bluuebunny/crossref_metadata_2025_split huggingface dataset:
Aragonite and magnesite in eclogites from the Jæren nappe, SW Norway: disequilibrium in the system CaCO3–MgCO3 and petrological implications
Authors: SMIT M. A. , BRÖCKER M. , SCHERER E. E. 
Published: November 2008

AbstractEclogites from the Jæren nappe in the Caledonian orogenic belt of SW Norway contain aragonite, magnesite and dolomite in quartz‐rich layers. The carbonates comprise composite grains that occur interstitially between phases of the eclogite facies assemblage: garnet + omphacite + zoisite + clinozoisite + quartz + apatite + rutile ± dolomite ± kyanite ± phengite. Pressure and temperature conditions for the main eclogite stage are estimated to be 2.3–2.8 GPa and 585–655 °C. Published ultrahigh pressure (UHP) experiments on CaO‐, MgO‐ and CO2‐bearing systems have shown that equilibrium assemblages of aragonite and magnesite form as a result of dolomite breakdown at pressures >5 GPa. As a result, recognition of magnesite and aragonite in eclogite facies rocks has been used as an indicator for UHP conditions. However, petrological testing showed that the samples studied here have not experienced such conditions. Aragonite and magnesite show disequilibrium textures that indicate replacement of magnesite by aragonite. This process is inferred to have occurred via a coupled dissolution–precipitation reaction. The formation of aragonite is constrained to eclogite facies conditions, which implies that the studied rocks have experienced metasomatic, reactive fluid flow during their residence at high pressure (HP) conditions. During decompression, the bimineralic carbonate aggregates were overgrown by rims of dolomite, which partially reacted with aragonite to form Mg‐calcite. The well‐preserved carbonate assemblages and textures observed in the studied samples provide a detailed record of the reaction series that affected the rocks during and after their residence at P–T conditions near the coesite stability field. Recognition of the HP mechanism of magnesite replacement by aragonite provides new insight into metasomatic processes that occur in subduction zones and illustrates how fluids facilitate HP carbonate reactions that do not occur in dry systems at otherwise identical physiochemical conditions. This study documents that caution is warranted in interpreting aragonite‐magnesite associations in eclogite facies rocks as evidence for UHP metamorphic conditions.
Graphitization of organic matter and fluid‐deposited graphite in Palaeoproterozoic (Birimian) black shales of the Kaya‐Goren greenstone belt (Burkina Faso, West Africa)
Authors: KŘÍBEK B. , SÝKOROVÁ I. , MACHOVIČ V. , LAUFEK F. 
Published: November 2008

AbstractPalaeoproterozoic black shales form an essential part of the Birimian volcanosedimentary belt in Burkina Faso, West Africa. The meanRmaxvalues and the atomicH/Cvalues of the bulk carbonaceous matter (BCM), together with rock structures and mineral assemblages, indicate that these carbon‐rich rocks were metamorphosed to sub‐greenschist and low‐grade greenschist facies. X‐ray diffraction reveals that the (002) ‘graphite’ peak width in half maximum (FWHM) ranges from 0.43 to 0.71 °2θ in sub‐greenschist facies and from 0.27 to 0.41 °2θ in greenschist facies rocks, but thed(002) values in both groups of rocks are approximately the same (∼3.35 Å). The BCM of individual samples is composed of particles with very variable shape, reflectance and Raman spectra. Type I particles that predominate in sub‐greenschist facies are fine‐grained, irregular or elongate bodies 1 to 3 μm in size. Their maximum reflectance (Rmax) ranges between 2.5% and 8.2%, and Raman parameters R1 and R2 range from 0.5 to 1.4 and 0.5 to 0.8, respectively. Type II particles are lath‐shaped, up to 40 μm large bodies, commonly arranged parallel to white mica flakes. The number of these particles increases from sub‐greenschist to greenschist facies. Maximum reflectance varies between 6% and 11.2% and R1 and R2 Raman parameters range from 0.05 to 0.7 and from 0.1 to 0.5, respectively. Type III particles occur in hydrothermally altered and sheared rocks; these are nodular aggregates composed of grains up to 10 μm in size. This type of particles has very high reflectance (Rmax = 11–15%) and its Raman spectra indicate a very high degree of structural ordering corresponding to well‐ordered graphite. Type I particles represent original organic matter in the metasediments. Type II particles are believed to have been formed eitherin situby solid‐state transformation of Type I particles or by crystallization from metamorphic fluids. Gradual graphitization of the Type I organic particles and the growth of lath‐shaped Type II particles from a fluid phase is assumed to have taken place under the peak metamorphic conditions associated with the burial of Birimian sediments during thrust tectonism, progressive tectonic accretion and crustal thickening during the D1 event of the Eburnean orogeny. The growth of equant, high‐reflectance postkinematic nodular aggregates of Type III particles is ascribed to the reduction of CO2‐rich fluids during a hydrothermal event associated with Late Eburnean D2 exhumation and strike–slip movements. Type I carbonaceous particles were only slightly affected by high‐temperature, low‐pressure contact metamorphism during intrusion of Late Eburnean magmatic bodies, whereas formation of Type II or III particles was not recorded in contact‐metamorphosed rocks at all.
Phenotypic and Genetic Analysis of a Large Family With Migraine‐Associated Vertigo
Authors: Lee Hane , Jen Joanna C. , Cha Yoon‐Hee , Nelson Stanley F. , Baloh Robert W. 
Published: November 2008

Objectives.— To describe a large multigenerational family with migraine‐associated vertigo (MAV) combining a detailed phenotypic and genetic analysis.Background.— Migraine‐associated vertigo is said to be highly prevalent in the general population and, like other migraine syndromes, its etiology is felt to have a strong genetic component. However, so far, there have been no reports of large families with MAV.Methods.— Detailed clinical study was conducted on a large multigenerational family with MAV. Genetic study using identical‐by‐descent analysis with dense single nucleotide polymorphism (SNP) arrays was performed to examine consistent inheritance pattern among the affecteds.Results.— Clinical features of MAV were variable although most had other migraine symptoms with at least some of their attacks. We did not find a region of the genome shared by all eight subjects with MAV indicating a polygenetic inheritance for MAV even in this single large family.Conclusions.— A region on 11q shared by most affected females may contain a susceptibility allele for MAV that is expressed exclusively or predominantly by women.
Divalproex Sodium Extended‐Release for the Prophylaxis of Migraine Headache in Adolescents: Results of a Stand‐Alone, Long‐Term Open‐Label Safety Study
Authors: Apostol George , Lewis Donald W. , Laforet Genevieve A. , Robieson Weining Z. , Fugate Julie M. , Abi‐Saab Walid M. , Saltarelli Mario D. 
Published: November 2008

Objective.—The objective of this long‐term open‐label study in adolescents was to assess the safety and tolerability of divalproex sodium extended‐release in the prophylaxis of migraine headaches.Background.—Two formulations of divalproex sodium have demonstrated efficacy in the prevention of migraine headaches in adults. However, no medications are currently approved for this indication in adolescents, and long‐term safety data on agents for migraine prevention are lacking for this younger population. Therefore, the current study was conducted to assess the long‐term safety and tolerability of divalproex extended‐release in adolescents with migraine headaches.Methods.—This was a 12‐month, phase 3, open‐label, multicenter study of adolescents aged 12 to 17 years with migraine headaches diagnosed by International Headache Society criteria. Divalproex sodium extended‐release was initiated at 500 mg/day for 15 days then increased to 1000 mg daily, with subsequent adjustments permitted within a dosing range of 250‐1000 mg daily. Study visits were conducted at days 1 and 15 and months 1, 2, 3, 6, 9, and 12. Safety was evaluated by adverse event collection, laboratory assessments, physical and neurological examinations, vital signs, electrocardiograms, the Udvalg for Kliniske Undersøgelser Side Effect Rating Scale, the Wechsler Abbreviated Scale of Intelligence, and the Behavioral Assessment Scale for Children. Efficacy was evaluated by following the number of migraine headache days reported in subjects' headache diaries over sequential 4‐week intervals for the duration of the trial.Results.—A total of 241 subjects were enrolled and treated. The most frequently reported adverse events were nausea (19%), vomiting (18%), weight gain (12%), nasopharyngitis (11%), migraine (10%), and upper respiratory tract infection (10%). Ten (4%) subjects experienced serious adverse events, and 40 (17%) subjects discontinued because of an adverse event. Increases in ammonia levels were observed. No other clinically significant changes were observed in laboratory values, vital signs, rating scales, or electrocardiograms. Median 4‐week migraine headache days decreased 75% between the first and the fourth months of the study (from 4.0 to 1.0) and remained at or below this level for the remainder of the study.Conclusions.—In this long‐term open‐label study of adolescents with migraine, the safety and tolerability profile of divalproex sodium extended‐release was consistent with findings from previous trials in adults, as well as 2 studies recently completed in adolescents. In general, divalproex sodium extended‐release was well‐tolerated in adolescents with migraine.
Multilocus Analyses Reveal Involvement of the ESR1, ESR2, and FSHR Genes in Migraine
Authors: Oterino Agustin , Toriello Maria , Cayón Amalia , Castillo Jesus , Colas Rafael , Alonson‐Arranz Ana , Ruiz‐Alegria Carlos , Quintela Estrella , Monton Fernando , Ruiz‐Lavilla Nuria , Gonzalez Felix , Pascual Julio 
Published: November 2008

Objective.— Female hormone genes have been investigated in migraine in recent years. Research in this field has been controversial, especially in regard to ESR1 gene findings. None of the reports have yet to approach the problem from a multigenic point of view.Methods.— We investigated 5 polymorphisms implicated in female hormone metabolism (FSHR, CYP19A1, ESR1, NRIP1, and ESR2) in a cohort of 730 subjects matched for age and sex. The effect of gene–gene interaction was assessed using the set association approach, and the corresponding haplotypes were studied with PM Plus software. To corroborate initial results, we analyzed the selected markers using a cohort of 134 families in which 168 trios were suitable for transmission‐disequilibrium test (TDT) analysis under the migraine with aura (MA) phenotype.Results.— A total of 356 consecutive migraine patients (198 with MA [76% females] and 158 migraine without aura [MO, 74% females], and 374 matched controls [71% females]) were genotyped. In the 2‐point analyses, the ESR1 and ESR2 polymorphisms showed nominal association under MA/MO phenotype, and this association was higher with the FSHR polymorphism in MA females (P = .004, uncorrected). Using the SUMSTAT program, we observed ESR2‐ESR1‐FSHR significant gene–gene interaction, suggesting association with the MA/MO phenotype (P = .005; P = .003 in females), and with MA alone (P = .021; P = .030 for females). We corroborated that ESR2‐ESR1‐FSHR haplotypes interacted for migraine under a model‐free hypothesis (empirical P = .010 for the whole sample; P = .001 for females), and the association was stronger for the MA phenotype alone (empirical P = 5.0e‐4, under the heterogeneity model; P = .001 for females). These results were corroborated using family‐based association approaches. We observed nominal association for ESR2 and ESR1 (P = .031 and .034, respectively) in the TDT study, and significant association for ESR1 using family‐based association test statistics. Haplotype‐TDT analyses showed further significant gene–gene interaction for ESR1‐ESR2 (global P = .009), ESR2‐FSHR (global P = .011), and nominally significant interaction for ESR2‐ESR1‐FSHR genes (global P = .037).Conclusion.— We found significant association of female hormone metabolism polymorphisms under the perspective of multigene approach.
Assessment of seizure susceptibility in pilocarpine epileptic and nonepileptic Wistar rats and of seizure reinduction with pentylenetetrazole and electroshock models
Authors: Blanco Miriam Marcela , Dos Santos Jr Jair Guilherme , Perez‐Mendes Patrícia , Kohek Silvia R. B. , Cavarsan Clarissa Fantin , Hummel Michele , Albuquerque Cristovão , Mello Luiz E. 
Published: November 2008

SummaryPurpose:  Pentylenetetrazole (PTZ) and maximal electroshock (MES) models are often used to induce seizures in nonepileptic control animals or naive animals. Despite being widely used to screen antiepileptic drugs (AEDs), both models have so far failed to detect potentially useful AEDs for treating drug‐resistant epilepsies. Here we investigated whether the acute induction of MES and PTZ seizures in epileptic rats might yield a distinct screening profile for AEDs.Methods:  Status epilepticus (SE) was induced in adult male Wistar rats by intraperitoneal pilocarpine injection (Pilo, 320 mg/kg, i.p.). One month later, controls or naive animals (Cont) that did not develop SE postpilocarpine (N‐Epi) and pilocarpine‐epileptic rats (Epi) received one of the following: phenobarbital (PB, 40 mg/kg), phenytoin (PHT, 50 mg/kg), or valproic acid (VPA, 400 mg/kg). Thirty min later the animals were challenged with either subcutaneous MES or PTZ (50 mg/kg, s.c.).Results:  VPA, PB, and PHT were able to prevent MES in all groups tested (Cont, N‐Epi, and Epi groups), whereas for the PTZ model, only the Cont group (naive animals) had seizure control with the same AEDs. In addition, Epi and N‐Epi groups when challenged with PTZ exhibited a higher incidence of severe seizures (scores IV‐IX) and SE (p < 0.05, Fisher's exact test).Conclusions:  Our findings suggest that the induction of acute seizures with PTZ, but not with MES, in animals pretreated with pilocarpine (regardless of SE induction) might constitute an effective and valuable method to screen AEDs and to study mechanisms involved in pharmacoresistant temporal lobe epilepsy (TLE).
Lamotrigine–valproic acid combination therapy for medically refractory epilepsy
Authors: Moeller Jeremy J. , Rahey Susan R. , Sadler R. Mark 
Published: November 2008

SummaryPurpose:  A retrospective study of lamotrigine (LTG)–valproic acid (VPA) combination therapy in medically refractory epilepsy.Methods:  Patients were identified with an adult epilepsy clinic database and were included if they had been on LTG–VPA combination therapy for at least 6 months. Patient demographics and information about epilepsy type, severity, and degree of medical intractability were obtained by retrospective chart review. The primary outcome measure was change in baseline seizure frequency, and patients were stratified into three groups: (i) seizure‐free, (ii) improved (at least 50% reduction in baseline seizure frequency), and (iii) not improved.Results:  Thirty‐five patients met all inclusion–exclusion criteria. Epilepsy type was generalized in 25 patients (71%) and partial in 10 patients (29%). Before LTG–VPA treatment, 27 of 35 (77%) experienced disabling seizures on a monthly basis, and 17 of 35 (49%) of patients had at least one disabling seizure per week. Patients had previously failed treatment with a median of five antiepileptic drugs (AEDs), alone or in combination. With LTG–VPA therapy, 18 (51.4%) remained completely seizure‐free, four (11.4%) were improved, and 13 (37.1%) were unimproved. Median follow‐up was 42 months. Of the 22 patients who improved, 11 had previously failed LTG and VPA monotherapy. There was no significant difference between improved and unimproved patients with respect to demographics, epilepsy type or severity, or number of previously failed AEDs.Discussion:  The combination of LTG and VPA should be considered in patients with medically refractory epilepsy. The effectiveness of this combination appears to be independent of epilepsy type or patient demographics.
A case report of a family with overlapping features of autosomal dominant febrile seizures and GEFS+
Authors: Hindocha Neeti , Nabbout Rima , Elmslie Frances , Makoff Andrew , Al‐Chalabi Ammar , Nashef Lina 
Published: November 2008

SummaryFamilial febrile seizures occur in both generalized epilepsy with febrile seizures plus (GEFS+) and autosomal dominant febrile seizures (ADFS). The literature largely separates families with GEFS+ from those with ADFS. However, there is clinical overlap, and families with ADFS also include individuals with afebrile seizures. The phenotypic spectrum of GEFS+ is broader now than when first described, resulting in unclear boundaries between these two familial syndromes. The purpose of this report is to highlight the phenotypic similarities of GEFS+ and ADFS. A multigenerational family with febrile and afebrile seizures is described and the clinical features are compared to those of previously reported GEFS+ and ADFS families. This family meets the requirements for both ADFS and the broader definition of GEFS+. Linkage analysis has shown no clear linkage to known febrile seizure or GEFS+ loci. Despite locus heterogeneity, identified mutations in reported GEFS+ have so far all been in sodium channel or γ‐aminobutyric acid (GABA)–receptor genes, with other modifier genes postulated to affect individual phenotypes. The two mutations identified in families with ADFS are in genes implicated in GEFS+, SCN1A, and GABRG2. We conclude that it is inappropriate to separate GEFS+ and ADFS at present given the clinical and genotypic overlap.
Status epilepticus in children with Alpers’ disease caused byPOLG1mutations: EEG and MRI features
Authors: Wolf Nicole I. , Rahman Shamima , Schmitt Bernhard , Taanman Jan‐Willem , Duncan Andrew J. , Harting Inga , Wohlrab Gabriele , Ebinger Friedrich , Rating Dietz , Bast Thomas 
Published: November 2008

SummaryPurpose: Refractory convulsive status epilepticus in infancy and childhood is a rare emergency situation. Metabolic disorders frequently underlie this condition, in particular Alpers' disease caused byPOLG1mutations. Status epilepticus may be the first symptom. A pathognomonic electroencephalography (EEG) signature may facilitate diagnosis of Alpers' disease and allow timely avoidance of valproic acid, which is contraindicated in this disorder because it may trigger fatal liver failure.Patients: We present five patients with Alpers' disease caused by mutations inPOLG1. Age of onset ranged from 7 months to 10 years. Three of the five children died after 3 to 12 months after onset of status epilepticus. Two of these had liver failure associated with use of valproic acid; liver transplantation in one child did not prevent a fatal neurologic outcome.Results: Convulsive status epilepticus was the first obvious sign of Alpers' disease in all children. All had focal clonic and complex‐focal seizures; four of them developed epilepsia partialis continua. In four children, initial EEG showed unilateral occipital rhythmic high‐amplitude delta with superimposed (poly)spikes (RHADS). Magnetic resonance imaging (MRI) revealed cortical and thalamic involvement in all, although there were only discrete abnormalities in one child. Metabolic investigations remained normal in three children.Conclusion: Alpers' disease is an important differential diagnosis in childhood refractory convulsive status epilepticus. Its EEG hallmark of RHADS is important for timely diagnosis, management, and counseling.
Three‐dimensional hippocampal atrophy maps distinguish two common temporal lobe seizure–onset patterns
Authors: Ogren Jennifer A. , Bragin Anatol , Wilson Charles L. , Hoftman Gil D. , Lin Jack J. , Dutton Rebecca A. , Fields Tony A. , Toga Arthur W. , Thompson Paul M. , Engel Jr. Jerome , Staba Richard J. 
Published: November 2008

SummaryPurpose:  Current evidence suggests that the mechanisms underlying depth electrode–recorded seizures beginning with hypersynchronous (HYP) onset patterns are functionally distinct from those giving rise to low‐voltage fast (LVF) onset seizures. However, both groups have been associated with hippocampal atrophy (HA), indicating a need to clarify the anatomic correlates of each ictal onset type. We used three‐dimensional (3D) hippocampal mapping to quantify HA and determine whether each onset group exhibited a unique distribution of atrophy consistent with the functional differences that distinguish the two onset morphologies.Methods:  Sixteen nonconsecutive patients with medically refractory epilepsy were assigned to HYP or LVF groups according to ictal onset patterns recorded with intracranial depth electrodes. Using preimplant magnetic resonance imaging (MRI), levels of volumetrically defined HA were determined by comparison with matched controls, and the distribution of local atrophy was mapped onto 3D hippocampal surface models.Results:  HYP and LVF groups exhibited significant and equivalent levels of HA ipsilateral to seizure onset. Patients with LVF onset seizures also showed significant contralateral volume reductions. On ipsilateral contour maps HYP patients exhibited an atrophy pattern consistent with classical hippocampal sclerosis (HS), whereas LVF atrophy was distributed more laterally and diffusely. Contralateral LVF maps also showed regions of subicular atrophy.Discussion:  The HS‐like distribution of atrophy and the restriction of HA to the ipsilateral hippocampus in HYP patients are consistent with focal hippocampal onsets, and suggest a mechanism utilizing intrahippocampal circuitry. In contrast, the bilateral distribution of nonspecific atrophy in the LVF group may reflect mechanisms involving both hippocampal and extrahippocampal networks.