bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hippocampal synaptic transmission and LTP in vivo are intact following bilateral vestibular deafferentation in the rat
Authors: Zheng Yiwen , Mason‐Parker Sara E. , Logan Barbara , Darlington Cynthia L. , Smith Paul F. , Abraham Wickliffe C. 
Published: June 2009

AbstractNumerous studies in animals and humans have shown that damage to the vestibular system in the inner ear results in spatial memory deficits, presumably because areas of the brain such as the hippocampus require vestibular input to accurately represent the spatial environment. Consistent with this hypothesis, studies in animals have demonstrated that complete bilateral vestibular deafferentation (BVD) causes a disruption of place cell firing as well as theta activity. The aim of this study was to investigate whether BVD in rats affects baseline field potentials (field excitatory postsynaptic potentials and population spikes) and long‐term potentiation (LTP) in CA1 and the dentate gyrus (DG) of awake freely moving rats up to 43 days post‐BVD and of anesthetized rats at 7 months post‐BVD. Compared to sham controls, BVD had no significant effect on either baseline field potentials or LTP in either condition. These results suggest that although BVD interferes with the encoding, consolidation, and/or retrieval of spatial memories and the function of place cells, these changes are not related to detectable in vivo decrements in basal synaptic transmission or LTP, at least in the investigated pathways. © 2009 Wiley‐Liss, Inc.
β‐Adrenergic receptors link NO/sGC/PKG signaling to BDNF expression during the consolidation of object recognition long‐term memory
Authors: Furini Cristiane R. , Rossato Janine I. , Bitencourt Lucas L. , Medina Jorge H. , Izquierdo Iván , Cammarota Martín 
Published: June 2009

AbstractThe nitric oxide (NO)/soluble guanylyl cyclase (sGC)/protein kinase G (PKG) pathway is important for memory processing, but the identity of its downstream effectors as well as its actual participation in the consolidation of nonaversive declarative long‐term memory (LTM) remain unknown. Here, we show that training rats in an object recognition (OR) learning task rapidly increased nitrites/nitrates (NOx) content in the CA1 region of the dorsal hippocampus while posttraining intra‐CA1 microinfusion of the neuronal NO synthase (nNOS) inhibitor L‐NN hindered OR LTM retention without affecting memory retrieval or other behavioral variables. The amnesic effect of L‐NN was not state dependent, was mimicked by the sGC inhibitor LY83583 and the PKG inhibitor KT‐5823, and reversed by coinfusion of the NO donorS‐nitroso‐N‐acetylpenicillamine (SNAP) and the PKG activator 8‐bromoguanosine 3′,5′‐cyclic monophosphate (8Br‐cGMP). SNAP did not affect the amnesic effect of LY83583 and KT‐5823. Conversely, 8Br‐cGMP overturned the amnesia induced by LY83583 but not that caused by KT‐5823. Intra‐CA1 infusion of the β‐adrenergic receptor blocker timolol right after training hindered OR LTM and, although coadministration of noradrenaline reversed the amnesia caused by L‐NN, LY83583, and KT5823, the amnesic effect of timolol was unaffected by coinfusion of 8Br‐cGMP or SNAP, indicating that hippocampal β‐adrenergic receptors act downstream NO/sGC/PKG signaling. We also found that posttraining intra‐CA1 infusion of function‐blocking anti‐brain‐derived neurotrophic factor (BDNF) antibodies hampered OR LTM retention, whereas OR training increased CA1 BDNF levels in a nNOS‐ and β‐adrenergic receptor‐dependent manner. Taken together, our results demonstrate that NO/sGC/PKG signaling in the hippocampus is essential for OR memory consolidation and suggest that β‐adrenergic receptors link the activation of this pathway to BDNF expression during the consolidation of declarative memories. © 2009 Wiley‐Liss, Inc.
A re‐examination of the stationarity of inflation
Authors: Cook Steven 
Published: June 2009

AbstractIn a recent examination of the integrated nature of inflation, Culver and Papell (Journal of Applied Econometrics, 1997) applied a range of unit root and stationarity tests to data from a panel of 13 OECD economies. The results obtained were mixed. While little evidence of stationarity was detected using univariate methods, rejection of the unit root hypothesis was observed under panel data unit root testing, although rejection was found to be sensitive to cross‐sectional variation. In this note the results of Culver and Papell are reconsidered in light of conditional heteroskedasticity detected in the inflation rate series. Using a more appropriate univariate testing procedure combining local‐to‐unity detrending and joint maximum likelihood estimation of a unit root testing equation and GARCH process, strong evidence in favour of stationarity is detected in 11 of 13 economies examined. In contrast to the univariate findings of Culver and Papell, the results obtained herein using an alternative univariate procedure provide evidence in support of their I(0) inference drawn using panel methods. Copyright © 2009 John Wiley & Sons, Ltd.
Neurobehavioral toxicity study of dibutyl phthalate on rats followingin uteroand lactational exposure
Authors: Li Yuanfeng , Zhuang Meizhu , Li Tao , Shi Nian 
Published: June 2009

AbstractTo investigate the neurobehavioral effects of dibutyl phthalate (DBP), an important endocrine disruptor known for reproductive toxicity, on rodent offspring followingin uteroand lactational exposure, pregnant Wistar rats were treated with DBP (0, 0.037, 0.111, 0.333 and 1% in the diet) from gestation day (GD) 6 to postnatal day (PND) 28, and selected developmental and neurobehavioral parameters of the offspring were measured. There were no significant effects of DBP on body weight gain of the dams during GD 6–20 or on the pups' ages of pinna detachment, incisor eruption or eye opening. Exposure to 1% DBP prolonged gestation period, decreased body weight in both male and female pups, depressed surface righting (PND 7) in male pups, shortened forepaw grip time (PND 10), enhanced spatial learning and reference memory (PND 35) in male pups. Exposure to 0.037% DBP also shortened forepaw grip time (PND 10), but inhibited spatial learning and reference memory in male pups. Sex × treatment effects were found in forepaw grip time (PND 10), spatial learning and reference memory, and the male pups appeared to be more susceptible than the females. However, all levels of DBP exposure did not significantly alter surface righting (PND 4), air righting (PND 16), negative geotaxis (PND 4 or 7), cliff avoidance (PND 7) or open field behavior (PND 28) in either sex. Overall, the dose level of DBP in the present study produced a few adverse effects on the neurobehavioral parameters, and it may alter cognitive abilities of the male rodent. Copyright © 2009 John Wiley & Sons, Ltd.
Shift of oxidants and antioxidants levels in rats as a reaction to exposure to sulfur mustard
Authors: Pohanka Miroslav , Stetina Rudolf 
Published: June 2009

AbstractAntixodants as well as oxidants levels were investigated in plasma of rats exposed to sulfur mustard in doses of 0 (control), 5, 20 and 80 mg kg−1body weight. Cyclic voltammetry performed on screen‐printed strips with platinum working electrode used as a tool for assaying oxidant and antioxidant levels. We found significant shifts in both examined analytes. A dose of sulfur mustard of 5 mg kg−1body weight caused only a small change in oxidant and antioxidant levels when compared with the control group. A dose of 20 mg kg−1body weight provided a significant increase in antioxidants as well oxidants; however, the ratio of both was similar to that in the control group. The most surprising facts were found when the highest dose of 80 mg kg−1body weight of sulfur mustard was applied. While antioxidants were significantly increased, oxidants were decreased on an extensive scale. Copyright © 2009 John Wiley & Sons, Ltd.
Doppler calibration method for Spectral Domain OCT spectrometers
Authors: Faber Dirk J. , Leeuwen Ton G. van 
Published: June 2009

AbstractWe present a calibration method for SD‐OCT domain spectrometers based on the M‐scan of a moving mirror. This method allows determination of the wavenumber sampling increment which determines the depth axis assigned to the structural image. It also allows wavelength calibration of individual pixels which ensures correct re‐sampling prior to Fast Fourier Transform. Determination of the spectrometer resolution, which determines sensitivity and resolution decay with depth, is also possible. The wavelength calibration results suggest that hardware calibration of the spectrometers is a necessary complement to the computational methods presented here. (© 2009 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
KiSS1 suppresses TNFα‐induced breast cancer cell invasion via an inhibition of RhoA‐Mediated NF‐κB activation
Authors: Cho Sung‐Gook , Li Dali , Stafford Lewis J. , Luo Jian , Rodriguez‐Villanueva Melissa , Wang Ying , Liu Mingyao 
Published: June 2009

AbstractTumor necrosis factor‐alpha (TNFα) induces cancer development and metastasis, which is prominently achieved by nuclear factor‐kappa B (NF‐κB) activation. TNFα‐induced NF‐κB activation enhances cellular mechanisms including proliferation, migration, and invasion. KiSS1, a key regulator of puberty, was initially discovered as a tumor metastasis suppressor. The expression of KiSS1 was lost or down‐regulated in different metastatic tumors. However, it is unclear whether KiSS1 regulates TNFα‐induced NF‐κB activation and further tumor cell migration. In this study, we demonstrate that KiSS1 suppresses the migration of breast cancer cells by inhibiting TNFα‐induced NF‐κB pathway and RhoA activation. Both KiSS1 overexpression and KP10 (kisspeptin‐10) stimulation inhibited TNFα‐induced NF‐κB activity, suppressed TNFα‐induced cell migration and cell attachment to fibronectin in breast cancer cells while KP10 has little effect on cancer cell proliferation. Furthermore, KP10 inhibited TNFα‐induced cell migration and RhoA GTPase activation. Therefore, our data demonstrate that KiSS1 inhibits TNFα‐induced NF‐κB activation via downregulation of RhoA activation and suppression of breast cancer cell migration and invasion. J. Cell. Biochem. 107: 1139–1149, 2009. © 2009 Wiley‐Liss, Inc.
Src and FAK mediate cell–matrix adhesion‐dependent activation of met during transformation of breast epithelial cells
Authors: Hui Angela Y. , Meens Jalna A. , Schick Colleen , Organ Shawna L. , Qiao Hui , Tremblay Eric A. , Schaeffer Erik , Uniyal Shashi , Chan Bosco M.C. , Elliott Bruce E. 
Published: June 2009

AbstractCell–matrix adhesion has been shown to promote activation of the hepatocyte growth factor receptor, Met, in a ligand‐independent manner. This process has been linked to transformation and tumorigenesis in a variety of cancer types. In the present report, we describe a key role of integrin signaling via the Src/FAK axis in the activation of Met in breast epithelial and carcinoma cells. Expression of an activated Src mutant in non‐neoplastic breast epithelial cells or in carcinoma cells was found to increase phosphorylation of Met at regulatory tyrosines in the auto‐activation loop domain, correlating with increased cell spreading and filopodia extensions. Furthermore, phosphorylated Met is complexed with β1 integrins and is co‐localized with vinculin and FAK at focal adhesions in epithelial cells expressing activated Src. Conversely, genetic or pharmacological inhibition of Src abrogates constitutive Met phosphorylation in carcinoma cells or epithelial cells expressing activated Src, and inhibits filopodia formation. Interestingly, Src‐dependent phosphorylation of Met requires cell–matrix adhesion, as well as actin stress fiber assembly. Phosphorylation of FAK by Src is also required for Src‐induced Met phosphorylation, emphasizing the importance of the Src/FAK signaling pathway. However, stimulation of Met phosphorylation by addition of exogenous HGF in epithelial cells is refractory to inhibition of Src family kinases, indicating that HGF‐dependent and Src/integrin‐dependent Met activation occur via distinct mechanisms. Together these findings demonstrate a novel mechanism by which the Src/FAK axis links signals from the integrin adhesion complex to promote Met activation in breast epithelial cells. J. Cell. Biochem. 107: 1168–1181, 2009. © 2009 Wiley‐Liss, Inc.
Characterization of myostatin/gdf8/11 in the starlet sea anemone Nematostella vectensis
Authors: Saina Michael , Technau Ulrich 
Published: June 2009

AbstractThe signaling molecule Myostatin, a member of the TGF‐β superfamily, is crucially involved in the control of muscle growth and development in triploblastic organisms. A homolog to vertebrate myostatin and gdf8/11 was isolated from a diploblastic cnidarian, the starlet sea anemone Nematostella vectensis. Here we provide a detailed characterization of the Nematostella myostatin/gdf8/11 gene and show the first analysis of gene expression in adult polyps. This analysis revealed that myostatin/gdf8/11 is expressed in the mesenteries, which are endodermal folds, and weakly in the body wall endoderm, but largely excluded from the areas of muscle formation, the retractor and the parietal muscle. Contrary to this, in vertebrates the muscle growth inhibitor myostatin is expressed in the muscle tissue. We therefore hypothesize that myostatin/gdf8/11 in Nematostella is involved in regulating nonmuscle cell differentiation, possibly by repressing muscle differentiation. J. Exp. Zool. (Mol. Dev. Evol.) 312B:780–788, 2009. © 2009 Wiley‐Liss, Inc.
Specific inhibition of epithelial Na+ channels by antisense oligonucleotides for the treatment of Na+ hyperabsorption in cystic fibrosis
Authors: Sobczak Katja , Segal Andrei , Bangel‐Ruland Nadine , Semmler Judith , Van Driessche Willy , Lindemann Hermann , Heermann Ralf , Weber Wolf‐Michael 
Published: June 2009

AbstractBackgroundCystic fibrosis (CF) respiratory epithelia are characterized by a defect Cl− secretion and an increased Na+ absorption through epithelial Na+ channels (ENaC). The present study aimed to find an effective inhibitor of human ENaC with respect to replacing amiloride therapy for CF patients. Therefore, we developed specific antisense oligonucleotides (AON) that efficiently suppress Na+ hyperabsorption by inhibiting the expression of the α‐ENaC subunit.MethodsWe heterologously expressed ENaC in oocytes of Xenopus laevis for mass screening of AON. Additionally, primary cultures of human nasal epithelia were transfected with AON and were used for Ussing chamber experiments, as well as biochemical and fluorescence optical analyses.ResultsScreening of several AON by co‐injection or sequential microinjection of AON and ENaC mRNA in X. laevis oocytes led to a sustained decrease in amiloride‐sensitive current and conductance. Using primary cultures of human nasal epithelia, we show that AON effectively suppress amiloride‐sensitive Na+ absorption mediated by ENaC in CF and non‐CF tissues. In western blot experiments, it could be shown that the amount of ENaC protein is effectively reduced after AON transfection.ConclusionsOur data comprise an initial step towards a preclinical test with AON to reduce Na+ hyperabsorption in CF epithelia. Copyright © 2009 John Wiley & Sons, Ltd.
Immunogenicity of intrathecal plasmid gene delivery: cytokine release and effects on transgene expression
Authors: Hughes Travis S. , Langer Stephen J. , Virtanen Salla I. , Chavez Raymond A. , Watkins Linda R. , Milligan Erin D. , Leinwand Leslie A. 
Published: June 2009

AbstractBackgroundOne method for the delivery of therapeutic proteins to the spinal cord is to inject nonviral gene vectors including plasmid DNA into the cerebrospinal fluid (CSF) that surrounds the spinal cord (intrathecal space). This approach has produced therapeutic benefits in animal models of disease and several months of protein expression; however, there is little information available on the immune response to these treatments in the intrathecal space, the relevance of plasmid CpG sequences to any plasmid‐induced immune response, or the effect of this immune response on transgene expression.MethodsIn the present study, coding or noncoding plasmids were delivered to the intrathecal space of the lumbar spinal region in rats. Lumbosacral CSF was then collected at various time points afterwards for monitoring of cytokines and transgene expression.ResultsThis work demonstrates, for the first time, increased tumor necrosis factor‐α and interleukin‐1 in response to intrathecal plasmid vector injection and provides evidence indicating that this response is largely absent in a CpG‐depleted vector. Transgene expression in the CSF is not significantly affected by this immune response. Expression after intrathecal plasmid injection is variable across rats but correlates with the amount of tissue associated plasmid and is increased by disrupting normal CSF flow.ConclusionsThe data obtained in the present study indicate that plasmid immunogenicity may affect intrathecal plasmid gene therapy safety but not transgene expression in the CSF. Furthermore, the development of methods to prevent loss of plasmid via CSF flow out of the central nervous system through the injection hole and/or natural outflow routes may increase intrathecal plasmid gene delivery efficacy. Copyright © 2009 John Wiley & Sons, Ltd.
Sulfoglucuronosyl paragloboside is a ligand for T cell adhesion: Regulation of sulfoglucuronosyl paragloboside expression via nuclear factor κB signaling
Authors: Dasgupta Somsankar , Silva Jeane , Wang Guanghu , Yu Robert K. 
Published: June 2009

AbstractInflammatory cytokines such as tumor necrosis factor (TNF)‐α and interleukin (IL)‐1β stimulate glucuronosyltransferase genes (S and P) in endothelial cells (ECs) and up‐regulate sulfoglucuronosyl paragloboside (SGPG) expression, which serves as a ligand for T cell adhesion. However, the mechanism of cytokine‐mediated gene up‐regulation has not been elucidated. To evaluate the precise mechanism of SGPG up‐regulation, we have specifically inhibited the SGPG synthesis in the cerebromicrovascular EC line (SV‐HCECs), a transformed brain ECs of human origin. SV‐HCECs were transfected with small interfering RNA designed to mimic the human natural killer epitope‐1 sulfotransferase (HNK‐1ST), the ultimate enzyme that transfers the sulfate group to glucuronic acid for SGPG synthesis. An inhibition of SGPG expression along with a reduction of human CD4+ cell adhesion was observed in siRNA HNK‐1ST (siHNK‐1)‐transfected cells after TNFα stimulation. A thorough screening of the signaling system confirmed that TNFα/IL‐1β stimulation up‐regulated nuclear factor κB (NFκB) signaling in SV‐HCECs. siHNK‐1 transfection interfered with the SGPG up‐regulation after TNFα/IL‐1β stimulation in transfected cells and reduced the T cell adhesion. Hence, our study indicates that T cell‐SGPG adhesion in SV‐HCECs may proceed through NFκB activation. In addition, siHNK‐1 transfection reduced the NFκB activity compared with cells that were transfected with scrambled siRNA, before and after TNFα/IL‐1β stimulation. This is the first report indicating that NFκB signaling is involved in SGPG gene expression in brain ECs by an unknown mechanism. Its down‐regulation by inhibiting HNK‐1ST expression may have a potential use in preventing the T cell invasion and consequently nerve damage during inflammation. © 2009 Wiley‐Liss, Inc.
Expression and distribution of cystic fibrosis transmembrane conductance regulator in neurons of the spinal cord
Authors: Guo Yong , Su Min , Su Meng , McNutt Michael A. , Gu Jiang 
Published: June 2009

AbstractTo verify the hypothesis that cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in neurons of the human spinal cord, we investigated the presence and distribution of CFTR protein and mRNA in different segments of the human spinal cord obtained from autopsies. The techniques employed included reverse transcriptase‐polymerase chain reaction (RT‐PCR) to detect CFTR gene expression, in situ hybridization to detect mRNA distribution, and immunohistochemistry to detect protein distribution. The specificity of these experiments was established with extensive controls. We found widespread and abundant expression of CFTR in neurons of the human spinal cord. CFTR protein and mRNA are localized to the cytoplasm of neurons in all segments of the spinal cord but not to glial fibrillary acidic protein (GFAP)‐positive cells. CFTR is a very important molecule, acting as a chloride channel and regulating many physiological functions, including salt transport, fluid flow, and intracellular ion concentrations. Its mutation causes cystic fibrosis. Our finding of abundant CFTR in the spinal cord suggests that this molecule may be significant in the normal function and pathology of the spinal cord. © 2009 Wiley‐Liss, Inc.
Fustin flavonoid attenuates β‐amyloid (1–42)‐induced learning impairment
Authors: Jin Chun‐Hui , Shin Eun‐Joo , Park Jae‐Bong , Jang Choon‐Gon , Li Zhengyi , Kim Min Soo , Koo Kyo Hwan , Yoon Hyoung‐Jong , Park Sang‐Jae , Choi Won‐Cheol , Yamada Kiyofumi , Nabeshima Toshitaka , Kim Hyoung‐Chun 
Published: June 2009

AbstractNatural flavonoids ameliorate amyloid‐β peptide (Aβ)‐induced neurotoxicity. We examined whether the fustin flavonoid affects Aβ‐induced learning impairment in mice. Repeated treatment with fustin significantly attenuated Aβ (1–42)‐induced conditioned fear and passive avoidance behaviors. This effect was comparable to that of EGb761, a standard extract of ginkgo. Fustin treatment significantly prevented decreases in acetylcholine (ACh) levels, choline acetyltransferase (ChAT) activity, and ChAT gene expression induced by Aβ (1–42). Fustin also consistently suppressed increases in acetyl cholinesterase (AChE) activity and AChE gene expression induced by Aβ (1–42). In addition, fustin significantly attenuated Aβ (1–42)‐induced selective decreases in muscarinic M1 receptor gene expression and muscarinic M1 receptor binding activity (as determined by [3H]pirenzepine binding) by modulating extracellular signal‐regulated kinase 1/2 (ERK 1/2) and cAMP response‐element binding protein (CREB) phosphorylation and brain‐derived neurotrophic factor (BDNF) expression. These effects of fustin were reversed by treatment with dicyclomine, a muscarinic M1 receptor antagonist, and SL327, a selective ERK inhibitor, but not by chelerythrine, a pan‐protein kinase C (PKC) inhibitor. Taken together, our results suggest that fustin attenuates Aβ (1–42)‐impaired learning, and that the ERK/CREB/BDNF pathway is important for the M1 receptor‐mediated cognition‐enhancing effects of fustin. © 2009 Wiley‐Liss, Inc.