bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasma membrane sphingomyelin hydrolysis increases hippocampal neuron excitability by sphingosine‐1‐phosphate mediated mechanisms
Authors: Norman Eric , Cutler Roy G. , Flannery Richard , Wang Yue , Mattson Mark P. 
Published: April 2010

J. Neurochem. (2010) 114, 430–439.AbstractProteins that control the excitability of neurons, including voltage‐dependent ion channels and neurotransmitter receptors, reside in a membrane lipid environment that includes sphingomyelin, but the influence of the metabolism of this lipid on excitability is unknown. Sphingomyelin in the plasma membrane can be cleaved by neutral sphingomyelinases (nSMase) to generate ceramides and sphingosine‐1‐phosphate (S1P) which have been shown to play a variety of roles in cellular signaling processes. We found that application of nSMase to hippocampal slices results in a selective enhancement in the population spike amplitude, resulting in fEPSP‐PS potentiation of the CA3‐CA1 schaeffer collateral synapse. Single cell recordings showed that nSMase activity increases action potential frequency in CA1 neurons in a reversible manner. Additional current clamp recordings showed that nSMase reduces the slow after‐hyperpolarization after a burst of action potentials. Mass spectrometry‐based measurements demonstrated that nSMase activity induces a rapid increase in the levels of ceramides and S1P in cells in hippocampal slices. The ability of nSMase to increase CA1 neuron excitability was blocked by an inhibitor of sphingosine kinase, the enzyme that converts ceramide to S1P. Moreover, direct intracellular application of S1P to CA1 neurons increased action potential firing. Our findings suggest roles for sphingomyelin metabolism and S1P in the positive regulation of the excitability of hippocampal neurons.
Plumbagin promotes the generation of astrocytes from rat spinal cord neural progenitors via activation of the transcription factor Stat3
Authors: Luo Yongquan , Mughal Mohamed R. , Ouyang Tae‐Gen Son Xin , Jiang Haiyang , Luo Weiming , Yu Qian‐Sheng , Greig Nigel H. , Mattson Mark P. 
Published: April 2010

J. Neurochem. (2010) 115, 1337–1349.AbstractPlumbagin (5‐hydroxy‐2‐methyl‐1,4 naphthoquinone) is a naturally occurring low molecular weight lipophilic phytochemical derived from roots of plants of the Plumbago genus. Plumbagin has been reported to have several clinically relevant biological activities in non‐neural cells, including anti‐atherosclerotic, anticoagulant, anticarcinogenic, antitumor, and bactericidal effects. In a recent screen of a panel of botanical pesticides, we identified plumbagin as having neuroprotective activity. In this study, we determined if plumbagin could modify the developmental fate of rat E14.5 embryonic neural progenitor cells (NPC). Plumbagin exhibited no cytotoxicity when applied to cultured NPC at concentrations below 1 μM. At a concentration of 0.1 μM, plumbagin significantly enhanced the proliferation of NPC as indicated by a 17% increase in the percentage of cells incorporating bromo‐deoxyuridine. Plumbagin at a concentration of 0.1 pM (but not 0.1 μM), stimulated the production of astrocytes as indicated by increased GFAP expression. Plumbagin selectively induced the proliferation and differentiation of glial progenitor cells without affecting the proliferation or differentiation of neuron‐restricted progenitors. Plumbagin (0.1 pM) rapidly activated the transcription factor signal transducer and activator of transcription 3 (Stat3) in NPC, and a Stat3 inhibitor peptide prevented both plumbagin‐induced astrocyte formation and proliferation. These findings demonstrate the ability of a low molecular weight naturally occurring phytochemical to control the fate of glial progenitor cells by a mechanism involving the Stat3 signaling pathway.
Dietary restriction mitigates cocaine‐induced alterations of olfactory bulb cellular plasticity and gene expression, and behavior
Authors: Xu Xiangru , Mughal Mohamed R. , Scott Hall F. , Perona Maria T. G. , Pistell Paul J. , Lathia Justin D. , Chigurupati Srinivasulu , Becker Kevin G. , Ladenheim Bruce , Niklason Laura E. , Uhl George R. , Cadet Jean Lud , Mattson Mark P. 
Published: April 2010

J. Neurochem.(2010)114, 323–334.AbstractBecause the olfactory system plays a major role in food consumption, and because ‘food addiction’ and associated morbidities have reached epidemic proportions, we tested the hypothesis that dietary energy restriction can modify adverse effects of cocaine on behavior and olfactory cellular and molecular plasticity. Mice maintained on an alternate day fasting (ADF) diet exhibited increased baseline locomotion and increased cocaine‐sensitized locomotion during cocaine conditioning, despite no change in cocaine conditioned place preference, compared with mice fedad libitum. Levels of dopamine and its metabolites in the olfactory bulb (OB) were suppressed in mice on the ADF diet compared with mice on the control diet, independent of acute or chronic cocaine treatment. The expression of several enzymes involved in dopamine metabolism including tyrosine hydroxylase, monoamine oxidases A and B, and catechol‐O‐methyltransferase were significantly reduced in OBs of mice on the ADF diet. Both acute and chronic administration of cocaine suppressed the production of new OB cells, and this effect of cocaine was attenuated in mice on the ADF diet. Cocaine administration to mice on the control diet resulted in up‐regulation of OB genes involved in mitochondrial energy metabolism, synaptic plasticity, cellular stress responses, and calcium‐ and cAMP‐mediated signaling, whereas multiple olfactory receptor genes were down‐regulated by cocaine treatment. ADF abolished many of the effects of cocaine on OB gene expression. Our findings reveal that dietary energy intake modifies the neural substrates underlying some of the behavioral and physiological responses to repeated cocaine treatment, and also suggest novel roles for the olfactory system in addiction. The data further suggest that modification of dietary energy intake could provide a novel potential approach to addiction treatments.
Microglial activation depends on beta‐amyloid conformation: role of the formylpeptide receptor 2
Authors: Heurtaux Tony , Michelucci Alessandro , Losciuto Sophie , Gallotti Christian , Felten Paul , Dorban Gauthier , Grandbarbe Luc , Morga Eleonora , Heuschling Paul 
Published: April 2010

J. Neurochem. (2010) 114, 576–586.AbstractAlzheimer’s disease (AD) is characterized by the presence of extracellular deposits referred to beta‐amyloid (Aβ) complexes or senile plaques. Aβ peptide is firstly produced as monomers, readily aggregating to form multimeric complexes, of which the smallest aggregates are known to be the most neurotoxic. In AD patients, abundant reactive microglia migrate to and surround the Aβ plaques. Though it is well known that microglia are activated by Aβ, little is known about the peptide conformation and the signaling cascades responsible for this activation. In this study, we have stimulated murine microglia with different Aβ(1‐42) forms, inducing an inflammatory state, which was peptide conformation‐dependent. The lightest oligomeric forms induced a more violent inflammatory response, whereas the heaviest oligomers and the fibrillar conformation were less potent inducers. BocMLF, a formylpeptide chemotactic receptor 2 antagonist, decreased the oligomeric Aβ‐induced inflammatory response. The Aβ‐induced signal transduction was found to depend on phosphorylation mechanisms mediated by MAPKs and on activator protein 1/nuclear factor kappa‐light‐chain‐enhancer of activated B cells pathways activation. These results suggest that the reactive microgliosis intensity during AD might depend on the disease progression and consequently on the Aβ conformation production. The recognition of Aβ by the formylpeptide chemotactic receptor 2 seems to be a starting point of the signaling cascade inducing an inflammatory state.
Aromaticl‐amino acid decarboxylase phosphorylation and activation by PKGIαin vitro
Authors: Duchemin Anne‐Marie , Neff Norton H. , Hadjiconstantinou Maria 
Published: April 2010

J. Neurochem.(2010)114, 542–552.AbstractBrain aromaticl‐amino acid decarboxylase (AAAD) is subject to regulation, and phosphorylation might be involved in the short‐term activation of the enzyme. Sites for serine/threonine phosphorylation are present in the deduced amino acid sequence of AAAD, and cAMP‐dependent protein kinase phosphorylates and activates neuronal AAADin vitro.We now report that cGMP‐dependent protein kinase (PKG) is able to phosphorylate and activate neuronal AAAD. In anin vitrokinase assay, immunoprecipitated native and recombinant mouse brain AAAD was rapidly phosphorylated by exogenous PKGIα. When added to striatal homogenates, PKGIα increased AAAD activity in a temporal fashion similar to phosphorylation. Recombinant AAAD was also activated by the kinase demonstrating a direct effect. Native enzyme activation was moderate and characterized by increasedVmaxandKmforl‐DOPA. A PKG peptide inhibitor prevented AAAD phosphorylation and activation providing specificity, and causally linking the two events. Together, the findings provide evidence for PKGIα‐dependent phosphorylation and activation of neuronal AAADin vitro, and introduce AAAD as a putative PKGIα substrate. Neuronal AAAD is best known for its role in the biosynthesis of catecholamines, indoleamines and trace amines in the nervous system, and the biological importance of PKGIα phosphorylation in these processes remains to be determined.
Chromogranins as regulators of exocytosis
Authors: Borges Ricardo , Díaz‐Vera Jésica , Domínguez Natalia , Arnau María Rosa , Machado José D. 
Published: April 2010

J. Neurochem.(2010)114, 335–343.AbstractChromogranins (Cgs) constitute the main protein component in the vesicular matrix of large dense core vesicles (LDCV). These acidic proteins have been implicated in several physiological processes such as vesicle sorting, the generation of bioactive peptides and the accumulation of soluble species inside LDCV. This latter feature of Cgs accounts for the ability of vesicles to concentrate catecholamines and Ca2+. Indeed, the low affinity and high capacity of Cgs to bind solutes at the low pH of the LDCV lumen seems to be behind the delay in the neurotransmitter exit towards the extracellular milieu after vesicle fusion. The availability of new mouse strains lacking Cgs in combination with the arrival of several techniques for the direct monitoring of exocytosis (like amperometry, patch‐amperometry and intracellular electrochemistry), have helped advance our understanding of how these granins concentrate catecholamines and Ca2+in LDCV, and how they influence the kinetics of exocytosis. In this review, we will discuss the roles of Cgs A and B in maintaining the intravesicular environment of secretory vesicles and in exocytosis, bringing together the most recent findings from adrenal chromaffin cells.
The Effect of the WIC Program on the Health of Newborns
Authors: Foster E. Michael , Jiang Miao , Gibson‐Davis Christina M. 
Published: April 2010

Objective.To determine the effect of the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) on birth outcomes.Data Source.The Child Development Supplement (CDS) of the Panel Study of Income Dynamics (PSID). The PSID provides extensive data on the income and well‐being of a representative sample of U.S. families from 1968 to present. The CDS collects information on the children in PSID families ranging from cognitive, behavioral, and health status to their family and neighborhood environment. The first two waves of the CDS were conducted in 1997 and 2002, respectively. We use information on 3,181 children and their mothers.Study Design.We use propensity score matching with multiple imputations to examine whether WIC program influences birth outcomes: birth weight, prematurity, maternal report of the infant's health, small for gestational age, and placement in the neonatal intensive care unit. Furthermore, we use a fixed‐effects model to examine the above outcomes controlling for mother‐specific unobservables.Principal Findings.After using propensity scores to adjust for confounding factors, WIC shows no statistically significant effects for any of six outcomes. Fixed‐effects models, however, reveal some effects that are statistically significant and fairly substantial in size. These involve preterm birth and birth weight.Conclusions.Overall, the WIC program had moderate effects, but findings were sensitive to the estimation method used.
Outcome from status epilepticus after portosystemic shunt attenuation in 3 dogs treated with propofol and phenobarbital
Authors: Gommeren Kris , Claeys Stéphanie , De Rooster Hilde , Hamaide Annick , Daminet Sylvie 
Published: April 2010

AbstractObjective
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To describe outcome of treatment with propofol and phenobarbital for status epilepticus (SE) after portosystemic shunt (PSS) attenuation.Case or Series Summary
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Three dogs without preceding seizure activity, were diagnosed with a single extrahepatic PSS. Following standard preoperative medical therapy, an ameroid constrictor was placed surgically. Recovery was uneventful until spontaneous SE developed 46–96 hours after surgery. After unsuccessful seizure control with benzodiazepines, dogs were treated with a bolus of propofol followed by a propofol constant rate infusion. Phenobarbital was concurrently administered and supportive care was optimized. All dogs recovered uneventfully over the next 7–9 days. Over the following months phenobarbital was slowly tapered. All dogs have been free from antiepileptic drugs for several months, without recurrence of neurologic signs.New or Unique Information Provided
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In this case series, we describe the treatment of 3 dogs with propofol and phenobarbital for refractory SE following attenuation of a single congenital PSS. After weaning of the propofol constant rate infusion, and tapering and discontinuation of phenobarbital over the following months, all dogs experienced a complete recovery. This study provides evidence that use of propofol in combination with phenobarbital may be efficacious for management of SE in dogs after PSS surgery.
A Quick Esthetic Remount Cast for All‐Ceramic Restorations
Authors: Hansen Paul A. , Gist Julie 
Published: April 2010

AbstractA technique is presented for the expedited fabrication of a remount cast for the alteration of all‐ceramic crowns and fixed partial dentures. The remount cast allows the laboratory technician to know the precise location of the gingival tissues and allows modification of all‐ceramic restorations.
Gender Differences in the Clinical Characteristics and Atrioventricular Nodal Conduction Properties in Patients With Atrioventricular Nodal Reentrant Tachycardia
Authors: SUENARI KAZUYOSHI , HU YU‐FENG , TSAO HSUAN‐MING , TAI CHING‐TAI , CHIANG CHERN‐EN , LIN YENN‐JIANG , CHANG SHIH‐LIN , LO LI‐WEI , TA‐CHUAN TUAN , LEE PI‐CHANG , TUNG NGUYEN HUU , HUANG SHIH‐YU , WU TSU‐JUEY , CHEN SHIH‐ANN 
Published: April 2010

Gender Differences in Patients With AVNRT. Introduction: The detailed electrophysiological characteristics of the gender differences associated with atrioventricular nodal reentrant tachycardia (AVNRT) have not been clarified. This study investigated the gender‐related electrophysiological differences in a large series of patients undergoing radiofrequency catheter ablation. Methods and Results: A total of 2,088 consecutive AVNRT patients (men/women 869/1,219) who underwent catheter ablation were enrolled in this study. We evaluated the gender differences in their electrophysiological characteristics. Women had a significantly younger age of onset, higher incidence of multiple jumps, shorter AH interval, atrial effective refractory period (ERP), anterograde fast pathway ERP, anterograde slow pathway ERP, and retrograde slow pathway ERP, and longer ventricular ERP than men. The incidence of baseline ventriculoatrial dissociation was lower in women than in men. Women needed less isoproterenol/atropine to induce AVNRT. No gender differences in the radiation exposure time, procedure time, complication rate, acute success rate, or second procedure rate were noted. Both typical and atypical AVNRT were more predominant in women. In the patients with atypical AVNRT, there was no significant gender difference in incidence of baseline ventriculoatrial dissociation; however, the retrograde slow pathway ERP was significantly shorter in women than in men. Women of premenopausal age (≤50 years old) had a significantly higher incidence of anterograde multiple jumps and a retrograde jump phenomenon, and a shorter anterograde slow pathway ERP and retrograde slow pathway ERP than those of women over 50 years old. Conclusion: Gender differences in the anterograde and retrograde AV nodal electrophysiology were noted in the patients with AVNRT. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1114‐1119)
Functional Properties of the Superior Vena Cava (SVC)‐Aorta Ganglionated Plexus: Evidence Suggesting an Autonomic Basis for Rapid SVC Firing
Authors: LU ZHIBING , SCHERLAG BENJAMIN J. , NIU GUODONG , LIN JIAXIONG , FUNG KAR‐MING , ZHAO LICHAO , YU LILEI , JACKMAN WARREN M. , LAZZARA RALPH , JIANG HONG , PO SUNNY S. 
Published: April 2010

Superior Vena Cava‐Aorta Ganglionated Plexus. Introduction: The mechanism underlying spontaneous rapid superior vena cava (SVC) firing that initiates atrial fibrillation (AF) remains poorly understood. We investigated the role of the SVC‐aorta‐ganglionated plexus (SVC‐Ao‐GP) in AF initiated by rapid firing from the SVC.
Methods and Results:
In 42 dogs, a circular catheter was positioned above the SVC‐atrial junction. Multielectrode catheters were sutured on atria, atrial appendages and pulmonary veins. The effective refractory period (ERP) and window of vulnerability (WOV) for AF were measured at all sites in the baseline state, during cervical vagosympathetic trunk stimulation and during SVC‐Ao‐GP stimulation, before and after SVC‐Ao‐GP ablation. AF inducibility was also assessed by delivering high‐frequency stimulation (HFS) within myocardial refractory period to the SVC before and after SVC‐Ao‐GP ablation. HFS applied to the SVC‐Ao‐GP slowed the sinus rate and/or atrioventricular conduction. HFS of the SVC‐Ao‐GP induced more significant shortening of ERP and a greater increase in WOV at the SVC than other sites. Ablation of the SVC‐Ao‐GP significantly increased the baseline ERP and decreased the baseline WOV only at the SVC. AF induced at the SVC by HFS during refractoriness was eliminated by ablation of the SVC‐Ao‐GP but was not altered by ablation of the 4 major atrial GP. Direct injection of acetylcholine into the SVC‐Ao‐GP initiated rapid firing from the SVC in every case.
Conclusions:
The SVC‐Ao‐GP preferentially modulates the electrophysiological function of the SVC sleeves and may contribute to rapid firing from the SVC. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1392‐1399, December 2010)
Repolarization Dynamics During Exercise Discriminate Between LQT1 and LQT2 Genotypes
Authors: SY RAYMOND W. , CHATTHA ISHVINDER S. , KLEIN GEORGE J. , GULA LORNE J. , SKANES ALLAN C. , YEE RAYMOND , BENNETT MATTHEW T. , KRAHN ANDREW D. 
Published: April 2010

Genotype and Exercise in LQTS. Background: Repolarization dynamics during exercise in patients with long‐QT Syndrome (LQTS) may be influenced by various factors such as a patient's genotype. We sought to systematically characterize the repolarization dynamics during exercise in patients with LQTS with a particular focus on the influence of genotype.
Methods:
Three groups of patients were studied on the basis of clinical status and genotype: LQT1, LQT2, and normal controls. Twenty‐five age‐ and gender‐matched patients were selected for each group. The QTc was measured during bicycle exercise testing and its dynamics were compared between the 3 groups.
Results:
The degree of QTc prolongation during exercise was greater in LQTS patients (LQT1 80 ± 47 ms, LQT2 64 ± 41 ms, Control 46 ± 20 ms, P = 0.02), with significant differences between LQT1 and LQT2 patients observed at heart rates ≥60% of the predicted maximum (P < 0.05). LQT1 patients demonstrated progressive or persistent QTc prolongation at higher heart rates, whereas LQT2 patients demonstrated maximum QTc prolongation at submaximal heart rates (∼50% of the predicted maximum) with subsequent QTc correction toward baseline values at higher heart rates. Importantly, these observations were consistent regardless of age, gender, or exercise type in subgroup analyses.
Conclusions:
Reduced repolarization reserve in LQTS is genotype and heart rate specific. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1242‐1246, November 2010)
Risk Factors for Recurrent Heart Failure Events in the Multicenter Automatic Defibrillator Implantation Trial II (MADIT‐II)
Authors: SZE EDWARD , MOSS ARTHUR J. , MCNITT SCOTT , BARSHESHET ALON , ANDREWS MARK L. , ZAREBA WOJCIECH , GOLDENBERG ILAN ,   for the Multicenter Automatic Defibrillator Implantation Trial‐II Investigators
Published: April 2010

Risk Factors for Recurrent Heart Failure. Background: This study was designed to identify risk factors for recurrent heart failure (HF) events in patients with ischemic left ventricular dysfunction enrolled in the Multicenter Automatic Defibrillator Implantation Trial II (MADIT‐II).
Methods and Results:
The Prentice, Williams, and Peterson (PWP) statistical model was utilized to identify and compare risk factors for 1 or ≥2 HF hospitalizations among 1,218 patients with ischemic left ventricular dysfunction enrolled in the MADIT‐II trial.Risk factors for a first HF hospitalization included treatment with an ICD (HR = 1.31; P = 0.05), New York Heart Association class >II (HR = 1.95; P < 0.001), female gender (HR = 1.38; P = 0.05), atrial fibrillation (HR = 1.90; P = 0.001), QRS >120 ms (HR = 1.41; P = 0.01), diabetes mellitus (HR = 1.51; P = 0.003), heart rate ≥80 (HR = 1.35; P = 0.04), diuretic therapy (HR = 1.82; P < 0.001), and the presence of prerenal azotemia (defined as blood urea nitrogen:creatinine >20; HR = 1.45; P = 0.01). In contrast, prerenal azotemia was the only risk factor that was independently associated with a significant increase in the risk of ≥2 HF hospitalizations (HR = 1.52; P = 0.027). The occurrence of 1 HF event after enrolment was associated with a 2.8‐fold (P < 0.001) increase in the risk of death, whereas after the occurrence of a second event there was a 6.7‐fold (P < 0.001) increase in the risk of subsequent mortality.
Conclusions:
In MADIT‐II, prerenal azotemia was the only significant and independent risk factor for HF progression after a first event, and recurrent HF was the most powerful predictor of mortality. These findings stress the importance of identifying risk factors for HF progression among patients who receive an ICD for primary prevention. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1217‐1223, November 2010)