bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of Herbicides for Restoring Native Grasses in Buffelgrass‐Dominated Grasslands
Authors: Tjelmeland Aaron D. , Fulbright Timothy E. , Lloyd‐Reilley John 
Published: September 2007

Abstract Buffelgrass (Pennisetum ciliare) is an exotic grass that threatens arid and semiarid ecosystems. The objective of this study was to determine effectiveness of several herbicides at reducing competition from buffelgrass to enhance establishment of planted native grasses. In Duval County, Texas, plots were delineated in two experiments in a buffelgrass‐dominated pasture and mowed on 2 September 2002. On 18 September 2002 and 7 October 2002, a 41% glyphosate (N‐(phosphonomethyl) glycine) herbicide was applied to all plots. A mixture of three native grasses—green sprangletop (Leptochloa dubia), plains bristlegrass (Setaria leucopila), and four‐flower trichloris (Chloris pluriflora)—was planted on 8 October 2002. On 9 October 2002, 1.12 and 2.24 kg/ha of a 80% tebuthiuron (N‐[5‐(1,1‐dimethyethyl)‐1,3,4‐thiadiazol‐2‐yl]‐N,N’‐dimethylurea) herbicide was applied preemergence to the first experiment, and all other herbicides were applied postemergence on 27 July 2003 to the second experiment. Percent canopy cover of vegetation was estimated with a 20 × 50–cm sampling frame during April, June, and October 2003 and August 2004. Postemergent herbicides had no significant effect on canopy cover of buffelgrass or planted species (p≥ 0.05). Canopy cover of native grasses did not exceed 8% on any treatment or sampling date, and buffelgrass cover returned to pre‐treatment conditions in less than 1 year; however, the 2.24 kg/ha rate of tebuthiuron suppressed (p < 0.05) canopy cover of buffelgrass compared with controls and increased (p < 0.05) native grasses almost 2 years past application. Tebuthiuron may have potential value in reducing buffelgrass canopy cover and increasing cover of native grasses, particularly Chloris spp.
Optimizing Hardwood Reforestation in Old Fields: The Effects of Treeshelters and Environmental Factors on Tree Seedling Growth and Physiology
Authors: Laliberté Etienne , Bouchard André , Cogliastro Alain 
Published: September 2007

AbstractStrong competition for water is largely recognized as the main factor explaining the resistance of herbaceous old fields to tree invasion. Therefore, site preparation as well as chemical and mechanical vegetation control are recommended when establishing hardwood tree plantations on such sites, but those methods are sometimes socially or ecologically inappropriate. The main objective of this study was to analyze whether treeshelters could improve early tree growth in herbaceous old fields, when mulching alone is used to partially control herbaceous competition. Our results indicate that treeshelters can facilitate tree growth in those conditions but that this was not caused by an improvement of tree water relations. Rather, it appeared to be related to an optimization of light levels inside the shelter, where light intensity was low enough to lead to a photosynthetic system less costly to maintain due to a greater specific leaf area but high enough to have no adverse effects on photosynthetic rates. Although treeshelters increased tree growth when surrounding herbaceous vegetation was low (either height or standing biomass), allowing high light levels, they reduced growth when surrounding vegetation was high and blocked a substantial quantity of light. Therefore, environmental factors such as light availability need to be considered to optimize the success of hardwood plantations when treeshelters are used in recently abandoned agricultural fields.
Intralesional recordings and epileptogenic zone in focal polymicrogyria
Authors: Chassoux Francine , Landre Elisabeth , Rodrigo Sebastian , Beuvon Frédéric , Turak Baris , Semah Franck , Devaux Bertrand 
Published: September 2007

Summary
Purpose: Polymicrogyria (PMG) is recognized as an epileptogenic lesion but few data concerning organization of the epileptogenic zone (EZ) are available.
Methods: We analyzed the distribution of the EZ according to Stereo‐EEG (SEEG) with intralesional recordings in four patients evaluated for intractable partial epilepsy associated with focal unilateral PMG, involving the posterior temporal region in two, the perisylvian area in one and the temporoparietal junction in the other. All had ictal scalp EEG, high‐resolution structural and functional MRI, fluorodeoxyglucose positron emission tomography (FDG‐PET), and SEEG. For each patient, several depth electrodes were implanted both within the PMG and in extralesional areas.
Results: In three patients, the PMG displayed high‐frequency spiking activity. However, interictal and ictal recordings demonstrated a large epileptogenic network, which was more widespread than the PMG, including the mesial temporal structures in two. In another patient, interictal spiking and seizure onset site were located within the hippocampus and outside of the PMG, although it was rapidly involved during seizure spread. Overall, EZ was considered to be larger than the PMG in all patients although hypometabolic areas detected by PET were concordant with EZ. Three patients underwent extensive surgery including the PMG and are seizure free with a follow‐up >2 years.
Discussion: Although intralesional recordings demonstrated intrinsic epileptogenicity in PMG, our data provide evidence that unilateral focal PMG belongs to a large epileptogenic network extending beyond the MRI lesion. SEEG may be helpful for planning surgery with favorable outcome, providing large resections are feasible, even in apparently focal PMG.
Generic Products of Antiepileptic Drugs (AEDs): Is It an Issue?
Authors: Bialer Meir 
Published: September 2007

Summary:  The availability of generic products of antiepileptic drugs (AEDs) has raised the following concerns: (1) Do generic AEDs work as well as brand AEDs in terms of their efficacy, safety and quality? (2) Can generic AEDs be used as substitutions for brand AEDs? and (3) Can generic products of AEDs be used interchangeably? The traditional average bioequivalence analysis addresses concern 1 but does not provide a complete adequate response to concerns 2 and 3. Drug interchangeability can be classified as drug prescribability or drug switchability. Drug prescribability refers to the situation where a patient is treated for the first time so that either a brand or a bioequivalent generic AED can be chosen. Drug switchability refers to the situation in which a brand AED is switched to a bioequivalent generic product of the same AED. The traditional average bioequivalence approach is sufficient to evaluate the prescribability of generic products, but does not ensure the switchability between prescribable formulations. The necessity of assuring switchability of two formulations can be addressed by individual bioequivalence.While the switch to generic AEDs is well tolerated by many patients and in general cost‐effective, seizure control should not be sacrificed on the basis of cost alone, as the major end point in treating epilepsy with AEDs is seizure control without side effects. Until we have individual (within patient) bioequivalence data on generic AEDs and/or the tools to a priori identify the subset of patients susceptible to the generic switch, a switch of AED products in seizure‐free patients is not recommended.
High Risk of Reading Disability and Speech Sound Disorder in Rolandic Epilepsy Families: Case–Control Study
Authors: Clarke Tara , Strug Lisa J. , Murphy Peregrine L. , Bali Bhavna , Carvalho Janessa , Foster Suzanne , Tremont Geoffrey , Gagnon Bernadine R. , Dorta Nelson , Pal Deb K. 
Published: September 2007

Summary
Purpose: Associations between rolandic epilepsy (RE) with reading disability (RD) and speech sound disorder (SSD) have not been tested in a controlled study. We conducted a case–control study to determine whether (1) RD and SSD odds are higher in RE probands than controls and (2) an RE proband predicts a family member with RD or SSD, hence suggesting a shared genetic etiology for RE, RD, and SSD.
Methods: Unmatched case–control study with 55 stringently defined RE cases, 150 controls in the same age range lacking a primary brain disorder diagnosis, and their siblings and parents. Odds ratios (OR) were calculated by multiple logistic regression, adjusted for sex and age, and for relatives, also adjusted for comorbidity of RD and SSD in the proband.
Results: RD was strongly associated with RE after adjustment for sex and age: OR 5.78 (95% CI: 2.86–11.69). An RE proband predicts RD in family members: OR 2.84 (95% CI: 1.38–5.84), but not independently of the RE proband's RD status: OR 1.30 (95% CI: 0.55–12.79). SSD was also comorbid with RE: adjusted OR 2.47 (95%CI: 1.22–4.97). An RE proband predicts SSD in relatives, even after controlling for sex, age and proband SSD comorbidity: OR 4.44 (95% CI: 1.93–10.22).
Conclusions: RE is strongly comorbid with RD and SSD. Both RD and SSD are likely to be genetically influenced and may contribute to the complex genetic etiology of the RE syndrome. Siblings of RE patients are at high risk of RD and SSD and both RE patients and their younger siblings should be screened early.
The effectiveness of low‐frequency stimulation for mapping cortical function
Authors: Zangaladze Andro , Sharan Ashwini , Evans James , Wyeth Dale H. , Wyeth Edmund G. , Tracy Joseph I. , Chervoneva Inna , Sperling Michael R. 
Published: September 2007

Summary
Objective: To establish the efficacy and safety of low‐frequency electrical stimulation for cortical brain mapping.
Methods: Cortical function was mapped using electrical stimulation in epilepsy patients with chronically implanted intracranial subdural electrodes. Contacts overlying motor, sensory, visual, and language cortex were stimulated at frequencies of 5, 10, and 50 Hz, using current levels ranging from 1 to 17.5 mA for 3–5 s. The current intensity and incidence at which functional alterations and afterdischarges (ADs) occurred were recorded. The modified McNemar test for nonindependent measures was used to analyze the data.
Results: 122 electrode contact pairs were electrically stimulated at least two different frequencies in 14 patients. Functional alterations were obtained at all stimulation frequencies (5, 10, and 50 Hz) at generally similar rates. The likelihood of producing an AD correlated with stimulation frequency, and lower‐frequency stimulation was less likely to provoke an AD. Higher current intensity was required to induce both functional responses and ADs at low‐frequency stimulation than high‐frequency stimulation. While overall rates of producing functional changes were similar, differences in functional response with regard to frequency were noted at individual cortical sites.
Conclusion: 5‐ and 10‐Hz stimulation are as effective for mapping cortical function as 50‐Hz stimulation and produce fewer ADs. We recommend that mapping of cortical function be started with 5‐Hz‐frequency stimulation. Higher frequencies should be used in suspect cortex if no symptoms or signs are produced with 5‐Hz stimulation.
Protective effect of topiramate on kainic acid–induced cell death in mice hippocampus
Authors: Park Hae Jeong , Kim Hak Jae , Park Hi Joon , Ra Jehyun , Zheng Long Tai , Yim Sung Vin , Chung Joo‐Ho 
Published: September 2007

Summary The protective effect of topiramate (TPM) on seizure‐induced neuronal injury is well known; however, its molecular basis has yet to be elucidated. We investigated the effect and signaling mediators of TPM on seizure‐induced hippocampal cell death in kainic acid (KA)‐treated ICR mice. KA‐induced hippocampal cell death was identified by terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling. Immunoreactivity (IR) of p‐Erk, p‐Jnk, p‐P38, and caspase‐3, and caspase‐3 activity were observed in the hippocampal region 3 h after KA (0.1 μg/5 μL, i.c.v.) administration, and/or TPM (100 mg/kg, i.p.) pretreatment. TPM attenuated seizure‐induced neuronal cell death and reduced KA‐induced p‐Erk IR in the CA3 region of the hippocampus, but did not affect p‐Jnk and p‐P38. In addition, TPM reduced caspase‐3 IR and activation by KA. KA‐induced seizures were also suppressed by TPM pretreatment. TPM inhibits seizures, and decreases Erk phosphorylation and caspase‐3 activation by KA, thereby contributing to protection from neuronal injury.
Pathways to discovery in epilepsy research: Rethinking the quest for cures
Authors: Lowenstein Daniel H. 
Published: September 2007

Summary This paper, based on the 4th Annual Hoyer Lecture presented at the 2006 annual meeting of the American Epilepsy Society, first provides a general view of the current limitations in therapies aimed at achieving the goal of “no seizures, no side effects” for patients living with epilepsy. Some of the seminal discoveries in epilepsy research over the past 100 years are then reviewed, with an emphasis on the pivotal role of basic and clinical/translational science in leading the way to new and effective means for diagnosing and treating for epilepsy. The paper concludes with a view of the future course of epilepsy research. Scientific advances will increasingly rely on the collaboration of multidisciplinary teams of reseachers using the analytic and storage capabilities of machines, and linked together by communication tools such as the Internet and related technologies.
Focal reduction of neuronal glutamate transporters in human neocortical epilepsy
Authors: Rakhade Sanjay N. , Loeb Jeffrey A. 
Published: September 2007

Summary
Purpose: To study the differential expression of excitatory amino acid transporters (EAATs) at localized epileptic foci compared to nonepileptic regions in human neocortical epilepsy. Decreased expression of EAATs, the predominant mechanism to remove synaptic‐released glutamate, may explain mechanisms of heightened excitability at these epileptic foci.
Methods: The differential expression of EAAT1‐4 at the mRNA and protein levels was measured in electrically mapped human neocortical tissues using quantitative real‐time PCR and immunoblotting. This required a novel way to prevent aggregation of EAAT proteins through cold solubilization. Layer‐specific neuronal densities were measured to control for potential differences in neuronal density.
Results: While focal epileptic brain regions show marked increases in immediate early genes, they have significant reductions in the neuronal glutamate transporter mRNAs (EAAT3 and EAAT4). These changes were not associated with changes in relative neuronal density, suggesting a reduction in EAAT mRNA per neuron. Immunohistochemical staining of epileptic human neocortex confirmed the presence of EAAT1 and EAAT2 proteins in astroglial cells and EAAT3 and EAAT4 proteins in human cortical neurons. At the protein level, western blots of the same epileptic and nonepileptic regions for a subset of these patients showed a similar decrease of EAAT3 and EAAT4. Despite no change in EAAT2 mRNA, EAAT2 protein expression was significantly reduced at epileptic foci.
Conclusion: Regional reductions in EAAT expression at human neocortical epileptic foci could produce increased local glutamate levels that in turn may contribute to both hyperexcitability and the spontaneous generation of epileptic discharges that characterize human epileptic foci.
Hypotheses, tests, methods, and innovation: The balancing act in research
Authors: Berg Anne T. 
Published: September 2007

Summary Clinical and epidemiological research studies are essential to advancing our understanding of human health conditions such as epilepsy. To be of value, studies must not only address important questions, they must do so in such a way as to contribute usefully to existing knowledge. Comprehensive understanding of the subject matter is only one component of successful research and research reports. A firm grasp of research methods and statistical issues and a scholarly command of the relevant and current literature are essential components to high‐quality research. No single study, however, is perfect nor can any single study definitively answer a given single research question. Studies must be designed and evaluated in light of historical, scientific, pragmatic, and ethical realities that may constrain them. Selected but essential methodological and statistical concepts are discussed along with the need to balance innovation and novelty against methodological rigor.
Surgery for medically intractable temporal lobe epilepsy during early life
Authors: Maton Bruno , Jayakar Prasanna , Resnick Trevor , Morrison Glenn , Ragheb John , Duchowny Michael 
Published: September 2007

Summary
Purpose: Temporal lobe epilepsy (TLE) in early life is often a catastrophic disorder with pharmacoresistant seizures and secondary neurological deterioration. There is little data available regarding epilepsy surgery performed in infants and young children and no prior study has focused on TLE.
Methods: We analyzed the results of temporal resection for epilepsy as the primary indication in children less than age 5 years who had at least 2 years of follow‐up.
Results: 20 children (14 males) were identified with a mean age at surgery of 26 months and a mean age at seizure onset of 12 months. Clinical presentation was diverse. Typical psychomotor seizures (n = 4; mean age at surgery 37 months) were followed by prominent motor changes (n = 7; 30 months) and were occasionally isolated (n = 3; 23 months). Epileptic spasms were noted in six patients and were frequently associated with lateralizing features. The interictal EEG was lateralizing in 15 patients and the ictal EEG was lateralizing in 18 patients. Brain MRI provided localizing value in 16 patients, ictal SPECT was concordant in 4/8 cases. Invasive EEG was employed in six cases. At mean follow‐up of 5.5 years, 65% of the children were seizure‐free and 15% had >90% seizure reduction. Morbidity included infection and hydrocephalus in one case and stroke‐related hemiparesis in two cases. Cortical dysplasia was identified in eight children, tumors in eight including two DNET, two ganglioglioma, and four malignant tumors. Hippocampal sclerosis was present in four cases, always as dual pathology.
Conclusion: TLE presents in early life with varied and severe manifestations. Excisional procedures in this age group are associated with favorable seizure reduction similar to older children and in adults.
Family‐Based Association Analyses of Alcohol Dependence Phenotypes Across DRD2 and Neighboring Gene ANKK1
Authors: Dick Danielle M. , Wang Jen C. , Plunkett Jevon , Aliev Fazil , Hinrichs Anthony , Bertelsen Sarah , Budde John P. , Goldstein Elianna L. , Kaplan Daniel , Edenberg Howard J. , Nurnberger John , Hesselbrock Victor , Schuckit Marc , Kuperman Sam , Tischfield Jay , Porjesz Bernice , Begleiter Henri , Bierut Laura Jean , Goate Alison 
Published: September 2007

Background:  There is an extensive and inconsistent literature on the association of the dopamine D2 receptor gene (DRD2) with alcohol dependence. Conflicting results have been attributed to differences in the severity of the alcohol dependence phenotype across studies, failure to exclude related disorders from comparison groups, and artifacts of population‐stratification. Recently the genetic polymorphism most widely analyzed in DRD2, Taq1A, has been discovered to reside in a neighboring gene, ankyrin repeat and kinase domain containing 1 (ANKK1), located 10 kb downstream from DRD2.Methods:  To more carefully characterize evidence for association across this region, we genotyped 26 single nucleotide polymorphisms (SNPs) spanning DRD2 and ANKK1 in a sample of 219 Caucasian families (n = 1,923) from the Collaborative Study on the Genetics of Alcoholism (COGA), making this the most extensive analysis to date of association between this region and alcohol dependence. We used family‐based analyses robust to population‐stratification, and we made use of rich phenotypic data to analyze alcohol dependence and subtypes hypothesized in the literature to be more directly influenced by DRD2.Results:  We found that the evidence for association is strongest in the 5′ linkage disequilibrium block of ANKK1 (that does not contain Taq1A), with weak evidence of association with a small number of SNPs in DRD2. The association in ANKK1 is strongest among the subsets of alcoholics with medical complications and with antisocial personality disorder.Conclusions:  More extensive genotyping across DRD2 and ANKK1 suggests that the association with alcohol dependence observed in this region may be due to genetic variants in the ANKK1 gene. ANKK1 is involved in signal transduction pathways and is a plausible biological candidate for involvement in addictive disorders.
Association of the Aldehyde Dehydrogenase 2 Promoter Polymorphism With Alcohol Consumption and Reactions in an American Jewish Population
Authors: Fischer Monika , Wetherill Leah Flury , Carr Lucinda G. , You Min , Crabb David W. 
Published: September 2007

Background:  Reduction in activity of the mitochondrial aldehyde dehydrogenase 2 (ALDH2) enzyme due to genetic deficiency causes reactions related to alcohol consumption and lowers the risk of alcoholism. ALDH2*2 is the only functionally significant polymorphism of the ALDH2 gene. An additional polymorphic locus in the promoter (G to A substitution approximately 360 bp from the translation start site) may influence ALDH2 activity through effects on transcriptional activity. The A allele is predicted to be less active transcriptionally than the G allele. Therefore, we hypothesized that individuals with 1 or 2 A alleles would have exaggerated reactions to alcohol.Methods:  Fifty‐three Jewish college students from a Midwestern University and 76 Jewish individuals living in a large Midwestern city (all of Ashkenazi descent) were tested for associations between ALDH2*G and ALDH2*A alleles and self‐reported alcohol consumption and responses to alcohol. Genotype determination was performed using PCR and slot‐blot hybridization. As alcohol drinking behavior differed substantially between the college students and the general population, as well as between males and females, the analyses were performed separately in each group.Results:  The frequency of the ALDH2*A allele was 0.87 in the 129 Jewish individuals tested. Among the general Jewish population, those who were homozygous for ALDH2*A drank fewer drinks per occasion than individuals who were not homozygous for the ALDH2*A allele, but did not drink significantly less frequently. When the other covariates (ADH1B genotype, gender, and population) were controlled for, there was a marginal association between ALDH2A genotype and quantity of alcohol consumed and the number of drinks consumed before feeling drowsy.Conclusion:  This study suggests that the ALDH2*A allele status may correlate with variations in alcohol consumption patterns among Jews, independent of the effect of ADH1B genotype.