bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fast‐track surgery for bariatric laparoscopic gastric bypass with focus on anaesthesia and peri‐operative care. Experience with 500 cases
Authors: BERGLAND A. , GISLASON H. , RAEDER J. 
Published: July 2010

Background: Bariatric surgery for morbid obesity implies challenges in anaesthesiological handling. We report our experience from 500 consecutive patients during 3 years.Methods: The patients were due for laparoscopic Roux–en–Y gastric bypass and enteral bypass. Sleep was induced after pre‐oxygenation with target control infusions (TCI) of remifentanil and propofol; vecuronium was supplied for facilitating endotracheal intubation. The propofol infusion was stopped and desflurane 3–6% was given for BIS‐titrated anaesthetic maintenance together with remifentanil TCI. Antiemetic prophylaxis was supplied with intravenous (IV) droperidol, ondansetron and dexamethasone; post‐operative pain prophylaxis was IV paracetamol, parecoxib and bupivacaine infiltration. The patients were extubated in the operating room and kept in the post‐operative care unit for 3–4 h, being tested for a 20 m walk before discharge to the ward.Results: The procedure was uncomplicated peri‐operatively in all 500 cases and in 497 patients (99.4%) post‐operatively. Three patients had one complication, which resolved without sequelae: oesophageal rupture from gastric tubing, reoperation for anastomosis leakage and pneumonia. The mean duration of surgery was 57 min (range 37–91). The mean time from the start of anaesthesia until the start of surgery and time from the end of surgery until the end of anaesthesia were both significantly reduced throughout the study period, from 23 to 7.8 and 5.8 to 1.9 min, respectively (P<0.001). The mean total hospital stay was reduced from 3 days at start to 2 days in the end of the series (P<0.05).Conclusion: Safe bariatric short‐stay surgery is feasible with a dedicated anaesthesiological concept in an expert surgical team.
An association study of 20 candidate genes with cryptorchidism in Siberian Husky dogs
Authors: Zhao X. , Du Z.‐Q. , Rothschild M.F. 
Published: July 2010

SummaryCryptorchidism (CO) as a common developmental defect in purebred dogs causes health concerns of reduced fertility and increases risk of testicular malignancies. A total of 49 single nucleotide polymorphisms (SNPs) discovered from 20 candidate genes was investigated to analyse their associations with CO in Siberian Huskies. The sibling‐transmission disequilibrium test on 38 discordant full‐sibs revealed seven SNPs in the collagen type II α 1 (COL2A1) gene were significantly (p < 0.05) or suggestively (p < 0.10) associated with CO. Further analyses showed that only one SNP (rs23358342) in this gene remained suggestively significant (p < 0.1) on a data set of full‐sibs with additional related dogs, but not significant on all 156 Siberian Huskies. Based on the statistical results and the involvement of COL2A1 in the testicle development and descent, we could not exclude COL2A1 as a potential candidate gene for CO in Siberian Huskies. Further studies are necessary to clarify these results from our relatively small sample size.
Proteomic analysis of human umbilical vein endothelial cells incubated with Cryptococcus neoformans var. neoformans
Authors: Wang Xiao‐Jun , Zhu Yuan‐Jie , Cui Jian‐Guo , Huang Xin , Gu Julin , Xu Hong , Wen Hai 
Published: July 2010

SummaryCryptococcus neoformans is a medically important fungus and can infect all the organs of the body. As vascular endothelial cell is an important target for C. neoformans to penetrate any organs, the differential protein expression of human umbilical vascular endothelial cell (HUVEC) after incubating with C. neoformans may be the key to penetration. The proteins of HUVECs incubated with C. neoformans and normal HUVECs were collected and purified. After two‐dimensional electrophoresis, the differential protein expression was identified by matrix‐assisted laser desorption/ionisation mass spectrometry. The mRNA levels of some proteins were measured by real‐time PCR. Three proteins were found significantly overexpressed in HUVECs incubated with C. neoformans, and nine other proteins were downregulated. The mRNA levels of S100A10 and peroxiredoxin I fluctuated with the protein levels. These results suggested that the expressions of peroxiredoxin I and S100A10 were regulated during the process of invasion of HUVECs by C. neoformans. We hypothesise that these proteins take part in the modifications of HUVEC cytoskeleton and the tolerance to oxidative stress, which may affect the process of invasion by C. neoformans.
Axonal projections of single auditory neurons in the thalamic reticular nucleus: implications for tonotopy‐related gating function and cross‐modal modulation
Authors: Kimura A. , Imbe H. , Donishi T. , Tamai Y. 
Published: July 2010

AbstractTonotopically comparable subfields of the primary auditory area (AI) and nonprimary auditory areas (non‐AI), i.e. posterodorsal area (PD) and ventral auditory area (VA), in the rat cortex have similar topographies in the projection to the ventral division of the medial geniculate nucleus (MGV), but reverse topographies in the projection to the thalamic reticular nucleus (TRN). In this study, we examined axonal projections of single auditory TRN cells, using juxtacellular recording and labeling techniques, to determine features of TRN projections and estimate how the TRN mediates corticofugal inhibition along with the reverse topographies of cortical projections to the TRN. Auditory TRN cells sent topographic projections to limited parts of the MGV in a manner that relays cortical inputs from tonotopically comparable subfields of the AI and non‐AI (PD and VA) to different parts of the MGV. The results suggest that corticofugal excitations from the AI and non‐AI modulate thalamic cell activity in the same part of the MGV, whereas corticofugal inhibitions via the TRN modulate cell activity in different parts of the MGV with regard to tonotopic organization. The AI and non‐AI could serve distinctive gating functions for auditory attention through the differential topography of inhibitory modulation. In addition, we obtained an intriguing finding that a subset of auditory TRN cells projected to the somatosensory but not to the auditory thalamic nuclei. There was also a cell projecting to the MGV and somatosensory nuclei. These findings extend the previously suggested possibility that TRN has a cross‐modal as well as an intramodal gating function in the thalamus.
Involvement of AMPA receptor phosphorylation in antidepressant actions with special reference to tianeptine
Authors: Svenningsson Per , Bateup Helen , Qi Hongshi , Takamiya Kogo , Huganir Richard L. , Spedding Michael , Roth Bryan L. , McEwen Bruce S. , Greengard Paul 
Published: July 2010

AbstractDepression is associated with abnormal neuronal plasticity. AMPA receptors mediate transmission and plasticity at excitatory synapses in a manner which is positively regulated by phosphorylation at Ser831‐GluR1, a CaMKII/PKC site, and Ser845‐GluR1, a PKA site. Treatment with the selective serotonin (5‐hydroxytryptamine; 5‐HT) reuptake inhibitor fluoxetine increases P‐Ser845‐GluR1 but not P‐Ser831‐GluR1. Here, it was found that treatment with another antidepressant, tianeptine, increased P‐Ser831‐GluR1 in the frontal cortex and the CA3 region of hippocampus and P‐Ser845‐GluR1 in the CA3 region of hippocampus. A receptorome profile detected no affinity for tianeptine at any monaminergic receptors or transporters, confirming an atypical profile for this compound. Behavioural analyses showed that mice bearing point mutations at both Ser831‐ and Ser845‐GluR1, treated with saline, exhibited increased latency to enter the centre of an open field and increased immobility in the tail‐suspension test compared to their wild‐type counterparts. Chronic tianeptine treatment increased open‐field locomotion and reduced immobility in wild‐type mice but not in phosphomutant GluR1 mice. P‐Ser133‐CREB was reduced in the CA3 region of hippocampus in phosphomutant mice, and tianeptine decreased P‐Ser133‐CREB in this region in wild‐type, but not in phosphomutant, mice. Tianeptine increased P‐Ser133‐CREB in the CA1 region in wild‐type mice but not in phosphomutant GluR1 mice. There were higher basal P‐Ser133‐CREB and c‐fos levels in frontal and cingulate cortex in phosphomutant GluR1 mice; these changes in level were counteracted by tianeptine in a GluR1‐independent manner. Using phosphorylation assays and phosphomutant GluR1 mice, this study provides evidence that AMPA receptor phosphorylation mediates certain explorative and antidepressant‐like actions under basal conditions and following tianeptine treatment.
Adenosine A1receptor‐mediated inhibition of dopamine release from rat striatal slices is modulated by D1dopamine receptors
Authors: O'Neill C. , Nolan B. J. , Macari A. , O'Boyle K. M. , O'Connor J. J. 
Published: July 2010

AbstractDopamine release is regulated by presynaptic dopamine receptors and interactions between adenosine and dopamine receptors have been well documented. In the present study, dopamine release from isolated striatal slices from Wistar rats was measured using fast cyclic voltammetry. Single‐pulse stimulation (0.1 ms, 10 V) was applied every 5 min over a 2‐h period. Superfusion with the adenosine (A)1receptor agonist N6‐cyclopentyladenosine (CPA), but not the A2receptor agonist 3‐[4‐[2‐[[6‐amino‐9‐[(2R,3R,4S,5S)‐5‐(ethylcarbamoyl)‐3,4‐dihydroxy‐oxolan‐2‐yl]purin‐2‐yl]amino]ethyl] phenyl]propanoic acid (CGS 21680), inhibited dopamine release in a concentration‐dependent manner (IC503.80 × 10−7 m;n = 10). The dose–response curve to CPA was shifted to the right (IC506.57 × 10−6 m;n = 6,P < 0.05 vs. control) by the A1receptor antagonist 8‐cyclopentyl‐1,3‐dipropylxanthine (DPCPX). Neither the D1agonist 6‐chloro‐APB nor the D1antagonist R‐(+)‐8‐chloro‐2,3,4,5‐tetrahydro‐3‐methyl‐5‐phenyl‐1H‐3‐ benzazepine‐7‐ol (SCH 23390) altered dopamine release on their own. However, SCH 23390 (3 µm) significantly attenuated the response to CPA (IC501.44 × 10−5 m;n = 6,P < 0.01 vs. control). Furthermore, the inhibitory effect of CPA was significantly increased in the presence of 6‐chloro‐APB (1 µm). In radioligand binding experiments, CPA interacted with high‐ and low‐affinity states of [3H]DPCPX‐lableled A1receptors. The high‐affinity agonist binding to A1receptors was inhibited by the stable guanosine triphosphate analogue Gpp(NH)p. In contrast, neither the proportion nor the affinity of high‐affinity A1receptors was altered by dopamine or SCH 23390. These results provide evidence that the inihibition of dopamine release by adenosine A1receptors is dependent, at least in part, on the simultaneous activation of D1dopamine receptors. While the mechanism underlying this interaction remains to be determined, it does not appear to involve an intramembrane interaction between A1and D1receptors.
Target regulation of V2R expression and functional maturation in vomeronasal sensory neurons in vitro
Authors: Muramoto Kazuyo , Hashimoto Mitsuhiro , Kaba Hideto 
Published: July 2010

AbstractVomeronasal receptors from the V1R and V2R gene families mediate the detection of chemical stimuli such as pheromones via the vomeronasal organ (VNO). The differential expression of vomeronasal receptors might contribute in part to a variety of pheromonal effects, which are different sexually, developmentally and even individually. However, little is known about the mechanisms controlling vomeronasal receptor expression. Cultured vomeronasal sensory neurons (VSNs) bear phenotypic resemblance to the intact VNO but they remain immature. Because indices of VSN maturation are increased by coculture with the target cells for VSNs, accessory olfactory bulb (AOB) neurons, AOB neurons may regulate vomeronasal receptor expression and functional maturation in VSNs. To test this hypothesis, we examined the expression of V2R‐type vomeronasal receptors (VR1 and VR4) and chemosensory responsiveness in VNOs cocultured with AOB neurons. Immunoblot and immunocytochemical analysis revealed that the coculture of VNOs with AOB neurons resulted in a greater expression of VR1 and VR4 after 10 days than VNOs cultured alone. Moreover, calcium imaging analysis showed that cocultured VNOs responded to urine components applied iontophoretically into their cavities with a time course similar to the V2R expression, in contrast to singly cultured VNOs that displayed no response. These results demonstrate that AOB neurons induce the expression of vomeronasal receptors in VSNs, allowing them to function.
A potential role for calcium / calmodulin‐dependent protein kinase‐related peptide in neuronal apoptosis: in vivo and in vitro evidence
Authors: Schenk Geert J. , Engels Bart , Zhang Yan‐Ping , Fitzsimons Carlos P. , Schouten Theo , Kruidering Marieke , Ron de Kloet E. , Vreugdenhil Erno 
Published: July 2010

AbstractPreviously, we have established that a product of the doublecortin‐like kinase (DCLK) gene, DCLK‐short, is cleaved by caspases during serum deprivation. Subsequently, the N‐terminal cleavage product of DCLK‐short facilitates apoptosis in the neuroblastoma cell line NG108. As this N‐terminal cleavage product is highly homologous to calcium/calmodulin‐dependent protein kinase‐related peptide (CARP), another DCLK gene splice variant, we aimed to determine the possible apoptotic properties of CARP in vivo and in vitro. We report highly specific CARP expression in apoptotic granule cells in the rat dentate gyrus after adrenalectomy relative to healthy granule cells. CARP is significantly upregulated in the suprapyramidal blade of the dentate gyrus, with varying levels of upregulation, depending on the extent of adrenalectomy‐induced apoptosis. Similar to the caspase‐cleaved N‐terminus of DCLK‐short, CARP overexpression itself facilitated apoptosis in serum‐deprived NG108 cells. Furthermore, CARP facilitated polymerization of tubulin in vitro and was capable of interacting with growth factor receptor‐bound protein 2, an intracellular protein involved in vesicle trafficking. Together, our data demonstrate a facilitating role for CARP in the apoptotic process in granule cell populations sensitive to adrenalectomy, and suggest that this proapoptotic effect is mediated by increasing the stability of the microtubule cytoskeleton.
Influence of macrophages and lymphocytes on the survival and axon regeneration of injured retinal ganglion cells in rats from different autoimmune backgrounds
Authors: Luo Jian‐Min , Zhi Ye , Chen Qing , Cen Ling‐Ping , Zhang Cheng‐Wu , Lam Dennis S. C. , Harvey Alan R. , Cui Qi 
Published: July 2010

AbstractThe immune response after neural injury influences the survival and regenerative capacity of neurons. In the primary visual pathway, previous studies have described beneficial effects of macrophages and T‐cells in promoting neural survival and axonal regeneration in some rat strains. However, the contributions of specific cell populations to these responses have been unclear. In adult Fischer (F344) rats, we confirm prior reports that intravitreal macrophage activation promotes the survival of retinal ganglion cells (RGCs) and greatly enhances axonal regeneration through a peripheral nerve graft. Neonatal thymectomy that results in elimination of T‐cell production enhanced RGC survival after axotomy, but diminished the effect of intravitreal macrophage activation on axon regeneration. Thus, in F344 rats, lymphocytes appear to suppress RGC survival but augment the pro‐regenerative effects of macrophages. The cytotoxic effect of lymphocytes on RGCs was confirmed in in vitro studies; coculture of retinal explants with lymphocytes led to a 60% reduction in viable RGCs. Similar in vivo results were obtained in Sprague Dawley rats. By comparison, in adult Lewis rats, neither RGC survival nor axonal regeneration was increased after intravitreal macrophage activation. Neonatal thymectomy had only a small beneficial effect on RGC survival, and although Lewis lymphocytes reduced RGC viability in culture, they did so to a lesser extent. Thus, in addition to a complex role of lymphocytes, particularly T‐cells, after central nervous system injury, the present results demonstrate that the impact of macrophages is also influenced by genetic background.
Epileptiform synchronization in the rat insular and perirhinal cortices in vitro
Authors: Sudbury Jessica R. , Avoli Massimo 
Published: July 2010

AbstractThe hippocampus plays a primary role in temporal lobe epilepsy, a common form of partial epilepsy in adults. Recent studies, however, indicate that extrahippocampal areas such as the perirhinal and insular cortices represent important participants in this epileptic disorder. By employing field potential recordings in the in vitro 4‐aminopyridine model of temporal lobe epilepsy, we have investigated here the contribution of glutamatergic and GABAergic signaling to epileptiform activity in these structures. First, we provide evidence of epileptiform synchronicity between the perirhinal and insular cortices, and resolve some pharmacological and network mechanisms involved in sustaining the interictal‐ and ictal‐like discharges recorded there. Second, we report that in the absence of ionotropic glutamatergic transmission, GABAergic networks produce synchronous potentials that spread between the perirhinal and insular cortices. Finally, we have established that such activity is modulated by activating µ‐opioid receptors. Our findings support clinical and experimental evidence concerning the involvement of the perirhinal and insular cortex networks in temporal lobe epilepsy, and provide observations that may impact research focussing on the role of the insular cortex in nociception.
Cognitive impairment and transmitter‐specific pre‐ and postsynaptic changes in the rat cerebral cortex during ageing
Authors: Majdi Maryam , Ribeiro‐da‐Silva Alfredo , Cuello A. Claudio 
Published: July 2010

AbstractRecent studies suggest that age‐related cognitive decline is correlated with an excitatory–inhibitory imbalance in synaptic discharges on pyramidal neurons. This study focuses on whether ageing and cognitive status correlates with relative numbers of excitatory and inhibitory presynaptic boutons. We investigated the density of excitatory and inhibitory presynaptic inputs across several areas of the rat cerebral cortex in young and aged male Fischer 344 rats. Aged animals were segregated into aged cognitively impaired (AI) and aged cognitively unimpaired (AU) groups using the Morris water maze. We applied immunohistochemistry to reveal the majority of excitatory and inhibitory presynaptic boutons captured with confocal microscopy and quantitative image analysis. A gradual decline in the density of excitatory and inhibitory presynaptic boutons occurred from young to AU to AI animals; however, the ratios of excitatory to inhibitory presynaptic bouton densities were not significantly altered. We further investigated the density of receptor scaffolding proteins representing key excitatory and inhibitory receptor postsynaptic sites, using antibodies against specific markers of excitatory and inhibitory postsynaptic densities, respectively. Significant changes in the ratios of excitatory to inhibitory postsynaptic densities were observed only in AI compared to young rats.
Regulated recycling and plasma membrane recruitment of the high‐affinity choline transporter
Authors: Ribeiro Fabiola M. , Pinthong Metta , Black Stefanie A. G. , Gordon Alexis C. , Prado Vania F. , Prado Marco A. M. , Rylett R. Jane , Ferguson Stephen S. G. 
Published: July 2010

AbstractThe high‐affinity choline transporter (CHT1) is responsible for uptake of choline from the synaptic cleft and supplying choline for acetylcholine synthesis. CHT1 internalization by clathrin‐coated vesicles is proposed to represent a mechanism by which high‐affinity choline uptake can be modulated. We show here that internalized CHT1 is rapidly recycled back to the cell surface in both human embryonic kidney cells (HEK 293 cells) and SH‐SY5Y neuroblastoma cells. This rapidly recycling pool of CHT1 comprises about 10% of total CHT1 protein. In the SH‐SY5Y neuroblastoma cell line K+‐depolarization promotes Ca2+‐dependent increase in the rate of CHT1 recycling to the plasma membrane without affecting the rate of CHT1 internalization. K+‐depolarization also increases the size of the pool of CHT1 protein that can be mobilized to the plasma membrane. Thus, the activity‐dependent increase in plasma membrane CHT1 localization appears to be regulated by two mechanisms: (i) an increase in the rate of externalization of the intracellular CHT1 pool; and (ii) the recruitment of additional intracellular transporters to the recycling pool.
Isolating endogenous visuo‐spatial attentional effects using the novel visual‐evoked spread spectrum analysis (VESPA) technique
Authors: Lalor Edmund C. , Kelly Simon P. , Pearlmutter Barak A. , Reilly Richard B. , Foxe John J. 
Published: July 2010

AbstractIn natural visual environments, we use attention to select between relevant and irrelevant stimuli that are presented simultaneously. Our attention to objects in our visual field is largely controlled endogenously, but is also affected exogenously through the influence of novel stimuli and events. The study of endogenous and exogenous attention as separate mechanisms has been possible in behavioral and functional imaging studies, where multiple stimuli can be presented continuously and simultaneously. It has also been possible in electroencephalogram studies using the steady‐state visual‐evoked potential (SSVEP); however, it has not been possible in conventional event‐related potential (ERP) studies, which are hampered by the need to present suddenly onsetting stimuli in isolation. This is unfortunate as the ERP technique allows for the analysis of human physiology with much greater temporal resolution than functional magnetic resonance imaging or the SSVEP. While ERP studies of endogenous attention have been widely reported, these experiments have a serious limitation in that the suddenly onsetting stimuli, used to elicit the ERP, inevitably have an exogenous, attention‐grabbing effect. Recently we have shown that it is possible to derive separate event‐related responses to concurrent, continuously presented stimuli using the VESPA (visual‐evoked spread spectrum analysis) technique. In this study we employed an experimental paradigm based on this method, in which two pairs of diagonally opposite, non‐contiguous disc‐segment stimuli were presented, one pair to be ignored and the other to be attended. VESPA responses derived for each pair showed a strong modulation at 90–100 ms (during the visual P1 component), demonstrating the utility of the method for isolating endogenous visuo‐spatial attention effects.