bluuebunny/crossref_metadata_2025_split huggingface dataset:
Postural orthostatic tachycardia syndrome: an underrecognized disorder
Authors: Pandian J. D. , Dalton K. , Henderson R. D. , McCombe P. A. 
Published: April 2007

AbstractBackground: Postural orthostatic tachycardia syndrome (POTS), a clinical syndrome of orthostatic intolerance characterized by excessive tachycardia and symptoms of cerebral hypoperfusion on standing, is not well recognized in Australia. The aim was to study the clinical symptomatology, results of autonomic testing and outcome in patients with POTS.Methods: Sixteen subjects from a tertiary referral centre who met the criteria for POTS were studied between January 2003 and January 2006. Ten of these patients consented to be interviewed using a validated autonomic symptom questionnaire. Heart rate responses to deep breathing and the Valsalva manoeuvre were measured using Colin BP‐508 machine (WR Medical Electronic Co., Stillwater, MN, USA). Tilt studies were carried out for 10 min to 80° of head‐up tilting. Patient outcome was assessed as functionally normal, able to stand 30 min without symptoms, able to work and carry out recreational activities or worse on follow up.Results: The mean age of 10 subjects was 24.9 ± 6.8 years, six being women. The mean duration of symptoms was 70.7 months (range 3–228 months). The common presenting orthostatic symptoms were light‐headedness (100%), palpitations (90%), pallor (90%), weakness (80%) and clammy skin (80%). The mean heart rate increment during the tilt study was 51.7 ± 14.3 b.p.m. The mean duration of follow up was 8.9 months (range 1–16 months). Only five patients were functioning normally at the follow‐up visit.Conclusion: POTS is an underrecognized but persistent autonomic disorder in young patients with a variety of symptoms and variable outcome.
Correlated species differences in the effects of cannabinoid ligands on anxiety and on GABAergic and glutamatergic synaptic transmission
Authors: Haller J. , Mátyás F. , Soproni K. , Varga B. , Barsy B. , Németh B. , Mikics É. , Freund T. F. , Hájos N. 
Published: April 2007

AbstractCannabinoid ligands show therapeutic potential in a variety of disorders including anxiety. However, the anxiety‐related effects of cannabinoids remain controversial as agonists show opposite effects in mice and rats. Here we compared the effects of the cannabinoid agonist WIN‐55,212 and the CB1 antagonist AM‐251 in CD1 mice and Wistar rats. Special attention was paid to antagonist–agonist interactions, which had not yet been studied in rats. In mice, WIN‐55,212 decreased whereas AM‐251 increased anxiety. The antagonist abolished the effects of the agonist. In contrast, WIN‐55,212 increased anxiety in rats. Surprisingly, the antagonist potentiated this effect. Cannabinoids affect both GABAergic and glutamatergic functions, which play opposite roles in anxiety. We hypothesized that discrepant findings resulted from species differences in the relative responsiveness of the two transmitter systems to cannabinoids. We investigated this hypothesis by studying the effects of WIN‐55,212 on evoked hippocampal inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs). IPSCs were one order of magnitude more sensitive to WIN‐55,212 in mice than in rats. In mice, IPSCs were more sensitive than EPSCs to WIN‐55,212. This is the first study showing that the relative cannabinoid sensitivity of GABA and glutamate neurotransmission is species‐dependent. Based on behavioural and electrophysiological findings, we hypothesize that WIN‐55,212 reduced anxiety in mice by affecting GABA neurotransmission whereas it increased anxiety in rats via glutamatergic mechanisms. In rats, AM‐251 potentiated this anxiogenic effect by inhibiting the anxiolytic GABAergic mechanism. We suggest that the anxiety‐related effects of cannabinoids depend on the relative cannabinoid responsiveness of GABAergic and glutamatergic neurotransmission.
The role of cingulate cortex in the detection of errors with and without awareness: a high‐density electrical mapping study
Authors: O'Connell Redmond G. , Dockree Paul M. , Bellgrove Mark A. , Kelly Simon P. , Hester Robert , Garavan Hugh , Robertson Ian H. , Foxe John J. 
Published: April 2007

AbstractError‐processing research has demonstrated that the brain uses a specialized neural network to detect errors during task performance but the brain regions necessary for conscious awareness of an error are poorly understood. In the present study we show that two well‐known error‐related event‐related potential (ERP) components, the error‐related negativity (ERN) and error positivity (Pe) have a differential relationship with awareness during performance of a manual response inhibition task optimized to examine error awareness. While the ERN was unaffected by the participants' conscious experience of errors, the Pe was only seen when participants were aware of committing an error. Source localization of these components indicated that the ERN was generated by a caudal region of the anterior cingulate cortex (ACC) while the Pe was associated with contributions from a more anterior ACC region and the posterior cingulate–precuneus. Tonic EEG measures of cortical arousal were correlated with individual rates of error awareness and showed a specific relationship with the amplitude of the Pe. The latter finding is consistent with evidence that the Pe represents a P3‐like facilitation of information processing modulated by subcortical arousal systems. Our data suggest that the ACC might participate in both preconscious and conscious error detection and that cortical arousal provides a necessary setting condition for error awareness. These findings may be particularly important in the context of clinical studies in which a proper understanding of self‐monitoring deficits requires an explicit measurement of error awareness.
Deficit of NMDA receptor activation in CA1 hippocampal area of aged rats is rescued byd‐cycloserine
Authors: Billard J‐M. , Rouaud E. 
Published: April 2007

AbstractActivation of the glycine modulatory site of theN‐methyl‐d‐aspartate glutamate receptor (NMDAR) may reduce cognitive impairments associated with normal ageing. In order to test this hypothesis, we assessed the effects of the partial agonistd‐cycloserine (DCS) on cellular activities involved in memory formation. This was performed in CA1 cellular networks of adult and aged Sprague–Dawley rat hippocampal slices using extracellular field excitatory postsynaptic potential recordings. Synaptic potentials specifically mediated by NMDAR were significantly reduced in aged animals. DCS increased the magnitude of these responses in both adult and old rats but this effect was significantly higher in the latter, thus reversing the age‐related decrease in NMDAR synaptic potentials. NMDAR‐mediated theta burst long‐term potentiation (TBS‐LTP) as well as long‐term depression (LTD) of synaptic transmission, prominent models for the cellular basis of learning and memory, were also weakened in aged animals. Age‐related alterations of both forms of synaptic plasticity were rescued by DCS. In addition, the DCS‐induced decrease in basal fast glutamatergic neurotransmission involving the activation of inhibitory glycinergic receptors, previously reported in young rats (Rouaud & Billard, 2003), was severely attenuated in aged animals. In summary, our results indicate that the facilitation of NMDAR activation through its glycine‐binding site rescues the age‐related deficit of cellular mechanisms of learning and memory. Such physiological evidences suggest that this modulation site of NMDAR represents an important target to alleviate cognitive deficits associated with normal ageing.
Hippocampal activity, but not plasticity, is required for early consolidation of fear conditioning with a short trace interval
Authors: Burman Michael A. , Gewirtz Jonathan C. 
Published: April 2007

AbstractThe dorsal hippocampus is required for explicit cue fear conditioning only when a temporal gap is inserted between conditioned stimulus (CS) termination and unconditioned stimulus (US) onset (trace fear conditioning). To examine the role of the dorsal hippocampus in associating temporally discontiguous stimuli and to minimize the potential contribution of contextual cues, fear conditioning was conducted using a relatively short (3‐s) trace interval. Inactivation of the dorsal hippocampus using the AMPA receptor antagonist NBQX (3 µg/hemisphere) or the GABAA agonist muscimol (5 µg/hemisphere) disrupted trace fear conditioning when conducted immediately following training. Trace conditioning was not disrupted significantly when NBQX was infused either before or 2 h after training. Similarly, NBQX infusions were not effective when the CS and US overlapped (delay conditioning). Moreover, trace conditioning was not impaired by intrahippocampal infusion of either the NMDA receptor antagonist AP5 (5 µg/hemisphere) or the L‐type voltage‐gated calcium channel (VGCC) blocker diltiazem (20 or 40 µg/hemisphere). These data suggest that the involvement of the dorsal hippocampus in short trace interval fear conditioning is largely restricted to the early period of memory consolidation, during which time it mediates the storage of long‐term memory in other brain regions.
Disruption of Kir6.2‐containing ATP‐sensitive potassium channels impairs maintenance of hypoxic gasping in mice
Authors: Miyake Akari , Yamada Katsuya , Kosaka Tomohiro , Miki Takashi , Seino Susumu , Inagaki Nobuya 
Published: April 2007

AbstractHypoxic gasping emerges under severe hypoxia/ischemia in various species, exerting a life‐protective role by assuring minimum ventilation even in loss of consciousness. However, the molecular basis of its generation and maintenance is not well understood. Here we found that mice lacking Kir6.2‐ but not Kir6.1‐containing ATP‐sensitive potassium (KATP) channels [knockout (KO) mice] exhibited few gaSPS when subjected to abrupt ischemia by decapitation, whereas wild‐type mice all exhibited more than 10 gaSPS. Under anesthesia, wild‐type mice initially responded to severe hypoxic insult with augmented breathing (tachypnea) accompanied by sighs and subsequent depression of respiratory frequency. Gasping then emerged and persisted stably (persistent gasping); if the hypoxia continued, several gaSPS with distinct patterns appeared (terminal gasping) before cessation of breathing. KO mice showed similar hypoxic responses but both depression and the two types of gasping were of much shorter duration than in wild‐type mice. Moreover, in the unanesthetized condition, the onset of terminal gasping in KO mice, which was always earlier than in wild‐type mice, was unaltered by decreasing O2 concentrations within the severe range (4.5–7.0%), whereas onset in wild‐type mice became earlier in response to lowered O2 concentrations. Thus, the mechanism responsible for regulating the hypoxic response in accordance with the severity of the hypoxia was dysfunctional in these KO mice, suggesting that Kir6.2‐containing KATP channels are critically involved in the maintenance rather than the generation of hypoxic gasping and depression of respiratory frequency.
Prenatal choline availability modulates hippocampal neurogenesis and neurogenic responses to enriching experiences in adult female rats
Authors: Glenn Melissa J. , Gibson Erin M. , Kirby Elizabeth D. , Mellott Tiffany J. , Blusztajn Jan K. , Williams Christina L. 
Published: April 2007

AbstractIncreased dietary intake of choline early in life improves performance of adult rats on memory tasks and prevents their age‐related memory decline. Because neurogenesis in the adult hippocampus also declines with age, we investigated whether prenatal choline availability affects hippocampal neurogenesis in adult Sprague–Dawley rats and modifies their neurogenic response to environmental stimulation. On embryonic days (ED) 12–17, pregnant rats ate a choline‐supplemented (SUP‐5 g/kg), choline sufficient (SFF‐1.1 g/kg), or choline‐free (DEF) semisynthetic diet. Adult offspring either remained in standard housing or were given 21 daily visits to explore a maze. On the last ten exploration days, all rats received daily injections of 5‐bromo‐2‐deoxyuridine (BrdU, 100 mg/kg). The number of BrdU+ cells was significantly greater in the dentate gyrus in SUP rats compared to SFF or DEF rats. While maze experience increased the number of BrdU+ cells in SFF rats to the level seen in the SUP rats, this enriching experience did not alter cell proliferation in DEF rats. Similar patterns of cell proliferation were obtained with immunohistochemical staining for neuronal marker doublecortin, confirming that diet and exploration affected hippocampal neurogenesis. Moreover, hippocampal levels of the brain‐derived neurotrophic factor (BDNF) were increased in SUP rats as compared to SFF and DEF animals. We conclude that prenatal choline intake has enduring effects on adult hippocampal neurogenesis, possibly via up‐regulation of BDNF levels, and suggest that these alterations of neurogenesis may contribute to the mechanism of life‐long changes in cognitive function governed by the availability of choline during gestation.
Brain‐derived neurotrophic factor prevents the nigrostriatal degeneration induced by human immunodeficiency virus‐1 glycoprotein 120 in vivo
Authors: Nosheny Rachel L. , Ahmed Farid , Yakovlev Alexander , Meyer Edwin M. , Ren Ke , Tessarollo Lino , Mocchetti Italo 
Published: April 2007

AbstractGlycoprotein 120 (gp120) from the T‐tropic strain of the human immunodeficiency virus type 1 has been shown to cause neuronal apoptosis through activation of the chemokine receptor CXCR4. Therefore, reducing CXCR4 expression may prevent gp120‐mediated apoptosis. Brain‐derived neurotrophic factor (BDNF) is known to reduce both gp120 neurotoxicity and CXCR4 expression in vitro. The scope of this work is to establish whether BDNF is neuroprotective against gp120 in vivo and, if so, whether this effect correlates with its ability to down‐regulate CXCR4. Serotype 2 adeno‐associated viral vector encoding for BDNF (rAAV‐BDNF) or control vector was microinjected into the striata of adult rats. Two weeks later gp120 was injected into the same striatum, and apoptosis determined. Pretreatment with rAAV‐BDNF prior to gp120 microinjection prevented caspase‐3 activation as well as in situ terminal deoxynucleotidyl transferase biotin–dUTP nick end labelling in the striatum and substantia nigra. In addition, rAAV‐BDNF reversed the loss of tyrosine hydroxylase immunoreactivity induced by gp120 in both areas. CXCR4 expression was then determined by immunohistochemistry and RT‐PCR, and found to be decreased in striata of rAAV‐BDNF‐treated rats. Conversely, BDNF heterozygous mice exhibited an increase in CXCR4 mRNA levels compared to wild‐type littermates. Our data suggest that down‐regulation of CXCR4 expression may contribute to the neuroprotective activity of BDNF against gp120 toxicity in the basal ganglia.
Optical glutamate sensor for spatiotemporal analysis of synaptic transmission
Authors: Namiki Shigeyuki , Sakamoto Hirokazu , Iinuma Sho , Iino Masamitsu , Hirose Kenzo 
Published: April 2007

AbstractImaging neurotransmission is expected to greatly improve our understanding of the mechanisms and regulations of synaptic transmission. Aiming at imaging glutamate, a major excitatory neurotransmitter in the CNS, we developed a novel optical glutamate probe, which consists of a ligand‐binding domain of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) receptor glutamate receptor GluR2 subunit and a small molecule fluorescent dye. We expected that such fluorescent conjugates might report the microenvironmental changes upon protein conformational changes elicited by glutamate binding. After more than 100 conjugates were tested, we finally obtained a conjugate named E (glutamate) optical sensor (EOS), which showed maximally 37% change in fluorescence intensity upon binding of glutamate with a dissociation constant of 148 nm. By immobilizing EOS on the cell surface of hippocampal neuronal culture preparations, we pursued in situ spatial mapping of synaptically released glutamate following presynaptic firing. Results showed that a single firing was sufficient to obtain high‐resolution images of glutamate release, indicating the remarkable sensitivity of this technique. Furthermore, we monitored the time course of changes in presynaptic activity induced by phorbol ester and found heterogeneity in presynaptic modulation. These results indicate that EOS can be generally applicable to evaluation of presynaptic modulation and plasticity. This EOS‐based glutamate imaging method is useful to address numerous fundamental issues about glutamatergic neurotransmission in the CNS.
Candidate pheromone receptors provide the basis for the response of distinct antennal neurons to pheromonal compounds
Authors: Große‐Wilde Ewald , Gohl Thomas , Bouché Elisabeth , Breer Heinz , Krieger Jürgen 
Published: April 2007

AbstractMales of the moth species Heliothis virescens are able to detect the female‐released pheromone with remarkable sensitivity and specificity, distinguishing between highly related pheromonal compounds. In the past, electrophysiological studies succeeded in assigning sensory hairs to identified compounds revealing three functional types of long sensilla trichodea housing neurons specifically responding to distinct semiochemicals. The specific responsiveness implies that the sensory neurons express different receptor types tuned to pheromone components. In this study we demonstrate that heterologously expressed candidate pheromone receptors from Heliothis responded to several pheromonal compounds, including the major sex‐pheromone component Z‐11‐hexadecenal indicating a limited specificity of each receptor type. Nonetheless, based on functional analysis and in situ hybridization studies the analysed receptor types could tentatively be assigned to types of long sensilla trichodea, containing the pheromone‐binding proteins (PBPs) HvirPBP1 and HvirPBP2 in the sensillum lymph. Substituting organic solvent with PBPs to solubilize the hydrophobic pheromone compounds in functional assays revealed an increase in sensitivity and especially specificity. It was found that in the presence of HvirPBP2, cells expressing the receptor type HR13 specifically responded to the main component of the sex pheromone blend only. The data provide further evidence that a combination of a distinct receptor type and binding protein underlie the specific response observed in the detection of a pheromone component in vivo.
The impact of Internet use for weight loss
Authors: Saperstein S. L. , Atkinson N. L. , Gold R. S. 
Published: April 2007

SummaryWith rising rates of obesity and obesity‐related health problems, finding additional means to help reduce obesity is critical. This review examined the impact of the Internet as a medium to deliver weight loss programs. Specifically, the review examined the public’s interest, the availability and the known efficacy of Internet‐based weight loss programs. Findings showed that the general public is turning to the Internet for diet and fitness information and has reported that information they found online has impacted their behaviour. Little is known about who is interested in using the Internet for weight loss and what their experiences have been. The programs most readily available to the general consumer tend to vary widely in quality, with few efficacy studies. However, researchers have shown that efficacious programs have been delivered via the Internet. Successful online programs included a structured approach to modifying energy balance, the use of cognitive‐behavioural strategies such as self‐monitoring, and individualized feedback and support. Implications include developing strategies to increase distribution of programs with known efficacy, determining the applicability of effective programs for diverse audiences, conducting media literacy education for the general public, and continued research into understanding who may be best served by online weight loss programming.
Childhood obesity: are we missing the big picture?
Authors: Maziak W. , Ward K. D. , Stockton M. B. 
Published: April 2007

SummaryChildhood obesity is increasing worldwide, raising alarm about future trends of cardiovascular disease, diabetes and cancer. This article discusses what may underlie our failure to respond effectively to the obesity epidemic, and presents a wider perspective for future research and public health agendas. So far targeting individual‐level determinants and clinical aspects of childhood obesity has produced limited success. There is growing interest in understanding the wider determinants of obesity such as the built environment (e.g. walkability), social interactions, food marketing and prices, but much needs to be learned. Particularly, we need to identify distal modifiable factors with multiple potential that would make them attractive for people and policymakers alike. For example, walking‐biking‐friendly cities can reduce obesity as well as energy cosumption, air pollution and traffic delays. Such agenda needs to be driven by strong evidence from research involving multi‐level influences on behaviour, as well as the study of wider politico‐economic trends affecting people’s choices. This article highlights available evidence and arguments for research and policy needed to curb the obesity epidemic. The upstream approach underlying these arguments aims to make healthy choices not only the most rational, but also the most feasible and affordable.
Disability and Development: Different Models, Different Places
Authors: McEwan Cheryl , Butler Ruth 
Published: April 2007

AbstractDebates about disability within geography, as well as in disability studies more generally, have been largely urban, Anglophone and Western‐centric. Not only have industrialised societies remained the predominant focus of attention, but the debates themselves are rooted within an often unacknowledged Western context. In the light of this, this article aims to bring together debates about disability and development, which have until relatively recently tended to be mutually exclusive, and provides a critical review of recent debates about disability issues in developing countries. By doing so, it furthers debates about the significance of geography in disability studies, challenges the Western‐centric focus of disability models and extends understanding of the shifting and complex landscapes of disability in developing countries.
Feminism and Geographic Information Systems: From a Missing Object to a Mapping Subject
Authors: Pavlovskaya Marianna , Martin Kevin St. 
Published: April 2007

AbstractAlthough feminism and the field of geographic information systems and science (GIS) have only recently begun speaking to each other, the feminist mapping subject is emerging across a variety of sites – academic, professional, and lay. However, it is most articulated in the work of critical GIS scholars. Both male and female, they are committed to nonpositivist practices of knowledge production and are sensitive to gender and other power hierarchies that produce social, economic, and cultural difference. These scholars have been creating ‘feminist cartographies’, practicing ‘feminist visualization’, and developing new mapping alternatives to mainstream cartographic and GIS representations. We begin by briefly re‐reading the history of women in cartography and GIS as a first step toward reclaiming mapping as a critical practice. We then review feminist theorizations of visual representation and geography that move beyond critique and posit a feminist deployment of such technologies. Finally, we reflect on explicitly feminist engagements with cartography and GIS and their implication for the discipline of geography and contemporary mapping practices in general. Throughout, we trace the evolution of a feminist mapping subject and her or his potential to disrupt the traditions of mapping and reclaim the power of maps and GIS‐based spatial analysis for critical intervention.