bluuebunny/crossref_metadata_2025_split huggingface dataset:
Method to Develop Health Care Peer Groups for Quality and Financial Comparisons Across Hospitals
Authors: Byrne Margaret M. , Daw Christina N. , Nelson Harlan A. , Urech Tracy H. , Pietz Kenneth , Petersen Laura A. 
Published: November 2008

Objective. To develop and explore the characteristics of a novel “nearest neighbor” methodology for creating peer groups for health care facilities.Data Sources. Data were obtained from the Department of Veterans Affairs (VA) databases.Statistical Methods and Findings. Peer groups are developed by first calculating the multidimensional Euclidean distance between each of 133 VA medical centers based on 16 facility characteristics. Each medical center then serves as the center for its own peer group, and the nearest neighbor facilities in terms of Euclidean distance comprise the peer facilities. We explore the attributes and characteristics of the nearest neighbor peer groupings. In addition, we construct standard cluster analysis‐derived peer groups and compare the characteristics of groupings from the two methodologies.Conclusions. The novel peer group methodology presented here results in groups where each medical center is at the center of its own peer group. Possible advantages over other peer group methodologies are that facilities are never on the “edge” of a group and group size—and thus group dispersion—is determined by the researcher. Peer groups with these characteristics may be more appealing to some researchers and administrators than standard cluster analysis and may thus strengthen organizational buy‐in for financial and quality comparisons.
Variation in Drug Prices at Pharmacies: Are Prices Higher in Poorer Areas?
Authors: Gellad Walid F. , Choudhry Niteesh K. , Friedberg Mark W. , Brookhart M. Alan , Haas Jennifer S. , Shrank William H. 
Published: November 2008

Objective. To determine whether retail prices for prescription drugs are higher in poorer areas.Data Sources. The MyFloridarx.com website, which provides retail prescription prices at Florida pharmacies, and median ZIP code income from the 2000 Census.Study Design. We compared mean pharmacy prices for each of the four study drugs across ZIP code income groups. Pharmacies were classified as either chain pharmacies or independent pharmacies.Data Collection. Prices were downloaded in November 2006.Principal Findings. Across the four study drugs, mean prices were highest in the poorest ZIP codes: 9 percent above the statewide average. Independent pharmacies in the poorest ZIP codes charged the highest mean prices.Conclusions. Retail prescription prices appear to be higher in poorer ZIP codes of Florida.
Relationship of Safety Climate and Safety Performance in Hospitals
Authors: Singer Sara , Lin Shoutzu , Falwell Alyson , Gaba David , Baker Laurence 
Published: November 2008

Objective. To examine the relationship between measures of hospital safety climate and hospital performance on selected Patient Safety Indicators (PSIs).Data Sources. Primary data from a 2004 survey of hospital personnel. Secondary data from the 2005 Medicare Provider Analysis and Review File and 2004 American Hospital Association's Annual Survey of Hospitals.Study Design. A cross‐sectional study of 91 hospitals.Data Collection. Negative binomial regressions used an unweighted, risk‐adjusted PSI composite as dependent variable and safety climate scores and controls as independent variables. Some specifications included interpersonal, work unit, and organizational safety climate dimensions. Others included separate measures for senior managers and frontline personnel's safety climate perceptions.Principal Findings. Hospitals with better safety climate overall had lower relative incidence of PSIs, as did hospitals with better scores on safety climate dimensions measuring interpersonal beliefs regarding shame and blame. Frontline personnel's perceptions of better safety climate predicted lower risk of experiencing PSIs, but senior manager perceptions did not.Conclusions. The results link hospital safety climate to indicators of potential safety events. Some aspects of safety climate are more closely related to safety events than others. Perceptions about safety climate among some groups, such as frontline staff, are more closely related than perceptions in other groups.
Anesthesia Provider Model, Hospital Resources, and Maternal Outcomes
Authors: Needleman Jack , Minnick Ann F. 
Published: November 2008

Objective. Determine the ability of anesthesia provider model and hospital resources to explain maternal outcome variation.Data Source/Study Setting. 1,141,641 obstetrical patients from 369 hospitals that reported at least one live birth in 2002 in six representative states.Study Design. Logistic regression of death, anesthesia complication, nonanesthesia maternal complication, and obstetrical trauma for all patients and those having cesarean deliveries on anesthesia provider model, obstetrical and anesthesia, and patient variables.Data Collection/Extraction Methods. Data was assembled from information given by hospitals to state agencies and from a 2004 survey of obstetrical organization resources.Principal Findings. Anesthesia complication rates in anesthesiologist‐only hospitals were 0.27 percent compared with 0.23 percent in certified registered nurse anesthetist (CRNA) only hospitals. Rates among other provider models varied from 0.24 to 0.37 percent with none statistically different from the anesthesiologist‐only hospitals. A similar pattern was observed for rates of other outcomes. Multivariate analysis found no systematic differences between hospitals with anesthesiologist‐only models and models using CRNAs. There was no consistent pattern of association of other hospital or patient characteristics with outcomes.Conclusion. Hospitals that use only CRNAs, or a combination of CRNAs and anesthesiologists, do not have systematically poorer maternal outcomes compared with hospitals using anesthesiologist‐only models.
Bilateral frontoparietal polymicrogyria, Lennox‐Gastaut syndrome, and GPR56 gene mutations
Authors: Parrini Elena , Ferrari Anna Rita , Dorn Thomas , Walsh Christopher A. , Guerrini Renzo 
Published: November 2008

SummaryPurpose:  Bilateral frontoparietal polymicrogyria (BFPP) has been reported in sporadic patients and in recessive pedigrees. Eleven mutations in GPR56, a gene encoding an evolutionarily dynamic G‐protein–coupled receptor, have been identified in 29 patients from 18 families. The clinical features of BFPP include severe mental retardation, motor and language impairment, and epilepsy. No detailed description of the epilepsy is available for the patients reported to date. We report three consanguineous families in which four affected individuals with BFPP and GPR56 mutations had Lennox‐Gastaut syndrome.Methods:  Family studies, brain magnetic resonance imaging (MRI), electroencephalography (EEG)‐video recordings, and mutation analysis.Results:  In Family 1, with one affected proband, we found an R565W change in the second extracellular loop of GPR56, involving a highly conserved aminoacidic residue. In Family 2, with one affected proband, we found an R79X change affecting the protein N‐terminus and predicted to cause a premature truncation with loss of the G‐protein–coupled receptor proteolytic site. In family 3, with two affected siblings, we found an R33P substitution in the protein N‐terminus, involving a highly conserved aminoacidic residue. Epilepsy, present in all four patients, had started between ages 1 and 8 years, with infantile spasms in one patient and with de novo Lennox‐Gastaut syndrome in the remaining three. All patients had Lennox‐Gastaut syndrome when last observed, at ages 13 to 32 years.Discussion:  Several genes, when mutated, can cause malformations of cortical development that have been associated with the Lennox‐Gastaut syndrome. BFPP caused by GPR56 mutations represents an additional, although rare, genetically determined cause of Lennox‐Gastaut syndrome.
History of the ketogenic diet
Authors: Wheless James W. 
Published: November 2008

Summary Fasting and other dietary regimens have been used to treat epilepsy since at least 500 BC. To mimic the metabolism of fasting, the ketogenic diet (KD) was introduced by modern physicians as a treatment for epilepsy in the 1920s. For two decades this therapy was widely used, but with the modern era of antiepileptic drug treatment its use declined dramatically. By the end of the twentieth century this therapy was available in only a small number of children's hospitals. Over the past 15 years, there has been an explosion in the use, and scientific interest in the KD. This review traces the history of one of the most effective treatments for childhood epilepsy.
The ketogenic diet—update on recent clinical trials
Authors: Cross J. Helen , Neal Elizabeth G. 
Published: November 2008

Summary The ketogenic diet (KD) has been used in the treatment of epilepsy for almost 100 years. Several cohort studies have emphasized its possible benefit, although use became less at the introduction of anticonvulsant medication. However, the KD has regained recognition over the past 15 years. Resources remain scarce and its availability for children may be limited. One argument has been the lack of evidence from suitably designed trials. Systematic reviews and meta‐analyses have revealed that studies are limited to class 3 and 4 data. A recently published randomized controlled trial has shown that the benefit of the KD is equivalent to any of the new anticonvulsant medications, emphasizing the need for more resources to ensure greater diet availability.
International consensus statement on clinical implementation of the ketogenic diet: Agreement, flexibility, and controversy
Authors: Kossoff Eric H. 
Published: November 2008

Summary The ketogenic diet (KD) is an established, effective nonpharmacologic treatment for intractable childhood epilepsy. The KD is provided differently throughout the world, with occasionally significant variations in its administration. There exists a need for more standardized protocols and management recommendations for clinical and research use. In December 2006, the Charlie Foundation commissioned a panel comprised of 26 pediatric epileptologists and dietitians with particular expertise in using the KD. This group was convened to create a consensus statement regarding the clinical management of the KD; the consensus statement has also been endorsed by the Child Neurology Society. Members were asked to write sections based on clinical interests and the full document was subsequently reviewed and approved by the entire group. Recommendations were made regarding evaluation of children before starting the diet, specifically in regards to ideal patient selection, pre‐KD counseling and testing, and choice of specific dietary therapy (ketogenic or less restrictive alternative diets). In addition, there was information provided regarding diet implementation (need for fasting and admission), supplementation, follow‐up management (frequency of visits as well as diet and laboratory evaluations while receiving the diet), adverse event monitoring, and timing and method of eventual KD discontinuation. This group effort highlights recommendations based on best evidence, including areas of agreement and controversy, unanswered questions, and future research.
KetoCalculator: A web‐based calculator for the ketogenic diet
Authors: Zupec‐Kania Beth 
Published: November 2008

Summary The classic ketogenic diet (KD) is a mathematically calculated diet with specific daily goals of fat, protein, and carbohydrate. Precise quantities of foods are then derived from these values which result in meal plans for the individual patient. The algebraic algorithm to determine a single meal requires approximately 35 calculations. This process is time consuming given that each individual requires many meals for variety and satisfaction. Computer applications can process multiple calculations in seconds. In 1997, a program was designed by this author with LifeTime Computing, a computer software company. This program was rebuilt into digital format in 2002, given the title KetoCalculator, and made available to registered dietitians on the World Wide Web (

Zupec‐Kania, 2002

).
Ketogenic ratio, calories, and fluids: Do they matter?
Authors: Wirrell Elaine C. 
Published: November 2008

Summary The ketogenic diet (KD) traditionally was initiated using specified ketogenic ratios, limited calories, and fluids. Recent work has shown that lower ketogenic ratio diets are frequently as efficacious as higher ones and result in fewer adverse effects. In animals, calorie restriction is anticonvulsant. In children, however, the need for calorie restriction is less clear, but avoidance of excessive calories may improve efficacy of the diet. There is no evidence that fluid restriction is a necessary component of the KD. Given the higher risk of nephrolithiasis, adequate fluid intake should be encouraged.
Assessing ketosis: Approaches and pitfalls
Authors: Carmant Lionel 
Published: November 2008

Summary Although the mechanism of action of the ketogenic diet (KD) remains unknown, ketones have been used as a marker of efficacy. Acetoacetate, acetone, and beta‐hydroxybutyrate can be measured in urine, blood, and breath. The value of these measures is reviewed in this paper. Future brain measures hold promise as markers of efficacy, but research focused on the mechanisms of the KD should help to develop more reliable markers of efficacy.
Long‐term health consequences of epilepsy diet treatments
Authors: Vining Eileen P. G. 
Published: November 2008

Summary The ketogenic diet (KD) typically provides a marginally healthy diet and in recent years has been used for more protracted courses of therapy. This results in concern about the impact of the diet on the general health of the child. Studies have demonstrated poor growth, dyslipidemia, kidney stones, and numerous other problems seen less frequently. Major areas of concern are reviewed as well as some emerging evidence of more beneficial long‐term health consequences beyond the expected control of seizures.
Use of the ketogenic diet in neonates and infants
Authors: Rubenstein James E. 
Published: November 2008

Summary The ketogenic diet (KD) is still viewed as virtually last‐line therapy in childhood epilepsies, and specifically as unsafe and difficult to initiate and maintain in neonates and infants. Information is presented to show that the KD is safe and efficacious in this population, and should be carefully studied to determine its real usefulness as first‐line or early therapy (one or fewer anticonvulsants) in the catastrophic epilepsies of infancy.
Medium‐chain triglyceride (MCT) ketogenic therapy
Authors: Liu Yeou‐mei Christiana 
Published: November 2008

Summary The medium‐chain triglyceride diet (MCTD) is a variant of the classic 4:1 ketogenic diet (KD) introduced in 1971 by Huttenlocher as an attempt to improve the palatability of the KD by allowing more carbohydrates yet preserving ketosis. Although initially found to be equally effective as the classic KD, use of the MCTD declined because of frequent gastrointestinal side effects such as cramps, diarrhea, and vomiting. Recently, we have used the MCTD in more than 50 patients. We have found excellent seizure control, similar to the classic KD, and with careful monitoring, we have encountered minimal side effects. The MCTD should remain a viable dietary option for children with refractory epilepsy who have large appetites, can tolerate more calories, or cannot accept the restrictions of the classic KD.
The Modified Atkins Diet
Authors: Kossoff Eric H. , Dorward Jennifer L. 
Published: November 2008

Summary In 2003, a case series was published describing the benefits of a less restrictive ketogenic diet (KD) started as an outpatient without a fast and without any restrictions on calories, fluids, or protein. This “Modified Atkins Diet” (MAD) restricts carbohydrates to 10 g/day (15 g/day in adults) while encouraging high fat foods. Now 5 years later, there have been eight prospective and retrospective studies published on this alternative dietary therapy, both in children as well as adults. In these reports, 45 (45%) have had 50–90% seizure reduction, and 28 (28%) >90% seizure reduction, which is remarkably similar to the traditional KD. This review will discuss basics and tips to best provide the MAD, evidence for its efficacy, suggestions about the role of ketosis in dietary treatment efficacy, and its side effect profile. Lastly, the possible future benefits of this treatment for new‐onset seizures, adults, neurologic conditions other than epilepsy, and developing countries of the world will be discussed.
Low glycemic index treatment: Implementation and new insights into efficacy
Authors: Pfeifer Heidi H. , Lyczkowski David A. , Thiele Elizabeth A. 
Published: November 2008

Summary Despite the substantial efficacy of the ketogenic diet (KD) in treating refractory epilepsy, use of the KD remains limited because of difficulties in implementation and tolerability. An effective alternative dietary approach is a low glycemic index treatment (LGIT), which liberalizes the extreme carbohydrate restriction of the KD but restricts the type of carbohydrate‐containing foods to those that produce relatively small changes in blood glucose. Foods with a “glycemic index” of less than 50 produce less than half the area‐under‐the‐curve elevation of blood glucose compared to a reference food. The LGIT approach produces comparable efficacy to the classic KD, but tolerability is improved and implementation is much simpler. The LGIT appears to be a viable first‐line dietary therapy for epilepsy.
Glucose transporter deficiency syndrome (GLUT1DS) and the ketogenic diet
Authors: Klepper Jörg 
Published: November 2008

Summary Glucose transporter type 1 (GLUT1) deficiency syndrome (GLUT1DS, OMIM 606777) is caused by impaired glucose transport into brain mediated by GLUT1, the glucose transporter at the blood–brain barrier. The condition is diagnosed by hypoglycorrhachia, impaired glucose uptake into erythrocytes, and heterozygous mutations in the SLC2A1 gene (OMIM 138140, gene map locus 1p35‐31.3). Patients present with early‐onset epilepsy, developmental delay, and a complex movement disorder. The phenotype is highly variable and several atypical variants have been described. The ketogenic diet (KD) provides ketones as an alternative fuel to the brain. Calculation, administration, supplements, and adverse effects of the KD in GLUT1DS do not differ from patients treated for intractable childhood epilepsy. In GLUT1DS, the KD should be introduced early to meet the energy demands of the developing brain and should be maintained into puberty. Seizures are effectively controlled, but the effects on neurodevelopment and on the movement disorder are less impressive. The KD remains the treatment of choice for GLUT1DS, but recent insights into anticonvulsive diet mechanisms, animal models for GLUT1DS, and the development of alternative KDs provide new opportunities to improve the treatment of this condition.
What constitutes a relevant animal model of the ketogenic diet?
Authors: Holmes Gregory L. 
Published: November 2008

Summary Animal models of human disease have been enormously important in improving our understanding of the pathophysiological basis and the development of novel therapies. In epilepsy, modeling using both in vivo and in vitro preparations has provided insight into fundamental neuronal mechanisms. Indeed, much of our understanding of seizure mechanisms comes from animal studies. The conceptual advances in understanding basic mechanisms of epilepsies have been largely validated in humans, attesting to the validity of the rationale and providing a basis for bridging the gaps between experimental and human data. While the ketogenic diet is clearly efficacious in a wide variety of seizure types and syndromes, the mechanism of action of the diet has not been established. Animal models will continue to be enormously important in furthering our understanding of how dietary therapy can help individuals with epilepsy.
Design of dietary treatment: Humans versus rodents
Authors: Eagles Douglas A. 
Published: November 2008

SummaryKetogenic diets (KDs) are designed to create the metabolic conditions of fasting, which was among the earliest therapies discovered for epilepsy. The major measures used to evaluate dietary effectiveness have been the levels of urinary ketone bodies and the successful reduction of seizure activity. Modifications of the “classical” animal fat KD have been used in an attempt to boost ketonuria or ketonemia, increase palatability and compliance, and reduce side effects. Studies of KDs in experimental animals have been largely confined to rodents (mice and rats) for reasons of cost and convenience, and both have been found to be protected against experimentally induced seizures following consumption of KDs. Most of these studies have been designed to test hypotheses about the mechanism(s) by which reductions in carbohydrate or increases in fat result in elevated seizure threshold, decreased seizure duration, and decreased seizure severity. So far, underlying mechanisms have proven elusive. Rodent studies have led to a degree of general agreement that ketone levels per se do not correlate well with seizure protection, that reduction of glucose levels is fundamentally important, and that calorie restriction is additive to high fat diets in providing seizure protection.
Genetic influences on ketogenic diet efficacy
Authors: Dutton Stacey B. B. , Escayg Andrew 
Published: November 2008

Summary An average of 15–20% of patients on the ketogenic diet (KD) experience a >50% reduction in seizure frequency; however, 10–40% discontinue the diet due to either a lack of response or adverse side effects. This variability in patient response raises the possibility that genetic factors may influence the efficacy of the KD. As a first step towards identifying these factors, we evaluated the ability of the KD to alter seizure thresholds in four commonly used inbred mouse strains: C57BL/6J, FVB/NJ, A/J, and DBA/2J. We observed strain‐specific differences, indicating that genetic factors are likely to influence efficacy.
Ketosis and brain handling of glutamate, glutamine, and GABA
Authors: Yudkoff Marc , Daikhin Yevgeny , Horyn Oksana , Nissim Ilana , Nissim Itzhak 
Published: November 2008

Summary We hypothesize that one mechanism of the anti‐epileptic effect of the ketogenic diet is to alter brain handling of glutamate. According to this formulation, in ketotic brain astrocyte metabolism is more active, resulting in enhanced conversion of glutamate to glutamine. This allows for: (a) more efficient removal of glutamate, the most important excitatory neurotransmitter; and (b) more efficient conversion of glutamine to GABA, the major inhibitory neurotransmitter.