bluuebunny/crossref_metadata_2025_split huggingface dataset:
Contrasting P–T–t paths for Neoproterozoic metamorphism in MacRobertson and Kemp Lands, east Antarctica
Authors: HALPIN J. A. , CLARKE G. L. , WHITE R. W. , KELSEY D. E. 
Published: July 2007

AbstractMineral equilibria modelling and electron microprobe chemical dating of monazite in granulite facies metapelitic assemblages from the MacRobertson Land coastline, Rayner Complex, east Antarctica, are consistent with an ‘anticlockwise’ Neoproterozoic P–T–t path. Metamorphism occurred at c. 990–970 Ma, achieving peak conditions of 850 °C and 5.6–6.2 kbar at Cape Bruce, and 900 °C and 5.4–6.2 kbar at the Forbes Glacier ∼50 km to the east. These peak metamorphic conditions preceded the emplacement of regionally extensive syntectonic charnockite. High temperature conditions are likely to have been sustained for 80 Myr by lithospheric thinning and repeated pluton emplacement; advection was accompanied by crustal thickening to maximum pressures of 6–7 kbar, followed by near‐isobaric cooling. This P–T–t path is distinct from that of rocks in adjacent Kemp Land, ∼50 km to the west, where a ‘clockwise’P–T–t path from higher‐P conditions at c. 940 Ma may reflect the response of a cratonic margin displaced from the main magma flux. In this scenario, crustal shortening was initially accommodated in younger, fertile crust (MacRobertson Land) involving metasediments and felsic plutons with the transfer of strain to adjacent older crust (Kemp Land) subsequent to charnockite emplacement.
In Vivo and In Vitro Effects of Pilocarpine: Relevance to Ictogenesis
Authors: Marchi Nicola , Oby Emily , Batra Ayush , Uva Laura , De Curtis Marco , Hernandez Nadia , Van Boxel‐Dezaire Anette , Najm Imad , Janigro Damir 
Published: July 2007

Summary
Objectives: A common experimental model of status epilepticus (SE) utilizes intraperitoneal administration of the cholinergic agonist pilocarpine preceded by methyl‐scopolamine treatment. Currently, activation of cholinergic neurons is recognized as the only factor triggering pilocarpine SE. However, cholinergic receptors are also widely distributed systemically and pretreatment with methyl‐scopolamine may not be sufficient to counteract the effects of systemically injected pilocarpine. The extent of such peripheral events and the contribution to SE are unknown and the possibility that pilocarpine also induces SE by peripheral actions is yet untested.
Methods: We measured in vivo at onset of SE: brain and blood pilocarpine levels, blood–brain barrier (BBB) permeability, T‐lymphocyte activation and serum levels of IL‐1β and TNF‐α. The effects of pilocarpine on neuronal excitability was assessed in vitro on hippocampal slices or whole guinea pig brain preparations in presence of physiologic or elevated [K+]out.
Results: Pilocarpine blood and brain levels at SE were 1400 ± 200 μM and 200 ± 80 μM, respectively. In vivo, after pilocarpine injection, increased serum IL‐1β, decreased CD4:CD8 T‐lymphocyte ratios and focal BBB leakage were observed. In vitro, pilocarpine failed to exert significant synchronized epileptiform activity when applied at concentrations identical or higher to levels measured in vivo. Intense electrographic seizure‐like events occurred only in the copresence of levels of K+ (6 mM) mimicking BBB leakage.
Conclusions: Early systemic events increasing BBB permeability may promote entry of cofactors (e. g. K+) into the brain leading to pilocarpine‐induced SE. Disturbance of brain homeostasis represents an etiological factor contributing to pilocarpine seizures.
Different Neuronal Networks Are Associated with Spikes and Slow Activity in Hypsarrhythmia
Authors: Siniatchkin Michael , Van Baalen Andreas , Jacobs Julia , Moeller Friederike , Moehring Jan , Boor Rainer , Wolff Stephan , Jansen Olav , Stephani Ulrich 
Published: July 2007

Summary
Purpose: West syndrome is a severe epileptic encephalopathy of infancy characterized by a poor developmental outcome and hypsarrhythmia. The pathogenesis of hypsarrhythmia is insufficiently understood.
Methods: We investigated eight patients with infantile spasms and hypsarrhythmia (group I) and 8 children with complex partial seizures (group II) using simultaneous recordings of electroencephalogram (EEG) and functional MRI. Hemodynamic responses to epileptiform discharges and slow wave activity (EEG delta power) were analyzed separately.
Results: In group I (mean age, 7.82 ± 2.87 months), interictal spikes within the hypsarrhythmia were associated with positive blood oxygenation level‐dependent (BOLD) changes in the cerebral cortex (especially occipital areas). This was comparable with cortical positive BOLD responses in group II (mean age, 20.75 ± 12.52 months). Slow wave activity in group I correlated significantly with BOLD signal in voxels, which were localized in brainstem, thalamus, as well as different cortical areas. There was no association between BOLD effect and EEG delta power in group II. Moreover, as revealed by group analysis, group I differed from group II according to correlations between BOLD signal and slow wave activity in putamen and brainstem.
Conclusions: This study demonstrates that multifocal interictal spikes and high‐amplitude slow wave activity within the hypsarrhythmia are associated with the activation of different neuronal networks. Although spikes caused a cortical activation pattern similar to that in focal epilepsies, slow wave activity produced a hypsarrhythmia‐specific activation in cortex and subcortical structures such as brainstem, thalamus, and putamen.
Life‐Threatening Status Epilepticus Following Gabapentin Administration in a Patient with Benign Adult Familial Myoclonic Epilepsy
Authors: Striano Pasquale , Coppola Antonietta , Madia Francesca , Pezzella Marianna , Zara Federico , Striano Salvatore 
Published: July 2007

Summary We report the case of a 57‐year‐old man who experienced life‐threatening myoclonic status after the administration of gabapentin. Based on familial data, the patient was determined to be a member of a previously described family with benign adult familial myoclonic epilepsy (BAFME). The myoclonic status did not respond to benzodiazepines, but resolved after discontinuing the gabapentin. As for other idiopathic generalized epilepsies, gabapentin may precipitate myoclonic status in a benign syndrome, such as BAFME, as is reported herein for the first time. A correct diagnosis and prompt discontinuation of the drug may reverse a potentially severe, life‐threatening condition.
EEG Characteristics Related to Educational Impairments in Children with Benign Childhood Epilepsy with Centrotemporal Spikes
Authors: Nicolai Joost , Van Der Linden Inge , Arends Johan B. A. M. , Van Mil Saskia G. M. , Weber Jacobiene W. , Vles Johan S. H. , Aldenkamp Albert P. 
Published: July 2007

SummaryPurpose:Learning and behavioral difficulties often occur in benign childhood epilepsy with centrotemporal spikes (BCECTS). In recent years, several electroencephalogram (EEG) characteristics have been related to the occurrence of learning and behavioral problems.Methods:From 28 children medical, school and psychological reports were present and children were rated according to a 4‐point scale for educational and behavioral impairment (Part 1). Thirty 24‐h EEG recordings were reanalyzed for spike frequency, the presence of atypical EEG criteria, and the presence of a nondipole spike. EEGs were scored during wakefulness, first hour of sleep and whole night sleep (minus the first hour of sleep) separately (Part 2).Results:The presence of I: an intermittent slow‐wave focus during wakefulness, II: a high number of spikes in the first hour of sleep (and during whole night sleep), and III: multiple asynchronous bilateral spike‐wave foci in the first hour of sleep correlates significantly with a sum score ≥ 3 which indicates a complicated course with educational or behavioral impairment. It is sufficient to analyze an EEG during wakefulness and a sleep EEG for only the first hour of sleep instead of a whole night recording to demonstrate those EEG criteria.Conclusions:On basis of our reanalysis we can possibly conclude that the aforementioned EEG characteristics correlate with educational impairments, and that analysing an EEG recording during wake and the first hour of sleep is sufficient to look adequately for those EEG criteria in children with BCECTS.
Aggravation of Seizures and/or EEG Features in Children Treated with Oxcarbazepine Monotherapy
Authors: Vendrame Martina , Khurana Divya S. , Cruz Marcos , Melvin Joseph , Valencia Ignacio , Legido Agustin , Kothare Sanjeev V. 
Published: July 2007

Summary
Purpose: Exacerbation of epilepsy may occur following initiation of therapy with antiepileptic drugs (AEDs). The aim of this study is to analyze the clinical and EEG characteristics of a group of pediatric patients with worsening of seizures and/or EEG deterioration while on oxcarbazepine (OXC).
Methods: A retrospective analysis of a clinical database was performed to identify patients with epilepsy treated with OXC over the past 3 years. History, neurological examination, and EEG findings were reviewed to identify any who had developed exacerbation of seizures or new abnormalities on EEG.
Results: Of 290 patients on OXC, we identified 12 patients with new onset seizures, all with initial normal neurological exam and normal EEG, who developed either worsening of preexisting seizures, new seizure types, and/or EEG deterioration following introduction of OXC monotherapy. EEG changes were primarily characterized by new onset of generalized epileptiform activity not reported on the initial baseline EEG. Following substitution of OXC with a broad spectrum AED, significant improvement of seizure control and improvement in the EEG was observed.
Conclusions: These findings suggest that OXC can aggravate seizures and/or worsen EEG features in children. Following initiation of therapy with OXC, monitoring of patients with follow‐up EEGs may be important, especially in patients who do not show adequate response to therapy.
Insulin and Insulin‐Like Growth Factor Resistance With Neurodegeneration in an Adult Chronic Ethanol Exposure Model
Authors: Cohen Ariel C. , Tong Ming , Wands Jack R. , De La Monte Suzanne M. 
Published: July 2007

Background: Previous studies linked cerebellar hypoplasia, neuronal loss, and impaired acetylcholine homeostasis to ethanol inhibition of insulin and insulin‐like growth factor signaling mechanisms in experimental models of fetal alcohol syndrome (FAS).Methods: To determine the extent to which similar abnormalities occur in mature brains, gene expression, ligand binding, and histopathological studies were performed with temporal lobe, hypothalamus, and cerebellar cortex from adult male Long Evans rats that were pair‐fed for 6 weeks with liquid diets containing 0% or 37% ethanol by caloric content.Results: Real time quantitative RT‐PCR analysis demonstrated that the chronic ethanol‐fed rats had significantly reduced insulin‐like growth factors (IGF)‐II receptor expression in all 3 regions and reduced insulin receptor expression in the temporal lobe. However, equilibrium binding assays revealed ethanol‐associated impairments in insulin and IGF‐I receptor binding in all 3 regions and reduced IGF‐II receptor binding in the cerebellum. These abnormalities were associated with decreased expression of Hu (neuronal loss) in the temporal lobe and cerebellum, and choline acetyltransferase (ChAT) in the hypothalamus and cerebellum, and increased expression of NADPH oxidase 3 in all 3 regions examined. Ethanol‐associated neuronal loss with increased indices of lipid peroxidation and DNA damage were demonstrated by histopathological, immunohistochemical, and enzyme linked immunosorbant assay studies.Conclusions: These results suggest that ethanol‐induced neurodegeneration in adults is mediated by insulin/IGF resistance, persistent oxidative stress, and impaired acetylcholine biosynthesis, similar to the findings in FAS. The reductions in ChAT gene expression most likely contribute to the cognitive and motor deficits that occur with chronic alcohol abuse.
Isoform‐Specific Enhancement of Adenylyl Cyclase Activity by n‐Alkanols
Authors: Kou Jinghong , Yoshimura Masami 
Published: July 2007

Background:  Numerous studies suggest that cAMP signaling pathways play important roles in the development of and predisposition to alcoholism. Our previous study showed that cAMP generation by various isoforms of adenylyl cyclase (AC) exhibits a broad spectrum of responses to ethanol in the human embryonic kidney (HEK) 293 cell system overexpressing individual AC isoforms. These findings suggest that the target of ethanol’s action in the cAMP‐generating system is AC. However, it is unknown if the action of ethanol is direct or indirect.Methods:  The effect of a series of n‐alkanols (ethanol to decanol) on dopamine (DA)–stimulated activity of AC isoforms type 6, 7, and 9 (AC6, AC7, and AC9) were examined in transfected HEK293 cells by cAMP accumulation assay.Results:  n‐Alkanols increased DA‐stimulated cAMP production in an AC isoform‐specific manner, and displayed the alcohol cutoff phenomenon (defined as the carbon chain length beyond which there is no further increase in the potency of an ascending series of n‐alkanols). The n‐alkanol cutoffs for AC6, AC7, and AC9 are butanol (C4), pentanol (C5), and equal to or greater than decanol (C10), respectively.Conclusion:  The results clearly indicate that, in the HEK293 expression system, the alcohol cutoff effect for n‐alkanol potentiation of DA‐stimulated AC activity is AC isoform specific. These results strongly suggest that alcohols interact directly with AC molecules.
Developmental Differences in Acute Ethanol Withdrawal in Adolescent and Adult Rats
Authors: Doremus‐Fitzwater Tamara L , Spear Linda P 
Published: July 2007

Background: Withdrawal from an acute high ethanol dose induces behaviors reminiscent of withdrawal from chronic ethanol exposure. While such “hangover”‐related anxiety has previously been shown to be considerably less pronounced in adolescent compared to adult male rats, ontogenetic studies are limited and few experiments have directly compared sex‐ and age‐related differences in sensitivity to ethanol hangover.Methods: The current experiments examined consequences of a previous ethanol challenge (4.0 g/kg i.p. injection, 20% v/v) on anxiety and exploratory behavior in the elevated plus‐maze (EPM) and holeboard (HB) tests, respectively, in adolescent and adult male and female Sprague–Dawley rats.Results: In Exp. 1, evidence of hangover‐related anxiety and withdrawal‐induced hypoactivity emerged at both ages and in both sexes. As several procedural variables were changed in Exp.1 relative to previous studies from our laboratory showing age‐related differences in these hangover measures, Exp. 2 explored the possible contribution of 2 variables to ontogenetic expression of withdrawal‐induced anxiogenesis: (1) isolation vs. social context during the postchallenge recovery period and (2) EPM testing alone or immediately following a 5 minute HB test. Results of Exp. 2 revealed few significant interactions of these variables with age‐ and ethanol exposure‐related anxiety measures, although sequential testing (HB before EPM) notably suppressed activity in the EPM and altered the major underlying component of EPM behavior from anxiety to activity as revealed in factor analyses of these data. Additional analyses conducted on animals tested only in the EPM revealed attenuations in withdrawal anxiogenesis among adolescents, along with withdrawal‐related decreases in activity at both ages.Conclusions: Taken together, these results suggest that adolescents do show an attenuated sensitivity to hangover‐induced anxiogenesis in the EPM, an age difference not evident under other pretest conditions. Therefore, caution should be exerted when using the EPM to index anxiety across age. The robustness of withdrawal‐related hypoactivity at both ages suggests that adolescents may not be globally insensitive to the consequences of previous binge‐like exposure to ethanol, but rather less likely to express certain hangover‐related consequences.
Acute Ethanol Has Biphasic Effects on Short‐ and Long‐Term Memory in Both Foreground and Background Contextual Fear Conditioning in C57BL/6 Mice
Authors: Gulick Danielle , Gould Thomas J. 
Published: July 2007

Background: Ethanol is a frequently abused, addictive drug that impairs cognitive function. Ethanol may disrupt cognitive processes by altering attention, short‐term memory, and/or long‐term memory. Interestingly, some research suggests that ethanol may enhance cognitive processes at lower doses. The current research examined the dose‐dependent effects of ethanol on contextual and cued fear conditioning. In addition, the present studies assessed the importance of stimulus salience in the effects of ethanol and directly compared the effects of ethanol on short‐term and long‐term memory.Methods: This study employed both foreground and background fear conditioning, which differ in the salience of contextual stimuli, and tested conditioning at 4 hours, 24 hours, and 1 week in order to assess the effects of ethanol on short‐term and long‐term memory. Foreground conditioning consisted of 2 presentations of a foot shock unconditioned stimulus (US) (2 seconds, 0.57 mA). Background conditioning consisted of 2 auditory conditioned stimulus (30 seconds, 85 dB white noise)–foot shock (US; 2 seconds, 0.57 mA) pairings.Results: For both foreground and background conditioning, ethanol enhanced short‐term and long‐term memory for contextual and cued conditioning at a low dose (0.25 g/kg) and impaired short‐term and long‐term memory for contextual and cued conditioning at a high dose (1.0 g/kg).Conclusions: These results suggest that ethanol has long‐lasting, biphasic effects on short‐term and long‐term memory for contextual and cued conditioning. Furthermore, the effects of ethanol on contextual fear conditioning are independent of the salience of the context.
Effects of Prenatal Ethanol Exposure on Basal Limbic–Hypothalamic–Pituitary–Adrenal Regulation: Role of Corticosterone
Authors: Glavas Maria M. , Ellis Linda , Yu Wayne K. , Weinberg Joanne 
Published: July 2007

Background:  Rats prenatally exposed to ethanol (E) exhibit hypothalamic–pituitary–adrenal (HPA) hyperresponsiveness and changes in central HPA regulation following exposure to stressors. Whether ethanol‐induced alterations in basal HPA regulation play a role in mediating HPA hyperresponsiveness remains unclear. We utilized adrenalectomy (ADX), with or without corticosterone (CORT) replacement, to investigate basal HPA function and the role of CORT in mediating ethanol‐induced alterations.Methods:  Adult males and females from prenatal E, pair‐fed (PF), and ad lib‐fed control (C) groups were terminated at the circadian peak, 7 days following sham surgery or ADX, with or without CORT replacement. Plasma levels of CORT and adrenocorticotropin (ACTH), and mRNA levels of corticotropin‐releasing hormone (CRH) and arginine vasopressin (AVP) in the paraventricular nucleus, CRH Type 1 receptor (CRH‐R1) and pro‐opiomelanocortin (POMC) in the anterior pituitary, and mineralocorticoid (MR) and glucocorticoid (GR) receptors in the dorsal hippocampus were determined.Results:  Adrenalectomy resulted in significantly greater plasma ACTH elevations in E and PF males, and parallel CRH mRNA elevations in both E and PF males and females compared with their C counterparts. In contrast, pituitary CRH‐R1 mRNA levels were lower in E compared with C males, with no differences in POMC. In addition, in response to ADX, E females showed a greater MR mRNA response, and E males showed a greater GR mRNA response compared with their C counterparts, and CORT replacement was ineffective in normalizing ADX‐induced alterations in ACTH levels in E and PF females, hippocampal MR mRNA levels in E males, and AVP mRNA levels in PF males and females.Conclusions:  Together, these data indicate that the prenatal ethanol exposure induces HPA dysregulation under basal conditions at multiple levels of the axis, resulting in alterations in both HPA drive and feedback regulation and/or in the balance between drive and feedback. While some effects may be nutritionally mediated, it appears that the mechanisms underlying basal HPA dysregulation may differ between E and PF animals rather than occurring along a continuum of effects on the same pathway. Altered basal HPA tone may play a role in mediating the HPA hyperresponsiveness to stressors observed in E offspring.
The blood bank: from provider to partner in treatment of massively bleeding patients
Authors: Johansson Pär I. 
Published: July 2007

BACKGROUND: Continued hemorrhage remains a major cause of mortality in massively transfused patients of whom many develop coagulopathy. Reviewing transfusion practice for these patients, we found that at our hospital more than 10 percent received a suboptimal transfusion therapy and that survivors had a higher platelet count than nonsurvivors. We therefore investigated whether the blood bank could improve its service and hence improve the outcome.METHODS: The blood bank introduced monitoring of the delivery of blood products and contacted the clinician provided there was an imbalance in the transfusion practice. For massively transfused patients, transfusion packages, including five red blood cells, five fresh‐frozen plasma, and two platelet concentrates, were introduced to improve hemostatic competence. The Thrombelastograph (TEG) Haemostatic System (Haemoscope Corp., Niles, IL) was implemented, aiding in the diagnosis and treatment of coagulopathy.RESULTS: The fraction of suboptimally transfused patients declined from more than 10 percent to less than 3 percent. The transfusion package administered intraoperatively to patients operated on for a ruptured abdominal aortic aneurysm resulted in decreased postoperative transfusion requirements and improved 30‐day survival (66% vs. 44%) compared with controls. Performing TEG alone in patients with significant bleeding as judged by the anesthetist reduced the number of analyses by approximately 85 percent, while those patients with coagulopathy remained identified. The TEG showed a 97 percent predictability in identifying a surgical cause of bleeding in postoperative patients. Ten percent of the massively bleeding trauma patients had hyperfibrinolysis as the major cause of bleeding, whereas 45 percent were hypercoagulable.CONCLUSION: The initiative from the blood bank has improved the transfusion practice and, hence, survival in massively transfused patients at our hospital.
Christian God‐Talk While Listening to Atheists, Pluralists, and Muslims
Authors: Peters Ted 
Published: July 2007

Abstract:In the global conversation over religious ideas, a de facto debate is raging between atheism, pluralism, and Islam. Pluralism respects the claim of every religion. Atheism respects the claim of no religion. Islam respects the claim of its own religion. How should a Christian theologian construct a doctrine of God that benefits from listening to this conversation yet stresses what is important in the gospel, namely, that the God of Jesus Christ is gracious in character? What is recommended here is to (1) investigate the truth question; (2) avoid putting God in the equations; (3) affirm what is essential; and (4) practice charity.
Nothing Less than Everything: Thoughts on a Sittler Legacy
Authors: Childs James M. 
Published: July 2007

Abstract:Universtiy of Chicago theologian Joseph Sittler has left a most valuable legacy. He was a “preacher's theologian.” He distinguished between a literal reading of the Bible from faith in the God of the Bible. He pioneered the interaction between Christology and ecology. Sittler was a pioneer, worthy of being remembered two decades after his death.