bluuebunny/crossref_metadata_2025_split huggingface dataset:
A 1H magnetic resonance spectroscopy study in patients with obstructive sleep apnea
Authors: Sarchielli P. , Presciutti O. , Alberti A. , Tarducci R. , Gobbi G. , Galletti F. , Costa C. , Eusebi P. , Calabresi P. 
Published: August 2008

Background and purpose:  Repeated episodes of hypoxia, hypercapnia and transient blood pressure elevation in obstructive sleep apnea syndrome (OSAS) may damage neutral structures and induce cerebral metabolic impairment. This study aimed to determine the impact of OSAS on cerebral metabolites measured by 1H magnetic resonance spectroscopy (1H ‐MRS).Methods:  Twenty OSAS patients underwent standard overnight polysomnography and 1H‐MRS separately. Proton volumes of interest (VOIs) were placed in frontal and midtemporal regions bilaterally.Results:  Significantly lower values of the N‐acetylaspartate (NAA)/creatine (Cr) ratio were found in frontal regions (P < 0.004) compared with 20 age‐matched control subjects. A significant increase in the myo‐inositol (Ins)/Cr ratio was evident bilaterally in temporal and frontal regions (P < 0.00002 and P < 0.04). Choline (Cho)/Cr ratio values were also significantly greater in temporal regions (P < 0.00001). A significant negative correlation (r = −0.51, P < 0.03) was found between the apnea‐hypopnea index (AHI) and NAA/Cr ratio in the frontal regions of OSAS patients.Conclusions:  Reduction in the NAA/Cr ratio in frontal regions of OSAS patients could be related to neural loss. Increase in the Cho/Cr ratio in temporal regions and Ins/Cr ratio in both frontal and temporal regions could be interpreted as evidence of membrane breakdown and reactive gliosis, respectively, consequent to repeated episodes of hypoxia in OSAS.
Cytokine IL‐1 beta but not IL‐1 alpha promoter polymorphism is associated with Alzheimer disease in a population from the Canary Islands, Spain
Authors: Déniz‐Naranjo M. C. , Muñoz‐Fernandez C. , Alemany‐Rodríguez M. J. , Pérez‐Vieitez M. C. , Aladro‐Benito Y. , Irurita‐Latasa J. , Sánchez‐García F. 
Published: August 2008

Aims:  Previous studies have reported the presence of low‐grade inflammation in Alzheimer disease (AD). Based on these data, our work attempts to investigate the effects of some promoter polymorphisms of pro‐inflammatory cytokines [interleukin (IL)‐1 alpha and IL‐1 beta] on AD.Patients and methods:  A PCR‐RFLP technique was used to analyze the promoter polymorphisms of both IL‐1 alpha (−889 C/T) and IL‐1 beta (−511 C/T) and the APOE genotype from the DNA samples of 282 patients (according to NINCDS‐ADRDA criteria) and 312 control subjects.Results:  (i) The risk of developing AD in our population was associated with the IL‐1 beta (−511 C/T) promoter polymorphism; (ii) such risk was independent of the risk factor allele in the APOE gene (APOE4); and (iii) the IL‐1 alpha promoter polymorphism (−889 C/T) was not associated with the disease.Conclusion:  In our population, IL‐1 beta promoter polymorphism (−511 C/T) is an independent risk factor for AD.
Lactoferrin induces cell surface retention of prion protein and inhibits prion accumulation
Authors: Iwamaru Yoshifumi , Shimizu Yoshihisa , Imamura Morikazu , Murayama Yuichi , Endo Ryo , Tagawa Yuichi , Ushiki‐Kaku Yuko , Takenouchi Takato , Kitani Hiroshi , Mohri Shirou , Yokoyama Takashi , Okada Hiroyuki 
Published: August 2008

AbstractPrion diseases are fatal neurodegenerative disorders, and the conformational conversion of normal cellular prion protein (PrPC) into its pathogenic, amyloidogenic isoform (PrPSc) is the essential event in the pathogenesis of these diseases. Lactoferrin (LF) is a cationic iron‐binding glycoprotein belonging to the transferrin (TF) family, which accumulates in the amyloid deposits in the brain in neurodegenerative disorders, such as Alzheimer’s disease and Pick’s disease. In the present study, we have examined the effects of LF on PrPSc formation by using cell culture models. Bovine LF inhibited PrPSc accumulation in scrapie‐infected cells in a time‐ and dose‐dependent manner, whereas TF was not inhibitory. Bioassays of LF‐treated cells demonstrated prolonged incubation periods compared with non‐treated cells indicating a reduction of prion infectivity. LF mediated the cell surface retention of PrPC by diminishing its internalization and was capable of interacting with PrPC in addition to PrPSc. Furthermore, LF partially inhibited the formation of protease‐resistant PrP as determined by the protein misfolding cyclic amplification assay. Our results suggest that LF has multifunctional antiprion activities.
IRS‐2 branch of IGF‐1 receptor signaling is essential for appropriate timing of myelination
Authors: Freude Susanna , Leeser Uschi , Müller Marita , Hettich Moritz M. , Udelhoven Michael , Schilbach Katharina , Tobe Kazuyuki , Kadowaki Takashi , Köhler Christoph , Schröder Hannsjörg , Krone Wilhelm , Brüning Jens C. , Schubert Markus 
Published: August 2008

AbstractInsulin‐like growth factor (IGF)‐1 increases proliferation, inhibits apoptosis and promotes differentiation of oligodendrocytes and their precursor cells, indicating an important function for IGF‐1 receptor (IGF‐1R) signaling in myelin development. The insulin receptor substrates (IRS), IRS‐1 and ‐2 serve as intracellular IGF‐1R adaptor proteins and are expressed in neurons, oligodendrocytes and their precursors. To address the role of IRS‐2 in myelination, we analyzed myelination in IRS‐2 deficient (IRS‐2−/−) mice and age‐matched controls during postnatal development. Interestingly, expression of the most abundant myelin proteins, myelin basic protein and proteolipid protein was reduced in IRS‐2−/− brains at postnatal day 10 (P10) as compared to controls. myelin basic protein immunostaining in P10‐IRS‐2−/− mice revealed a reduced immunostaining, but an unchanged regional distribution pattern. In cerebral myelin isolates at P10 unaltered relative expression of different myelin proteins was found, indicating quantitatively reduced but not qualitatively altered myelination. Interestingly, up‐regulation of IRS‐1 expression and increased IGF‐1R signaling were observed in IRS‐2−/− mice at P10‐14, indicating a compensatory mechanism to overcome IRS‐2 deficiency. Adult IRS‐2−/− mice showed unaltered myelination and motor function. Furthermore, in neuronal/brain‐specific insulin receptor knockout mice myelination was unchanged. Thus, our experiments reveal that IGF‐1R/IRS‐2 mediated signals are critical for appropriate timing of myelination in vivo.
Differential migration, LPS‐induced cytokine, chemokine, and NO expression in immortalized BV‐2 and HAPI cell lines and primary microglial cultures
Authors: Horvath Ryan J. , Nutile‐McMenemy Nancy , Alkaitis Matthew S. , DeLeo Joyce A. 
Published: August 2008

AbstractMicroglial cells are hematopoietically derived monocytes of the CNS and serve important neuromodulatory, neurotrophic, and neuroimmune roles. Following insult to the CNS, microglia develop a reactive phenotype, migrate to the site of injury, proliferate, and release a range of proinflammatory, anti‐inflammatory, and neurotrophic factors. Isolation of primary microglial cell cultures has been an integral step in elucidating the many roles of these cells. In addition to primary microglial cells, several immortalized cell lines have been created to model primary microglia in vitro, including murine‐derived BV‐2 cells and rat derived highly aggressive proliferating immortalized (HAPI) cells. Here, we compare rat primary microglial, BV‐2, and HAPI cells in experiments assessing migration, expression of activation markers, and production and release of nitric oxide, cytokines, and chemokines. BV‐2 and HAPI cells responded similarly to primary microglia in experiments assessing migration, ionized calcium binding adaptor molecule 1 expression, and nitric oxide release. However, BV‐2 and HAPI cells did not model primary microglia in experiments assessing tumor necrosis factor‐α, interleukin‐1β, interleukin‐6, and monocyte chemoattractant protein‐1 expression and release and phospho‐extracellular signal‐regulated kinase 44/42 expression following lipopolysaccharide treatment. These results indicate that BV‐2 and HAPI cell cultures only partially model primary microglia and that their use should therefore be carefully considered.
Values of the balanced decision making between supply chain partners
Authors: Kim Bowon , Kim Jongjoo 
Published: August 2008

AbstractCoordination between supply chain partners is critical to effective supply chain management. In this paper, we consider two cases of decision‐making structure for a simple supply chain consisting of two players: the first case in which a supply chain partner dominates the decision‐making process, and the other in which two players share the decision‐making process equally. According to the literature, we knowa priorithat the balanced decision making forges a better (financial) outcome than the dominating case does. Therefore, our primary research objective is to analyze detailed dynamics of resource allocation and sources of the benefit of the balanced decision making. Our analysis indicates that the value of the balanced decision making arises from more effective resource utilization than the dominating case does: each of the cooperative partners knows how to optimize its resource utilization better than the other does.
The ALGACEA‐1 method for the capacitated vehicle routing problem
Authors: Faulin Javier , Juan Angel A. 
Published: August 2008

AbstractWe base the ALGACEA‐1 method on Clarke–Wright's savings estimates, using Monte Carlo techniques for node selection. This procedure controls the assigned probabilities for node selection using a bounded Entropy function. Similarly, we have discussed the parameter tuning for this method with the purpose of obtaining a good algorithm performance. Finally, some computational results are given to show the quality of the solutions provided by ALGACEA‐1 in a real case and in some benchmarking instances.
Peliosis hepatis and hemoperitoneum in a dog with diphacinone intoxication
Authors: Beal Matthew W. , Doherty Arin M. , Curcio Keith 
Published: August 2008

AbstractObjective: To describe the clinical course of a dog presented with peliosis hepatis and hemoperitoneum in concert with anticoagulant rodenticide intoxication.Case summary: A 7.75‐year‐old spayed female Shetland Sheepdog presented with clinical signs consistent with hypovolemia, hemoperitoneum, and a history of bright green stool 3 days before the onset of clinical signs. Initial packed cell volume/total solids were consistent with acute hemorrhage. A coagulation profile showed prolongation in activated clotting time and prolongation of both prothrombin and activated partial thromboplastin time, suggesting abnormal coagulation. Abdominal hemorrhage persisted in the face of normalization of the hemodynamic status and coagulation profile, and treatment with Vitamin K1. Abdominal ultrasound revealed multiple patchy hypoechoic areas throughout the caudate liver lobe. An exploratory laparotomy was performed 24 hours after presentation and revealed the caudate liver lobe as the source of the hemorrhage. Histopathologic examination of a specimen of the liver was consistent with peliosis hepatis. Toxicologic testing identified diphacinone levels in the blood consistent with anticoagulant rodenticide intoxication. Postoperative recovery was uneventful, and within 48 hours the dog was discharged. The dog returned to full function and a hepatic ultrasound performed 15 months postoperatively showed no significant abnormalities.New or unique information provided: Exposure to anticoagulant rodenticides may be associated with the development of peliosis hepatis in dogs.
Decreased expression of synaptic vesicle protein 2A, the binding site for levetiracetam, during epileptogenesis and chronic epilepsy
Authors: Van Vliet Erwin A. , Aronica Eleonora , Redeker Sandra , Boer Karin , Gorter Jan A. 
Published: August 2008

SummaryPurpose:  We previously showed that gene expression of synaptic vesicle protein 2A (SV2A), the binding site for the antiepileptic drug levetiracetam, is reduced during epileptogenesis in the rat. Since absence of SV2A has been associated with increased epileptogenicity, changes in expression of SV2A could have consequences for the progression of epilepsy. Therefore we investigated hippocampal SV2A protein expression of temporal lobe epilepsy (TLE) patients and in rats during epileptogenesis and in the chronic epileptic phase.Methods:  SV2A immunocytochemistry and Western blot analysis were performed on the hippocampus of autopsy controls, patients that died from status epilepticus (SE), and pharmacoresistant TLE patients. In addition, in epileptic rats, SV2A expression was determined after SE during the acute, latent, and chronic epileptic phase.Results:  In control tissue, presynaptic SV2A was expressed in all hippocampal subfields, with strongest expression in mossy fiber terminals. SV2A positive puncta were distributed in a patchy pattern over the somata and dendrites of neurons. SV2A decreased throughout the hippocampus of TLE patients with hippocampal sclerosis (HS), compared to autopsy control, SE, and non‐HS tissue. In most rats, SV2A was already decreased in the latent period especially in the inner molecular layer and stratum lucidum. Similarly as in humans, SV2A was also decreased throughout the hippocampus of chronic epileptic rats, specifically in rats with a progressive form of epilepsy.Discussion:  These data support previous findings that reduced expression of SV2A could contribute to the increased epileptogenicity. Whether this affects the effectiveness of levetiracetam needs to be further investigated.
Imaging seizure activity: A combined EEG/EMG‐fMRI study in reading epilepsy
Authors: Salek‐Haddadi Afraim , Mayer Thomas , Hamandi Khalid , Symms Mark , Josephs Oliver , Fluegel Dominique , Woermann Friedrich , Richardson Mark P. , Noppeney Uta , Wolf Peter , Koepp Matthias J. 
Published: August 2008

SummaryPurpose:  To characterize the spatial relationship between activations related to language‐induced seizure activity, language processing, and motor control in patients with reading epilepsy.Methods:  We recorded and simultaneously monitored several physiological parameters [voice‐recording, electromyography (EMG), electrocardiography (ECG), electroencephalography (EEG)] during blood oxygen level‐dependent (BOLD) functional magnetic resonance imaging (fMRI) in nine patients with reading epilepsy. Individually tailored language paradigms were used to induce and record habitual seizures inside the MRI scanner. Voxel‐based morphometry (VBM) was used for structural brain analysis. Reading‐induced seizures occurred in six out of nine patients.Results:  One patient experienced abundant orofacial reflex myocloni during silent reading in association with bilateral frontal or generalized epileptiform discharges. In a further five patients, symptoms were only elicited while reading aloud with self‐indicated events. Consistent activation patterns in response to reading‐induced myoclonic seizures were observed within left motor and premotor areas in five of these six patients, in the left striatum (n = 4), in mesiotemporal/limbic areas (n = 4), in Brodmann area 47 (n = 3), and thalamus (n = 2). These BOLD activations were overlapping or adjacent to areas physiologically activated during language and facial motor tasks. No subtle structural abnormalities common to all patients were identified using VBM, but one patient had a left temporal ischemic lesion.Discussion:  Based on the findings, we hypothesize that reflex seizures occur in reading epilepsy when a critical mass of neurons are activated through a provoking stimulus within corticoreticular and corticocortical circuitry subserving normal functions.
Preoperative amygdala fMRI in temporal lobe epilepsy
Authors: Bonelli Silvia B. , Powell Robert , Yogarajah Mahinda , Thompson Pamela J. , Symms Mark R. , Koepp Matthias J. , Duncan John S. 
Published: August 2008

SummaryPurpose:  Anterior temporal lobe resections (ATLR) benefit 70% of patients with refractory mesial temporal lobe epilepsy (TLE), but may be complicated by emotional disturbances. We used functional magnetic resonance imaging (fMRI) to investigate the role of the amygdala in processing emotions in TLE and whether this may be a potential preoperative predictive marker for emotional disturbances following surgery.Methods:  We studied 54 patients with refractory mesial TLE due to hippocampal sclerosis (28 right, 26 left) and 21 healthy controls using a memory encoding fMRI paradigm, which included viewing fearful and neutral faces. Twenty‐one TLE patients (10 left, 11 right) subsequently underwent ATLR. Anxiety and depression were assessed preoperatively and 4 months postoperatively using the Hospital Anxiety and Depression Scale.Results:  On viewing fearful faces, healthy controls demonstrated left lateralized, while right TLE patients showed bilateral amygdala activation. Left TLE patients had significantly reduced activation in left and right amygdalae compared to controls and right TLE patients. In right TLE patients, left and right amygdala activation was significantly related to preoperative anxiety and depression levels, and preoperative right amygdala activation correlated significantly with postoperative change of anxiety and depression scores, characterized by greater increases in anxiety and depression in patients with greater preoperative activation. No such correlations were seen for left TLE patients.Discussion:  The fearful face fMRI paradigm is a reliable method for visualizing amygdala activation in controls and patients with mesial TLE. Activation of the right amygdala preoperatively was predictive of emotional disturbances following right ATLR.
A blinded, crossover study of the efficacy of the ketogenic diet
Authors: Freeman John M. , Vining Eileen P.G. , Kossoff Eric H. , Pyzik Paula L. , Ye Xiaobu , Goodman Steven N. 
Published: August 2008

SummaryDespite over 80 years of use, the ketogenic diet (KD) has never been tested in a blinded manner. Twenty children with intractable Lennox‐Gastaut syndrome (LGS) were fasted 36 h and then randomized to receive the classic KD in conjunction with a solution containing either 60 g/day of glucose or saccharin. Parents and physicians were blinded to both the solution composition and level of ketosis. A crossover to the KD with the alternate solution occurred following the sixth day and a repeat fast. A 24‐h electroencephalography (EEG) was obtained at baseline and after each arm. After administration of the solution, there was moderate evidence of a reduction in parent‐reported seizures between the glucose and saccharin arms, with a median difference of 1.5 seizures per day (p = 0.07). There was no reduction in the number of EEG‐identified events, with a median reduction of 7 events per day (p = 0.33). Ketosis was not completely eliminated in the glucose‐added arm.
Two novel ALDH7A1 (antiquitin) splicing mutations associated with pyridoxine‐dependent seizures
Authors: Striano Pasquale , Battaglia Silvia , Giordano Lucio , Capovilla Giuseppe , Beccaria Francesca , Struys Eduard A. , Salomons Gajja S. , Jakobs Cornelis 
Published: August 2008

SummaryPyridoxine‐dependent seizures (PDS) is a rare autosomal recessive disorder causing intractable seizures in neonates and infants. Patients are typically resistant to conventional anticonvulsants but respond well to the administration of pyridoxine. We report two unrelated patients affected with PDS as a result of α‐aminoadipic semialdehyde (α‐AASA) dehydrogenase deficiency caused by pathogenic ALDH7A1/antiquitin mutations. Two of the three reported mutations are novel and result in erroneous splicing, as showed by messenger RNA (mRNA) studies.So far, the vast majority of the patients clinically diagnosed as PDS show α‐AASA dehydrogenase deficiency, caused by mutations in the ALDH7A1 gene. However, despite the availability of reliable biomarkers, early consideration of a pyridoxine trial is still the most important issue in a child with therapy‐resistant seizures.
Source localization of scalp‐EEG interictal spikes in posterior cortex epilepsies investigated by HR‐EEG and SEEG
Authors: Gavaret Martine , Trébuchon Agnès , Bartolomei Fabrice , Marquis Patrick , McGonigal Aileen , Wendling Fabrice , Regis Jean , Badier Jean‐Michel , Chauvel Patrick 
Published: August 2008

SummaryPurpose:  To determine the validity of scalp‐electroencephalography (EEG)‐interictal spike (IIS) source localization in posterior cortex epilepsies (PCE).Methods:  Eleven patients with drug‐resistant PCE were studied with high‐resolution EEG (HR‐EEG) and stereoelectroencephalography (SEEG). Sixty‐four scalp channels, a realistic head model, and different algorithms [multiple signal classification (MUSIC) and equivalent current dipoles] were used. Results were compared to intracerebral SEEG recordings. For SEEG, a semiautomatic detection of intracerebral IIS was used, allowing a classification of intracerebral IIS into one of three groups: Medial, lateral, and mediolateral.Results:  In the medial group (two patients), scalp‐EEG IIS were usually absent for one patient whereas for the other, scalp‐EEG was misleading. Indeed, scalp‐EEG IIS had a posterior projection, predominantly contralateral to the source. In the lateral group (two patients), scalp‐EEG IIS were subcontinuous and accurately localized. In the mediolateral group (seven patients), intracerebral interictal distribution was complex and bilateral for four of seven patients. Source localizations were able to determine only a part, whether lateral or medial, of the intracerebral interictal distribution.Discussion:  The accuracy of scalp‐EEG IIS source localization is dependant on the type of intracerebral interictal distribution. In the most frequent type of PCE, patients proved to have a complex interictal distribution between both medial and lateral cortices, and source localizations always underestimated intracerebral IIS. In cases where intracranial sources were quite focal, surface EEG sources were localized with accuracy, even in medial occipital lobe structures.
Oxcarbazepine, not its active metabolite, potentiates GABAA activation and aggravates absence seizures
Authors: Zheng Thomas , Clarke Alison L. , Morris Margaret J. , Reid Christopher A. , Petrou Steven , O'Brien Terence J. 
Published: August 2008

SummaryPurpose:  Studies in genetic absence epileptic rats from Strasbourg (GAERS) indicate that enhancement of γ aminobutyric acid (GABAA) receptor activity is a critical mechanism in the aggravation of seizures by carbamazepine (CBZ). We examined whether structural analogs of CBZ, oxcarbazepine (OXC), and its active metabolite, monohydroxy derivative (MHD), also potentiate GABAA receptor current and aggravate seizures.Methods:  In vitro studies in Xenopus oocytes compared the three drugs' effect on GABAA receptor currents. In vivo studies compared seizure activity in GAERS after intraperitoneal drug administration.Results:  OXC potentiated GABAA receptor current and aggravated seizures in GAERS, similarly to the effect of CBZ. Conversely, MHD showed only a minor potentiation of GABAA receptor current and did not aggravate seizures.Discussion:  A hydroxyl group at the C‐10 position on the CBZ tricyclic structure in MHD reduces GABAA receptor potentiation and seizure aggravation. Reports of the aggravation of absence seizures in patients taking OXC may result from circulating unmetabolized OXC rather than MHD.