bluuebunny/crossref_metadata_2025_split huggingface dataset:
Controls on metamorphic equilibration: the importance of intergranular solubilities mediated by fluid composition
Authors: Carlson W. D. , Hixon J. D. , Garber J. M. , Bodnar R. J. 
Published: October 2014

AbstractA dramatic demonstration of the role of intergranular solubility in promoting chemical equilibration during metamorphism is found in the unusual zoning of garnet in pelitic schist exposed at Harpswell Neck, Maine, USA. Many garnet crystals have irregular, patchy distributions of Mn, Cr, Fe and Mg in their inclusion‐rich interiors, transitioning to smooth, concentric zoning in their inclusion‐poor outer rims; in contrast, zoning of Ca and Y is comparatively smooth and concentric throughout. We re‐assess the disputed origin of these zoning features by examining garnet growth in the context of the thermal and structural history of the rocks, and by evaluating the record of fluid–rock interaction revealed in outcrop‐scale veining and fluid‐inclusion assemblages. The transition in the character of garnet zoning correlates with the onset of a synkinematic, simple‐shear‐dominated phase of garnet growth and with a shift in the composition of the intergranular fluid from CO2‐rich to H2O‐rich. Compositional variations in garnet are therefore best explained by a two‐stage growth history in which intergranular diffusive fluxes reflect differences in the concentration of dissolved species in these two contrasting fluids. Interiors of garnet crystals grew in the presence of a CO2‐rich fluid, in which limited solubility for Mn and Cr (and perhaps Fe and Mg) produced patchy disequilibrium overprint zoning, while appreciable solubility for Ca and Y permitted their rock‐wide equilibration. Rims grew in the presence of an H2O‐rich fluid, in which high intergranular concentrations for all elements except Cr enabled diffusion over length scales sufficient for rock‐wide equilibration. This striking example of partial chemical equilibrium during reaction and porphyroblast growth implies that thermal effects may commonly be subsidiary in importance to solubilities in the intergranular medium as determinants of length scales for metamorphic equilibration.
Aging and brain rejuvenation as systemic events
Authors: Bouchard Jill , Villeda Saul A. 
Published: October 2014

AbstractThe effects of aging were traditionally thought to be immutable, particularly evident in the loss of plasticity and cognitive abilities occurring in the aged central nervous system (CNS). However, it is becoming increasingly apparent that extrinsic systemic manipulations such as exercise, caloric restriction, and changing blood composition by heterochronic parabiosis or young plasma administration can partially counteract this age‐related loss of plasticity in the aged brain. In this review, we discuss the process of aging and rejuvenation as systemic events. We summarize genetic studies that demonstrate a surprising level of malleability in organismal lifespan, and highlight the potential for systemic manipulations to functionally reverse the effects of aging in the CNS. Based on mounting evidence, we propose that rejuvenating effects of systemic manipulations are mediated, in part, by blood‐borne ‘pro‐youthful’ factors. Thus, systemic manipulations promoting a younger blood composition provide effective strategies to rejuvenate the aged brain. As a consequence, we can now consider reactivating latent plasticity dormant in the aged CNS as a means to rejuvenate regenerative, synaptic, and cognitive functions late in life, with potential implications even for extending lifespan.
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We review evidence of brain rejuvenation focusing on several systemic manipulations – exercise, caloric restriction, heterochronic parabiosis, and young plasma administration – and their ability to restore regenerative capacity, synaptic plasticity, and cognitive function in the brain.
Hypoxia interferes with aryl hydrocarbon receptor pathway in hCMEC/D3 human cerebral microvascular endothelial cells
Authors: Jacob Aude , Potin Sophie , Saubaméa Bruno , Crete Dominique , Scherrmann Jean‐Michel , Curis Emmanuel , Peyssonnaux Carole , Declèves Xavier 
Published: October 2014

AbstractThe expression of aryl hydrocarbon receptor (AhR) transcription factor was detected at transcript level in freshly isolated human brain microvessels and in the hCMEC/D3 human cerebral microvascular endothelial cell line. Recent studies have demonstrated that AhR pathway is able to crosstalk with other pathways such as hypoxia signaling pathway. Therefore, we used the hCMEC/D3 cell line to investigate the potential crosstalk between AhR and hypoxia signaling pathways. First, we performed two different hypoxia‐like procedures in hCMEC/D3 cells; namely, exposition of cells to 150 μM deferoxamine or to glucose and oxygen deprivation for 6 h. These two procedures led to hypoxia‐inducible factor (HIF)‐1α and HIF‐2α proteins accumulation together with a significant induction of the two well‐known hypoxia‐inducible genes VEGF and GLUT‐1. Both HIF‐1α and ‐2α functionally mediated hypoxia response in the hCMEC/D3 cells. Then, we observed that a 6 h exposure to 25 nM 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin, a strong AhR ligand, up‐regulated CYP1A1 and CYP1B1 expression, and that this effect was AhR dependent. Regarding AhR and hypoxia crosstalk, our experiments revealed that an asymmetric interference between these two pathways effectively occurred in hCMEC/D3 cells: hypoxia pathway interfered with AhR signaling but not the other way around.
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We studied the putative crosstalk of AhR and hypoxia pathways in hCMEC/D3 human cerebral microvascular endothelial cells. While hypoxia decreased the expression of the two AhR target genes CYP1A1 and CYP1B1, AhR activation results in no change in hypoxia target gene expression. This is the first sign of AhR and hypoxia pathway crosstalk in an in vitro model of the human cerebral endothelium.
The effects of nesfatin‐1 in the paraventricular nucleus on gastric motility and its potential regulation by the lateral hypothalamic area in rats
Authors: Guo Fei‐fei , Xu Luo , Gao Sheng‐li , Sun Xiang‐rong , Li Zhi‐ling , Gong Yan‐ling 
Published: October 2014

AbstractThe current study investigated the effects of nesfatin‐1 in the hypothalamic paraventricular nucleus (PVN) on gastric motility and the regulation of the lateral hypothalamic area (LHA). Using single unit recordings in the PVN, we show that nesfatin‐1 inhibited the majority of the gastric distention (GD)‐excitatory neurons and excited more than half of the GD‐inhibitory (GD‐I) neurons in the PVN, which were weakened by oxytocin receptor antagonist H4928. Gastric motility experiments showed that administration of nesfatin‐1 in the PVN decreased gastric motility, which was also partly prevented by H4928. The nesfatin‐1 concentration producing a half‐maximal response (EC50) in the PVN was lower than the value in the dorsomedial hypothalamic nucleus, while nesfatin‐1 in the reuniens thalamic nucleus had no effect on gastric motility. Retrograde tracing and immunofluorescent staining showed that nucleobindin‐2/nesfatin‐1 and fluorogold double‐labeled neurons were observed in the LHA. Electrical LHA stimulation changed the firing rate of GD‐responsive neurons in the PVN. Pre‐administration of an anti‐ nucleobindin‐2/nesfatin‐1 antibody in the PVN strengthened gastric motility and decreased the discharging of the GD‐I neurons induced by electrical stimulation of the LHA. These results demonstrate that nesfatin‐1 in the PVN could serve as an inhibitory factor to inhibit gastric motility, which might be regulated by the LHA.image
Nesfatin‐1 regulated the gastric distension (GD)‐responsive neurons and reduced gastric motility in the paraventricular nucleus (PVN), which were partly blocked by H4928. Electrical stimulation of the lateral hypothalamic area (LHA) increased the firing activities of GD‐responsive neurons in the PVN and promoted the gastric motility. NUCB2/nesfatin‐1/fluorogold double‐labeled neurons were identified in the LHA, indicating that nesfatin‐1 in the PVN could play a pivotal role in the central control of gastric motility and the LHA may participate in the regulatory process. NUCB2 = nucleobindin‐2
Work–family conflict and social undermining behaviour: An examination of PO fit and gender differences
Authors: Scott Kristin L. , Ingram Amy , Zagenczyk Thomas J. , Shoss Mindy K. 
Published: October 2014

In this study, we develop and test a novel theoretical model that addresses the relationship between work–family conflict (WFC), sex, PO fit perceptions (PO fit) and social undermining behaviour. Drawing on the source attribution perspective and role theory, we hypothesize that WFC is positively associated with social undermining behaviour at a later point in time and this relationship is explained in part by diminished PO fit perceptions. Furthermore, we argue that female employees reporting high levels of WFC are more likely to engage in undermining behaviour relative to men when PO fit is considered as a mediating variable. Specifically, we assert that PO fit is depleted to a larger extent for female than for male workers and, subsequently, is associated with higher levels of undermining behaviour. In a sample of over 300 full‐time working adults employed across a variety of occupations, we found support for each of our predictions. Implications for research and practice are addressed.Practitioner points

Work–family conflict contributes to co‐worker‐directed social undermining behaviour because it weakens person–organization fit perceptions – especially among women.

Organizational leaders can create a stronger sense of community among employees, offer avenues for support as well as resources that can help workers cope with the difficulties associated with WFC.

Leaders implementing interventions should try to maintain a sense of ‘fit’ and belongingness within the organization and let workers know they are valued even in the face of high levels of work‐related demands and challenges.
Rehabilitation of oral function with removable dentures – still an option?
Authors: Xie Q. , Ding T. , Yang G. 
Published: October 2014

SummaryTooth loss is a chronic disability, which makes it difficult for patients to perform essential tasks such as eating, communicating with others and socialising. Numerous studies have revealed and addressed the recent rapid development of various prosthodontic materials and treatment patterns. Oral rehabilitation with dentures exerts a great influence on people's daily life and has tremendous social implications. Dentures help to restore an individual's sense of normality and ability to interact normally. With the introduction and progression of implant technology, many troublesome issues can now be solved simply. Nowadays, more and more attention has been paid to new trends (implant‐assisted restoration and fixed prostheses). However, removable dentures may be a more appropriate solution under some circumstances, such as if they are a patient's preferred option, if remaining oral tissues are in poor condition, or if they provide the most cost‐effective form of treatment. Thus, removable dentures are still an option for the rehabilitation of oral function. The purpose of this article was to retrospectively review the applications of removable dentures and to emphasise their indispensable status.
Relationship Between Degenerative Joint Disease, Pain, and Bartonella spp. Seroreactivity in Domesticated Cats
Authors: Tomas A. , Pultorak E.L. , Gruen M.E. , Breitschwerdt E.B. , Lascelles B.D.X. 
Published: October 2014

BackgroundRecently, a potential association was identified between Bartonella exposure and arthritides in mammalian species other than cats.Hypothesis/ObjectivesWe hypothesized that Bartonella exposure is associated with more severe degenerative joint disease (DJD) and a greater burden of DJD‐associated pain in client‐owned cats.AnimalsNinety‐four client‐owned cats (6 months to 20 years old), ranging from clinically unaffected to severely lame because of DJD.MethodsUsing physical examination and radiography, pain and radiographic scores were assigned to each part of the bony skeleton. Sera were tested for Bartonella henselae, B. koehlerae, and B. vinsonii subsp. berkhoffii (genotypes I, II, and III) antibodies using immunofluorescence antibody assays. Variables were categorized and logistic regression used to explore associations.ResultsSeropositivity to Bartonella was identified in 33 (35.1%) cats. After multivariate analysis controlling for age, total DJD score (OR, 0.51; 95% CI, 0.26–0.97; P = .042), appendicular pain score (OR, 0.33; 95% CI, 0.17–0.65; P = .0011), and total pain score (OR, 0.35; 95% CI, 0.17–0.72; P = .0045) were significantly inversely associated with Bartonella seroreactivity status, indicating that cats with higher DJD and pain scores were less likely to be Bartonella seropositive.Conclusions and Clinical ImportanceBased upon this preliminary study, Bartonella spp. seropositivity was associated with decreased severity of DJD and decreased DJD‐associated pain in cats. Additional studies are needed to verify these findings, and if verified, to explore potential mechanisms.
Antiarrhythmic and Electrophysiologic Effects of Flecainide on Acutely Induced Atrial Fibrillation in Healthy Horses
Authors: Haugaard M.M. , Pehrson S. , Carstensen H. , Flethøj M. , Hesselkilde E.Z. , Præstegaard K.F. , Diness J.G. , Grunnet M. , Jespersen T. , Buhl R. 
Published: October 2014

BackgroundOnly few pharmacologic compounds have been validated for treatment of atrial fibrillation (AF) in horses. Studies investigating the utility and safety of flecainide to treat AF in horses have produced conflicting results, and the antiarrhythmic mechanisms of flecainide are not fully understood.ObjectivesTo study the potential of flecainide to terminate acutely induced AF of short duration (≥15 minutes), to examine flecainide‐induced changes in AF duration and AF vulnerability, and to investigate the in vivo effects of flecainide on right atrial effective refractory period, AF cycle length, and ventricular depolarization and repolarization.AnimalsNine Standardbred horses. Eight received flecainide, 3 were used as time‐matched controls, 2 of which also received flecainide.MethodsProspective study. The antiarrhythmic and electrophysiologic effects of flecainide were based on 5 parameters: ability to terminate acute pacing‐induced AF (≥15 minutes), and drug‐induced changes in atrial effective refractory period, AF duration, AF vulnerability, and ventricular depolarization and repolarization times. Parameters were assessed at baseline and after flecainide by programmed electrical stimulation methods.ResultsFlecainide terminated all acutely induced AF episodes (n = 7); (AF duration, 21 ± 5 minutes) and significantly decreased the AF duration, but neither altered atrial effective refractory period nor AF vulnerability significantly. Ventricular repolarization time was prolonged between 8 and 20 minutes after initiation of flecainide infusion, but no ventricular arrhythmias were detected.Conclusions and Clinical ImportanceFlecainide had clear antiarrhythmic properties in terminating acute pacing‐induced AF, but showed no protective properties against immediate reinduction of AF. Flecainide caused temporary prolongation in the ventricular repolarization, which may be a proarrhythmic effect.
Conservation genomics of anadromous Atlantic salmon across its North American range: outlier loci identify the same patterns of population structure as neutral loci
Authors: Moore Jean‐Sébastien , Bourret Vincent , Dionne Mélanie , Bradbury Ian , O'Reilly Patrick , Kent Matthew , Chaput Gérald , Bernatchez Louis 
Published: October 2014

AbstractAnadromous Atlantic salmon (Salmo salar) is a species of major conservation and management concern in North America, where population abundance has been declining over the past 30 years. Effective conservation actions require the delineation of conservation units to appropriately reflect the spatial scale of intraspecific variation and local adaptation. Towards this goal, we used the most comprehensive genetic and genomic database for Atlantic salmon to date, covering the entire North American range of the species. The database included microsatellite data from 9142 individuals from 149 sampling locations and data from a medium‐density SNP array providing genotypes for >3000 SNPs for 50 sampling locations. We used neutral and putatively selected loci to integrate adaptive information in the definition of conservation units. Bayesian clustering with the microsatellite data set and with neutral SNPs identified regional groupings largely consistent with previously published regional assessments. The use of outlier SNPs did not result in major differences in the regional groupings, suggesting that neutral markers can reflect the geographic scale of local adaptation despite not being under selection. We also performed assignment tests to compare power obtained from microsatellites, neutral SNPs and outlier SNPs. Using SNP data substantially improved power compared to microsatellites, and an assignment success of 97% to the population of origin and of 100% to the region of origin was achieved when all SNP loci were used. Using outlier SNPs only resulted in minor improvements to assignment success to the population of origin but improved regional assignment. We discuss the implications of these new genetic resources for the conservation and management of Atlantic salmon in North America.
The NOTCH3ECD cascade hypothesis of cerebral autosomal‐dominant arteriopathy with subcortical infarcts and leukoencephalopathy disease
Authors: Joutel Anne 
Published: October 2014

AbstractBackgroundCerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy, with an autosomal dominant mode of transmission, is an archetypal small vessel disease of the brain that has emerged as the most common heritable cause of stroke and vascular dementia worldwide.Aims and methodsHere we review the current knowledge on the pathogenesis of this disease.ResultsThe disease is caused by highly stereotyped missense mutations that alter the number of cysteine residues in the extracellular domain of NOTCH3, a transmembrane receptor that undergoes a series of proteolytic cleavages on ligand binding that release the extracellular domain, and ultimately enable the intracellular domain to translocate to the nucleus, where it acts as a transcriptional activator. NOTCH3 is predominantly expressed in vascular smooth muscle cells, and is critical for the structure and function of small vessels of the brain. Mutations differentially affect NOTCH3 transcriptional activity; however, it is still debated whether a reduction in NOTCH3 activity might contribute to the disease process. In contrast, all disease associated NOTCH3 mutations are associated with an early accumulation, aggregation and deposition of the extracellular domain at the plasma membrane of smooth muscle cells, in extracellular deposits called granular osmiophilic material. Importantly, recent work identified a novel mechanism in which excess of the extracellular domain of NOTCH3 promotes the abnormal recruitment of proteins of the extracellular matrix that might cause multifactorial toxicity in the brain vessels.ConclusionRecent studies lend support to a NOTCH3ECD cascade hypothesis in in Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy that posits that the deposition of NOTCH3 extracellular domain in the brain vessels initiates a sequence of events that ultimately lead to stroke and dementia.
Chronic inflammatory demyelinating polyneuropathy triggered by interferon‐α for chronic hepatitis B virus infection
Authors: Sakaguchi Hideya , Yamashita Satoshi , Ueda Akihiko , Sada Hiromi , Ikeda Tokunori , Hirahara Tomoo , Honda Shoji , Kimura En , Yamashita Taro , Maeda Yasushi , Hirano Teruyuki , Uchino Makoto 
Published: October 2014

AbstractInterferon‐α has been widely used for treatment of chronic hepatitis and some malignancies. Several autoimmune diseases have been reported to be induced by interferon‐α, but chronic inflammatory demyelinating polyneuropathy is rare. Here, we report a chronic hepatitis B patient who developed chronic inflammatory demyelinating polyneuropathy after receiving interferon‐α treatment. After withdrawal of interferon‐α, neurological symptoms continued to progress, but the symptoms improved after intravenous immunoglobulin treatment. This case provides further immunological insight into the correlation between chronic inflammatory demyelinating polyneuropathy and interferon‐α.
Spinocerebellar ataxia type 6: Lessons from faithful knock‐in mouse models
Authors: Watase Kei 
Published: October 2014

AbstractSpinocerebellar ataxia type 6 is a dominantly inherited neurodegenerative disorder characterized by slowly progressive ataxia, slurred speech and nystagmus. The molecular pathogenesis of spinocerebellar ataxia type 6 has attracted considerable attention, because it is caused by the small expansion of a CAG trinucleotide repeat encoding a polyglutamine tract within the Cav2.1 voltage‐gated Ca++ channel. To recreate the characteristics of spinocerebellar ataxia type 6, we produced several lines of knock‐in mice carrying normal or mutant CAG repeat tracts in the Cacna1a locus. The mice expressing a hyperexpanded polyglutamine (Sca684Q) developed late‐onset progressive motor impairment and neuronal inclusion formation in the cytoplasm of cerebellar Purkinje cells. The electrophysiological analysis of the Sca684Q Purkinje cells showed that the repeat expansion did not affect the intrinsic properties of the channel. MPI‐118Q knock‐in mice, which expressed a hyperexpanded channel at modestly enhanced levels because of the insertion of a splice‐site mutation, recapitulated many features of spinocerebellar ataxia type 6, including selective Purkinje cell degeneration. An analysis of the cytoplasmic neuronal inclusions showed the lysosomal localization of accumulated mutant Cav2.1 channels. The lack of cathepsin B, a major lysosomal cysteine proteinase, increased the loss of the Purkinje cells and was accompanied by an acceleration of neuronal inclusion formation in this model. These results suggest that the spinocerebellar ataxia type 6 mutation exerts its neurotoxicity through a mechanism associated with age‐dependent accumulation of the expanded polyglutamine protein, and the pathogenesis of spinocerebellar ataxia type 6 involves the endolysosomal degradation pathway.
Cardioembolic stroke in the cardiac variant of Fabry disease
Authors: Nishimura Kazutaka , Uehara Toshiyuki , Ishibashi‐Ueda Hatsue , Anzai Toshihisa , Toyoda Kazunori 
Published: October 2014

AbstractWe describe herein the case of a 71‐year‐old man with the cardiac variant of Fabry disease presenting with cardioembolic stroke. Stroke is one of the most well‐known manifestations of Fabry disease, and lacunar stroke is a widely recognized etiology. However, little is known about stroke in patients with the cardiac variant of Fabry disease. The cardiac variant of Fabry disease should be considered as a potential cardiac source of embolic stroke.