bluuebunny/crossref_metadata_2025 huggingface dataset:
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.
Bodies, bombs and barricades: geographies of conflict and civilian (in)security
Authors: Fluri Jennifer L
Published: December 2010

This article critically examines the entanglements between ‘security’ and the geopolitical and geo‐economic formations that assist in the cyclical continuation of conflict. The author questions the biopolitical configurations of state and private forms of militarised security. The author’s approach to this research addresses the spatial and corporeal aspects of civilian security in contemporary conflicts zones – with a specific focus on Afghanistan. Drawing on the work of feminist political geographers, this article highlights the corporeal as a key site of analysis for the everyday and seemingly apolitical spaces occupied by civilians living amidst political conflict. This descriptive analysis of security and insecurity focuses on four specific areas: (1) Afghan civilian security measures, (2) domestic spaces as sites of security and violence, (3) mobile forms of security and insecurity and (4) the divergent perceptions and experiences of security/insecurity between international civilian workers living in Afghanistan and Afghan civilian citizens. While macro‐scale analyses of security and civilian agency in various locations are important for geographic inquiry, it remains imperative that geographers and other social scientists examine the particularities of specific conflict sites and situations in order to avoid one‐size‐fits‐all responses to or analyses of political conflict – and subsequently flattening civilian experiences through aggregated forms of knowledge production. This paper seeks to investigate several key aspects of feminist political geography by examining the multiple and varied experiences of the everyday within this conflict zone.
“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

In 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

Voltage‐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

γ‐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

γ‐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

Glutamate 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

Neuronal 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

Seizure 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

Recent 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

The 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

The 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

The 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

Very 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

This 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

Neonatal 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

Epilepsy 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).
Cell death after single and repeated brief seizures
Authors: Henshall David C. , Meldrum Brian S.
Published: December 2010

We review the experimental evidence from animal models that suggest that brief, evoked seizures can result in neuronal death while spontaneous seizures normally do not, as well as human data showing damage may progress in certain patients, and we describe the cell death and survival pathways regulating these processes. 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).
Circuit mechanisms of acquired epileptogenesis
Authors: Dudek F. Edward , Staley Kevin J.
Published: December 2010

The time course of development of spontaneous recurrent seizures is a sigmoid function of time after status epilepticus or perinatal stroke, which reflects underlying mechanisms of epileptogenesis. The increase in recurrent excitation after axon sprouting, along with death of specific γγ‐aminobutyric acid (GABA)ergic interneurons, may contribute to this temporal pattern of epileptogenesis. 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).
Abnormal dentate gyrus network circuitry in temporal lobe epilepsy
Authors: Sloviter Robert S. , Bumanglag Argyle V. , Schwarcz Robert , Frotscher Michael
Published: December 2010

Patients with temporal lobe epilepsy exhibit developmental and acquired hippocampal abnormalities that include abnormally developed structure, neuron loss, aberrant neurogenesis, synaptic reorganization, granule cell dispersion, and gliosis. Determining which features play causal roles in epileptogenesis, and which features affect other aspects of the disorder, is a central challenge of epilepsy research. 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).
Seizure‐induced basal dendrites on granule cells
Authors: Ribak Charles E. , Shapiro Lee A. , Yan Xiao‐Xin , Dashtipour Khashayar , Nadler J. Victor , Obenaus Andre , Spigelman Igor , Buckmaster Paul S.
Published: December 2010

Seizure‐induced hilar basal dendrites on dentate granule cells are observed in several rodent models of temporal lobe epilepsy. Ultrastructural evidence showed that basal dendrites receive predominantly excitatory synapses, including many from mossy fibers. Such highly interconnected granule cells with basal dendrites are suggested to enhance hyperexcitability within the dentate network. 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).
Neurogenesis and epilepsy
Authors: Parent Jack M. , Kron Michelle M.
Published: December 2010

Persistent neural stem cells generate dentate granule cells (DGCs) throughout life. Evidence suggests that aberrant neurogenesis contributes to epileptic structural abnormalities, but that normally integrating adult‐born DGCs may restore inhibition. Current research focuses on how epileptogenic insults alter neurogenesis, and whether restoring normal neurogenesis will attenuate epilepsy or its comorbidities. 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).
Temporal lobe epilepsy and the BDNF receptor, TrkB
Authors: McNamara James O. , Scharfman Helen E.
Published: December 2010

Brain derived neurotrophic factor (BDNF) regulates diverse neuronal functions and plasticity, and its expression is increased by seizures. Here we review the evidence that actions of BDNF at TrkB receptors contribute to temporal lobe epilepsy. In addition, regulation of BDNF by steroid hormones might explain syndromes such as catamenial 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).
GABAA receptor plasticity in status epilepticus
Authors: Joshi Suchitra , Kapur Jaideep
Published: December 2010

Seizures become self‐sustaining during status epilepticus (SE) in part due to altered inhibitory neurotransmission mediated by γ‐aminobutyric acid (GABAA) receptors (GABAARs). This chapter reviews mechanisms of altered GABAAR function during SE. 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).
Plasticity of GABAA receptors relevant toneurosteroid actions
Authors: Mody Istvan
Published: December 2010

It is now widely accepted that phasic (synaptic) and tonic (extrasynaptic) γ‐aminobutyric acid (GABA)ergic influences on neuronal excitability are mediated by different receptors with different pharmacologic profiles. This article focuses on the plasticity of the neurosteroid‐sensitive δ subunit containing GABAA receptors(δ‐GABAARs) in animal models of temporal lobe epilepsies (TLEs) and its possible consequences for modulating the excitability of the dentate gyrus. 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).
Regulation of GABAA receptor gene expression and epilepsy
Authors: Brooks‐Kayal Amy R. , Russek Shelley J.
Published: December 2010

Although multiple genes drive epileptogenesis, uncovering the mechanisms controlling expression of GABAA receptors (GABAARs), the brain’s major inhibitory receptors, may have far‐reaching therapeutic implications. In this review, we describe how seizure‐induced changes in GABAARs result from brain‐derived neurotrophic factor (BDNF)‐induced changes in Janus kinase/Signal Transducer and Activators of Transcription (JAK/STAT), cAMP response element binding protein/inducible cAMP early repressor (CREB/ICER), and early growth factor (Egr3) signaling, and discuss implications for prevention and treatment. 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).
Study of the genetically complex epilepsies
Authors: Ottman Ruth , Risch Neil
Published: December 2010

Identifying the genes that influence risk for genetically complex epilepsies is a major challenge for the next decade. This chapter reviews possible biologic mechanisms, methodologic approaches, and findings from recent studies aimed at gene identification in complex epilepsies, and approaches for clarifying phenotype definition for genetic research on 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).
Potassium channelopathies of epilepsy
Authors: Brenner Robert , Wilcox Karen S.
Published: December 2010

The potassium channel family represents a large group with diverse functional roles. Not surprisingly, the list of potassium channelopathies contributing to human epilepsy has greatly expanded. The focus of this chapter will be the causative role in epilepsy of mutations in potassium channels and associated regulatory proteins. 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).
Nicotinic acetylcholine receptor mutations
Authors: Steinlein Ortrud K. , Kaneko Sunao , Hirose Shinichi
Published: December 2010

Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is characterized by clusters of brief motor seizures. This rare syndrome is caused by mutations in at least two subunit genes of the neuronal nicotinic acetylcholine receptor (nAChR). Some of these mutations seem to increase the risk for additional neurologic symptoms. 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).
Gene interactions and modifiers in epilepsy
Authors: Meisler Miriam H.
Published: December 2010

The onset, progression, and severity of epilepsy vary between family members with identical mutations in primary disease genes. The background of genetic variation unique to each individual genome contributes to clinical variation. Known examples of gene interactions in human families and mouse models provide insight into underlying molecular mechanisms. 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).
Rare genetic causes of lissencephaly may implicate microtubule‐based transport in the pathogenesis of cortical dysplasias
Authors: Liu Judy S. , Walsh Christopher A.
Published: December 2010

The causative genes for lissencephaly—including LIS1, DCX, and TUBA1A—highlight the importance of a microtubule‐based transport pathway in cortical development and potentially in pathogenesis of focal cortical dysplasias. 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).
The generation of cortical interneurons
Authors: Rubenstein John L.R.
Published: December 2010

The developmental origins of cortical and hippocampal interneurons in the rodent are discussed, in addition to a description of the transcriptional mechanisms that control their specification and differentiation. 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).
Genes in infantile epileptic encephalopathies
Authors: Depienne Christel , Gourfinkel‐An Isabelle , Baulac Stéphanie , LeGuern Eric
Published: December 2010

Patients with infantile epileptic encephalopathies are often isolated cases with or without a limited familial history of epilepsy, suggesting a complex mode of inheritance. However, recent data, for example regarding Dravet syndrome, show that these sporadic rare diseases can result from a monogenic cause. 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).
Haploinsufficiency of STXBP1 and Ohtahara syndrome
Authors: Saitsu Hirotomo , Kato Mitsuhiro , Matsumoto Naomichi
Published: December 2010

Ohtahara syndrome (OS) is one of the most severe and earliest forms of epilepsy. De novo heterozygous mutations and a microdeletion of STXBP1 have been found in individuals with OS. STXBP1 encodes MUNC18‐1, which is essential in synaptic vesicle release, highlighting aberration of synaptic vesicle release in pathogenesis 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).
mTOR and epileptogenesis in developmental brain malformations
Authors: Wong Michael , Crino Peter B.
Published: December 2010

Tuberous sclerosis complex and related malformations of cortical development represent common developmental causes of intractable epilepsy. Abnormalities in the mammalian target of rapamycin pathway may be central to the pathophysiology of epilepsy and other neurologic deficits in these disorders and serve as a rational target for antiepileptogenic or disease‐modifying therapies. 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).
ELP4 in rolandic epilepsy and BRD2 in juvenile myoclonic epilepsy
Authors: Pal Deb K. , Strug Lisa J. , Veliskova Jana , Chachua Tamar , Velisek Libor , Greenberg David A.
Published: December 2010

The common forms of idiopathic epilepsies have complex genetic inheritance and are likely to include genes in biologic pathways other than “channelopathies,” the most frequent cause of their rare Mendelian counterparts. Recent analyses of ELP4 and BRD2 indicate that subtle genetically determined neurodevelopmental deviations may play a part in the pathogenesis of rolandic epilepsy and juvenile myoclonic 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).
Epilepsy in autism spectrum disorders
Authors: Stafstrom Carl E. , Hagerman Paul J. , Pessah Isaac N.
Published: December 2010

Epilepsy occurs frequently in individuals with autism spectrum disorders (ASDs). However, the mechanisms responsible for increased seizure susceptibility in ASDs are largely unknown. Clues to neural hyperexcitability in the autistic brain might be derived from disorders in which single gene mutations cause both epilepsy and an autistic phenotype, such as fragile X syndrome. 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).
Calcium channel α2δ subunits in epilepsy and as targets for antiepileptic drugs
Authors: Dolphin Annette C.
Published: December 2010

The α2δ proteins are auxiliary subunits of voltage‐gated calcium channels, but may also have other functions. Four mammalian α2δ genes have been cloned. There are several links between α2δ proteins and disease, including mice with mutated α2δ‐2, which exhibit spike‐wave epilepsy. Furthermore, the gabapentinoid drugs bind to α2δ‐1 and α2δ‐2. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (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).
Neurosteroids as endogenous regulators of seizure susceptibility and use in the treatment of epilepsy
Authors: Reddy Doodipala S. , Rogawski Michael A.
Published: December 2010

Neurosteroids such as allopregnanolone are positive allosteric modulators of γ‐aminobutyric acid (GABA)A receptors with powerful antiseizure activity in diverse animal models. Neurosteroids may be endogenous regulators of seizure susceptibility, for example, in catamenial epilepsy. Clinical trials with the synthetic neurosteroid analog ganaxolone in the treatment of refractory partial seizures and infantile spasms have been encouraging. Neurosteroids and analogs such as ganaxolone show promise in the treatment of diverse forms of epilepsy. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (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).
Animal models for evaluating antiepileptogenesis
Authors: White H. Steve
Published: December 2010

The development of any new therapy for the treatment of a human disorder or disease depends heavily on the demonstration of efficacy in a validated animal model. The need for finding a therapy that would prevent or delay the development of epilepsy in the susceptible individual is evident, and many of the required tools have been developed in recent years. However, there are many practical challenges and hurdles that must be overcome before a “cure” can be realized. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (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).
A treatment paradigm for neonatal seizures based on the ontogeny of neuronal chloride/cation cotransporter expression in the human cortex
Authors: Kahle Kristopher T. , Staley Kevin J.
Published: December 2010

Neonatal seizures are a common problem inadequately treated with standard γ‐aminobutyric acid (GABA)ergic anticonvulsants. Understanding how the ontogeny of neuronal cation/chloride cotransporter expression renders GABAergic signaling excitatory in the neonatal brain has helped explain the increased seizure propensity and poor efficacy of GABAergic anticonvulsants in newborns, and is the rational underlying the polypharmaceutical approach to treating neonatal seizures with bumetanide and phenobarbital. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (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).
Drug resistance in epilepsy
Authors: Gorter Jan , Potschka Heidrun
Published: December 2010

Drug resistance remains one of the major challenges in epilepsy therapy. Identification of factors that contribute to therapeutic failure is crucial for future development of novel drugs and therapeutic strategies for difficult‐to treat epilepsies. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (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).
Neural stem cell therapy for temporal lobe epilepsy
Authors: Shetty Ashok K.
Published: December 2010

Neural stem cells (NSCs) are one of the candidates for grafting in the realm of cell‐based therapy for temporal lobe epilepsy (TLE). Because NSCs can produce neurons synthesizing the inhibitory neurotransmitter γ‐aminobutyric acid (GABA) and cells secreting multiple neurotrophic factors, NSC grafting therapy has promise for restraining seizures and easing cognitive dysfunction in TLE. 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).
Embryonic stem cell therapy for intractable epilepsy
Authors: Naegele Janice R. , Vemuri Mohan C. , Studer Lorenz
Published: December 2010

Stem cell therapies are envisioned for severe neurologic disorders and intractable epilepsy. Methods to maintain and derive neural cells from embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) are providing insights into human nervous system development from stem cells and the future of stem cell therapy for epilepsy. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (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).
Restarting arrested neurodevelopment
Authors: Manent Jean‐Bernard , LoTurco Joseph J.
Published: December 2010

Malformations of cortical development (MCDs) are common causes of seizures and developmental delay. Although considered to be irreversible, recent observations in animal models suggest that MCDs may remain responsive to corrective manipulations during prolonged time periods after malformations are formed. These findings may change our understanding of MCDs and open new therapeutic avenues. For an expanded treatment of this topic, see Jasper’s basic mechanisms of the epilepsies. 4th ed. (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).
Adenosine augmentation therapy for epilepsy
Authors: Boison Detlev
Published: December 2010

Deficiency of the brain’s endogenous anticonvulsant adenosine is a pathologic hallmark of epilepsy. Consequently, focal adenosine augmentation therapies (AATs) constitute a rational approach for seizure suppression. Focal adenosine augmentation and resulting seizure suppression can be realized by implanting adenosine‐releasing stem cells or polymers into epileptogenic brain regions. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (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).
Detection of human platelet antigen‐1a alloantibodies in cases of fetomaternal alloimmune thrombocytopenia using recombinant β3 integrin fragments coupled to fluorescently labeled beads
Authors: Chong Winnie , Metcalfe Paul , Mushens Rosey , Lucas Geoff , Ouwehand Willem H. , Navarrete Cristina V.
Published: December 2010

BACKGROUND: Testing for alloantibodies against human platelet antigens (HPAs) is essential for the clinical diagnosis of fetomaternal alloimmune thrombocytopenia (FMAIT), posttransfusion purpura, and platelet (PLT) refractoriness. Most of the methods currently used for HPA alloantibody detection rely on the availability of panels of HPA‐typed PLTs and some rely on validated monoclonal antibodies (MoAbs) against the PLT glycoproteins. Recombinant β3 integrins displaying the HPA‐1a (rHPA‐1a) or HPA‐1b (rHPA‐1b) epitopes have been produced as an alternative source of antigen. The suitability of these integrin fragments was evaluated for the development of an HPA‐1a alloantibody screening assay, using Luminex xMAP technology.

STUDY DESIGN AND METHODS: A 3‐plex bead assay was developed by coupling biotinylated rHPA‐1a, rHPA‐1b, and recombinant glycoprotein VI to LumAvidin microspheres. Forty patient samples referred for FMAIT diagnostic testing, which were previously screened by the MoAb‐specific immobilization of PLT antigens (MAIPA) assay, were used to assess the assay.

RESULTS: The rHPA‐1a‐ and rHPA‐1b‐coupled beads were able to detect HPA‐1a and HPA‐1b alloantibodies in all patient samples tested that were previously confirmed to contain HPA‐1‐specific antibodies. Furthermore, HLA Class I antibodies did not cross‐react with the coupled beads.

CONCLUSION: The 3‐plex bead assay can be used to detect HPA‐1a antibodies with sufficient specificity and sensitivity for use in the clinical setting of FMAIT. The development of other recombinant integrin fragments with the use of Luminex xMAP technology may assist in providing more rapid HPA antibody detection, enabling prompt diagnosis of alloimmune PLT disorders.
Emotional Intelligence and Dispute Mediation in Escalating and De‐Escalating Situations
Authors: Boland Michael J. , Ross William H.
Published: December 2010

A scenario‐based laboratory experiment investigated how emotional intelligence (EI) influences informal mediation. A 2 × 2 factorial design varied subjects' EI level (high vs. low) and whether disputant hostility was escalating or de‐escalating. Dependent variables included mediation goals and tactics. Results indicated that high EI mediators were more likely than low EI mediators to pursue the goal of achieving an overall mutually satisfactory agreement. High EI mediators were more likely than low EI mediators to report a willingness to use a larger number of mediation tactics to promote a compromise. By contrast, low EI mediators were more likely to endorse using pressing, compensating, and inaction techniques. Results suggest that individual differences in EI should be considered in future mediation research.
Interactive Effects of Caffeine Consumption and Stressful Circumstances on Components of Stress: Caffeine Makes Men Less, But Women More Effective as Partners Under Stress
Authors: St. Claire Lindsay , Hayward Robert C. , Rogers Peter J.
Published: December 2010

We tested whether increased caffeine consumption exacerbates stress and disrupts team performance, and we explored whether “tend and befriend” characterizes women's coping. We gave decaffeinated coffees, half of which contained added caffeine, to coffee drinkers in same‐sex, same‐aged dyads. We measured individual cognitive appraisals, emotional feelings, bodily symptoms, coping, and performance evaluations, together with dyad memory, psychomotor performance, and negotiation skills under higher or lower stressful conditions. Evidence consistent with the first hypothesis was weak, but we found that women performed better than did men on collaborative tasks under stress, provided caffeine had been consumed. The usefulness of multi component, cognitive‐relational approaches to studying the effects of caffeine on stress is discussed, together with special implications of the effects for men.
Still an American? Mortality Salience and Treatment of Suspected Terrorists
Authors: Kugler Matthew B. , Cooper Joel
Published: December 2010

In today's post‐9/11 world, it is important to consider the psychological factors related to beliefs about the proper treatment of those suspected of terrorist involvement. We report 2 experiments on the impact of mortality salience on people's willingness to deny procedural protections to terror suspects. Reminders of mortality led participants to extend more procedural protections to an American terrorism suspect, but fewer toward a Saudi Arabian. In Study 2, we replicated and extended the results of Study 1 by showing that support of extreme interrogation measures was specific to members of enemy out‐groups (e.g., Saudis), as opposed to non‐enemy out‐groups (e.g., Bulgarians). The results are discussed in terms of terror‐management theory.
The Influence of Emotional Dissonance on Subjective Health and Job Satisfaction: Testing the Stress–Strain–Outcome Model
Authors: Cheung Francis , Tang Catherine
Published: December 2010

We adopted the stress–strain–outcome model (Koeske & Koeske, 1993) to examine the influence of work stressors on subjective health and job satisfaction among Chinese service employees. Two independent studies were reported. In the first study, 271 employees provided cross‐sectional data on work characteristics, emotional dissonance, work strain, and job satisfaction. Structural equation modeling showed that work characteristics were related to emotional dissonance, which, in turn, was associated with work strain, with the latter eventually predicting job satisfaction. Study 2 was a 3‐month longitudinal survey with a separate sample of 155 call‐center and retail‐shop representatives. Longitudinal data showed that emotional dissonance at Time 1 significantly predicted work strain at Time 2, which predicted job satisfaction at Time 2.
Biodiversity influences ecosystem functioning in aquatic angiosperm communities
Authors: Gustafsson Camilla , Boström Christoffer
Published: December 2010

Knowledge of the connection between aquatic plant diversity and ecosystem processes is still limited. To examine how plant species diversity affects primary productivity, plant nutrient use, functional diversity of secondary producers and population/community stability, we manipulated submerged angiosperm species diversity in a field experiment lasting 15 weeks. Plant richness increased the shoot density for three of four species. Polyculture biomass production was enhanced by increasing richness, with positive complementarity and selection effects causing positive biodiversity effects. Species richness enhanced the community stability for biomass production and shoot density. Sediment ammonium availability decreased with plant diversity, suggesting improved nutrient usage with increasing plant richness. Interestingly, positive multitrophic effects of plant species richness on structural and functional diversity of macrobenthic secondary producers were recorded. The results suggest that mixed seagrass meadows play an important role for ecosystem functioning and thus contribute to the provision of goods and services in coastal areas.