bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of intraurethral captopril gel on the recurrence of urethral stricture after direct vision internal urethrotomy: Phase II clinical trial
Authors: Shirazi Mehdi , Khezri Abdolaziz , Samani Soleiman Mohammadi , Monabbati Ahmad , Kojoori Javad , Hassanpour Abbas 
Published: April 2007

Objective:  The purpose of this study is to evaluate the effect of intraurethral captopril gel as an antifibrotic agent on patients with urethral stricture.Materials and Methods:  In the first phase of clinical trial, 13 rabbits were included and local side‐effects of captopril gel were evaluated. In the second phase, 56 patients were enrolled from April 2004 to January 2006. After internal urethrotomy the patients were classified into three patient groups: (i) received placebo gel (group I); (ii) received 0.1% captopril gel (group II); and (iii) instilled 0.5% captopril gel intraurethrally (group III).Results:  In phase I, no significant local side‐effects were seen in the urethra of rabbits. In phase II, the mean age of the patients was 39.5 and the mean follow‐up duration was 16 months. The most common etiology of the urethral stricture in the patients was iatrogenic (35.7%), most of their strictures had a depth of 0.5 cm or less (67.8%), and the length of most strictures was between 1 and 2 cm (41.1%). The patients' maximum urine flow increased more in groups II and III, than in group I (P < 0.04, P < 0.05, respectively). The recurrence rate was less in groups II and III than in group I (P < 0.05). In terms of the maximal urine flow and recurrence rate, no significant difference was seen between group II and group III (P = 0.13, P = 0.21, respectively).Conclusion:  Captopril gel is a safe, effective and non‐toxic agent for decreasing the recurrence rate of the urethral stricture after internal urethrotomy. However, more studies, including more cases and a longer follow up, are needed to prove the effect of captopril gel on patients' urethra.
Effects of opioid subtypes on detrusor overactivity in rats with cerebral infarction
Authors: Nagasaka Yasuhiro , Yokoyama Osamu , Komatsu Kazuto , Ishiura Yoshiyuki , Nakamura Yasuo , Namiki Mikio 
Published: April 2007

Aim:  In order to determine the influence of different opioid receptor subtypes on detrusor overactivity after left middle cerebral artery (MCA) occlusion, cystometric recordings were obtained in conscious rats.Methods:  Female Sprague‐Dawley rats were used in this study. Control cystometrography was followed by left MCA occlusion. The sham‐operated (SO) rats underwent the same procedures except for MCA occlusion. [D‐Ala2, Phe4, Gly5]‐enkephalin (DAGO; μ‐opioid agonist), [D‐Pen2,5]‐enkephalin (DPDPE; δ1‐opioid agonist), deltorpin II (δ2‐opioid agonist), and U‐50488 (κ‐opioid agonist) were administered intracerebroventricularly at graded doses. The bladder capacity, residual volume, micturition threshold pressure, and bladder contraction pressure were determined. Finally, the volume of the infarction was measured.Results:  The intracerebroventricular administration of DAGO and DPDPE significantly increased the bladder capacity in the cerebrally infarcted (CI) and SO rats, but differences in the changes in bladder capacity between the CI and SO rats were not significant. Deltorpin II did not produce any changes in the bladder capacity in the CI or SO rats at any dose examined. However, the intracerebroventricular administration of U‐50488 significantly increased the bladder capacity in the CI rats but not in the SO rats. None of the drugs affected the residual volume, micturition threshold pressure or bladder contraction pressure at any dosage examined. The mean infarcted volumes were not significantly different from those in the vehicle‐treated rats.Conclusion:  These results suggest that the opioid receptor subtypes, μ and δ1 in the brain, are related to the micturition reflex. Furthermore, the κ opioid agonist might be useful for the suppression of detrusor overactivity caused by cerebral infarction.
Search for fMRI BOLD signals in networks of spiking neurons
Authors: Amit Daniel J. , Romani Sandro 
Published: April 2007

AbstractIn a recent experiment, functional magnetic resonance imaging blood oxygen level‐dependent (fMRI BOLD) signals were compared in different cortical areas (primary‐visual and associative), when subjects were required covertly to name images in two protocols: sequences of images, with and without intervening delays. The amplitude of the BOLD signal in protocols with delay was found to be closer to that without delays in associative areas than in primary areas. The present study provides an exploratory proposal for the identification of the neural activity substrate of the BOLD signal in quasi‐realistic networks of spiking neurons, in networks sustaining selective delay activity (associative) and in networks responsive to stimuli, but whose unique stationary state is one of spontaneous activity (primary). A variety of observables are ‘recorded’ in the network simulations, applying the experimental stimulation protocol. The ratios of the candidate BOLD signals, in the two protocols, are compared in networks with and without delay activity. There are several options for recovering the experimental result in the model networks. One common conclusion is that the distinguishing factor is the presence of delay activity. The effect of NMDAr is marginal. The ultimate quantitative agreement with the experiment results depends on a distinction of the baseline signal level from its value in delay‐period spontaneous activity. This may be attributable to the subjects' attention. Modifying the baseline results in a quantitative agreement for the ratios, and provided a definite choice of the candidate signals. The proposed framework produces predictions for the BOLD signal in fMRI experiments, upon modification of the protocol presentation rate and the form of the response function.
Metabolic progression markers of neurodegeneration in the transgenic G93A‐SOD1 mouse model of amyotrophic lateral sclerosis
Authors: Niessen Heiko G. , Debska‐Vielhaber Grazyna , Sander Kerstin , Angenstein Frank , Ludolph Albert C. , Hilfert Liane , Willker Wieland , Leibfritz Dieter , Heinze Hans‐Jochen , Kunz Wolfram S. , Vielhaber Stefan 
Published: April 2007

AbstractAmyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by a progressive loss of motor neurons. Visualizing corresponding metabolic changes in the brain of patients with ALS with proton magnetic resonance spectroscopy (1H‐MRS) may provide surrogate markers for an early disease detection, for monitoring the progression and for evaluating a treatment response. The primary objective of our study was to evaluate whether modifications in MR metabolite levels occur before clinical disease onset, and whether these changes are directly linked to a distinct spatial progression pattern in the CNS. Therefore, age‐dependent alterations in the cerebral and spinal metabolic profile in the mouse model of ALS overexpressing the mutated human G93A‐superoxide dismutase 1 (G93A‐SOD1) were determined by high‐resolution MRS of tissue extracts at 14.1 Tesla. Both non‐transgenic mice (control mice) and transgenic mice overexpressing the non‐mutated human SOD1 (tg‐SOD1) served as controls. In the spinal cord of G93A‐SOD1 mice significantly decreased levels of N‐acetyl aspartate were already detected 34 days postpartum, i.e. about 60 days before the average disease onset caused by motor neuron decline. In addition, glutamine and γ‐aminobutyric acid concentrations were significantly diminished at Day 75, which is still in the presymptomatic phase of the disease. These metabolic changes were further progressive in the course of the disease and started to involve the brainstem at Day 75. Overall, high‐resolution 1H‐MRS allows a sensitive spatial and temporal metabolite profiling in the presymptomatic phase of ALS even before significant neuronal cell loss occurs.
Maintenance of superior learning and memory function in NR2B transgenic mice during ageing
Authors: Cao Xiaohua , Cui Zhenzhong , Feng Ruiben , Tang Ya‐Ping , Qin Zhenxia , Mei Bing , Tsien Joe Z. 
Published: April 2007

AbstractBrain ageing represents a general and evolutionarily conserved phenomenon and is marked by gradual declines in cognitive functions such as learning and memory. As a synaptic coincidence detector, the N‐methyl‐d‐aspartate (NMDA) receptor is known to be essential for the induction of synaptic plasticity and memory formation. Here, we test the hypothesis that up‐regulation of NR2B expression is beneficial for learning and memory in the aged animals. Our in vitro recordings show that the aged transgenic mice with the forebrain‐specific overexpression of the NR2B subunit indeed exhibit more robust hippocampal long‐term potentiation (LTP) induced by either high‐frequency stimulation or theta‐stimulation protocol. Furthermore, those aged NR2B transgenic mice consistently outperform their wild‐type littermates in five different learning and memory tests, namely, novel object recognition, contextual and cued fear conditioning, spatial reference memory, and spatial working memory T‐maze task. Thus, we conclude that increased expression of NR2B in the forebrain improves learning and memory function in the aged brain.
Cholinergic modulation incorporated with a tone presentation induces frequency‐specific threshold decreases in the auditory cortex of the mouse
Authors: Chen Ganling , Yan Jun 
Published: April 2007

AbstractLearning‐induced or experience‐dependent auditory cortical plasticity has often been characterized by frequency‐specificity. Studies have revealed the critical role of the cholinergic basal forebrain and acoustic guidance. Cholinergic facilitation of specific thalamocortical inputs potentially determines such frequency‐specificity but this issue requires further clarification. To examine the cholinergic effects on thalamocortical circuitry of specific frequency channels, we recorded the responses of cortical neurons while pairing basal forebrain activation or acetylcholine (ACh) microiontophoresis with tone presentations at 10 dB below the neuronal response threshold. We found that both basal forebrain activation and acetylcholine microiontophoresis paired with a tone induced a significant decrease in response threshold of the recorded cortical neurons to the frequency of the paired tone, and that this threshold decrease could be eliminated by atropine microiontophoresis. Our data suggest that cortical acetylcholine specifically facilitates thalamocortical circuitry tuned to the frequency of a presented tone; it is the first, fundamental step towards frequency‐specific cortical plasticity evoked by auditory learning and experience.
Evidence from gene knockout studies implicates Asc‐1 as the primary transporter mediating d‐serine reuptake in the mouse CNS
Authors: Rutter A. Richard , Fradley Rosa L. , Garrett Elizabeth M. , Chapman Kerry L. , Lawrence Jason M. , Rosahl Thomas W. , Patel Smita 
Published: April 2007

AbstractIn the mammalian central nervous system, transporter‐mediated reuptake may be critical for terminating the neurotransmitter action of d‐serine at the strychnine insensitive glycine site of the NMDA receptor. The Na+ independent amino acid transporter alanine–serine–cysteine transporter 1 (Asc‐1) has been proposed to account for synaptosomal d‐serine uptake by virtue of its high affinity for d‐serine and widespread neuronal expression throughout the brain. Here, we sought to validate the contribution of Asc‐1 to d‐serine uptake in mouse brain synaptosomes using Asc‐1 gene knockout (KO) mice. Total [3H]d‐serine uptake in forebrain and cerebellar synaptosomes from Asc‐1 knockout mice was reduced to 34 ± 5% and 22 ± 3% of that observed in wildtype (WT) mice, respectively. When the Na+ dependent transport components were removed by omission of Na+ ions in the assay buffer, d‐serine uptake in knockout mice was reduced to 8 ± 1% and 3 ± 1% of that measured in wildtype mice in forebrain and cerebellum, respectively, suggesting Asc‐1 plays a major role in the Na+ independent transport of d‐serine. Potency determination of d‐serine uptake showed that Asc‐1 mediated rapid high affinity Na+ independent uptake with an IC50 of 19 ± 1 µm. The remaining uptake was mediated predominantly via a low affinity Na+ dependent transporter with an IC50 of 670 ± 300 µm that we propose is the glial alanine–serine–cysteine transporter 2 (ASCT2) transporter. The results presented reveal that Asc‐1 is the only high affinity d‐serine transporter in the mouse CNS and is the predominant mechanism for d‐serine reuptake.
Interactions of cannabidiol with endocannabinoid signalling in hippocampal tissue
Authors: Ryan Duncan , Drysdale Alison J. , Pertwee Roger G. , Platt Bettina 
Published: April 2007

AbstractThe phytocannabinoid cannabidiol (CBD) possesses no psychotropic activity amid potentially beneficial therapeutic applications. We here characterized interactions between CBD (1 µm) and the endocannabinoid system in cultured rat hippocampal cells. The CBD‐induced Ca2+ rise observed in neurons and glia was markedly reduced in the presence of the endogenous cannabinoid anandamide in neurons, with no alteration seen in glia. Neuronal CBD responses were even more reduced in the presence of the more abundant endocannabinoid 2‐arachidonyl glycerol, this action was maintained in the presence of the CB1 receptor antagonist AM281 (100 nm). Neuronal CBD responses were also reduced by pre‐exposure to glutamate, expected to increase endocannabinoid levels by increasing in [Ca2+]i. Application of AM281 at 1 µm elevated CBD‐induced Ca2+ responses in both cell types, further confirming our finding that endocannabinoid‐mediated signalling is negatively coupled to the action of CBD. However, upregulation of endogenous levels of endocannabinoids via inhibition of endocannabinoid hydrolysis (with URB597 and MAFP) could not be achieved under resting conditions. Because Δ9‐tetrahydrocannabinol did not mimic the endocannabinoid actions, and pertussis toxin treatment had no effect on CBD responses, we propose that the effects of AM281 were mediated via a constitutively active signalling pathway independent of CB1 signalling. Instead, signalling via Gq/11 and phospholipase C appears to be negatively coupled to CBD‐induced Ca2+ responses, as the inhibitor U73122 enhanced CBD responses. Our data highlight the interaction between exogenous and endogenous cannabinoid signalling, and provide evidence for the presence of an additional pharmacological target, sensitive to endocannabinoids and to AM281.
Functional presynaptic HCN channels in the rat globus pallidus
Authors: Boyes Justin , Bolam J. Paul , Shigemoto Ryuichi , Stanford Ian M. 
Published: April 2007

AbstractHyperpolarization‐activated, cyclic nucleotide‐gated cation (HCN) channels are expressed postsynaptically in the rodent globus pallidus (GP), where they play several important roles in controlling GP neuronal activity. To further elucidate the role of HCN channels in the GP, immunocytochemical and electrophysiological approaches were used to test the hypothesis that HCN channels are also expressed presynaptically on the local axon collaterals of GP neurons. At the electron microscopic level, immunoperoxidase labelling for HCN1 and HCN2 was localized in GP somata and dendritic processes, myelinated and unmyelinated axons, and axon terminals. One population of labelled terminals formed symmetric synapses with somata and proximal dendrites and were immunoreactive for parvalbumin, consistent with the axon collaterals of GABAergic GP projection neurons. In addition, labelling for HCN2 and, to a lesser degree, HCN1 was observed in axon terminals that formed asymmetric synapses and were immunoreactive for the vesicular glutamate transporter 2. Immunogold labelling demonstrated that HCN1 and HCN2 were located predominantly at extrasynaptic sites along the plasma membrane of both types of terminal. To determine the function of presynaptic HCN channels in the GP, we performed whole‐cell recordings from GP neurons in vitro. Bath application of the HCN channel blocker ZD7288 resulted in an increase in the frequency of mIPSCs but had no effect on their amplitude, implying that HCN channels tonically regulate the release of GABA. Their presence, and predicted role in modulating transmitter release, represents a hitherto unidentified mechanism whereby HCN channels influence the activity of GP neurons.
Segregated pathways to the vomeronasal amygdala: differential projections from the anterior and posterior divisions of the accessory olfactory bulb
Authors: Mohedano‐Moriano Alicia , Pro‐Sistiaga Palma , Úbeda‐Bañón Isabel , Crespo Carlos , Insausti Ricardo , Martinez‐Marcos Alino 
Published: April 2007

AbstractApically and basally located receptor neurons in the vomeronasal sensory epithelium express Gi2α‐ and Goα‐proteins, V1R and V2R vomeronasal receptors, project to the anterior and posterior accessory olfactory bulb and respond to different stimuli, respectively. The extent to which secondary projections from the two portions of the accessory olfactory bulb are convergent in the vomeronasal amygdala is controversial. This issue is addressed by using anterograde and retrograde tract‐tracing methods in rats including electron microscopy. Injections of dextran‐amines, Fluoro Gold, cholera toxin‐B subunit and Fast Blue were delivered to the anterior and posterior accessory olfactory bulb, bed nucleus of the stria terminalis, dorsal anterior amygdala and bed nucleus of the accessory olfactory tract/anteroventral medial amygdaloid nucleus. We have demonstrated that, apart from common vomeronasal‐recipient areas, only the anterior accessory olfactory bulb projects to the bed nucleus of the stria terminalis, medial division, posteromedial part, and only the posterior accessory olfactory bulb projects to the dorsal anterior amygdala and deep cell layers of the bed nucleus of the accessory olfactory tract and the anteroventral medial amygdaloid nucleus. These results provide evidence that, excluding areas of convergence, the V1R and V2R vomeronasal pathways project to specific areas of the amygdala. These two vomeronasal subsystems are therefore anatomically and functionally separated in the telencephalon.
Region‐specific tolerance to cocaine‐regulated cAMP‐dependent protein phosphorylation following chronic self‐administration
Authors: Edwards Scott , Graham Danielle L. , Bachtell Ryan K. , Self David W. 
Published: April 2007

AbstractChronic cocaine self‐administration can produce either tolerance or sensitization to certain cocaine‐regulated behaviours, but whether differential alterations develop in the biochemical response to cocaine is less clear. We measured cocaine‐induced phosphorylation of multiple cAMP‐dependent and ‐independent protein substrates in mesolimbic dopamine terminal regions following chronic self‐administration. Changes in self‐administering rats were compared to changes produced by passive yoked injection to identify reinforcement‐related regulation, whereas acute and chronic yoked groups were compared to identify the development tolerance or sensitization in the biochemical response to cocaine. Microwave‐fixed brain tissue was collected immediately following 4 h of intravenous cocaine administration, and subjected to Western blot analysis of phosphorylated and total protein substrates. Chronic cocaine produced region‐ and substrate‐specific tolerance to cAMP‐dependent protein phosphorylation, including phosphorylation in striatal and amygdala subregions and phosphorylation in the CA1 subregion of the hippocampus. Tolerance also developed to cAMP‐independent phosphorylation in the prefrontal cortex. In contrast, sensitization to presynaptic regulation of synapsinS9 phosphorylation developed in the hippocampal CA3 subregion while cAMP‐dependent tyrosine hydroxylaseS40 phosphorylation decreased in striatal dopamine terminals. Cocaine‐induced ERK and CREBS133 phosphorylation were dissociated in many brain regions and failed to develop either tolerance or sensitization with chronic administration. Positive reinforcement‐related correlations between cocaine intake and protein phosphorylation were found only in self‐administering animals, while negative dose‐related correlations were found primarily with yoked administration. These regional‐ and substrate‐specific adaptations in cocaine‐induced protein phosphorylation are discussed in view of their potential impact on the development of cocaine addiction.
Perioperative management for surgical correction of frontoethmoidal encephalomeningocele in children: a review of 102 cases
Authors: LEELANUKROM RUENREONG , WACHARASINT PETCH , KAEWANUCHIT AREERAT 
Published: April 2007

SummaryBackground:  Frontoethmoidal encephalomeningocele (FEEM) is a congenital neural tube defect characterized by herniation of brain and meninges through an anterior skull defect. The extruding mass results in a cutaneous expanding lesion and facial deformity. The objective of this study was to review perioperative management for surgical correction of this condition.Methods:  We reviewed the charts of FEEM children who were treated by surgical correction in King Chulalongkorn Memorial Hospital during 1995–2005. The collected data were categorized into preoperative, intraoperative and postoperative data. In addition, average blood loss was calculated.Results:  A total of 102 charts were reviewed.Preoperative data: The mean age of the patients was 4.62 years. Forty‐six patients (45%) were smaller than average weight or height. Preoperative‐associated abnormal conditions were found in 69 cases (68%).Intraoperative data: The mean duration of the anesthesia and surgery were 6.35 h and 5.51 h, respectively. The estimated mean red cell mass loss was 13.04 ml·kg−1. There is one case of difficult intubation. No major anesthetic complication was found.Postoperative data:  The average intensive care unit stay and hospital stay were 1.55 days and 11.51 days, respectively. The main postoperative complications were tonic–clonic seizure and serious infection including septic shock from wound infection and meningitis.Conclusions:  We reported perioperative management in 102 FEEM children. Comprehensive care during preoperative, intraoperative and postoperative period is essential for successful outcome.