bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of a structured asthma education program on hospitalized asthmatic children: A randomized controlled study
Authors: NG DANIEL KK , CHOW POK‐YU , LAI WAI‐PING , CHAN KIT‐CHING , AND BO‐LING TSANG , SO HANG‐YIN 
Published: April 2006

AbstractBackground: The aim of this study was to compare the effectiveness of an intensive asthma education program (group B) with that of a standard asthma education program (group A).Methods: A prospective randomized single blinded study was conducted in the pediatric department of a public hospital in Hong Kong. Children aged 2–15 years admitted to the pediatric department with an acute attack of asthma were recruited. A standard asthma education program (group A) or an intensive asthma education program (group B) for children were offered. The main outcome measures include the number of visits to the emergency department and the number of hospitalization for asthma during the 3 month follow‐up period.Results: A total of 45 children were in group A and 55 in group B. Group B had statistically significant reductions in the number of visits to the emergency department and the number of hospitalizations. Drug compliance was also significantly improved in group B. Parents’ satisfaction rate was also higher in group B.Conclusion: The intensive asthma education program might be more cost effective than the standard asthma education program in the management of asthmatic children admitted to hospital in Hong Kong.
Sedation with intravenous ketamine and midazolam for painful procedures in children
Authors: KARAPINAR BÜLENT , YILMAZ DENIZ , DEMIRAĞ KUBILAY , KANTAR MEHMET 
Published: April 2006

AbstractBackground: Children often require relief of pain and anxiety when undergoing painful procedures. The purpose of this study is to evaluate the effectiveness and safety of painful pediatric procedures performed by pediatric intensivist, using the combination of intravenous ketamine and midazolam for sedation and analgesia.Methods: The records of the patients who received intravenous ketamine‐midazolam combination for painful procedures in the pediatric sedation unit of a university hospital over a 3 year period were retrospectively reviewed to determine indications, dosing, assesment of the level of sedation, adverse events, and recovery time for each procedural sedation and analgesia.Results: A total of 227 children aged 4 months to 18 years were admitted to the pediatric sedation unit for a total of 356 procedures. The indications for procedural sedation and analgesia included bone marrow aspiration or biopsy (50.8%), central venous catheter insertion (27%), and others (22%). A total of 46 adverse events (12.9%) were observed. These adverse events included SpO2 below 85% without apnea (n = 14), apnea (n = 3), transient stridor (n = 2), hypertension and tachycardia (n = 8), hypersalivation (n = 6), vomiting (n = 5), hallucinatory emergence reaction (n = 4), and rash (n = 4). There were no adverse outcomes attributable to ketamine and midazolam combination.Conclusion: Skilled pediatric intensivists can safely and effectively administer ketamine and midazolam to facilitate painful procedures outside the operating room setting.
Prevalence of trachoma and diabetes‐related eye disease among a cohort of adult Aboriginal patients screened over the period 1999–2004 in remote South Australia
Authors: Durkin Shane R , Casson Robert , Newland Henry S , Selva Dinesh 
Published: April 2006

AbstractBackground:  To determine the prevalence of trachoma and diabetes‐related eye disease within the adult Aboriginal population screened by the South Australian Eye Health Program between 1999 and 2004 inclusive.Methods:  The South Australian Eye Health Program visited 22 Aboriginal communities in remote South Australia. Visiting ophthalmologists and optometrists systematically collected data on the cohort of adult patients seen over the period 1999–2004. Prevalence and grade of trachoma according to World Health Organization classification and the prevalence and degree of diabetic retinopathy according to the Early Treatment Diabetic Retinopathy Study and National Health and Medical Research Council guidelines were recorded.Results:  A population of 1651 Aboriginal patients was examined. Sixty‐two per cent were female and 38% were male. Twenty patients (1.2%) had evidence of active trachoma with 260 (15.7%) patients having either lid scarring, trichiasis or corneal opacity. There was no significant association between gender and the prevalence of trachoma (P = 0.48). Seven hundred and seventy‐one patients within the examined population had diabetes mellitus (46.70%). Significantly more women than men were affected and prevalence increased with age (P < 0.0001). One hundred and sixty‐nine patients (22%) with diabetes mellitus had features of diabetic retinopathy, and of these patients 77 had background diabetic retinopathy (46%) and 92 (54%) had either proliferative diabetic retinopathy or maculopathy. Prevalence of clinically significant macula oedema among those with maculopathy (14 of 50 patients) was 28%.Conclusions:  The data suggest that although trachoma is still endemic in this South Australian Aboriginal population the prevalence and severity are less than previously reported. Diabetes mellitus has a high prevalence within this population and great potential for detrimental visual sequelae.
Firing cell repertoire during carbachol‐induced theta rhythm in rat hippocampal formation slices
Authors: Konopacki Jan , Eckersdorf Barbara , Kowalczyk Tomasz , Gołębiewski Henryk 
Published: April 2006

AbstractOne hundred and seven cells were recorded extracellularly in hippocampal formation (HPC) slices during carbachol‐induced theta. The data obtained provided evidence of a population of HPC neurons which, when activated cholinergically, participate in the generation ofin vitrotheta. The activity patterns ofin vitrorecorded theta‐related cells were shown to be similar to those of theta‐related cells recordedin vivoand cells recordedin vitroduring cholinergically induced theta, and non‐theta intervals were successfully classified according to previously developed criteria forin vivorecorded theta‐related cells. The currentin vitroexperiments showed that, in addition to theta‐on and theta‐off cells, the HPC contained cells that were probably involved in programming the appearance and duration of theta epochs and the intervals between theta epochs. These novel types of cells were termed ’gating cells’.
Cerebellar granule cell: ascending axon and parallel fiber
Authors: Huang Chi‐ming , Wang Lucase , Huang Rosa H. 
Published: April 2006

AbstractMorphometric data have indicated that most (> 95%) of the granule cell axonal synapses are located along the parallel fibers. The ascending axons of granule cells, however, exert powerful excitatory effects on the activities of Purkinje cells. To resolve this apparent conflict, we propose that some of the parallel fiber synapses overlying a functionally homogeneous granule cell patch can discharge in close synchrony with the ascending axon synapses from that same granule cell patch, thereby augmenting the excitatory action from ascending axons. Moreover, we also propose that age may be an important factor in the ascending axon synapses. We examined the synaptic varicosities along the ascending axons and parallel fibers in the anterior lobe of the male NIA C57BL/6j mouse. Between 2.5 and 10 months, the fraction of synaptic varicosities anatomically associated with the ascending axons increased from 2.6% to 6.6% whereas the fraction of synaptic varicosities that can discharge in synchrony with ascending axon synapses (including some parallel fiber synapses) increased from 17.3% to 39% (assuming a granule cell patch of 300 × 300 µm). The results of the present study may be relevant to understanding the role of the ascending axon vs. the parallel fibers. Differential age‐related synaptic changes in these two portions of the granule cell axons may constitute an important age‐dependent synaptic remodeling in the granule cell–Purkinje cell synaptic system.
Sleep spindle‐related activity in the human EEG and its relation to general cognitive and learning abilities
Authors: Schabus M. , Hödlmoser K. , Gruber G. , Sauter C. , Anderer P. , Klösch G. , Parapatics S. , Saletu B. , Klimesch W. , Zeitlhofer J. 
Published: April 2006

AbstractStage 2 sleep spindles have been previously viewed as useful markers for the development and integrity of the CNS and were more currently linked to ‘offline re‐processing’ of implicit as well as explicit memory traces. Additionally, it had been discussed if spindles might be related to a more general learning or cognitive ability. In the present multicentre study we examined the relationship of automatically detected slow (< 13 Hz) and fast (> 13 Hz) stage 2 sleep spindles with: (i) the Raven's Advanced Progressive Matrices (testing ‘general cognitive ability’); as well as (ii) the Wechsler Memory scale‐revised (evaluating memory in various subdomains). Forty‐eight healthy subjects slept three times (separated by 1 week) for a whole night in a sleep laboratory with complete polysomnographic montage. Whereas the first night only served adaptation and screening purposes, the two remaining nights were preceded either by an implicit mirror‐tracing or an explicit word‐pair association learning or (corresponding) control task. Robust relationships of slow and fast sleep spindles with both cognitive as well as memory abilities were found irrespectively of whether learning occurred before sleep. Based on the present findings we suggest that besides being involved in shaping neuronal networks after learning, sleep spindles do reflect important aspects of efficient cortical‐subcortical connectivity, and are thereby linked to cognitive‐ and memory‐related abilities alike.
Electrophysiology in ischemic neocortical brain slices: species differences vs. influences of anaesthesia and preparation
Authors: Wölfer Johannes , Bantel Carsten , Köhling Rüdiger , Speckmann Erwin‐Josef , Wassmann Hansdetlef , Greiner Christoph 
Published: April 2006

AbstractIschemia models are indispensable for the evaluation of measures to be clinically applied to brain trauma or stroke patients. Slice models provide good control over experimental parameters and allow for comparative examinations of human and animal brain tissue. Experimental tissue, however, may be altered by anaesthesia, preparatory technique, and, in the case of human tissue, by underlying diseases. These influences on tissue behaviour under ischemia were examined electrophysiologically. Native rat tissue slices were prepared either immediately after decapitation (n = 13), during short ether/barbiturate narcosis (n = 18), or after two hours of inhalation anaesthesia (n = 12) imitating clinical narcosis. Tissue from rats in which generalized amygdala‐kindled seizures had been triggered by electric stimulation (n = 10) was prepared according to the decapitation protocol, while human tissue (n = 10) was obtained during epilepsy or tumour surgery. Electrophysiological data (latency and amplitude of anoxic depolarization, recovery of evoked potentials) were recorded during ischemia simulation. Neither details of preparation or anaesthesia nor a history of epileptic fits were associated with significant changes of electrophysiological reactions under ischemia. Human tissue showed a significantly higher ability to uphold transmembrane ion gradients under ischemia. The ability of brain tissue to withstand ischemia is obviously species dependent. For the transfer of experimental results into clinical use it is important that interspecies differences alone can bring about a significant change of tissue behaviour.
Stress‐induced sensitization of the limbic system in ovariectomized rats is partly restored by cyclic 17β‐estradiol administration
Authors: Gerrits Marjolein , Bakker Petra L. , Koch Tineke , Ter Horst Gert J. 
Published: April 2006

AbstractChronic stress induces neurobiological alterations which have consequences for subsequent stress handling. In the current experiment, ovariectomized rats were subjected daily to a stressor for 21 days. Thereafter, the rats were treated for 21 days with 17β‐estradiol benzoate (10 µg/250 g, once every 4 days) or mirtazapine (10 mg/kg, daily). In this way, we were able to evaluate the ability of these compounds to reverse chronic stress‐induced changes in the activity of the limbic system. After 21 days of recovery and treatment, the rats were re‐exposed to the adverse environment of the initial stressor and perfused 2 h later. Ovariectomized rats displayed increased numbers of c‐Fos‐positive nuclei, after re‐exposure to the stressor, in the paraventricular nucleus of the hypothalamus, dentate gyrus, medial prefrontal cortex and central and medial amygdala. Cyclic estradiol treatment attenuated the sensitization of the paraventricular nucleus and central amygdala. Mirtazapine increased the number of c‐Fos‐positive nuclei in the central amygdala and dentate gyrus. Long‐term transcriptional changes induced by chronic stress were determined with ΔFosB immunoreactivity. The medial prefrontal cortex showed an increased number of ΔFosB‐positive nuclei after chronic stress and this was not affected by estradiol or mirtazapine administration during recovery. In conclusion, cyclic estradiol administration reversed chronic stress‐induced sensitization in the limbic system, the paraventricular nucleus and central amygdala of female rats, output regions of the limbic system involved in fear responses. Mirtazapine did not achieve this reversal of stress‐induced aberrations in the limbic system after 21 days of treatment.
Estrogen receptor‐β gene disruption potentiates estrogen‐inducible aggression but not sexual behaviour in male mice
Authors: Nomura Masayoshi , Andersson Sandra , Korach Kenneth S. , Gustafsson Jan‐Åke , Pfaff Donald W. , Ogawa Sonoko 
Published: April 2006

AbstractAggressive behaviour of gonadally intact male mice is increased by estrogen receptor (ER)‐β gene disruption, whereas sexual behaviour remains unchanged. The elevated aggression levels following ER‐β gene disruption is pronounced during repeated aggression tests in young animals and the first aggression test in adults. In the present study, the roles of ER‐β activation in the regulation of aggressive and sexual behaviour were investigated in gonadectomized ER‐β knockout (βERKO) and wild‐type (WT) male mice treated with various doses of estrogen. Overall, estradiol benzoate (EB) treatment induced higher levels of aggression in βERKO mice than in WT mice. In WT mice, the levels of aggression induced by EB were highest in the lowest‐dose (2.5 µg/day) group and gradually decreased in higher‐dosage groups. On the other hand, equally high levels of aggressive behaviour were induced by all three doses of EB in βERKO mice. A marked genotype difference in dose responses is inferred, such that the ER‐α‐mediated facilitatory action of estrogen is more pronounced at lower and physiological doses and the ER‐β‐mediated inhibitory action is only unveiled at higher doses of estrogen. In contrast to aggression, the levels of sexual behaviour induced by EB were not different between βERKO and WT at either dose of EB (2.5 and 12.5 µg/day) examined. These findings support the notion that ER‐β activation may exert an attenuating action on male aggression induced by estrogen through ER‐α‐mediated brain mechanisms, whereas its effect on male sexual behaviour is relatively small.
Transfer of interfered motor patterns to self from others
Authors: Pierno Andrea C. , Becchio Cristina , Wall Matthew B. , Smith Andrew T. , Castiello Umberto 
Published: April 2006

AbstractPrevious behavioural and neuroimaging data on humans demonstrated that kinematics and the level of brain activity vary according to whether participants reach towards and grasp a target object presented in isolation or flanked by a distractor object. Here we seek to explore whether a differential activation can be revealed by the mere observation of another person grasping an object in isolation or alongside a distractor. To this end we used event‐related functional magnetic resonance imaging to localize neural activity related to action observation that was influenced by the presence of a distractor object. We found that observing a human model reaching‐to‐grasp a three‐dimensional target alongside a distractor elicits a differential level of activation in a network of areas typically involved during action observation: the dorsal sectors of the premotor cortex and the inferior frontal gyrus. Whereas our previous understanding of the human action observation system has been restricted to actions directed to single objects, we provide compelling evidence that areas within this network modulate with respect to the context in which the observed action takes place. This may prove to be a fundamental process for our understanding of how others' actions can be represented at a neural level.
Metaplasticity of the late‐phase of long‐term potentiation: a critical role for protein kinase A in synaptic tagging
Authors: Young Jennie Z. , Isiegas Carolina , Abel Ted , Nguyen Peter V. 
Published: April 2006

AbstractThe late‐phase of long‐term potentiation (L‐LTP) in hippocampal area CA1 requires gene expression and de novo protein synthesis but it is expressed in an input‐specific manner. The ‘synaptic tag’ theory proposes that gene products can only be captured and utilized at synapses that have been ‘tagged’ by previous activity. The mechanisms underlying synaptic tagging, and its activity dependence, are largely undefined. Previously, we reported that low‐frequency stimulation (LFS) decreases the stability of L‐LTP in a cell‐wide manner by impairing synaptic tagging. We show here that a phosphatase inhibitor, okadaic acid, blocked homosynaptic and heterosynaptic inhibition of L‐LTP by prior LFS. In addition, prior LFS homosynaptically and heterosynaptically impaired chemically induced synaptic facilitation elicited by forskolin/3‐isobutyl‐1‐methylxanthine, suggesting that there is a cell‐wide dampening of cAMP/protein kinase A (PKA) signaling concurrent with phosphatase activation. We propose that prior LFS impairs expression of L‐LTP by inhibiting synaptic tagging through its actions on the cAMP/PKA pathway. In support of this notion, we show that hippocampal slices from transgenic mice that have genetically reduced hippocampal PKA activity display impaired synaptic capture of L‐LTP. An inhibitor of PKA, KT‐5720, also blocked synaptic capture of L‐LTP. Moreover, pharmacological activation of the cAMP/PKA pathway can produce a synaptic tag to capture L‐LTP expression, resulting in persistent synaptic facilitation. Collectively, our results show that PKA is critical for synaptic tagging and for input‐specific L‐LTP. PKA‐mediated signaling can be constrained by prior episodes of synaptic activity to regulate subsequent L‐LTP expression and perhaps control the integration of multiple synaptic events over time.
Learning‐induced oscillatory activities correlated to odour recognition: a network activity
Authors: Martin Claire , Gervais Rémi , Messaoudi Belkacem , Ravel Nadine 
Published: April 2006

AbstractIn trained behaving rats, the expression of a prominent beta oscillatory activity in the olfactory system was previously identified as a correlate of odour recognition. The aim of the present study was to assess the putative role of a functional coupling between the olfactory bulb (OB) and higher structures in this activity. We performed a unilateral inactivation of the medial part of the olfactory peduncle by lidocaine infusion. Inactivation deprived the OB from most of its centrifugal afferences, including feedback connections from the piriform cortex (PC) while sparing the ascending fibres from the OB to higher cortical structures. This treatment reduced the amplitude of odour‐induced oscillatory beta responses both in OB and PC. In parallel, gamma activity classically observed in these two structures during spontaneous activity displayed a strong enhancement. Results suggest that odour‐induced oscillatory response could be the emergent feature of an olfactory functional network set up through learning.
Neurogenesis in the R6/1 transgenic mouse model of Huntington's disease: effects of environmental enrichment
Authors: Lazic Stanley E. , Grote Helen E. , Blakemore Colin , Hannan Anthony J. , van Dellen Anton , Phillips Wendy , Barker Roger A. 
Published: April 2006

AbstractPrevious work has demonstrated that the transgenic R6/1 mouse model of Huntington's disease has decreased proliferation of neural precursor cells (NPCs) in the dentate gyrus of the hippocampus. This study therefore examined the survival and differentiation of NPCs in presymptomatic and symptomatic R6/1 mice and the effects of environmental enrichment on these variables. Here it is demonstrated that the survival of bromodeoxyuridine‐positive (BrdU+) NPCs in the dentate gyrus is decreased in the transgenic mice. In addition, the number of doublecortin‐positive (DCX+) cells is greatly reduced in these mice, as is the total number of new mature neurons, while the proportion of BrdU+ cells differentiating into mature neurons was not significantly different between genotypes. Furthermore, the DCX+ cells in the R6/1 mice had smaller and irregular‐shaped somas, shorter neurites, and migrated a shorter distance into the granular cell layer compared with wild‐type mice. Older symptomatic mice housed in an enriched environment had an increased number of BrdU+ and DCX+ cells as well as longer neurites and increased migration of DCX+ cells. There was no significant difference between genotypes or environments in the number of BrdU+ cells in the subventricular zone. These results suggest that decreased neurogenesis might be responsible, in part, for the hippocampal deficits observed in these mice and that environmental enrichment produces morphological changes in newborn granule neurons in both wild‐type and R6/1 mice, which could underlie some of the beneficial effects of enrichment.
Plasma membrane ion permeability induced by mutant α‐synuclein contributes to the degeneration of neural cells
Authors: Furukawa Katsutoshi , Matsuzaki‐Kobayashi Michiko , Hasegawa Takafumi , Kikuchi Akio , Sugeno Naoto , Itoyama Yasuto , Wang Yue , Yao Pamela J. , Bushlin Ittai , Takeda Atsushi 
Published: April 2006

AbstractMutations in α‐synuclein cause some cases of familial Parkinson's disease (PD), but the mechanism by which α‐synuclein promotes degeneration of dopamine‐producing neurons is unknown. We report that human neural cells expressing mutant α‐synuclein (A30P and A53T) have higher plasma membrane ion permeability. The higher ion permeability caused by mutant α‐synuclein would be because of relatively large pores through which most cations can pass non‐selectively. Both the basal level of [Ca2+]i and the Ca2+ response to membrane depolarization are greater in cells expressing mutant α‐synuclein. The membrane permeable Ca2+ chelator BAPTA‐AM significantly protected the cells against oxidative stress, whereas neither l‐type (nifedipine) nor N‐type (ω‐conotoxin‐GVIA) Ca2+ channel blockers protected the cells. These findings suggest that the high membrane ion permeability caused by mutant α‐synuclein may contribute to the degeneration of neurons in PD.