bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of cytochrome P450 2C19 genetic polymorphism and dosage of rabeprazole on accuracy of proton‐pump inhibitor testing in Chinese patients with gastroesophageal reflux disease
Authors: Lee Yi‐Chia , Lin Jaw‐Town , Wang Hsiu‐Po , Chiu Han‐Mo , Wu Ming‐Shiang 
Published: June 2007

AbstractBackground and Aim:  To evaluate the optimal dosage of rabeprazole for proton‐pump inhibitor (PPI) testing of gastroesophageal reflux disease (GERD) and to test the influence of cytochrome P450 (CYP) 2C19 polymorphism in a population with a high prevalence of people who metabolize PPI poorly.Methods:  In this randomized, open‐label trial, patients with symptoms suggestive of GERD were randomized to receive a 2‐week test with 20‐ or 40‐mg rabeprazole after diagnostic endoscopy. Symptom response was assessed with a four‐grade daily record; in addition, DNA from peripheral blood leukocytes was genotyped for CYP2C19 polymorphism with the polymerase chain reaction–restriction fragment length polymorphism technique.Results:  Of the 164 patients who completed the study, 69 (42.1%) were endoscopically positive for esophagitis; the remaining 95 (57.9%) were diagnosed with endoscopy‐negative reflux disease. Based on the best cut‐off value for 50% symptom reduction, the sensitivity, specificity, positive predictive value, negative predictive value, and accuracy for detecting erosive esophagitis were 68%, 70%, 66%, 72%, and 69%, respectively, for the 20‐mg regimen, and 84%, 71%, 64%, 88%, and 76%, respectively, for the 40‐mg regimen, a non‐significant difference. Regarding the genotype, 60 (39%) patients had two wild‐type alleles, 63 (40.9%) had one variant allele, and 31 (20.1%) had two variant CYP2C19 alleles. The presence of a variant allele did not alter the diagnostic efficacy of PPI testing.Conclusions:  Both dose levels of rabeprazole proved efficacious in the diagnosis of GERD. Various measures of test accuracy were unrelated to the status of the CYP2C19 genotype.
Helicobacter pylori eradication improves gastric histology and decreases serum gastrin, pepsinogen I and pepsinogen II levels in patients with duodenal ulcer
Authors: Pimanov Sergey I , Makarenko Elena V , Voropaeva Alla V , Matveenko Maya E , Voropaev Eugen V 
Published: June 2007

AbstractBackground and Aim:  The aim of this study was to assess the gastric histopathology and serum gastrin‐17 and pepsinogens profiles in patients with duodenal ulcer before and after Helicobacter pylori eradication in a population with a very high prevalence of H. pylori. At the same time we assessed the role of H. pylori density on these variables.Methods:  Eighty Caucasian patients with H. pylori–associated duodenal ulcer before treatment and 1 year after randomized eradication were studied. Among patients with unsuccessful eradication two groups were distinguished according to the data obtained after treatment: the group with negative rapid urease test and decreased bacterial density according to morphological score (partial elimination group); the group with positive rapid urease test and high bacterial density (failed eradication group).Results:  One year after successful eradication, serum levels of gastrin‐17, pepsinogen I and pepsinogen II decreased. Similar changes of serum pepsinogen I and pepsinogen II levels were observed in patients with partial elimination of H. pylori infection. In the group with successful eradication, inflammation, activity, atrophy and number of lymphoid follicles in the antral mucosa fell. In the group with partial elimination, antral mucosa activity and H. pylori score reduced. Other morphological changes were statistically non‐significant.Conclusion:  Patients with duodenal ulcer after successful eradication have improvement of morphological and functional characteristics of gastric mucosa.
Comparison of three different second‐line quadruple therapies including bismuth subcitrate in Turkish patients with non‐ulcer dyspepsia who failed to eradicate Helicobacter pylori with a 14‐day standard first‐line therapy
Authors: Uygun Ahmet , Ozel A Melih , Yildiz Oguzhan , Aslan Murat , Yesilova Zeki , Erdil Ahmet , Bagci Sait , Gunhan Omer 
Published: June 2007

AbstractBackground and Aim:  Many studies have reported poor results with standard first‐line treatment for Helicobacter pylori. Second‐line regimens that may overcome bacterial resistance can minimize side‐effects and optimize compliance. The aim of this study was to evaluate the efficacy of proton pump inhibitor (PPI) and bismuth subcitrate‐based quadruple therapy, after failure of a PPI plus clarithromycin and amoxicillin as first‐line therapy.Methods:  Patients who failed to eradicate the infection after initial therapy were randomly separated into three groups. The first group received lansoprazole, bismuth subcitrate, metronidazole and amoxicillin (LBMA); in the second group metronidazole was replaced by tetracycline (LBTA); and the third group was given metronidazole and tetracycline in addition to same doses of lansoprazole and bismuth subcitrate (LBMT).Results:  In the LBMA group, the eradication rate was 74.7% and was significantly related to sex, with no relationship to age. In the LBTA group the eradication rate was 81.5% with similar rates in males and females. No relation to sex or age was observed. In the LBMT group the eradication rate was 82.1% with no difference between women and men and it was not related to age, either. Eradication rates in study groups were similar (P > 0.05).Conclusion:  A‐14‐day regimen of lansoprazole, bismuth subcitrate and antibiotic pairs, tetracycline–amoxicillin and tetracycline–metronidazole, is an effective quadruple therapy after one failed course of standard triple therapy. The evaluation of tolerability of and compliance with quadruple therapy needs further studies.
Synaptic organization and input‐specific short‐term plasticity in anterior cingulate cortical neurons with intact thalamic inputs
Authors: Lee Chia‐Ming , Chang Wei‐Chih , Chang Kung‐Bo , Shyu Bai‐Chuang 
Published: June 2007

AbstractThe absence of a slice preparation with intact thalamocortical pathways has held back elucidation of the cellular and synaptic mechanisms by which thalamic signals are differentially transmitted to and processed in the anterior cingulate cortex (ACC). In this report we introduce an innovative mouse brain slice preparation in which it is possible to explore the electrophysiological properties of ACC neurons with intact long‐distance inputs from medial thalamic (MT) nuclei by intracellular recordings; this MT–ACC neuronal pathway plays an integral role in information transmission. Biocytin‐labeled fibers in a functional slice could be traced anterogradely or retrogradely from the MT via the reticular thalamic nuclei, striatum and corpus callosum to the cingulate cortical areas. Eighty‐seven cells downstream of the thalamic projections in 49 slices were recorded intracellularly. Intracellular recordings in the ACC showed that thalamocingulate transmission involves both α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA)/kainate and N‐methyl‐d‐aspartate (NMDA) subtypes of glutamate receptors. Thalamus‐evoked responses recorded extracellularly in the ACC were activated and progressed along a deep–superficial–deep trajectory loop across the ACC layers. We observed enhanced paired‐pulse facilitation and tetanic potentiation of thalamocingulate synapses, suggestive of input‐specific ACC plasticity and selective processing of information relayed by thalamocingulate pathways. Furthermore, we observed differential responses of ACC neurons to thalamic burst stimulation, which underscores the importance of MT afferents in relaying sensory information to the ACC. This new slice preparation enables the contribution of MT‐evoked ACC synaptic transmission to short‐term plasticity in the neuronal circuitry underlying sensory information processing to be examined in detail.
Directing neurotransmitter identity of neurones derived from expanded adult neural stem cells
Authors: Berninger Benedikt , Guillemot François , Götz Magdalena 
Published: June 2007

Abstract In‐vitro expanded neural stem cells (NSCs) of the adult subependymal zone (SEZ) may serve as a source for replacing degenerating neurones in disease and trauma. Crucial for the viability of this approach is the ability to selectively generate specific types of neurones from these cells. Here we show that NSCs derived from the adult mouse SEZ and expanded in vitro as neurosphere cells lose their in‐vivo specification and generate a mixture of progeny comprising both GABAergic and also, surprisingly, glutamatergic neurones. When forced to express the pro‐neural transcription factor neurogenin 2, virtually all progeny of in‐vitro expanded adult NSCs acquire a glutamatergic identity, whereas only GABAergic neurones are generated upon expression of the transcription factor Mash1. Respecification of expanded NSCs from the adult SEZ by neurogenin 2 was accompanied by upregulation of the T‐box transcription factor Tbr1, suggesting that their progeny had acquired a dorsal telencephalic identity. Thus, in‐vitro expanded adult NSCs have the competence to become directed towards distinct functional neurotransmitter phenotypes when the appropriate transcriptional cues are provided.
Ferroportin1 and hephaestin are involved in the nigral iron accumulation of 6‐OHDA‐lesioned rats
Authors: Wang Jun , Jiang Hong , Xie Jun‐Xia 
Published: June 2007

AbstractElevated iron levels in the substantia nigra (SN) participate in neuronal death in Parkinson's disease (PD). While the mechanisms underlying the increased iron are still unknown, some iron transport proteins may be involved. The nigral iron accumulation could be a result of either increased import or decreased export. The mechanisms of iron import have received considerable attention, but little is known about iron export mechanisms. Ferroportin1 (FP1) and hephaestin (HP), two newly discovered iron export proteins, cooperate in the iron export in the gut. Here, we investigated their expression in the SN of rats lesioned by 6‐hydroxydopamine (6‐OHDA). Using immunofluorescence, we showed that FP1 and HP were both expressed on astrocytes, microglia, oligodendrocytes and neurons in the SN. By immunohistochemistry, we showed that 1 day after 6‐OHDA lesion, the expression of the two proteins decreased compared with the control. When rats began showing rotation behaviour induced by apomorphine, usually 6 weeks after 6‐OHDA lesion, they are considered PD models. In these PD models, a further decrease in the two proteins was observed. Reverse transcriptase‐polymerase chain reaction showed that the mRNA levels of FP1 and HP decreased 1 day after 6‐OHDA lesion compared with the control, and further decrease was also observed in the PD model rats. These results show for the first time that FP1 and HP co‐localize in the rat brain, and suggest that decreased expression of these transporters in the SN can account for the increased iron levels.
EphB1 null mice exhibit neuronal loss in substantia nigra pars reticulata and spontaneous locomotor hyperactivity
Authors: Richards A. Brent , Scheel Tracy A. , Wang Kan , Henkemeyer Mark , Kromer Lawrence F. 
Published: June 2007

AbstractThe molecular mechanisms that regulate basal ganglia development are largely unknown. Eph receptor tyrosine kinases are potential participants in this process as they regulate development of other CNS regions and are expressed in basal ganglia nuclei, such as the substantia nigra (SN) and striatum. To address the role of Eph receptors in the development of these nuclei, we analysed anatomical changes in the SN and striatum of mice with null mutations for EphB1. These mice express β‐galactosidase as a marker for cells normally expressing EphB1. In situ hybridization data and a direct comparison of SN neurons expressing tyrosine hydroxylase (TH) and/or the β‐gal marker for EphB1 revealed that EphB1 is not expressed in TH+ neurons of pars compacta (SNc), but is restricted to neurons in pars reticulata (SNr). Consistent with this, we find that EphB1 null mice exhibit a significant decrease in the volume and number of neurons (40% decrease) in SNr, whereas the volume and number of TH+ neurons in SNc is not significantly affected nor are there changes in the distribution of nigrostriatal dopamine neurons. Although EphB1 is expressed in the striatum, EphB1–/– mice exhibit no significant changes in striatal volume and TH fiber density, and have no obvious alterations in striatal patch/matrix organization. Behavioral evaluation of EphB1 null mice in an open‐field environment revealed that these mice exhibited spontaneous locomotor hyperactivity. These results suggest that EphB1 is necessary for the proper formation of SNr, and that neuronal loss in SNr is associated with altered locomotor functions.
Desensitization and binding properties determine distinct α1β2γ2 and α3β2γ2 GABAA receptor‐channel kinetic behavior
Authors: Barberis Andrea , Mozrzymas Jerzy W. , Ortinski Pavel I. , Vicini Stefano 
Published: June 2007

AbstractGABAA receptor subtypes comprising the α1 and α3 subunits change with development and have a specific anatomical localization in the adult brain. These receptor subtypes have been previously demonstrated to greatly differ in deactivation kinetics but the underlying gating mechanisms have not been fully elucidated. Therefore, we expressed rat α1β2γ2 and α3β2γ2 receptors in human embryonic kidney 293 cells and recorded current responses to ultrafast GABA applications at macroscopic and single‐channel levels. We found that the slow deactivation of α3β2γ2‐mediated currents is associated with a relatively small rate and extent of apparent desensitization. In contrast, responses mediated by α1β2γ2 receptors had faster deactivation and stronger desensitization. α3β2γ2 receptors had faster recovery in the paired‐pulse agonist applications than α1β2γ2 channels. The onset of currents mediated by α3β2γ2 receptors was slower than that of α1β2γ2 for a wide range of GABA concentrations. Single‐channel analysis did not reveal differences in the opening/closing kinetics of α1β2γ2 and α3β2γ2 channels but burst durations were longer in α3β2γ2 receptors. Simulation with a previously reported kinetic model was used to explore the differences in respective rate constants. Reproduction of major kinetic differences required a smaller desensitization rate as well as smaller binding and unbinding rates in α3β2γ2 compared with α1β2γ2 receptors. Our work describes the mechanisms underlying the kinetic differences between two major GABAA receptor subtypes and provides a framework to interpret data from native GABA receptors.
LTP‐like changes induced by paired associative stimulation of the primary somatosensory cortex in humans: source analysis and associated changes in behaviour
Authors: Litvak Vladimir , Zeller Daniel , Oostenveld Robert , Maris Eric , Cohen Ayala , Schramm Axel , Gentner Reinhard , Zaaroor Menashe , Pratt Hillel , Classen Joseph 
Published: June 2007

AbstractPaired associative stimulation (PAS), which combines repetitive peripheral nerve stimulation with transcranial magnetic stimulation (TMS), may induce neuroplastic changes in somatosensory cortex (S1), possibly by long‐term potentiation‐like mechanisms. We used multichannel median nerve somatosensory evoked potential (MN‐SSEP) recordings and two‐point tactile discrimination testing to examine the location and behavioural significance of these changes. When TMS was applied to S1 near‐synchronously to an afferent signal containing mechanoreceptive information, MN‐SSEP changes (significant at 21–31 ms) could be explained by a change in a tangential source located in Brodmann area 3b, with their timing and polarity suggesting modification of upper cortical layers. PAS‐induced MN‐SSEP changes between 28 and 32 ms were linearly correlated with changes in tactile discrimination. Conversely, when the near‐synchronous afferent signal contained predominantly proprioceptive information, PAS‐induced MN‐SSEP changes (20–29 ms) were shifted medially, and tactile performance remained stable. With near‐synchronous mechanoreceptive stimulation subtle differences in the timing of the two interacting signals tended to influence the direction of tactile performance changes. PAS performed with TMS delivered asynchronously to the afferent pulse did not change MN‐SSEPs. Hebbian interaction of mechanoreceptive afferent signals with TMS‐evoked activity may modify synaptic efficacy in superficial cortical layers of Brodmann area 3b and is associated with timing‐dependent and qualitatively congruent behavioural changes.
How does a short history of spinal cord injury affect movement‐related brain potentials?
Authors: Castro Antonio , Díaz Fernando , Van Boxtel Geert J. M. 
Published: June 2007

AbstractBrain plasticity following spinal cord injury (SCI) has been studied by a wide range of neurofunctional techniques, which tend to have low temporal resolution or overlook cognitive preparatory processes. This study tried to overcome both limitations by recording the movement‐related brain potentials using an experimental task somewhat similar to the contingent negative variation paradigm. The aim was to look for amplitude or topographic distribution changes at an early stage of the SCI. Hence, the brain electrical activity of patients who had a clinical history of less than 6 months of paraplegia was recorded and compared with that of two groups of healthy volunteers. None of the patients was able to move their toes, but they were asked to prepare to carry out this movement and to try to execute it in the same way as one of the control groups. The other control group was instructed to prepare to conduct the same movement but not to execute it. Results did not show significant differences in the readiness potential between patients with paraplegia and both controls. However, the readiness potential topography observed in patients was more similar to that of healthy participants who conducted the movement, whereas a greater similarity was found in the motor potential between patients and healthy participants who did not carry out the movement. These findings suggest that neurofunctional changes that take place in the brain after a SCI may be shown earlier by the motor potential than by the readiness potential.
Synaptic activation of GABAB receptors regulates neuronal network activity and entrainment
Authors: Brown Jon T. , Davies Ceri H. , Randall Andrew D. 
Published: June 2007

AbstractIn the mammalian central nervous system, GABAB receptors mediate slow pre‐ and postsynaptic inhibition. Using rat hippocampal slices we investigated the role of synaptic GABAB receptors in regulating kainate‐induced subthreshold neuronal network oscillations in the gamma frequency range (25–80 Hz). The GABAB receptor agonist baclofen largely eliminated gamma oscillations. The GABAB receptor antagonist CGP55845 reversed this action of baclofen but alone did not alter the power or frequency of ongoing oscillations. To examine the role of synaptically released GABA on network activity, we electrically stimulated stratum radiatum of CA3 whilst recording gamma oscillations from stratum pyramidale. Single stimuli produced a pronounced transient (up to 1 s in duration) inhibition of gamma frequency oscillations. This stimulus‐induced shutdown of network activity was enhanced by the GABA uptake inhibitor tiagabine and largely inhibited by CGP55845. Multiple stimuli delivered at frequencies of 1–3 Hz resulted in an activity‐dependent fatigue of the inhibition of gamma activity, such that, after a number of stimuli, oscillations could be detected tens of milliseconds after the stimulus. Interestingly, this activity‐dependent fatigue of inhibition uncovered a stimulus‐dependent temporal entrainment of the gamma oscillations. Furthermore, the amount of repetitive synaptic input that was required to cause this entrainment was dramatically reduced by GABAB receptor antagonism such that it was evident within just a few stimuli. These data suggest that convergent afferent synaptic activity can alter the precise temporal arrangement of neuronal network activity. Furthermore, the flow of such information into a functioning neuronal network is highly regulated by GABAB receptor‐mediated synaptic inhibition.
Shedding light on circadian clock resetting by dark exposure: differential effects between diurnal and nocturnal rodents
Authors: Mendoza Jorge , Revel Florent G. , Pévet Paul , Challet Etienne 
Published: June 2007

AbstractThe master circadian clock in mammals, located in the suprachiasmatic nuclei (SCN) of the hypothalamus, is entrained by light and behavioural stimulation. In addition, the SCN can be reset by dark pulses in nocturnal rodents under constant light conditions. Here, the shifting effects of a dark pulse on the SCN clock were detailed at both a behavioural and molecular level in a nocturnal rodent (Syrian hamster), and were compared to those of a diurnal rodent (Arvicanthis ansorgei). Four‐hour dark pulses led to phase advances in the circadian rhythm of locomotor activity from subjective midday to dusk in hamsters, but from subjective dusk to midnight in Arvicanthis. Moreover, dark pulses had no resetting effect during the middle of the subjective night in hamsters, while such a dead shifting zone occurred during most of the subjective day in Arvicanthis. The behavioural phase advances in both hamsters and Arvicanthis were most often accompanied by marked downregulation of the clock genes Per1 and/or Per2 in the SCN, and also by changes in the transforming growth factor‐α expression, a neuropeptide that suppresses daytime activity in nocturnal mammals. Despite that both hamsters and Arvicanthis showed dark‐induced phase advances at circadian time‐12, Per1 gene and its protein PER1 were downregulated in Arvicanthis but not in hamsters. Altogether these results show that dark resetting of the SCN is always associated with downregulation of Per1 and/or Per2 expression, and mostly occurs during resting. Thus, the circadian window of sensitivity to dark differs between nocturnal and diurnal rodents.
Dexterity is impaired at both hands following unilateral subcortical middle cerebral artery stroke
Authors: Nowak Dennis A. , Grefkes Christian , Dafotakis Manuel , Küst Jutta , Karbe Hans , Fink Gereon R. 
Published: June 2007

AbstractDexterity was investigated in right‐handed subjects in the subacute phase of a first unilateral subcortical middle cerebral artery stroke affecting the left or right hemisphere and right‐handed healthy subjects. Dexterity was quantified at both hands by kinematic recordings of finger and hand tapping, a reach‐to‐grasp movement, quantitative analysis of grip forces in a grasp‐lift task and clinical rating scales. Stroke subjects exhibited significant deficits in timing and coordination of tapping movements at both the contralesional and ipsilesional hands, irrespective of the hemisphere affected. Likely for the reach‐to‐grasp and grasp‐lift movements a bilateral impairment was found in stroke subjects. In particular, slowing of hand transport towards the object, deficient timing and scaling of grasp formation, discoordination between grip and lift forces and inefficient scaling of grip forces were observed. The severity of impairment was independent of the hemisphere affected and evident for both the reach (involving more proximal muscles of the arm) and grasp (involving more distal muscles of the arm and hand) components of the task. Strong correlations were found between clinical scores of hand function and loss of sensibility with the deficits in timing, coordination and efficiency of movement of the contralesional and ipsilesional hand. These data provide evidence that dexterity is impaired at both hands after subcortical middle cerebral artery stroke.