bluuebunny/crossref_metadata_2025_split huggingface dataset:
Curcumin attenuates cerebral edema following traumatic brain injury in mice: a possible role for aquaporin‐4?
Authors: Laird Melissa D. , Sukumari‐Ramesh Sangeetha , Swift Andrew E. B. , Meiler Steffen E. , Vender John R. , Dhandapani Krishnan M. 
Published: February 2010

J. Neurochem.(2010)113, 637–648.AbstractTraumatic brain injury is a devastating neurological injury associated with significant morbidity and mortality. Medical therapies to limit cerebral edema, a cause of increased intracranial hypertension and poor clinical outcome, are largely ineffective, emphasizing the need for novel therapeutic approaches. In the present study, pre‐treatment with curcumin (75, 150 mg/kg) or 30 min post‐treatment with 300 mg/kg significantly reduced brain water content and improved neurological outcome following a moderate controlled cortical impact in mice. The protective effect of curcumin was associated with a significant attenuation in the acute pericontusional expression of interleukin‐1β, a pro‐inflammatory cytokine, after injury. Curcumin also reversed the induction of aquaporin‐4, an astrocytic water channel implicated in the development of cellular edema following head trauma. Notably, curcumin blocked IL‐1β‐induced aquaporin‐4 expression in cultured astrocytes, an effect mediated, at least in part, by reduced activation of the p50 and p65 subunits of nuclear factor κB. Consistent with this notion, curcumin preferentially attenuated phosphorylated p65 immunoreactivity in pericontusional astrocytes and decreased the expression of glial fibrillary acidic protein, a reactive astrocyte marker. As a whole, these data suggest clinically achievable concentrations of curcumin reduce glial activation and cerebral edema following neurotrauma, a finding which warrants further investigation.
Mitochondrial respiration and respiration‐associated proteins in cell lines created through Parkinson’s subject mitochondrial transfer
Authors: Esteves A. Raquel , Lu Jane , Rodova Mariana , Onyango Isaac , Lezi E , Dubinsky Richard , Lyons Kelly E. , Pahwa Rajesh , Burns Jeffrey M. , Cardoso Sandra M. , Swerdlow Russell H. 
Published: February 2010

J. Neurochem. (2010) 113, 674–682.AbstractParkinson’s disease (PD) is associated with perturbed mitochondrial function. Studies of cytoplasmic hybrid (cybrid) cell lines containing mitochondria from PD subjects suggest complex I dysfunction in particular is a relatively upstream biochemical defect. To evaluate potential downstream consequences of PD mitochondrial dysfunction, we used a cybrid approach to model PD mitochondrial dysfunction; our cybrid cell lines were generated via transfer of PD or control subject platelet mitochondria to mtDNA‐depleted NT2 cells. To confirm our PD cybrid mitochondria did indeed differ from control cybrid mitochondria we measured complex I Vmax activities. Consistent with other PD cybrid reports, relative to control cybrid cell lines the PD cybrid cell line mean complex I Vmax activity was reduced. In this validated model, we used an oxygen electrode to characterize PD cybrid mitochondrial respiration. Although whole cell basal oxygen consumption was comparable between the PD and control cybrid groups, the proton leak was increased and maximum respiratory capacity was decreased in the PD cybrids. PD cybrids also had reduced SIRT1 phosphorylation, reduced peroxisome proliferator‐activated receptor‐γ coactivator‐1α levels, and increased NF‐kB activation. We conclude mitochondrial respiration and pathways influenced by aerobic metabolism are altered in NT2 cybrid cell lines generated through transfer of PD subject platelet mitochondria.
The WldS mutation delays anterograde, but not retrograde, axonal degeneration of the dopaminergic nigro‐striatal pathway in vivo
Authors: Cheng Hsiao‐Chun , Burke Robert E. 
Published: February 2010

J. Neurochem. (2010) 113, 683–691.AbstractFor many neurodegenerative disorders, such as Parkinson’s disease, there is evidence that the disease first affects axons and terminals of neurons that are selectively vulnerable. This would suggest that it may be possible to forestall progression by targeting the cellular mechanisms of axon degeneration. While it is now clear that these mechanisms are distinct from the pathways of programmed cell death, they are less well known. Compelling evidence of the distinctiveness of these mechanisms has derived from studies of the WldS mutation, which confers resistance to axon degeneration. Little is known about how this mutation affects degeneration in dopaminergic axons, those that are affected in Parkinson’s disease. We have characterized the WldS phenotype in these axons in four models of injury: two that utilize the neurotoxin 6‐hydroxydopamine or axotomy to induce anterograde degeneration, and two that use these methods to induce retrograde degeneration. For both 6‐hydroxydopamine and axotomy, WldS provides protection from anterograde, but not retrograde degeneration. This protection is observed as preserved immunostaining for tyrosine hydroxylase in axons and striatum, and by structural integrity visualized by GFP in tyrosine hydroxylase‐GFP mice. Therefore, WldS offers axon protection, but it reveals fundamentally different processes underlying antero‐ and retrograde degeneration in this system.
NPY augments the proliferative effect of FGF2 and increases the expression of FGFR1 on nestin positive postnatal hippocampal precursor cells, via the Y1 receptor
Authors: Rodrigo Chamira , Zaben Malik , Lawrence Timothy , Laskowski Alexandra , Howell Owain W. , Gray William P. 
Published: February 2010

J. Neurochem. (2010) 113, 615–627.AbstractWe have shown that neuropeptide Y (NPY), a peptide neurotransmitter released by hippocampal interneurons, is proliferative for hippocampal neural stem progenitor cells (NSPCs) via the Y1 receptor. Fibroblast growth factor (FGF) 2, released predominantly by astrocytes, is also a powerful mitogen for postnatal and adult NSPCs, via the FGFR1 receptor. Knockout studies show that NPY and FGF2 are individually necessary, but not sufficient, for seizure‐induced neurogenesis, suggesting a possible interaction. Here, we examined for interactions between NPY and FGF2 on NSPCs from the postnatal hippocampus and report that the combination of NPY and FGF2 significantly shortens the cell cycle time of nestin positive NSPCs, more than either factor alone. This augmentation of proliferation rate is NPY Y1 receptor mediated, and Y1 receptor activation increases both FGFR1 mRNA and protein in NSPC cultures. NSPCs immunostain for both Y1 and FGFR1 receptors and the interaction is specific for dentate NSPCs. This is the first report of a proliferative factor that augments the proliferative effect of FGF2 and is the first evidence of a positive proliferative interaction between a glial growth factor and a neuronal transmitter, identifying a novel neural activity driven mechanism for modulating the proliferation of hippocampal NSPCs.
Tumour necrosis factor alpha induces rapid reduction in AMPA receptor‐mediated calcium entry in motor neurones by increasing cell surface expression of the GluR2 subunit: relevance to neurodegeneration
Authors: Rainey‐Smith Stephanie R , Andersson David A , Williams Robert J , Rattray Marcus 
Published: February 2010

J. Neurochem.(2010)113, 692–703.AbstractThe α‐amino‐3‐hydroxyl‐5‐methyl‐4‐isoxazole‐propionate receptor (AMPAR) subunit GluR2, which regulates excitotoxicity and the inflammatory cytokine tumour necrosis factor alpha (TNFα) have both been implicated in motor neurone vulnerability in amyotrophic lateral sclerosis/motor neurone disease. TNFα has been reported to increase cell surface expression of AMPAR subunits to increase synaptic strength and enhance excitotoxicity, but whether this mechanism occurs in motor neurones is unknown. We used primary cultures of mouse motor neurones and cortical neurones to examine the interaction between TNFα receptor activation, GluR2 availability, AMPAR‐mediated calcium entry and susceptibility to excitotoxicity. Short exposure to a physiologically relevant concentration of TNFα (10 ng/mL, 15 min) caused a marked redistribution of both GluR1 and GluR2 to the cell surface as determined by cell surface biotinylation and immunofluorescence. Using fura‐2‐acetoxymethyl ester microfluorimetry, we showed that exposure to TNFα caused a rapid reduction in the peak amplitude of AMPA‐mediated calcium entry in a PI3‐kinase and p38 kinase‐dependent manner, consistent with increased insertion of GluR2‐containing AMPAR into the plasma membrane. This resulted in a protection of motor neurones against kainate‐induced cell death. Our data therefore, suggest that TNFα acts primarily as a physiological regulator of synaptic activity in motor neurones rather than a pathological drive in amyotrophic lateral sclerosis.
Effects of T‐type calcium channel blockers and thalidomide on contractions of rat vas deferens
Authors: Seto Sai Wang , Docherty James R. 
Published: February 2010

Background and purpose:  In rat vas deferens, nerve mediated‐contractions to a single electrical stimulus consist of an early purinergic and a later adrenergic component with differing sensitivities to L‐type calcium channel blockers. We have investigated the effects of the T‐type calcium channel blockers mibefradil and (1S, 2S)‐2‐[2‐[[3‐(1H‐benzimidazol‐2‐yl)propyl]methylamino]ethyl]‐6‐fluoro‐1,2,3,4‐tetrahydro‐1‐(1‐methylethyl)‐2‐naphthalenyl cyclopropanecarboxylic dihydrochloride (NNC 55‐0396) against contractions in rat vas deferens. In addition, the actions of thalidomide were examined.Experimental approach:  Prostatic and epididymal portions of rat vas deferens were stimulated with a single electrical stimulus every 5 min, and mouse whole vas deferens was stimulated with 40 pulses at 10 Hz every 5 min.Key results:  Both mibefradil and NNC 55‐0396 (100 µM) produced inhibition of contractions of epididymal portions (42 ± 13%, n= 7, and 43 ± 4%, n= 15, of control respectively). However, both agents produced small inhibitions of responses in prostatic portions, presumably by L‐type calcium channel block. Thalidomide (100 µM) inhibited contractions in epididymal (55 ± 4% of control, n= 17) but not in prostatic portions of rat vas deferens. Thalidomide (10–100 µM) also inhibited contractions in mouse vas deferens.Conclusions and implications:  The T‐type calcium channel blockers mibefradil and NNC 55‐0396 block particularly the adrenoceptor‐mediated, nifedipine‐resistant response to nerve stimulation in rat vas deferens, and this may suggest that this component involves T‐type calcium channels. In addition, thalidomide has actions that resemble those of the T‐type calcium channel blockers, in that it blocks nifedipine‐resistant contractions in epididymal portions.
Activation of cardiac muscarinic M3 receptors induces delayed cardioprotection by preserving phosphorylated connexin43 and up‐regulating cyclooxygenase‐2 expression
Authors: Zhao Jinlong , Su Yue , Zhang Yong , Pan Zhenwei , Yang Lili , Chen Xichuang , Liu Yan , Lu Yanjie , Du Zhimin , Yang Baofeng 
Published: February 2010

Background and purpose:  Activation of muscarinic M3 mucarinic acetylcholine receptors (M3‐mAChRs) has been previously shown to confer short‐term cardioprotection against ischaemic injuries. However, it is not known whether activation of these receptors can provide delayed cardioprotection. Consequently, the present study was undertaken to investigate whether stimulation of M3‐mAChRs can induce delayed preconditioning in rats, and to characterize the potential mechanism.Experimental approach:  Rats were pretreated (24 h), respectively, with M3‐mAChRs agonist choline, M3‐mAChRs antagonist 4‐DAMP or M2‐mAChRs antagonist methoctramine followed by the administration of choline. This was followed by 30 min of ischaemia and then 3 h of reperfusion. Ischaemia‐induced arrhythmias and ischaemia–reperfusion (I/R)‐induced infarction were determined. The phosphorylation status of connexin43 (Cx43) after 30 min ischaemia, and the expression level of Hsp70, cyclooxygenase‐2 (COX‐2) and iNOS effected by administration of choline were also measured.Key results:  Compared to the control group, pretreatment with choline significantly decreased ischaemia‐induced arrhythmias, reduced the total number of ventricular premature beats, the duration of ventricular tachycardia episodes and markedly reduced I/R‐induced infarct size. Furthermore, choline attenuated ischaemia‐induced dephosphorylation of Cx43, and up‐regulated the expression of Hsp70 and COX‐2. Administration of 4‐DAMP abolished these changes, while methoctramine had no effect.Conclusions and implications:  Our results suggest that stimulation of M3‐mAChRs with choline elicits delayed preconditioning, which we propose is the result of up‐regulation of the expression of COX‐2 and inhibition of the ischaemia‐induced dephosphorylation of Cx43. Therefore, M3‐mAChRs represent a promising target for rendering cardiomyocytes tolerant to ischaemic injury.
Markedly reduced toxicity of a hydrogen sulphide‐releasing derivative of naproxen (ATB‐346)
Authors: Wallace John L , Caliendo Giuseppe , Santagada Vincenzo , Cirino Giuseppe 
Published: February 2010

Background and purpose:  Hydrogen sulphide is an important mediator of gastric mucosal defence. The use of non‐steroidal anti‐inflammatory drugs continues to be limited by their toxicity, particularly in the upper gastrointestinal tract. We evaluated the gastrointestinal safety and anti‐inflammatory efficacy of a novel hydrogen sulphide‐releasing derivative of naproxen, ATB‐346 [2‐(6‐methoxy‐napthalen‐2‐yl)‐propionic acid 4‐thiocarbamoyl‐phenyl ester].Experimental approach:  The ability of ATB‐346 versus naproxen to cause gastric damage was evaluated in healthy rats and in rats with compromised gastric mucosal defence. Effects on the small intestine and on the healing of ulcers were also assessed. The ability of ATB‐346 to inhibit cyclooxygenase‐1 and 2 and to reduce inflammation in vivo was also evaluated.Key results:  ATB‐346 suppressed gastric prostaglandin E2 synthesis as effectively as naproxen, but produced negligible damage in the stomach and intestine. In situations in which the gastric mucosa was rendered significantly more susceptible to naproxen‐induced damage (e.g. ablation of sensory afferent nerves, inhibition of endogenous nitric oxide or hydrogen sulphide synthesis, co‐administration with aspirin, antagonism of KIR6.x channels), ATB‐346 did not cause significant damage. Unlike naproxen and celecoxib, ATB‐346 accelerated healing of pre‐existing gastric ulcers. In a mouse airpouch model, ATB‐346 suppressed cyclooxygenase‐2 activity and inhibited leukocyte infiltration more effectively than naproxen. ATB‐346 was as effective as naproxen in adjuvant‐induced arthritis in rats, with a more rapid onset of activity. Unlike naproxen, ATB‐346 did not elevate blood pressure in hypertensive rats.Conclusions and implications:  ATB‐346 exhibits anti‐inflammatory properties similar to naproxen, but with substantially reduced gastrointestinal toxicity.
What is ‘Catholic Enlightenment’?
Authors: Lehner Ulrich L. 
Published: February 2010

AbstractRecent research has demonstrated not only the existence of a variety of Enlightenments, but also the importance of the religious aspect to this worldwide process. In particular, special interest has been paid to the long‐neglected Catholic Enlightenment, which entailed many strands of thought by Catholic intellectuals and political leaders who attempted to renew and reform Catholicism from the middle of the 18th to the early 19th century. This renewal was an apologetic endeavor designed to defend the essential dogmas of Catholic Christianity by explaining their rationality in modern terminology and by reconciling Catholicism with modern culture. The Catholic Enlightenment was in dialog with contemporary culture, not only by developing new hermeneutical approaches to the Council of Trent or to Jansenist ideas, but also by implementing some of the core values of the overall European Enlightenment process that tried to ‘renew’ and ‘reform’ the whole of society, and thus truly deserves the label Enlightenment.
Radicalism in Civil War and Interregnum England
Authors: Baker Philip 
Published: February 2010

AbstractIn recent decades, the subject of civil war and interregnum radicalism has provoked a vexed and tendentious scholarship within early modern English history. This article charts the subject’s historiographical fortunes since the 1970s and addresses a series of crucial interpretive and definitional issues. In addition to providing an overview of the existing field, the article also suggests a new approach to mid‐17th‐century radicalism that encompasses a much broader spectrum of individuals, groups and ideas than those found in both Marxist and revisionist accounts. Drawing on this approach and the recent insights of other scholars, this article identifies a number of possible avenues for future research and suggests how the subject might be developed in original ways.
Women, Gender, and Religion in the Early Americas
Authors: Lindman Janet Moore 
Published: February 2010

AbstractThe historical study of women and religion in the early Americas has garnered substantial scholarship in the last 30 years. The influence of women’s history and feminist studies has generated great interest on the topic of gender and religion. Scholars have analyzed women’s religious history using indices of race, class, and gender to produce nuanced histories. This work has shown the complex contours of female spirituality in the early Americas. Female laity both accepted and questioned male religious leadership and sought meaningful spiritual experiences in myriad contexts, such as the sanctuary, household, and community. Studies have been done on a wide range of topics relating to women and religion, such as conversion, preaching, mysticism, speech, healing, domesticity, monasticism, witchcraft, sexuality, and the body. Women in Protestant, Catholic, and Jewish traditions have been examined, as have Native American, African American, and mixed race women in Spanish, French, and British America. Their historical experience reveals an ongoing tension between religious hierarchy and female pursuits of piety. Scholarly literature on ‘women religious’, that is, Catholic nuns, demonstrates that they exercised power, even while working under a male‐dominated ecclesiastical authority, in both North and South American settlements from the 16th to the 19th centuries. Female members of radical Protestant groups, such as the Quakers, Shakers, and Moravians, participated in communities that promoted gender ideologies divergent from the dominant culture. The study of women’s religious history will continue to ponder the multiple meanings and interactions of spirituality, gender, and power within early American societies.
Book‐History Approaches to India: Representations of the Subcontinent in the Novel and Verse, 1780–1823
Authors: Malhotra Ashok 
Published: February 2010

AbstractLiterary representations of India in verse and novels written by British authors during the period 1780–1823 have been approached by contemporary scholars either from the postcolonial perspective of relating the fiction to the shifting relationship between colonizer or colonized, or to correlating portrayals to elitist political debates taking place within the metropole. The argument proposes that forthcoming scholarship should adopt a book‐history approach to the topic which would add an important contextual dimension to the readings of fictional texts and understanding of a whole set of British cultural attitudes towards Indians. To this end, it proposes that further critical analysis of British India fictions could situate recurring tropes about India in relation to the demands and prevailing fashions of the literary marketplace, and determine how the varying perceived cultural status and the internal development of the two literary modes affect portrayals of the subcontinent.
Interictal cerebral blood flow abnormality in cryptogenic West syndrome
Authors: Hamano Shin‐ichiro , Higurashi Norimichi , Koichihara Reiko , Oritsu Tomotaka , Kikuchi Kenjiro , Yoshinari Satoshi , Tanaka Manabu , Minamitani Motoyuki 
Published: February 2010

SummaryPurpose:  To elucidate the abnormality of interictal regional cerebral blood flow (rCBF) of West syndrome at the onset.Methods:  Quantitative measurement of rCBF with an autoradiography method using N‐isopropyl‐(123I) p‐iodoamphetamine single photon emission computed tomography (SPECT) was performed on 14 infants with cryptogenic West syndrome. Regions of interest (ROIs) for rCBF were placed automatically using an automated ROI analysis software (three‐dimensional stereotactic ROI template), and were grouped into 12 segments: callosomarginal, precentral, central, parietal, angular, temporal, posterior cerebral, pericallosal, lenticular nucleus, thalamus, hippocampus, and cerebellum. We compared rCBF between the patients and seven age‐matched infants with cryptogenic focal epilepsy as a control group. The patients were divided into two groups according to the duration from onset to SPECT, to compare rCBF.Results:  Quantitative analysis revealed cerebral hypoperfusion in cryptogenic West syndrome with normal SPECT images under visual inspection. In bilateral central, posterior cerebral, pericallosal, lenticular nucleus, and hippocampus, and in the left parietal, temporal, and cerebellum, and in the right angular and thalamus segments there were statistical differences (p < 0.05). Compared with the duration from onset to SPECT, there were no significant differences of rCBF in all segments.Discussion:  Broad cerebral hypoperfusion with posterior predominance involving the hippocampus and lenticular nucleus implies that even cryptogenic West syndrome has a widespread cerebral dysfunction at least transiently, which would correspond to clinical manifestations of hypsarrhythmia and epileptic spasms. Hippocampal hypoperfusion suggests the dysfunction of hippocampal circuitry in the brain adrenal axis, and may contribute to subsequent cognitive impairment of cryptogenic West syndrome.
Importance of Catheter Contact Force During Irrigated Radiofrequency Ablation: Evaluation in a Porcine Ex Vivo Model Using a Force‐Sensing Catheter
Authors: THIAGALINGAM ARAVINDA , D’AVILA ANDRE , FOLEY LORI , GUERRERO J. LUIS , LAMBERT HENDRIK , LEO GIOVANNI , RUSKIN JEREMY N. , REDDY VIVEK Y. 
Published: February 2010

Effect of Ablation Electrode Contact Force. Introduction: Ablation electrode–tissue contact has been shown to be an important determinant of lesion size and safety during nonirrigated ablation but little data are available during irrigated ablation. We aimed to determine the importance of contact force during irrigated‐tip ablation.
Methods and Results:
Freshly excised hearts from 11 male pigs were perfused and superfused using fresh, heparinized, oxygenated swine blood in an ex vivo model. One‐minute ablations were placed using one of 3 different power control strategies (impedance control—15 Ω target impedance drop, and 20 W or 30 W fixed power) and 3 different contact forces (2 g, 20 g, and 60 g) to give a grid of 9 ablation groups. The force sensing catheter (Tacticath™, Endosense SA) was irrigated at 17 mL/min for all of the ablations.Of a total 101 ablations, no thrombus formation was noted but popping was seen in 17 lesions. The lesion depth and incidence of pops was 5.0 ± 1.3 mm /0%, 5.0 ± 1.6 mm /10% and 6.7 ± 2.5 mm /45% for the 15 Ω, 20 W, and 30 W groups (P < 0.01), respectively, and 4.4 ± 1.8 mm /3%, 5.8 ± 1.6 mm /17% and 6.6 ± 2.0 mm /37% for the 2 g, 20 g, and 60 g groups, respectively (P < 0.01). The impedance drop in the first 5 seconds was significantly correlated to catheter contact force: 9.7 ± 9.9 Ω, 22.3 ± 11.0 Ω, and 41.7 ± 22.1 Ω, respectively, for the 2 g, 20 g, and 60 g groups (Pearson's r = 0.65, P < 0.01).
Conclusion:
Catheter contact force has an important impact on both ablation lesion size and the incidence of pops. (J Cardiovasc Electrophysiol, Vol. pp. 806‐811, July 2010)