bluuebunny/crossref_metadata_2025_split huggingface dataset:
NOV/CCN3 upregulates CCL2 and CXCL1 expression in astrocytes through β1 and β5 integrins
Authors: Le Dréau G. , Kular L. , Nicot A.B. , Calmel C. , Melik‐Parsadaniantz S. , Kitabgi P. , Laurent M. , Martinerie C. 
Published: June 2010

AbstractIncreasing evidence suggests that CCN matricellular proteins play important roles in inflammation. One of the major cell types that handle inflammation in the brain is the astrocyte, which, upon activation, dramatically increases its production of cytokines and chemokines. Here, we report that NOV/CCN3, added to primary cultured rat brain astrocytes, markedly increased the expression of CCL2 and CXCL1 chemokines, as indicated by ELISA and RT‐qPCR assays. This effect was selective, as the production of thirteen other cytokines and chemokines was not affected by NOV. NOV expression by astrocytes was demonstrated by immunocytochemistry and Western blot analysis, and astrocyte transfection with NOV small interfering RNA (siRNA) markedly decreased CXCL1 and CCL2 production, indicating that endogenous NOV played a major role in the control of astrocytic chemokine synthesis. NOV was shown to mediate several of its actions through integrins. Here, we observed that siRNAs against integrins β1 and β5 decreased basal and abrogated NOV‐stimulated astrocyte expression of CCL2 and CXCL1, respectively. Using a panel of kinase inhibitors, we demonstrated that NOV action on CCL2 and CXCL1 production involved a Rho/ROCK/JNK/NF‐κB and a Rho/qROCK/p38/NF‐κB pathway, respectively. Thus, distinct integrins and signaling mechanisms are involved in NOV‐induced production of CCL2 and CXCL1 in astrocytes. Finally, astrocytic expression of NOV was detected in rat brain tissue sections, and NOV intracerebral injection increased CCL2 and CXCL1 brain levels in vivo. Altogether, our data shed light on the signaling pathways operated by NOV and strongly suggest that NOV mediates astrocyte activation and, therefore, might play a role in neuroinflammation. © 2010 Wiley‐Liss, Inc.
Neural processes for intentional control of perceptual switching: A magnetoencephalography study
Authors: Shimono Masanori , Kitajo Keiichi , Takeda Tsunehiro 
Published: June 2010

AbstractThis article reports an interesting link between the psychophysical property of intentional control of perceptual switching and the underlying neural activities. First, we revealed that the timing of perceptual switching for a dynamical dot quartet can be controlled by the observers' intention, without eye movement. However, there is a clear limitation to this control, such that each animation frame of the stimulus must be presented for a sufficiently long time length; in other words, the frequency of the stimulus alternation must be sufficiently slow for the control. The typical stimulus onset asynchrony for a 50% level of success was about 275 ms for an average of 10 observers. On the basis of psychophysical property, we designed three experiments for investigating the neural process with a magnetoencephalography. They revealed that: (1) a peak component occurring about 300 ms after a reversal was stronger when the direction of perceived motion was switched intentionally than when it was not switched, and (2) neural components about 30–40 ms and 240–250 ms after the reversal of the stimulus animation were stronger when perception was altered intentionally than when it was switched unintentionally. The 300 ms component is consistent with a previous study about passive perceptual switching (Struber and Herrmann [ 2002]: Cogn Brain Res 14:370–382), but the intentional effect was seemed to be a different component from the well‐known P300 component. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Cognitive impairment and EEG background activity in adults with Down's syndrome: A topographic study
Authors: Velikova Svetla , Magnani Giuseppe , Arcari Claudia , Falautano Monica , Franceschi Massimo , Comi Giancarlo , Leocani Letizia 
Published: June 2010

AbstractObjective: Studies correlating electroencephalographic (EEG) data and cognitive performance in Down's syndrome (DS) showed conflicting results. The aims of this study were to investigate the sources of EEG rhythms in adults with DS at three dimensional representation of current source density (CSD) using exact/standard Low Resolution Electromagnetic Tomography (e/sLORETA), and their correlation with cognitive performance. Methods: Twenty‐five adults with DS underwent a neuropsychological battery and 5 min of resting, eye‐closed 29‐channel EEG were recorded. After e/sLORETA analysis, data were compared with those from age and gender‐matching control subjects as following: absolute and relative power in delta (1–3 Hz), theta (4–7 Hz), alpha1 (8–9 Hz), alpha2 (10–12 Hz), beta1 (13–18 Hz), beta2 (19–21 Hz), beta3 (22–30 Hz); alpha and theta bands adjusted to individual alpha peak frequency (IAF). Current source activities in DS group in regions showing significant differences compared with controls underwent correlation analysis with psychometric scores. Results: In DS, IAF was shifted to lower frequencies and correlated positively with Wechsler Adult Intelligence Scale and Mini‐Mental State examination. Compared with controls, DS showed increased CSD in: theta, alpha‐1, and beta1 classical bands and in IAF‐adjusted bands, while relative alpha2 was decreased. A negative correlation between cognitive performance and theta/alpha CSD in the right frontal lobe and right posterior cingulate cortex was found. The relative alpha2 correlated positively with cognitive tests. Conclusions: Increased CSD in DS, correlating with cognitive performance, for both slow and fast rhythms suggests involving of cortical and subcortical mechanisms. LORETA might be useful for objective measure of cognitive decline in DS. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Detection and localization of hippocampal activity using beamformers with MEG: A detailed investigation using simulations and empirical data
Authors: Quraan Maher A. , Moses Sandra N. , Hung Yuwen , Mills Travis , Taylor Margot J. 
Published: June 2010

AbstractThe ability to detect neuronal activity emanating from deep brain structures such as the hippocampus using magnetoencephalography has been debated in the literature. While a significant number of recent publications reported activations from deep brain structures, others reported their inability to detect such activity even when other detection modalities confirmed its presence. In this article, we relied on realistic simulations to show that both sides of this debate are correct and that these findings are reconcilable. We show that the ability to detect such activations in evoked responses depends on the signal strength, the amount of brain noise background, the experimental design parameters, and the methodology used to detect them. Furthermore, we show that small signal strengths require contrasts with control conditions to be detected, particularly in the presence of strong brain noise backgrounds. We focus on one localization technique, the adaptive spatial filter (beamformer), and examine its strengths and weaknesses in reconstructing hippocampal activations, in the presence of other strong brain sources such as visual activations, and compare the performance of the vector and scalar beamformers under such conditions. We show that although a weight‐normalized beamformer combined with a multisphere head model is not biased in the presence of uncorrelated random noise, it can be significantly biased in the presence of correlated brain noise. Furthermore, we show that the vector beamformer performs significantly better than the scalar under such conditions. We corroborate our findings empirically using real data and demonstrate our ability to detect and localize such sources. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Motor callosal disconnection in early relapsing‐remitting multiple sclerosis
Authors: Wahl Mathias , Hübers Annemarie , Lauterbach‐Soon Birgit , Hattingen Elke , Jung Patrick , Cohen Leonardo G. , Ziemann Ulf 
Published: June 2010

AbstractIn relapsing‐remitting multiple sclerosis (RRMS) the corpus callosum (CC) is often and early affected by macroscopic lesions when investigated by conventional MRI. We sought to determine to which extent microstructural and effective disconnection of the CC are already present in RRMS patients at the earliest stages of the disease prior to evidence of macroscopic CC lesion. We compared 16 very early RRMS patients (median expanded disability status scale (EDSS), 1.5; range, 0–2.0) to an age‐matched group of healthy controls and focused analysis to the motor CC, i.e. that part of the CC relaying interhemispheric motor information. A combined functional magnetic resonance imaging/diffusion tensor imaging fiber‐tracking procedure was applied to identify the callosal motor fibers (CMFs) connecting the hand areas of the primary motor cortices of the two hemispheres. Fractional anisotropy (FA) within the motor CC (FA‐CC) assessed the CMF microstructural integrity. Bifocal paired transcranial magnetic stimulation (TMS) tested short‐interval interhemispheric inhibition (S‐IHI), an established measure of CMF effective connectivity. FA‐CC and S‐IHI were significantly reduced in early RRMS compared to healthy controls. Furthermore, a significant linear correlation between microstructure (FA‐CC) and function (S‐IHI) in the controls was broken down in the patients. These abnormalities were obtained in the absence of macroscopic CMF lesion in conventional MRI, and whilst motor hand/arm function in the nine‐hole‐peg test and corticospinal conduction time were normal. Findings suggest that reductions in FA and S‐IHI may serve as surrogate markers of motor callosal disconnection at the earliest stages of RRMS prior to development of macroscopic lesion. Hum Brain Mapp, 2011. © 2010 Wiley‐Liss, Inc.
Co‐overexpression of p21 and Ki‐67 in head and neck squamous cell carcinoma relative to a significantly poor prognosis
Authors: Fischer Claude A. , Jung Minoa , Zlobec Inti , Green Edith , Storck Claudio , Tornillo Luigi , Lugli Alessandro , Wolfensberger Markus , Terracciano Luigi M. 
Published: June 2010

AbstractBackground.Head and neck squamous cell carcinomas (HNSCC) are treated by surgery or radiotherapy. Tumor cell death–related markers, such as p21 and Ki‐67, may predict response to therapy and improve treatment choice. We evaluated and compared the effect of their coexpression between patients treated by surgery or radiotherapy.Methods.Immunohistochemistry for p21 and Ki‐67 expression in 144 pharyngeal and laryngeal HNSCC samples was analyzed and correlated with follow‐up parameters.Results.p21 expression correlated significantly with positive cN classification (p < .001), locoregional relapse (p = .031), and poor overall survival (p = .016), and Ki‐67 positivity with poor survival only (p = .025). Coexpressing tumor phenotypes showed the worst survival (p = .009), observed primarily in patients treated by radiotherapy (p = .077).Conclusions.Coexpression of p21/Ki‐67 is a strong negative prognostic factor in HNSCC and could be of particular relevance in tumors treated by primary radiotherapy. © 2010 Wiley Periodicals, Inc. Head Neck, 2011
Lectin Complement Pathway Gene Profile of Donor and Recipient Determine the Risk of Bacterial Infections After Orthotopic Liver Transplantation†,‡
Authors: de Rooij Bert-Jan F. , van Hoek Bart , ten Hove Rogier W. , Roos Anja , Bouwman Lee H. , Schaapherder Alexander F. , Porte Robert J. , Daha Mohamed R. , van der Reijden Johan J. , Coenraad Minneke J. , Ringers Jan , Baranski Andrzej G. , Hepkema Bouke G. , Hommes Daniel W. , Verspaget Hein W. 
Published: June 2010

Abstract

Infectious complications after orthotopic liver transplantation (OLT) are a major clinical problem. The lectin pathway of complement activation is liver-derived and a crucial effector of the innate immune defense against pathogens. Polymorphisms in lectin pathway genes determine their functional activity. We assessed the relationship between these polymorphic genes and clinically significant bacterial infections, i.e., sepsis, pneumonia, and intra-abdominal infection, and mortality within the first year after OLT, in relation to major risk factors in two cohorts from different transplant centers. Single-nucleotide polymorphisms in the mannose-binding lectin gene (

MBL2

), the ficolin-2 gene (

FCN2

), and the MBL-associated serine protease gene (

MASP2

) of recipients and donors were determined. Recipients receiving a donor liver in the principal cohort with polymorphisms in all three components i.e.,

MBL2

(XA/O; O/O),

FCN2

+6359T, and

MASP2

+371A, had a cumulative risk of an infection of 75% as compared to 18% with wild-type donor livers (

P

= 0.002), an observation confirmed in the second cohort (

P

= 0.04). In addition, a genetic (mis)match between donor and recipient conferred a two-fold higher infection risk for each separate gene. Multivariate Cox analysis revealed a stepwise increase in infection risk with the lectin pathway gene profile of the donor (hazard ratio = 4.52;

P

= 8.1 × 10−6) and the donor-recipient (mis)match genotype (hazard ratio = 6.41;

P

= 1.9 × 10−7), independent from the other risk factors sex and antibiotic prophylaxis (hazard ratio > 1.7 and

P

< 0.02). Moreover, patients with a lectin pathway gene polymorphism and infection had a six-fold higher mortality (

P

= 0.9 × 10−8), of which 80% was infection-related.

Conclusion:

Donor and recipient gene polymorphisms in the lectin complement pathway are major determinants of the risk of clinically significant bacterial infection and mortality after OLT.
Serum Cholesterol and Statin Use Predict Virological Response to Peginterferon and Ribavirin Therapy†,‡
Authors: Harrison Stephen A. , Rossaro Lorenzo , Hu Ke-Qin , Patel Keyur , Tillmann Hans , Dhaliwal Sandeep , Torres Dawn M. , Koury Kenneth , Goteti Venkata S. , Noviello Stephanie , Brass Clifford A. , Albrecht Janice K. , McHutchison John G. , Sulkowski Mark S. 
Published: June 2010

Abstract

Elevated low-density lipoprotein (LDL) levels and statin use have been associated with higher sustained virological response (SVR) rates in patients receiving chronic hepatitis C therapy. However, these relationships have not been well characterized in randomized controlled trials. Furthermore, little is known about the relationship between high-density lipoprotein (HDL) and virological response. To determine whether baseline LDL or HDL levels and statin use affect SVR rates, we retrospectively evaluated the IDEAL (Individualized Dosing Efficacy Versus Flat Dosing to Assess Optimal Pegylated Interferon Therapy) trial, in which 3070 treatment-naive, hepatitis C virus (HCV) genotype 1–infected patients were treated for up to 48 weeks in one of the following arms: (1) peginterferon (PEG-IFN) alfa-2b at 1.5 μg/kg/week with ribavirin (RBV) at 800 to 1400 mg/day, (2) PEG-IFN alfa-2b at 1.0 μg/kg/week with RBV at 800 to 1400 mg/day, or (3) PEG-IFN alfa-2a at 180 μg/week with RBV at 1000 to 1200 mg/day. Virological responses were assessed by pretreatment statin use and baseline elevated LDL levels (≥130 mg/dL) or low HDL levels (<40 mg/dL for men and <50 mg/dL for women). In 1464 patients with baseline elevated LDL levels or low HDL levels, the SVR rate was significantly higher than that in patients with normal levels (44.9% versus 34.0%,

P

< 0.001). In 66 patients receiving a statin pretreatment, the SVR rate was higher than the rate of those not receiving it (53.0% versus 39.3%,

P

= 0.02). In a multivariate logistic regression analysis using the stepwise selection method with baseline characteristics, a high LDL level [odds ratio (OR) = 1.6, 95% confidence interval (CI) = 1.4-1.8,

P

< 0.001], a low HDL level (OR = 0.5, 95% CI = 0.3-0.8,

P

= 0.004), and statin use (OR = 2.0, 95% CI = 1.1-3.7,

P

= 0.02) were independently associated with SVR. Conclusion: Baseline elevated LDL levels or low HDL levels and preemptive statin usage were associated with higher SVR rates. Prospective studies may be considered to explore the biological impact of these factors on HCV RNA replication and treatment response.
Liver Enzymes, Nonalcoholic Fatty Liver Disease, and Incident Cardiovascular Disease: A Narrative Review and Clinical Perspective of Prospective Data†
Authors: Ghouri Nazim , Preiss David , Sattar Naveed 
Published: June 2010

Abstract

In recent years, a strong link has been established between nonalcoholic fatty liver disease (NAFLD) and the pathogenesis of type 2 diabetes mellitus. The potential role of NAFLD in cardiovascular disease (CVD) has also attracted interest. Published studies have tended to use biochemical and imaging surrogate markers of NAFLD, such as elevated gamma glutamyl transpeptidase (GGT) and alanine aminotransferase (ALT) and fatty liver on ultrasound, when investigating associations with incident CVD events. Positive associations between both baseline GGT and temporal change in GGT, as well as cardiovascular events and cardiovascular mortality independent of alcohol intake, have been reported in several prospective studies. However, adjustment for confounders is often incomplete, and there is scant evidence of improvement in cardiovascular risk prediction beyond established risk scores when incorporating such data. There also appears to be a strong and underrecognized age interaction, with associations between GGT and incident coronary heart disease (CHD) being strong in young individuals but relatively weak in the elderly. By contrast, ALT appears to be only weakly associated with incident CHD and may exhibit a U-shaped association with total mortality. Finally, although some studies have linked imaging-defined and biopsy-confirmed NAFLD with CVD risk, the evidence is inconsistent, with few incident events and/or insufficient potential confounders.

Conclusion:

A diagnosis of NAFLD is insufficient to consider patients as being at high risk for CVD. The presence of NAFLD should be a clear indication for diabetes screening, but cardiovascular risk screening should be performed with the use of existing risk calculators and should be guided by established cardiovascular risk factors.
Dentate gyrus and hilus transection blocks seizure propagation and granule cell dispersion in a mouse model for mesial temporal lobe epilepsy
Authors: Pallud Johan , Häussler Ute , Langlois Mélanie , Hamelin Sophie , Devaux Bertrand , Deransart Colin , Depaulis Antoine 
Published: June 2010

AbstractEpilepsy‐associated changes of the anatomical organization of the dentate gyrus and hilus may play a critical role in the initiation and propagation of seizures in mesial temporal lobe epilepsy (MTLE). This study evaluated the role of longitudinal projections in the propagation of hippocampal paroxysmal discharges (HPD) in dorsal hippocampus by performing a selective transection in a mouse model for MTLE obtained by a single unilateral intrahippocampal injection of kainic acid (KA). Full transections of the dentate gyrus and hilus were performed in the transverse axis at 22 days after KA injection when spontaneous HPD were fully developed. They: (i) significantly reduced the occurrence of HPD; (ii) increased their duration at the KA injection site; (iii) abolished their spread along the longitudinal axis of the hippocampal formation and; (iv) limited granule cell dispersion (GCD) of the dentate gyrus posterior to the transection. These data suggest that: (i) longitudinal projections through the dentate gyrus and hilus are involved in HPD spread; (ii) distant hippocampal circuits participate in the generation and cessation of HPD and; (iii) GCD requires continuous HPD to develop, even when seizures are established. Our data reveal a critical role for longitudinal projections in the generation and spread of hippocampal seizures. © 2010 Wiley‐Liss, Inc.
Acute nicotine treatment prevents rem sleep deprivation‐induced learning and memory impairment in rat
Authors: Aleisa A.M. , Helal G. , Alhaider I.A. , Alzoubi K.H. , Srivareerat M. , Tran T.T. , Al‐Rejaie S.S. , Alkadhi K.A. 
Published: June 2010

AbstractRapid eye movement (REM) sleep deprivation (SD) is implicated in impairment of spatial learning and memory and hippocampal long‐term potentiation (LTP). An increase in nicotine consumption among habitual smokers and initiation of tobacco use by nonsmokers was observed during SD. Although nicotine treatment was reported to attenuate the impairment of learning and memory and LTP associated with several mental disorders, the effect of nicotine on SD‐induced learning and memory impairment has not been studied. Modified multiple platform paradigm was used to induce SD for 24 or 48 h during which rats were injected with saline or nicotine (1 mg kg−1 s.c.) twice a day. In the radial arm water maze (RAWM) task, 24‐ or 48‐h SD significantly impaired learning and short‐term memory. In addition, extracellular recordings from CA1 and dentate gyrus (DG) regions of the hippocampus in urethane anesthetized rats showed a significant impairment of LTP after 24‐ and 48‐h SD. Treatment of normal rats with nicotine for 24 or 48 h did not enhance spatial learning and memory or affect magnitude of LTP in the CA1 and DG regions. However, concurrent, acute treatment of rats with nicotine significantly attenuated SD‐induced impairment of learning and STM and prevented SD‐induced impairment of LTP in the CA1 and DG regions. These results show that acute nicotine treatment prevented the deleterious effect of sleep loss on cognitive abilities and synaptic plasticity. © 2010 Wiley‐Liss, Inc.
Hippocampal granule cells opt for early retirement
Authors: Alme C.B. , Buzzetti R.A. , Marrone D.F. , Leutgeb J.K. , Chawla M.K. , Schaner M.J. , Bohanick J.D. , Khoboko T. , Leutgeb S. , Moser E.I. , Moser M.‐B. , McNaughton B.L. , Barnes C.A. 
Published: June 2010

AbstractIncreased excitability and plasticity of adult‐generated hippocampal granule cells during a critical period suggests that they may “orthogonalize” memories according to time. One version of this “temporal tag” hypothesis suggests that young granule cells are particularly responsive during a specific time period after their genesis, allowing them to play a significant role in sculpting CA3 representations, after which they become much less responsive to any input. An alternative possibility is that the granule cells active during their window of increased plasticity, and excitability become selectively tuned to events that occurred during that time and participate in later reinstatement of those experiences, to the exclusion of other cells. To discriminate between these possibilities, rats were exposed to different environments at different times over many weeks, and cell activation was subsequently assessed during a single session in which all environments were revisited. Dispersing the initial experiences in time did not lead to the increase in total recruitment at reinstatement time predicted by the selective tuning hypothesis. The data indicate that, during a given time frame, only a very small number of granule cells participate in many experiences, with most not participating significantly in any. Based on these and previous data, the small excitable population of granule cells probably correspond to the most recently generated cells. It appears that, rather than contributing to the recollection of long past events, most granule cells, possibly 90–95%, are effectively “retired.” If granule cells indeed sculpt CA3 representations (which remains to be shown), then a possible consequence of having a new set of granule cells participate when old memories are reinstated is that new representations of these experiences might be generated in CA3. Whatever the case, the present data may be interpreted to undermine the standard “orthogonalizer” theory of the role of the dentate gyrus in memory. © 2010 Wiley‐Liss, Inc.