bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of the BCR sequential extraction for trace elements in European reference volcanic soils
Authors: Hernández‐Moreno J. M. , Rodríguez‐González J. I. , Espino‐Mesa M. 
Published: February 2007

SummaryTrace metal behaviour in volcanic ash soils displays distinctive features related to the soils’ large contents of metal‐binding phases and to the rapid release of trace metals from glasses and weatherable minerals. In this work, the BCR (Community Bureau of Reference) sequential extraction scheme (exchangeable + weak acid soluble, reducible, oxidizable, and non‐extractable metal fractions) was applied to selected COST‐622 European reference volcanic soils to determine partitioning of zinc and copper between various solid‐phase constituents, along with the major elements Al, Fe and Mn. The total extracted Al (ΣAl) was strongly correlated with acid ammonium oxalate extractable Al (Alo) (ΣAl = 0.985Alo+ 0.11, R2= 0.98), while the total extracted Fe clearly underestimated the amorphous fraction. Large values for the non‐extractable Al fraction were associated with the presence of gibbsite and phyllosilicates. Although the Zn and Cu contents of the soils were generally large, total amounts extracted (the potentially mobilizable fraction) were small, especially for Zn and for soils with crystalline secondary minerals. The fraction of the total Cu which was potentially mobilizable generally exceeded that of Zn. In the potentially mobilizable Cu the oxidizable fraction was generally dominant. Biocycling appears to play an important role in the surface enrichment of potentially mobilizable Zn and Mn. Although further methodological research seems necessary, the BCR sequential extraction appears to be a valuable tool for studies on metal dynamics in soils with andic properties.
Angiotensin converting enzyme inhibitor and angiotensin receptor blockade use in relation to outcomes in anticoagulated patients with atrial fibrillation
Authors: Lip G. Y. H. , Frison L. , Grind M. ,   on Behalf of the SPORTIF Investigators and the SPORTIF Executive Steering Committee
Published: February 2007

Abstract.Background.  The renin‐angiotensin‐aldosterone‐system (RAAS) plays an important role in atrial fibrillation (AF). Evidence shows that blocking the RAAS with angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) has a definite role in preventing new onset AF and in maintaining sinus rhythm in recurrent AF. Our aim was to determine if ACEI/ARB treatment was associated with clinical outcomes [stroke/systemic embolic events (SEE), mortality] in a controlled, anticoagulated AF population.Methods.  An ancillary retrospective cross‐sectional and longitudinal analysis of participants in the Stroke Prevention using an ORal Thrombin Inhibitor in AF (SPORTIF) III and V trials, in relation to use (or nonuse) of ACEI/ARBs.Results.  Rates of stroke/SEEs, mortality or major bleeding were no different between users and nonusers in the whole cohort, or in relation to the presence/absence of hypertension, coronary artery disease and previous stroke/transient ischaemic attack, nor amongst those aged <75 years. Patients aged ≥75 years taking ACEIs or ARBs had lower mortality (HR 0.71, 95% CI 0.52–0.95), but no significant influence on other end‐points was noted. Diabetics and those with left ventricular dysfunction on ximelagatran had a higher odds ratio of abnormal liver enzyme levels. There was no apparent benefit of ACEIs or ARBs on other event rates.Conclusions.  This analysis from two large randomized trials of anticoagulation has not demonstrated a significant benefit of ACEI or ARB use amongst AF patients, except amongst elderly subjects.
Lhx3, a LIM domain transcription factor, is regulated by Pou4f3 in the auditory but not in the vestibular system
Authors: Hertzano Ronna , Dror Amiel A. , Montcouquiol Mireille , Ahmed Zubair M. , Ellsworth Buffy , Camper Sally , Friedman Thomas B. , Kelley Matthew W. , Avraham Karen B. 
Published: February 2007

AbstractA dominant mutation of the gene encoding the POU4F3 transcription factor underlies human non‐syndromic progressive hearing loss DFNA15. Using oligonucleotide microarrays to generate expression profiles of inner ears of Pou4f3ddl/ddl mutant and wild‐type mice, we have identified and validated Lhx3, a LIM domain transcription factor, as an in vivo target gene regulated by Pou4f3. Lhx3 is a hair cell‐specific gene expressed in all hair cells of the auditory and vestibular system as early as embryonic day 16. The level of Lhx3 mRNA is greatly reduced in the inner ears of embryonic Pou4f3 mutant mice. Our data also show that the expression of Lhx3 is regulated differently in auditory and vestibular hair cells. This is the first example of a hair cell‐specific gene expressed both in auditory and in vestibular hair cells, with differential regulation of expression in these two closely related systems.
A model for mammalian cochlear hair cell differentiation in vitro: effects of retinoic acid on cytoskeletal proteins and potassium conductances
Authors: Helyer R. , Cacciabue‐Rivolta D. , Davies D. , Rivolta M. N. , Kros C. J. , Holley M. C. 
Published: February 2007

AbstractWe have established a model for the in‐vitro differentiation of mouse cochlear hair cells and have used it to explore the influence of retinoic acid on proliferation, cytoskeletal proteins and voltage‐gated potassium conductances. The model is based on the conditionally immortal cell line University of Sheffield/ventral otocyst‐epithelial cell line clone 36 (US/VOT‐E36), derived from ventral otic epithelial cells of the mouse at embryonic day 10.5 and transfected with a reporter for myosin VIIa. Retinoic acid did not increase cell proliferation but led to up‐regulation of myosin VIIa and formation of prominent actin rings that gave rise to numerous large, linear actin bundles. Cells expressing myosin VIIa had larger potassium conductances and did not express the cyclin‐dependent kinase inhibitor p27kip1. US/VOT‐E36 endogenously expressed the voltage‐gated potassium channel α‐subunits Kv1.3 and Kv2.1, which we subsequently identified in embryonic and neonatal hair cells in both auditory and vestibular sensory epithelia in vivo. These subunits could underlie the embryonic and neonatal delayed‐rectifiers recorded in nascent hair cells in vivo. Kv2.1 was particularly prominent on the basolateral membrane of cochlear inner hair cells. Kv1.3 was distributed throughout all hair cells but tended to be localized to the cuticular plates. US/VOT‐E36 recapitulates a coherent pattern of cell differentiation under the influence of retinoic acid and will provide a convenient model for screening the effects of other extrinsic factors on the differentiation of cochlear epithelial cell types in vitro.
Neuronal differentiation of the early embryonic auditory hindbrain of the chicken in primary culture
Authors: Kuenzel Thomas , Mönig Benedikt , Wagner Hermann , Mey Jörg , Luksch Harald 
Published: February 2007

AbstractNeurons in the auditory hindbrain pathway of the chicken are physiologically and morphologically highly specialized. It remains unclear to what extent independent differentiation vs. activity‐dependent mechanisms determines the development of this system. To address this question we established a primary culture system of the early auditory hindbrain neurons. Primary cultures of neurons from nucleus magnocellularis and nucleus laminaris were prepared from embryonic day 6.5 chicken. These cells developed in culture under serum‐free conditions for up to 15 days. Immunocytochemical staining and whole‐cell patch recordings were used to characterize the development of the neurons. A stable expression of the calcium‐binding protein calretinin, which serves as a characteristic marker of the auditory pathway, was found at all stages. A voltage‐gated potassium channel (Kv3.1b) with a specific function in the auditory system was also expressed after about 1 week in culture. Electrophysiological recordings showed a general maturation of the neuronal phenotype as reflected by an increase in the mean resting membrane potential, a decrease in the mean input resistance as well as a maturation of action potential parameters. Four groups of neurons that generate action potentials could be distinguished. One of these showed the phasic firing pattern of auditory brainstem neurons known from slice preparations. In older cultures we demonstrated functional synaptogenesis in vitro by recording postsynaptic activity elicited by extracellular stimulation and styryl dye loading of vesicles. Thus, isolated neurons from the auditory region of the avian brainstem differentiate to specific neuronal subtypes and autonomously develop synaptic connections in vitro.
Alteration of the cell adhesion molecule L1 expression in a specific subset of primary afferent neurons contributes to neuropathic pain
Authors: Yamanaka Hiroki , Obata Koichi , Kobayashi Kimiko , Dai Yi , Fukuoka Tetsuo , Noguchi Koichi 
Published: February 2007

AbstractThe cell adhesion molecule L1 (L1‐CAM) plays important functional roles in the developing and adult nervous systems. Here we show that peripheral nerve injury induced dynamic post‐transcriptional alteration of L1‐CAM in the rat dorsal root ganglia (DRGs) and spinal cord. Sciatic nerve transection (SCNT) changed the expression of L1‐CAM protein but not L1‐CAM mRNA. In DRGs, SCNT induced accumulation of the L1‐CAM into the surface of somata, which resulted in the formation of immunoreactive ring structures in a number of unmyelinated C‐fiber neurons. These neurons with L1‐CAM‐immunoreactive ring structures were heavily colocalized with phosphorylated p38 MAPK. Western blot analysis revealed the increase of full‐length L1‐CAM and decrease of fragments of L1‐CAM after SCNT in DRGs. Following SCNT, L1‐CAM‐immunoreactive profiles in the dorsal horn showed an increase mainly in pre‐synaptic areas of laminae I–II with a delayed onset and colocalized with growth‐associated protein 43. In contrast to DRGs, SCNT increased the proteolytic 80‐kDa fragment of L1‐CAM and decreased full‐length L1‐CAM in the spinal cord. The intrathecal injection of L1‐CAM antibody for the extracellular domain of L1‐CAM inhibited activation of p38 MAPK and emergence of ring structures of L1‐CAM immunoreactivity in injured DRG neurons. Moreover, inhibition of extracellular L1‐CAM binding by intrathecal administration of antibody suppressed the mechanical allodynia and thermal hyperalgesia induced by partial SCNT. Collectively, these data suggest that the modification of L1‐CAM in nociceptive pathways might be an important pathomechanism of neuropathic pain.
Neuropeptide Y suppresses absence seizures in a genetic rat model primarily through effects on Y2 receptors
Authors: Morris Margaret J. , Gannan Emma , Stroud Leanne M. , Beck‐Sickinger Annette G. , O'Brien Terence J. 
Published: February 2007

AbstractNeuropeptide Y (NPY) potently suppresses absence seizures in a model of genetic generalized epilepsy, genetic absence epilepsy rats of Strasbourg (GAERS). Here we investigated the Y‐receptor subtype(s) on which NPY exerts this anti‐absence effect. A dual in vivo approach was used: the cumulative duration of seizures was quantified in adult male GAERS in 90‐min electroencephalogram recordings following intracerebroventricular (i.c.v.) injection of: (i) subtype‐selective agonists of Y1 ([Leu31Pro34]NPY, 2.5 nmol), Y2 (Ac[Leu28,31]NPY24–36, 3 nmol), Y5 receptors [hPP1−17,Ala31,Aib32]NPY, 4 nmol), NPY (3 nmol) or vehicle; and following (ii) i.c.v. injection of antagonists of Y1 (BIBP3226, 20 nmol), Y2 (BIIE0246, 20 nmol) and Y5 (NPY5RA972, 20 nmol) receptors or vehicle, followed by NPY (3 nmol). Injection of the Y1‐ and Y5‐selective agonists resulted in significantly less mean seizure suppression (37.4% and 53.9%, respectively) than NPY (83.2%; P < 0.05), while the Y2 agonist had similar effects to NPY (62.3% suppression, P = 0.57). Food intake was not increased following injection of the Y2 agonist, while significant increases in food intake were seen following NPY and the other Y‐subtype agonists. Compared with vehicle, NPY injection suppressed seizures following the Y1 and Y5 antagonists (45.3% and 80.1%, respectively, P < 0.05), but not following the Y2 antagonist (5.1% suppression, P = 0.46). We conclude that NPY Y2 receptors are more important than Y1 and Y5 receptors in mediating the effect of NPY to suppress absence seizures in a genetic rat model. Y2 receptor agonists may represent targets for novel drugs against genetic generalized epilepsies without resulting in appetite stimulation.
Plasticity of inhibitory synaptic network interactions in the lateral amygdala upon fear conditioning in mice
Authors: Szinyei Csaba , Narayanan Rajeevan T. , Pape Hans‐Christian 
Published: February 2007

AbstractAfter fear conditioning, plastic changes of excitatory synaptic transmission occur in the amygdala. Fear‐related memory also involves the GABAergic system, although no influence on inhibitory synaptic transmission is known. In the present study we assessed the influence of Pavlovian fear conditioning on the plasticity of GABAergic synaptic interactions in the lateral amygdala (LA) in brain slices prepared from fear‐conditioned, pseudo‐trained and naïve adult mice. Theta‐burst tetanization of thalamic afferent inputs to the LA evoked an input‐specific potentiation of inhibitory postsynaptic responses in projection neurons; the cortical input was unaffected. Philanthotoxin (10 µm), an antagonist of Ca2+‐permeable AMPA receptors, disabled this plastic phenomenon. Surgical isolation of the LA, extracellular application of a GABAB receptor antagonist (CGP 55845A, 10 µm) or an NMDA receptor antagonist (APV, 50 µm), or intracellular application of BAPTA (10 mm), did not influence the plasticity. The plasticity also showed as a potentiation of monosynaptic excitatory responses in putative GABAergic interneurons. Pavlovian fear conditioning, but not pseudo‐conditioning, resulted in a significant reduction in this potentiation that was evident 24 h after training. Two weeks after training, the potentiation returned to control levels. In conclusion, a reduction in potentiation of inhibitory synaptic interactions occurs in the LA and may contribute to a shift in synaptic balance towards excitatory signal flow during the processes of fear‐memory acquisition or consolidation.
Spontaneous depolarization waves of multiple origins in the embryonic rat CNS
Authors: Momose‐Sato Yoko , Sato Katsushige , Kinoshita Masae 
Published: February 2007

AbstractDuring development, correlated neuronal activity plays an important role in the establishment of the central nervous system (CNS). We have previously reported that a widely propagating correlated neuronal activity, termed the depolarization wave, is evoked by various sensory inputs. A remarkable feature of the depolarization wave is that it spreads broadly through the brain and spinal cord. In the present study, we examined whether the depolarization wave occurs spontaneously in the embryonic rat CNS and, if so, where it originates. In E15–16 rat embryos, spontaneous optically‐revealed signals appeared in association with the rhythmic discharges of cranial motoneurons and propagated widely with similar characteristics to the evoked depolarization wave. At E15, the spontaneous wave mostly originated in the cervical to upper lumbar cords. At E16, the wave was predominantly generated in the lumbosacral cord although a wave associated with the second oscillatory burst was initiated in the rostral cord. At E16, a few waves also originated in the rostral ventrolateral medulla and the dorsomedial pons. When the influence of the caudal cord was removed by transecting the spinal cord, the contribution of the medulla and pons became more significant. These results show that the depolarization wave can be triggered by the spontaneous activity of multiple neuronal populations which are distributed widely from the pons to the lumbosacral cord, although the spinal cord usually plays a predominant role. This network possibly works as a self‐distributing system that maintains the incidence and complicated patterns of the correlated activity in the developing CNS.
Developmental changes in cell–extracellular matrix interactions limit proliferation in the mammalian inner ear
Authors: Davies Dawn , Magnus Christopher , Corwin Jeffrey T. 
Published: February 2007

AbstractHair cell losses can produce severe hearing and balance deficits in mammals and nonmammals alike, but nonmammals recover after epithelial supporting cells divide and give rise to replacement hair cells. Here, we describe cellular changes that appear to underlie the permanence of hair cell deficits in mammalian vestibular organs. In sensory epithelia isolated from the utricles of embryonic day 18 (E18) mice, supporting cells readily spread and proliferated, but spreading and proliferation were infrequent in supporting cells from postnatal day 6 (P6) mice. Cellular spreading and proliferation were dependent on α6 integrin, which disappeared from lateral cell membranes by P6 and colocalized with β4 integrin near the basement membrane at both ages. In the many well‐spread, proliferating E18 supporting cells, β4 was localized at cell borders, but it was localized to hemidesmosome‐like structures in the columnar, nondividing supporting cells that were prevalent in P6 cultures. We treated cultures with phorbol myristate acetate (PMA) to activate protein kinase C (PKC) in an initial test of the possibility that maturational changes in supporting cell cytoskeletons or their anchorage might restrict the proliferation of these progenitor cells in the developing mammalian inner ear. That treatment triggered the disassembly of the hemidesmosome‐like β4 structures and resulted in significantly increased cellular spreading and S‐phase entry in the P6 epithelia. The results suggest that maturational changes in cytoskeletal organization and anchorage restrict proliferation of mammalian supporting cells whose counterparts are the progenitors of replacement hair cells in nonmammals, thereby leaving mammals vulnerable to persistent sensory deficits caused by hair cell loss.
Preliminary sex differences in human cortical BOLD fMRI activity during the preparation of increasingly complex visually guided movements
Authors: Gorbet Diana J. , Sergio Lauren E. 
Published: February 2007

AbstractIn the past it has often been assumed that the cortical networks for visually guided movement are the same for males and females. Here we use functional magnetic resonance imaging (fMRI) to show significant sex‐related differences in human brain activity during visual‐to‐motor transformation tasks. Although the behavioural performance of the male and female groups did not differ, sex‐related differences in levels of blood oxygen level‐dependent fMRI activity are apparent in several cortical areas that have previously been demonstrated to be important for visually guided movements. These areas include the primary sensorimotor, dorsal premotor, superior parietal and lateral sulcus regions. Furthermore, the data indicate that the nature of these sex differences depends on the spatial mapping between a visual cue and the motor response that it guides.
Differential neurogenesis in the adult rat dentate gyrus: an identifiable zone that consistently lacks neurogenesis
Authors: Melvin Neal R. , Spanswick Simon C. , Lehmann Hugo , Sutherland Robert J. 
Published: February 2007

AbstractThe dentate gyrus continues to produce new neurons in adult rodents. The possibility of differential regulation of neurogenesis within regions of the dentate gyrus is largely unexplored, despite several other aspects of this phenomenon being well characterized in a large number of studies. In this report, we describe an area located at the anterior pole of the dentate gyrus that consistently lacks neurogenesis. This neurogenically quiescent zone invariably lacks expression of the neuroblast marker doublecortin (DCX), bromodeoxyuridine and Ki‐67, though DCX expression can be elicited in response to a combined paradigm of environmental enrichment and wheel running. We propose that this region may provide a valuable model system to discern the factors that regulate the process of neurogenesis.
Synchrony of spontaneous calcium activity in mouse neocortex before synaptogenesis
Authors: Platel Jean‐Claude , Dupuis Alain , Boisseau Sylvie , Villaz Michel , Albrieux Mireille , Brocard Jacques 
Published: February 2007

AbstractSpontaneous calcium activity can be detected in embryonic mouse cortical slices as fluorescence intensity variations, in the presence of a fluorescent calcium indicator. Current methods to detect and quantify these variations depend heavily on experimenters whose judgement may interfere with measurement. In the present work, we developed new software called CalSignal for automatic detection and tracking of cellular bodies and quantification of spontaneous calcium activity on time‐series of confocal fluorescence images. Analysis of 28 neocortical slices revealed that 21.0% of detected cells displayed peaks of fluorescence corresponding to spontaneous activity, with a mean frequency of one peak per 4 min. This activity was blocked in the absence of extracellular calcium but was not modified after depletion of calcium stores with thapsigargin or blockade of voltage‐gated calcium channels with Ni2+. Further, statistical analysis of calcium activity revealed concomitant activation of distant cells in 24 slices, and the existence of a significant network of synchrony based on such coactivations in 17 slices out of 28. These networks enclosed 84.3% of active cells, scattered throughout the neocortical wall (mean distance between cellular bodies, 111.7 µm). Finally, it was possible to identify specific cells which were synchronously active with more neighbouring cells than others. The identity of these nodal cells remains to be investigated to fully comprehend the role of spontaneous calcium activity, before synaptogenesis, in shaping cortical neurogenesis.
Disruption of noradrenergic transmission and the behavioural response to a novel environment in NK1R–/– mice
Authors: Fisher Amy S. , Stewart R. John , Yan Ting , Hunt Stephen P. , Stanford S. Clare 
Published: February 2007

AbstractThe behaviour of neurokinin‐1‐receptor gene knockout (NK1R–/–) mice, which lack functional, substance P‐preferring receptors, resembles that of NK1R+/+ mice treated with an antidepressant. Because all antidepressants increase central monoamine transmission, we have investigated whether noradrenergic transmission is increased in NK1R–/– mice and, if so, whether this could influence their behaviour. In anaesthetized subjects, the concentration of extracellular noradrenaline in NK1R–/– mice was two–fourfold greater than in NK1R+/+ mice. Systemic administration of the α2‐adrenoceptor antagonist, 2‐(2,3‐dihydro‐2‐methoxy‐1,4‐benzodioxan‐2‐yl)‐4,5‐dihydro‐1H‐imidazoline (RX 821002), in anaesthetized or freely moving animals increased extracellular noradrenaline in NK1R+/+ mice only. This suggests that the function of α2a‐autoreceptors, which modulate noradrenergic transmission, is impaired in NK1R–/– mice. Consistent with this, [35S]GTPγS binding to activated α2a‐adrenoceptors was lower (−70%) in the locus coeruleus, but not the frontal cortex, of NK1R–/– mice compared with their NK1R+/+ counterparts. RX 821002‐pretreatment, followed by retrodialysis of the noradrenaline reuptake inhibitor, desipramine, into the frontal cortex of anaesthetized mice increased extracellular noradrenaline to the same extent in the two genotypes. Western blots confirmed that there was no difference in the amount of noradrenaline transporter protein in NK1R–/– and NK1R+/+ mice. Finally, the effects of RX 821002 on certain behaviours in a light/dark exploration box were blunted in NK1R–/– mice, but there was no consistent effect on anxiety‐like behaviour in the two genotypes. It is concluded that the greater basal efflux of noradrenaline in NK1R–/– mice is explained by increased transmitter release, coupled with desensitization of somatodendritic α2a‐adrenoceptors. These changes could contribute to the difference in the behavioural phenotypes.