bluuebunny/crossref_metadata_2025_split huggingface dataset:
CheckViz: Sanity Check and Topological Clues for Linear and Non‐Linear Mappings
Authors: Lespinats Sylvain , Aupetit Michaël 
Published: December 2010

AbstractMultidimensional scaling is a must‐have tool for visual data miners, projecting multidimensional data onto a two‐dimensional plane. However, what we see is not necessarily what we think about. In many cases, end‐users do not take care of scaling the projection space with respect to the multidimensional space. Anyway, when using non‐linear mappings, scaling is not even possible. Yet, without scaling geometrical structures which might appear do not make more sense than considering a random map. Without scaling, we shall not make inference from the display back to the multidimensional space. No clusters, no trends, no outliers, there is nothing to infer without first quantifying the mapping quality. Several methods to qualify mappings have been devised. Here, we propose CheckViz, a new method belonging to the framework of Verity Visualization. We define a two‐dimensional perceptually uniform colour coding which allows visualizing tears and false neighbourhoods, the two elementary and complementary types of geometrical mapping distortions, straight onto the map at the location where they occur. As examples shall demonstrate, this visualization method is essential to help users make sense out of the mappings and to prevent them from over interpretations. It could be applied to check other mappings as well.
The effect of disgust on oral immune function
Authors: Stevenson Richard J. , Hodgson Deborah , Oaten Megan J. , Barouei Javad , Case Trevor I. 
Published: December 2010

AbstractDisgust motivates avoidance of pathogen sources, but whether its role in disease avoidance extends into activating the immune system is unexplored. This was tested here by comparing oral immune markers before and after a disgust induction, relative to neutral and negative induction control groups. The disgust group, but not controls, revealed an oral inflammatory response, with increased salivary tumor necrotizing factor alpha and albumin, as well as a down‐regulation of immunoglobulin A (SIgA) secretion. It has been hypothesized that disgust evolved in animals to clear toxins from the oral cavity by gaping and increased salivary flow. Our data suggest down‐regulated SIgA secretion may be a vestige of this response so as to conserve protein, while the inflammatory reaction may reflect an adaptive response to disease threat, selectively triggered by disgust. The broader implications of these data for a discrete neuro‐gut‐immune axis are examined.
Images and the ethics of inclusion and exclusion: learning through participatory photography in education
Authors: Kaplan Ian , Miles Susie , Howes Andy 
Published: December 2010

Participatory research methods directly engage with the topics that they set out to address. It is therefore no surprise that participatory research practice on the topic of educational inclusion and exclusion raises ethical issues for the participatory researcher that are themselves about inclusion and exclusion. This paper describes and analyses a pilot postgraduate course on the use of participatory photography in this area, and uses this analysis to illustrate the value of sensitive and reflexive participative research as a powerful educational practice.A multi‐ethnic and multinational group of students attended the course and explored the use of images as a qualitative research tool as a means to further developing their own sociocultural perspectives on inclusion.As a method, participatory photography was able to support students to represent their own perspectives on issues such as inclusion and diversity. Just as importantly, it facilitated inclusive teaching and learning, making it easy for students to take an active role in ongoing evaluation of the course and in devising their own assessment criteria. More significantly still, a deep exploration of practices of inclusion and exclusion was facilitated by the ethical issues that were raised and addressed during the research process.
Methamphetamine oxidatively damages parkin and decreases the activity of 26S proteasomein vivo
Authors: Moszczynska Anna , Yamamoto Bryan K. 
Published: December 2010

J. Neurochem. (2011)116, 1005–1017.AbstractMethamphetamine (METH) is toxic to dopaminergic (DAergic) terminals in animals and humans. An early event in METH neurotoxicity is an oxidative stress followed by damage to proteins and lipids. The removal of damaged proteins is accomplished by the ubiquitin‐proteasome system (UPS) and the impairment of this system can cause neurodegeneration. Whether dysfunction of the UPS contributes to METH toxicity to DAergic terminals has not been determined. The present investigation examined the effects of METH on functions of parkin and proteasome in rat striatal synaptosomes. METH rapidly modified parkin via conjugation with 4‐hydroxy‐2‐nonenal (4‐HNE) to decrease parkin levels and decreased the activity of the 26S proteasome while simultaneously increasing chymotrypsin‐like activity and 20S proteasome levels. Prior injections of vitamin E diminished METH‐induced changes to parkin and the 26S proteasome as well as long‐term decreases in DA and its metabolites’ concentrations in striatal tissue. These results suggest that METH causes lipid peroxidation‐mediated damage to parkin and the 26S proteasome. As the changes in parkin and 26S occur before the sustained deficits in DAergic markers, an early loss of UPS function may be important in mediating the long‐term degeneration of striatal DAergic terminals via toxic accumulation of parkin substrates and damaged proteins.
Relationships between coping, coping resources and quality of life in patients with chronic illness: a pilot study
Authors: Kristofferzon Marja‐Leena , Lindqvist Ragny , Nilsson Annika 
Published: December 2010

Scand J Caring Sci; 2011; 25; 476–483

Relationships between coping, coping resources and quality of life in patients with chronic illness: a pilot study Background:  In Sweden there are approximately about 3500 end‐stage renal disease (ESRD) and 250 000 chronic heart failure (CHF) patients.Objectives:  The original purpose of the study was to determine differences between two groups of patients with chronic illness (ESRD and CHF) regarding the following study variables: coping, sense of coherence (SOC), self‐efficacy and quality of life (QOL). Following this, the aim was to explore the relationships between demographic variables (sex, age, educational level and living area) and QOL as well as between coping, SOC, self‐efficacy and QOL for the combined sample of patients with ESRD and CHF.Methods:  A comparative and correlative design was used with a sample of 100 patients (n = 41 ESRD, n = 59 CHF). The data were collected during 2004, using four standardized questionnaires and regression analyses were conducted.Results:  No significant differences were found between the two groups. Positive correlations were identified between SOC, general self‐efficacy and QOL, whereas negative correlations emerge between emotion‐focused coping, SOC, general self‐efficacy and QOL. SOC, general self‐efficacy and emotion‐focused coping explained 40% of the variance in QOL. Those with low SOC and general self‐efficacy showed negative correlations between emotion‐focused coping and QOL, whereas no such correlations were shown for those with high values on SOC and general self‐efficacy.Conclusions:  The present results on coping and QOL correspond with previous research regarding how other groups with chronic illness handled their daily life. Preliminary results indicate that how individuals tackle their present situation is more important than which chronic illness they have. Women used more emotion‐focused coping than men, which constitute an important finding for further research.
Surgical nurses’ different understandings of their interactions with patients: a phenomenographic study
Authors: Jangland Eva , Larsson Jan , Gunningberg Lena 
Published: December 2010

Scand J Caring Sci; 2011; 25; 533–541

Surgical nurses’ different understandings of their interactions with patients: a phenomenographic study The aim of this study was to identify and describe different ways surgical nurses understand their roles and interactions with patients and their families in a surgical care setting. The surgical nurse has an important role in supporting and encouraging the patient during the hospital stay. It can be a challenge for the nurse to quickly establish a trustful relationship with the patient. The assumption is that nurses’ interactions with patients are affected by their understanding and expectations of the roles in the nurse–patient relationship. A qualitative interview approach was used and the interviews were analysed using the phenomenographic method. A strategic sample of 17 registered nurses in two hospitals in Sweden was interviewed. In the analysis four ways of understanding the nurse’s role in interactions with the patient were identified: (A) Focusing on medical treatment, following prescribed instructions, and maintaining routines; (B) Providing information, giving service, and coordinating care and treatment; (C) Seeing patients as vulnerable people and helping and supporting them as individuals; and (D) Inviting patients to participate in the caring process and encouraging them to take responsibility in their own care. Seeing each patient as a person with individual needs and personal resources. The first way of understanding, A, focuses on the work task; the other three understandings focus on the patients, but differ in how the nurses see them as people. Understanding A represents a restricted and task‐oriented approach, whereas the others are more patient‐focused, but also more complex. To realise patient‐centred care, nurses should pay attention to all aspects of the interaction. Nurses need to have time at ward meetings or in supervision to discuss and become aware of different ways of understanding their interactions and relationships with patients. In this way new areas of professional development may be opened up.
“Jasper’s Basic Mechanisms of the Epilepsies” Workshop
Authors: Noebels Jeffrey L. , Avoli Massimo , Rogawski Michael , Olsen Richard , Delgado‐Escueta Antonio V. 
Published: December 2010

SummaryIn 1969, H.H. Jasper, A.A. Ward, and A. Pope and the Public Health Service Advisory Committee on the Epilepsies of the National Institutes of Health (NIH) published the first edition on Basic Mechanisms of the Epilepsies (BME). Since then, basic and clinical researchers in epilepsy have gathered together each decade to assess where epilepsy research has been, what it has accomplished, and where it should go. In 1999, the third edition of BME was named in honor of H.H. Jasper. Projected for publication in 2011, the fourth edition of Jasper’s BME will (1) synthesize the role of interactions between neurons, synapses, and glia in the initiation, spread, and arrest of seizures; (2) examine the molecular, cellular, and network plasticity mechanisms that subserve excitability, seizure susceptibility, and ultimately epileptogenesis; (3) provide a framework for expanding the genome of rare mendelian epilepsies and understanding the complex heredity responsible for common epilepsies; (4) explore cellular mechanisms of the two main groups of presently known Mendelian epilepsy genes, namely ion channelopathies and developmental epilepsy genes; and (5) for the first time, describe the current efforts to translate the discoveries in epilepsy disease mechanisms into molecular and cellular therapeutic strategies in order to repair and cure the epilepsies. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Voltage‐gated Na+ channels and epilepsy
Authors: Mantegazza Massimo , Catterall William A. 
Published: December 2010

SummaryVoltage‐gated Na+ (NaV) channels are key mediators of neuronal function and essential for neuronal excitability. Their abnormal activity is implicated in the generation of seizures, both in acquired and genetic epilepsy. Several of the most widely used antiepileptic drugs inhibit NaV activity by binding to a common receptor site. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Phasic GABAA‐mediated inhibition
Authors: Cherubini Enrico 
Published: December 2010

Summaryγ‐Aminobutyric acid (GABA) is the main inhibitory transmitter in the central nervous system (CNS) and regulates via GABAA receptors tonic and phasic inhibition. This review focuses on the sequential steps leading to phasic inhibition, including vesicle exocytosis, dynamics of GABA transient in the synaptic cleft, binding to GABAA receptors, opening of anionic channels, and neurotransmitter clearance. For an expanded treatment of this topic see Cherubini E. in Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds), published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Tonic GABAA receptor–mediated signaling
Authors: Kullmann Dimitri M. , Walker Matthew C. 
Published: December 2010

Summaryγ‐Aminobutyric acid (GABA) mediates both fast synaptic inhibition and a tonic form of signaling that depends on high‐affinity, extrasynaptic GABAA receptors. Tonic inhibition may contribute to the generation of spike‐wave discharges. Because they have a profound effect on circuit excitability, tonically active GABAA receptors represent an important therapeutic target. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Glutamatergic mechanisms related to epilepsy: Ionotropic receptors
Authors: Dingledine Raymond 
Published: December 2010

SummaryGlutamate receptor channels mediate transmission at most excitatory synapses throughout the brain, and are thus essential for seizure propagation. Calcium entry through N‐methyl‐d‐aspartate (NMDA) and possibly kainate receptors also triggers many plastic changes that contribute to epileptogenesis. Glutamate receptor structure and function are reviewed in the context of epilepsy. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Neocortical synchronization
Authors: Timofeev Igor , Bazhenov Maksim , Seigneur Joseé , Sejnowski Terrence 
Published: December 2010

SummaryNeuronal synchronization occurs when two or more neuronal events are coordinated across time. Local synchronization produces field potentials. Long‐range synchronization between distant brain sites contributes to the electroencephalogram. Neuronal synchronization depends on synaptic (chemical/electrical), ephaptic, and extracellular interactions. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Neuronal network synchronization and limbic seizures
Authors: Jefferys John G.R. , de Curtis Marco , Avoli Massimo 
Published: December 2010

SummarySeizure discharges involving hippocampus and parahippocampal structures are the hallmark of temporal lobe epilepsy (TLE). Herein we discuss neuronal synchronization in limbic networks from control and epileptic brains under conditions that are inductive for the generation of seizure‐like discharges. In particular, we address the paradoxic role played by inhibitory mechanisms in supporting epileptiform hypersynchrony. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Interictal epileptiform discharges in partial epilepsy: Neurobiologic mechanisms based on clinical and experimental evidence
Authors: de Curtis Marco , Avoli Massimo 
Published: December 2010

SummaryRecent evidence in humans and in experimental animal models indicates that epileptiform interictal events in partial epileptic disorders show a variety of different features. Cellular, network, and pharmacologic mechanisms that underlie interictal events are here reviewed, with particular attention to their relation with ictal activity. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Mechanisms of excitability in the thalamocortical circuit
Authors: Huguenard John 
Published: December 2010

SummaryThe thalamocortical system consists of widespread excitatory connections between cortical and subcortical structures. Synaptic excitation and inhibition play subcircuit‐specific roles in its function. Generalized absence seizures result from either increased/decreased inhibition or excitation, depending on the subcircuit, yet a common feature of absence seizures in thalamus is net increased inhibition, with therapeutic implications. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Brainstem networks: Reticulocortical synchronization
Authors: Faingold Carl L. 
Published: December 2010

SummaryThe brainstem reticular formation (BRF) is important in generalized tonic–clonic convulsive seizures (GTCS). Audiogenic kindling (AK) in genetically epilepsy‐prone rats (GEPR‐9s) induces seizures closely mimicking GTCS. Unkindled GEPR‐9 seizure network requires only brainstem nuclei. After AK, the seizure network permanently expands into forebrain, involving N‐methyl‐d‐aspartate (NMDA) receptor–mediated cAMP changes in amygdala. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
On the basic mechanisms of infantile spasms
Authors: Swann John W. , Moshe Solomon L. 
Published: December 2010

SummaryThe neurobiologic basis for infantile spasms has long been debated but with little resolution. The very recent development of several animal models of this disorder should provide a paradigm shift in our understanding of this disorder. This chapter outlines unresolved questions and suggests experimental approaches to answering them. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Epileptic fast oscillations and synchrony in vitro
Authors: Traub Roger D. , Whittington Miles A. , Cunningham Mark O. 
Published: December 2010

SummaryVery fast oscillations (VFOs; >70–80 Hz) precede and superimpose upon electrographic seizures. Knowing the cellular mechanisms of VFOs may offer clues to therapy. In vitro models, and ultrastructural and network modeling data, suggest that VFOs are generated by electrical coupling between principal neurons, and that VFOs are favored by the suppression of chemical neurotransmission. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Computer modeling of epilepsy
Authors: Case Marianne J. , Morgan Rob J. , Schneider Calvin J. , Soltesz Ivan 
Published: December 2010

SummaryThis chapter reviews current computational models and proposes future directions for computational modeling in the field of epilepsy. The models include single cells with mutated ion channels; small‐ and large‐scale networks of detailed cells; and macroscopic, mean‐field models of network dynamics. In addition, we consider the potential therapeutic applications of modeling. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AC, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Epileptogenesis in the immature brain: Neonatal seizures in hypoxic/ischemic encephalopathy
Authors: Jensen Frances E. 
Published: December 2010

SummaryNeonatal hypoxic/ischemic encephalopathy is the most common cause of neonatal seizures, and these seizures are refractory to conventional antiseizure drugs and can lead to later life epilepsy and congitive deficits. Data from human tissue studies as well as rodent models suggest unique age‐specific mechanisms underlying these neonatal seizure and their consequences, and are leading to a number of new therapeutic targets. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AC, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Role of blood–brain barrier injury in epileptogenesis
Authors: Friedman Alon , Heinemann Uwe 
Published: December 2010

SummaryEpilepsy is common following various brain insults. We review experimental and clinical data supporting the involvement of a primary blood–brain barrier (BBB) injury in seizures and epileptogenesis. These data point to novel signaling cascades, which may offer new therapeutic targets for the prevention and treatment of epilepsy. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).