bluuebunny/crossref_metadata_2025_split huggingface dataset:
RENAL nephrometry score predicts surgical outcomes of laparoscopic partial nephrectomy
Authors: Hayn Matthew H. , Schwaab Thomas , Underwood Willie , Kim Hyung L. 
Published: December 2010

Study Type – Therapy (case series)Level of Evidence 4What’s known on the subject? and What does the study add?For small renal tumours, partial nephrectomy provides excellent cancer control and preserves renal function. The RENAL Nephrometry Score is useful for quantifying anatomic features relevant to surgical decision‐making.In patients undergoing laparoscopic partial nephrectomy, this study shows a correlation between RENAL Nephrometry Score and estimated blood loss, warm ischemia time, and length of hospital stay, suggesting that the RENAL Nephrometry Score may be useful for predicting the technical challenge posed by a renal tumour.OBJECTIVE• To assess the use of the RENAL Nephrometry Score (RNS), which has been proposed as an anatomical classification system for renal masses, aiming to predict surgical outcomes for patients undergoing laparoscopic partial nephrectomy (LPN).MATERIALS AND METHODS• In the present study, 159 consecutive patients who underwent LPN were reviewed and RNS was calculated for 141 patients with solitary renal masses who had complete radiographic data.• Renal tumours were categorized by RNS as low (nephrometry sum 4–6), intermediate (sum 7–9) and high (sum 10–12).RESULTS• Of the 141 patients, there were 43 (30%) low, 91 (65%) intermediate and seven (5%) high score lesions. There was no statistically significant difference in the demographics of the three groups.• There was a significant difference in warm ischaemia time (16 vs 23 vs 31 min; P < 0.001), estimated blood loss (163 vs 312 vs 317 mL; P= 0.034) and length of hospital stay (1.2 vs 1.9 vs 2.3 days; P < 0.001) between the low, intermediate and high score groups, respectively. There was no difference in overall operative time (P= 0.862), transfusion rate (P= 0.665), complication rate (P= 0.419), preoperative creatinine clearance (P= 0.888) or postoperative creatinine clearance (P= 0.473) between the groups.• Sixty‐one lesions (43%) were anterior and 80 (57%) were posterior. No difference was found among any intra‐operative, pathological or postoperative outcomes when comparing anterior vs posterior lesions.CONCLUSIONS• In patients undergoing LPN, a higher RNS was significantly associated with an increased estimated blood loss, warm ischaemia time and length of hospital stay.• The RNS may stratify tumours based on the technical difficulty of performing LPN.
Local recurrence after tumour enucleation for renal cell carcinoma with no ablation of the tumour bed: results of a prospective single‐centre study
Authors: Minervini Andrea , Serni Sergio , Tuccio Agostino , Raspollini Maria Rosaria , Di Cristofano Claudio , Siena Giampaolo , Vittori Gianni , Saleh Omar , Lapini Alberto , Carini Marco 
Published: December 2010

Study Type – Therapy (individual cohort)  Level of Evidence 2b What’s known on the subject? and What does the study add? Tumour enucleation was demonstrated to be an oncologically safe conservative treatment for small renal masses in agreement with the EAU guidelines. Nevertheless, the theoretical increased risk of positive surgical margins and local recurrence, led some authors to hypothesize a possible key role of laser or diathermy ablation of the tumour bed to free the kidney parenchyma from any tumour cells that extended in the kidney parenchyma.Our pathological and clinical results showed that tumour enucleation with no ablation of the tumour bed (e.g. diathermy, argon beam or Nd‐YAG laser) can ensure negative surgical margins and it is not associated with an increased risk of local recurrence.OBJECTIVE

To prospectively evaluate the risk of positive surgical margins and local recurrence after blunt tumour enucleation (TE) with no ablation of the tumour bed.

PATIENTS AND METHODS

Between 2005 and 2007, data were gathered prospectively from 201 consecutive patients who had open TE with no ablation of the tumour bed.
Overall, 164 consecutive patients had TE for single sporadic renal cell carcinoma (RCC).
All patients had an abdominal computed tomography (CT) at the last follow‐up visit.

RESULTS

The pathological review showed that 70.2% of tumours were pT1a, 18.9% were pT1b, 1.8% were pT2 and 9.1% were pT3a.
The mean (range, interquartile range) tumour greatest dimension was 3.5 (0.5–12.5, 2.4–4.1) cm.
Although no deliberate attempt to resect normal parenchyma was performed, the pathological analysis showed the presence of a thin layer of parenchyma with a mean (range) thickness of 0.97 (0.31–1.60) mm, around the tumour. None of the patients had positive surgical margins.
At a mean (median, range) follow up of 40 (38, 25–62) months, three (1.8%) patients had local recurrence, of whom one (0.6%) had a true local recurrence at the enucleation site detected 35 months after surgery, while two had kidney recurrence elsewhere associated with concurrent systemic metastases diagnosed 16 and 13 months after surgery.

CONCLUSIONS

TE with no ablation of the tumour bed is a safe technique with a local recurrence rate of 0.6%.
The histopathological analysis showed the presence of a minimal tumour‐free surgical margin, although no deliberate attempt to resect normal parenchyma is performed.
Exploring the perceptual spaces of faces, cars and birds in children and adults
Authors: Tanaka James W. , Meixner Tamara L. , Kantner Justin 
Published: December 2010

AbstractWhile much developmental research has focused on the strategies that children employ to recognize faces, less is known about the principles governing the organization of face exemplars in perceptual memory. In this study, we tested a novel, child‐friendly paradigm for investigating the organization of face, bird and car exemplars. Children ages 3–4, 5–6, 7–8, 9–10, 11–12 and adults were presented with 50/50 morphs of typical and atypical face, bird and car parent images. Participants were asked to judge whether the 50/50 morph more strongly resembled the typical or the atypical parent image. Young and older children and adults showed a systematic bias to the atypical faces and birds, but no bias toward the atypical cars. Collectively, these findings argue that by the age of 3, children encode and organize faces, birds and cars in a perceptual space that is strikingly similar to that of adults. Category organization for both children and adults follows Krumhansl’s (1978) distance‐density principle in which the similarity between two exemplars is jointly determined by their physical appearance and the density of neighboring exemplars in the perceptual space.
Ferrans and Powers’ Quality of life index applied in urinary incontinence research – a pilot study
Authors: Rannestad Toril , Skjeldestad Finn Egil 
Published: December 2010

Scand J Caring Sci; 2011; 25; 410–416

Ferrans and Powers’ Quality of life index applied in urinary incontinence research – a pilot study Background:  The aim of this study was to explore the usefulness of applying a global, evaluation‐based quality of life (QoL) questionnaire in assessing the impact of urinary incontinence (UI) on women’s lives.Methods:  The study population comprised long‐term gynaecological cancer survivors (n = 160) and controls from the general population (n = 493). The presence of UI was assessed by the question ‘Do you leak urine?’ while UI perceived as a problem was assessed on a five‐point scale from ‘No problem’ to ‘A very large problem’. QoL was measured by Ferrans & Powers’ QoL index (QLI), generic version II.Results:  UI was distributed equally among women with a history of gynaecological cancer and among women from the general population (34%). UI has a negative impact on overall QLI as well as a wide range of items. Approximately 20% of the incontinent women defined UI as no problem, with QLI scores similar to continent women. Only 5% experienced UI as a large/very large problem; with exceptionally low QLI scores. The psychometric testing of QLI (acceptability, internal consistency reliability and known‐group validity) supports the use of QLI in UI‐studies.Conclusions:  The Ferrans & Powers’ QLI is considered an acceptable tool for UI research, but further psychometric testing is required.
Large‐Sample Evidence on Firms’ Year‐over‐Year MD&A Modifications
Authors: BROWN STEPHEN V. , TUCKER JENNIFER WU 
Published: December 2010

ABSTRACTThe Securities and Exchange Commission (SEC) has expressed concern about the informativeness of firms’ Management Discussion and Analysis (MD&A) disclosures. A firm's MD&A is potentially uninformative if it does not change appreciably from the previous year after significant economic changes at the firm. We introduce a measure for narrative disclosure—the degree to which the MD&A differs from the previous disclosure—and provide three findings on the usefulness of MD&A disclosure. First, firms with larger economic changes modify the MD&A more than those with smaller economic changes. Second, the magnitude of stock price responses to 10‐K filings is positively associated with the MD&A modification score, but analyst earnings forecast revisions are unassociated with the score, suggesting that investors—but not analysts—use MD&A information. Finally, MD&A modification scores have declined in the past decade even as MD&A disclosures have become longer; the price reaction to MD&A modification scores has also weakened, suggesting a decline in MD&A usefulness.
HCN channelopathy in epilepsy
Authors: Poolos Nicholas P. 
Published: December 2010

SummaryHyperpolarization‐activated, cyclic nucleotide‐gated (HCN) channels are voltage‐gated ion channels that influence neuronal excitability in brain regions implicated in both focal and generalized epilepsies. Dysregulation of HCN channel function occurs in many animal models of epilepsy; understanding HCN channel regulation may lead to novel therapies for the prevention and treatment of human 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).
Imaging of hippocampal circuits in epilepsy
Authors: Takano Hajime , Coulter Douglas A. 
Published: December 2010

SummarySeizures and epilepsy are fundamentally neuronal circuit phenomena. This article describes the development and application of multiple dynamic imaging techniques that, in combination, facilitate the elucidation of hippocampal circuit function in animal models of epilepsy. This combined approach has significant promise in furthering our understanding of the mechanisms underlying 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 posttraumatic epileptogenesis
Authors: Prince David A. , Parada Isabel , Li Huifang , McDonald Whitney , Graber Kevin 
Published: December 2010

SummaryDevelopment of new excitatory connectivity and decreases in γ‐aminobutyric acid (GABA)ergic inhibition are mechanisms underlying posttraumatic epileptogenesis in animal models. Experimental strategies that interfere with these processes, applied between the trauma and seizure onset, are antiepileptogenic in the laboratory, and have promise for prophylaxis of epileptogenesis after cortical injury in humans. 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) National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Head trauma and epilepsy
Authors: Pitkänen Asla , Bolkvadze Tamuna 
Published: December 2010

SummaryPosttraumatic epilepsy (PTE) is defined as a recurrent seizure disorder due to injury to the brain following head trauma. Traumatic brain injury (TBI) accounts for 20% of symptomatic epilepsy in the general population and 5% of all epilepsy. Prevention or suppression of the development of PTE is a major unmet challenge in medicine. 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).
Fever, febrile seizures, and epileptogenesis
Authors: Dubé Céline M. , McClelland Shawn , Choy ManKin , Brewster Amy L. , Noam Yoav , Baram Tallie Z. 
Published: December 2010

SummaryFebrile seizures (FS) are common and are associated with increased probability of temporal lobe epilepsy (TLE). However, whether FS can provoke TLE in the nonpredisposed brain is unknown. Using an immature rat model, we established that long FS cause TLE, and that duration of FS governed the severity of epilepsy. Epileptogenesis was accompanied, perhaps causally, by ion channel dysfunction and inflammatory changes. Because FS are a prevalent antecedent of TLE, studying the epileptogenesis that follows them provides powerful insight and potential therapies for 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 AC, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Alterations in synaptic function in epilepsy
Authors: Bernard Christophe 
Published: December 2010

SummaryEpilepsy often results from a brain insult. Herein, I describe the complex time‐dependent alterations in glutamatergic and γ‐aminobutyric acid (GABA)ergic circuitry triggered by the initial insult. I will relate these modifications to the occurrence of the first spontaneous seizure, the development of epileptogenic networks, and associated cognitive deficits. 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 alcohol withdrawal
Authors: Olsen Richard W. , Spigelman Igor 
Published: December 2010

SummaryChronic intermittent ethanol (CIE) treatment and withdrawal in rats produces behavioral changes that models human alcohol dependence, including increased seizure susceptibility, and can be explained by plastic changes in inhibitory neurotransmission involving γ‐aminobutyric acid (GABA)A receptors. 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).
Chloride homeostasis and GABA signaling in temporal lobe epilepsy
Authors: Kaila Kai , Miles Richard 
Published: December 2010

SummaryTwo electron‐neutral, cation‐chloride cotransporters control intraneuronal chloride ion concentration (Cl−). The Na‐K‐2Cl cotransporter‐1 mediates Cl− influx while the K‐Cl cotransporter‐2 (KCC2) extrudes Cl−, assuring that γ‐aminobutyric acid (GABA)ergic signals hyperpolarize neurons. KCC2 is downregulated in pyramidal cells from human temporal lobe epilepsy and experimental focal epilepsy, inducing a depolarizing shift in response to GABA. 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).
Glia–neuron interactions: Neurosteroids
Authors: Biagini Giuseppe , Avoli Massimo 
Published: December 2010

SummaryGlial cells have both beneficial and detrimental effects on recovery from brain damage and play a role in epileptogenesis. Herein, we summarize evidence indicating that the ability of astrocytes to produce neurosteroids that reinforce γ‐aminobutyric acid receptor A (GABAA) functions impinge on epileptogenesis, as shown in temporal lobe epilepsy models. 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).
Na+ channel mutations and epilepsy
Authors: Catterall William A. 
Published: December 2010

SummaryVoltage‐gated Na+ channels are the molecular targets for mutations that cause several epilepsy syndromes. Mutations that impair the function of NaV1.1 channels cause reduced Na+ currents and failure of electrical excitability in γγ‐aminobutyric acid (GABA)ergic interneurons, providing a potential mechanism for hyperexcitability in a spectrum of Na+ channel epilepsy syndromes. 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 calcium channel mutations andabsence epilepsy
Authors: Noebels Jeffrey L. 
Published: December 2010

SummarySpontaneous mutation of the gene encoding theP/Q voltage‐gated calcium ion channel alpha subunit proved to be the first identified cause of absence epilepsy, and subsequent exploration of other members within this gene family has had a major impact on our understanding of how inherited errors of single genes lead to specific epileptic phenotypes. 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 GABAAγ2(R43Q) mouse model of humangenetic epilepsy
Authors: Petrou Steven 
Published: December 2010

Summaryγ‐Aminobutyric acid (GABA)A receptors mediate phasic and tonic inhibition in the brain, and epilepsy‐associated mutations are found in GABAA genes. This chapter discusses a mouse model of human genetic epilepsy and how it has informed our understanding of the role of GABAA receptor dysfunction in patients. 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).
Genetic epilepsies and GABAA receptor mutations
Authors: Macdonald Robert L. , Kang Jing‐Qiong , Gallagher Martin J. 
Published: December 2010

SummaryIdiopathic generalized epilepsy (IGE) syndromes are associated with ion channel gene mutations including GABAA receptor subunit gene (GABR) mutations. GABAA receptors are the primary mediators of central nervous system (CNS) inhibitory synaptic transmission, and GABR mutations have been shown to produce GABAergic disinhibition by altering GABAA receptor function and/or impairing receptor biogenesis. 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).
Aristaless‐related homeobox mutations
Authors: Marsh Eric D. , Golden Jeffrey A. 
Published: December 2010

SummaryMutations in the Aristaless‐related homeobox gene (ARX) are linked to infantile spasms and other developmental epilepsies. How loss of Arx leads to epilepsy is not well understood. This review will discuss the spectrum of Arx disorders and the emerging evidence, from animal models, of the function of Arx during development and the potential role in generating an epilepsy phenotype. 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).
Myoclonin1/EFHC1 disease mechanisms in JME
Authors: Grisar Thierry , LoTurco Joseph , Daga Andrea , Delgado‐Escueta Antonio V. 
Published: December 2010

Summary Myoclonin1/EFHC1 mutations cause 9% of juvenile myoclonic epilepsy (JME) by impairing apoptosis in neurons/synapses where R type voltage dependent calcium channel function is altered, imbuing susceptibility to myoclonic and grand mal seizures. By disrupting mitotic spindle assembly and radial migration of neuroblasts, mutations could produce abnormal intracortical architecture upon which epileptogenesis is established. 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).
Unverricht‐Lundborg disease and ceroid lipofuscinoses
Authors: Lehesjoki Anna‐Elina , Gardiner Richard Mark 
Published: December 2010

SummaryUnverricht‐Lundborg disease is a neurodegenerative disorder characterized by stimulus‐sensitive myoclonus, epileptic seizures, and ataxia. It is associated with mutations in the Cystatin B gene. The neuronal ceroid lipofuscinoses are a heterogeneous group of disorders characterized by the intracellular accumulation of autofluorescent lipopigment. Mutations in eight genes have been identified. 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).
Migraine and epilepsy: Shared mechanisms?
Authors: Rogawski Michael A. 
Published: December 2010

SummaryMigraine and epilepsy are comorbid conditions that have many clinical similarities. There are also cellular physiologic similarities, and some antiepileptic drugs are prophylactic in migraine, suggesting common pathophysiologic elements. The most compelling evidence comes from familial hemiplegic migraine, in which migraine and epilepsy can be caused by mutations in the same gene. 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).
Targeting SV2A for discovery of antiepileptic drugs
Authors: Kaminski Rafal M. , Gillard Michel , Klitgaard Henrik 
Published: December 2010

SummaryLevetiracetam’s (Keppra) binding site and its subsequent identification as the synaptic vesicle protein 2A (SV2A) enabled the discovery of high affinity SV2A ligands with promising anticonvulsant properties. Among these, brivaracetam was selected for further development. SV2A represents an important antiepileptic drug target validated in both preclinical and clinical studies. 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).