have potential for new applications in biocatalysis.
Detection of glial fibrillary acidic protein (GFAP) and vimentin (Vim) by immunoelectron microscopy of the glial cells in the central nervous system of the snail Megalobulimus abbreviatus
Authors: Dos Santos Paula C. , Gehlen Günther , Faccioni‐Heuser M. Cristina , Achaval Matilde 
Published: September 2005

AbstractWhen examined under an electron microscope, the central nervous system of Megalobulimus abbreviatus showed two types of glial cells: firstly, protoplasmic glial cells which displayed a nucleus with peripheral heterochromatin, scanty or no intermediate filaments, a developed Golgi complex, rough and smooth endoplasmic reticula, mitochondria and polymorphic lysosomes that indicate phagocytic activity of debris from the extracellular space; and, secondly, fibrous glial cells which showed numerous glial fibrillary acidic protein (GFAP) and vimentin immunoreactive intermediate filament bundles, a discrete Golgi complex, mitochondria, endoplasmic reticulum, lipid droplets and lysosomes. The contacts between the glial cells consisted of desmosomes and puncta adherentia, while those between the glial cells and the basal lamina consisted of hemidesmosomes. Both glial cell types were located in the cortex and medullary regions, however, the protoplasmic glial cells prevailed in the cortical region, while the fibrous glial cells prevailed in the medullar region. As the nervous tissue is avascular, the passage of nutrients and waste products may be facilitated by the glial labyrinthic system which is located in the cortical region. Glial processes adjacent to large and giant neurones formed a trophospongium, which seemed to be involved in a metabolic exchange between these cells. Thus, this evidence suggests that glial cells of M. abbreviatus are involved in structural support, isolation of different ganglionic areas, the formation of a microcirculatory system and an intimate metabolic relationship with neurones.
Altered expression of neprilysin family members in the pituitary gland of sleep‐disturbed rats, an animal model of severe fatigue
Authors: Ogawa Tokiko , Kiryu‐Seo Sumiko , Tanaka Masaaki , Konishi Hiroyuki , Iwata Nobuhisa , Saido Takaomi , Watanabe Yasuyoshi , Kiyama Hiroshi 
Published: September 2005

AbstractAlterations of the expression of some peptidases in the pituitary gland of a fatigued rat model were identified. Rats were kept in a cage filled with water to a height of 1.5 cm to disturb deep sleep. After 24‐h sleep disturbance, expression of neutral endopeptidase 24.11 (neprilysin) mRNA was increased in the intermediate lobe of the pituitary gland, whereas the mRNA expression of another family member, damage‐induced neuronal endopeptidase, which is normally expressed in a subgroup of anterior pituitary cells, was significantly suppressed. These alterations were demonstrated by RT‐PCR, northern blotting and in situ hybridization. Other family members, such as neprilysin 2 and endothelin converting enzyme‐1, did not show any change in mRNA expression. An increase of neprilysin mRNA expression was not seen in any other tissues of the sleep‐disturbed rats. The enzymatic activity of neprilysin was also increased in the pituitary. The augmentation of neprilysin expression and activity was prolonged as long as the sleep disturbance continued (up to 5 days), and returned to the basal level when rats were allowed to sleep freely. These results suggest that peptide processing and degradation in the pituitary may be an influential factor in fatigued states such as sleep disturbance.
The blood–brain barrier transmigrating single domain antibody: mechanisms of transport and antigenic epitopes in human brain endothelial cells
Authors: Abulrob Abedelnasser , Sprong Hein , En Henegouwen Paul Van Bergen , Stanimirovic Danica 
Published: September 2005

AbstractAntibodies against receptors that undergo transcytosis across the blood–brain barrier (BBB) have been used as vectors to target drugs or therapeutic peptides into the brain. We have recently discovered a novel single domain antibody, FC5, which transmigrates across human cerebral endothelial cells in vitro and the BBB in vivo. The purpose of this study was to characterize mechanisms of FC5 endocytosis and transcytosis across the BBB and its putative receptor on human brain endothelial cells. The transport of FC5 across human brain endothelial cells was polarized, charge independent and temperature dependent, suggesting a receptor‐mediated process. FC5 taken up by human brain endothelial cells co‐localized with clathrin but not with caveolin‐1 by immunochemistry and was detected in clathrin‐enriched subcellular fractions by western blot. The transendothelial migration of FC5 was reduced by inhibitors of clathrin‐mediated endocytosis, K+ depletion and chlorpromazine, but was insensitive to caveolae inhibitors, filipin, nystatin or methyl‐β‐cyclodextrin. Following internalization, FC5 was targeted to early endosomes, bypassed late endosomes/lysosomes and remained intact after transcytosis. The transcytosis process was inhibited by agents that affect actin cytoskeleton or intracellular signaling through PI3‐kinase. Pretreatment of human brain endothelial cells with wheatgerm agglutinin, sialic acid, α(2,3)‐neuraminidase or Maackia amurensis agglutinin that recognizes α(2,3)‐, but not with Sambucus nigra agglutinin that recognizes α(2,6) sialylgalactosyl residues, significantly reduced FC5 transcytosis. FC5 failed to recognize brain endothelial cells‐derived lipids, suggesting that it binds luminal α(2,3)‐sialoglycoprotein receptor which triggers clathrin‐mediated endocytosis. This putative receptor may be a new target for developing brain‐targeting drug delivery vectors.
Induction of endogenous pathways by antiepileptics and clinical implications
Authors: Strolin Benedetti M. , Ruty B. , Baltes E. 
Published: September 2005

AbstractThe aim of this study was to review modifications of the endogenous pathways (e.g. enzyme elevations, normal body constituent depletion or higher formation/excretion of endogenous metabolites) which could be ascribed to enzyme induction by antiepileptic drugs (AEDs). Information on older (e.g. phenobarbital, phenytoin and carbamazepine) and newer drugs (where information is available) is discussed together with clinical implications. The enzymes involved in the endogenous pathways and induced by the AEDs will not be limited to the hepatic microsomal enzymes; extrahepatic enzymes and/or enzymes present in other subcellular fractions will also be discussed, if pertinent. The induction of endogenous pathways by AEDs has been taken into account in the past, but much less emphasis has been given compared with the extensive literature on induction by AEDs of the metabolism of concomitantly administered drugs, either of the same or of different classes. Not all of the endogenous pathways examined and induced by AEDs appear to result in serious clinical consequences (e.g. induction of hepatic ALP, increased excretion of d‐glucaric acid or of 6β‐hydroxycortisol). In some cases, induction of some pathways (e.g. increase of high‐density lipoprotein cholesterol or of conjugated bilirubin) might even be a beneficial side‐effect, however enzyme induction is considered rather a detrimental aspect for an AED, as induction is generally a broad and a non‐specific phenomenon. The new AEDs have generally less induction potential than the older agents. Yet some (felbamate, topiramate, oxcarbazepine and lamotrigine) have the potential for inducing enzymes, whereas others (levetiracetam, gabapentin and vigabatrin) appear to be completely devoid of enzyme inducing characteristics, at least as far as the enzymes investigated are concerned.
Topiramate prevents ecstasy consumption: a case report
Authors: Akhondzadeh Shahin , Hampa Ali Daliri 
Published: September 2005

AbstractThe last decade has witnessed a development in the phenomenon ‘ecstasy’. Several substances, with more or less the same effects, are grouped together by the term ecstasy, the best‐known one being 3,4‐methylenedioxymethamphetamine (MDMA). The psychopathological consequences of MDMA in humans are relatively poorly understood. In addition, the treatment approach is complicated by the lack of documented studies. Topiramate is an antiepileptic drug that has a broad spectrum of antiseizure effects, which appear to be the result of several neurostabilizing pharmacological mechanisms including facilitation of GABAergic neurotransmission and inhibition of glutametergic activity at AMPA/kainate receptors. As both GABAergic and glutametergic neurons appear to be important modulators of the brain reward system, it was postulated that topiramate would be an effective treatment for reducing MDMA consumption through the attenuation of MDMA‐induced euphoria. The case of an ecstasy consumer, who started to discontinue ecstasy under topiramate treatment is presented here. Antiepileptics/mood stabilizers with glutamate inhibition activity like topiramate may present a promising new approach for challenging the consequence of drug abuse.
l‐Arginine and melatonin interaction in rat intestinal ischemia–reperfusion
Authors: Arslan S. Oktay , Gelir Ethem , Sayan Hale , Haktan Ozacmak V. 
Published: September 2005

AbstractWe investigated the combinative effects of l‐arginine and melatonin on the contractile responses of terminal ileum after the intestinal ischemia–reperfusion (I/R), in vivo. Male rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (180 min). We have observed a dramatic decrease in spontaneous basal activity and Ach‐induced contractile response. Our data clearly showed that the contractility decrease was ameliorated by l‐arginine but not by l‐NAME. Melatonin has reversed the inhibition of contractility caused by I/R injury in part. We did not observe an augmentation in the contractility of ileum when we use melatonin and l‐arginine in combination, in fact, melatonin decreased the protective effect of l‐arginine in intestinal I/R injury.
Welfare to Work, Wages and Wage Growth*
Authors: Lydon Reamonn , Walker Ian 
Published: September 2005

AbstractThis paper attempts to uncover the effects of a UK welfare‐to‐work programme on individual wage growth by exploiting an expansion to this welfare programme. The conventional wisdom is that such programmes trap recipients into low‐wage, low‐quality work – this comes from the simple argument that the ‘poverty trap’, which a wage subsidy for low‐income workers induces, reduces thebenefitsto investments, such as on‐the‐job training, and so reduces wage growth. In fact, a wage subsidy will also reduce thecostsof, at least, general training because we would normally expect workers to pay for their own general training in the form of lower gross wages. So a wage subsidy is a way of sharing these costs with the taxpayer. Thus, the net effect on wage progression depends on whether it reduces costs by more or less than it reduces the benefits.
Measuring Diagnoses: ICD Code Accuracy
Authors: O'Malley Kimberly J. , Cook Karon F. , Price Matt D. , Wildes Kimberly Raiford , Hurdle John F. , Ashton Carol M. 
Published: September 2005

Objective. To examine potential sources of errors at each step of the described inpatient International Classification of Diseases (ICD) coding process.Data Sources/Study Setting. The use of disease codes from the ICD has expanded from classifying morbidity and mortality information for statistical purposes to diverse sets of applications in research, health care policy, and health care finance. By describing a brief history of ICD coding, detailing the process for assigning codes, identifying where errors can be introduced into the process, and reviewing methods for examining code accuracy, we help code users more systematically evaluate code accuracy for their particular applications.Study Design/Methods. We summarize the inpatient ICD diagnostic coding process from patient admission to diagnostic code assignment. We examine potential sources of errors at each step and offer code users a tool for systematically evaluating code accuracy.Principle Findings. Main error sources along the “patient trajectory” include amount and quality of information at admission, communication among patients and providers, the clinician's knowledge and experience with the illness, and the clinician's attention to detail. Main error sources along the “paper trail” include variance in the electronic and written records, coder training and experience, facility quality‐control efforts, and unintentional and intentional coder errors, such as misspecification, unbundling, and upcoding.Conclusions. By clearly specifying the code assignment process and heightening their awareness of potential error sources, code users can better evaluate the applicability and limitations of codes for their particular situations. ICD codes can then be used in the most appropriate ways.