bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessing the efficacy of reintroduction programmes by modelling adult survival: the example of Hermann's tortoise
Authors: Bertolero A. , Oro D. , Besnard A. 
Published: August 2007

AbstractAlthough reintroduction programmes are often implemented for recovering animal populations, projects seldom monitor the long‐term survival of released animals. In addition, although many releases may occur in the same area, little is known about how the survival of successive release batches is affected by the presence of conspecifics and density dependence. Here, we use multi‐state capture–recapture modelling (combining information from recaptures and recoveries) to analyse the survival of two batches of Hermann's tortoise Testudo hermanni hermanni released in a 10‐year interval and monitored for 18 years at the Ebro Delta (western Mediterranean). We also tested whether the released animals experienced lower survival (i.e. a release cost) before becoming familiar with the new environment. Although we used a hard‐release method, neither group experienced a short‐term release cost. Annual survival of both groups differed and was not negatively affected by density‐dependent factors. Annual survivorship of the first group of released tortoises was constant and very high (0.945, se=0.011), and similar to that estimated from several natural populations. The presence of a terrestrial predator in 1 year (before the release of the second group) significantly decreased the survival of tortoises (0.819, se=0.073). Strikingly, survival of the second batch was significantly lower than that of the first group after the first years of release (0.775, se=0.049). Although survivorship for the first group suggested that habitat quality was high, the second group seemed not to acclimate well to the new environment, possibly due to the presence of resident tortoises. From a management perspective, reintroduction programmes of the Hermann's tortoise are a successful strategy for its recovery. Nevertheless, it seems advisable to avoid: (1) the release of tortoises at the core of well‐established populations and (2) areas with a high density of predators, which can jeopardize the reintroduction success, especially when the number of released individuals is small.
Contribution of endothelial cells to organogenesis: a modern reappraisal of an old Aristotelian concept
Authors: Crivellato E. , Nico B. , Ribatti D. 
Published: August 2007

AbstractIt is well established that many tissue‐derived factors are involved in blood vessel formation, but evidence is now emerging that endothelial cells themselves represent a crucial source of instructive signals to non‐vascular tissue cells during organ development. Thus, endothelial cell signalling is currently believed to promote fundamental cues for cell fate specification, embryo patterning, organ differentiation and postnatal tissue remodelling. This review article summarizes some of the recent advances in our understanding of the role of endothelial cells as effector cells in organ formation.
Beyond drinking: the role of wine in the life of the UK consumer
Authors: Ritchie Caroline 
Published: August 2007

AbstractSince the development of wine sales via supermarkets in the UK in the 1970s wine consumption has more than doubled so now the UK is the largest wine import market (by value) in the world. Wine is now consumed by approximately 61% of the UK adult population on a regular basis. For many social wine consumption has become part of their lifestyle. Given the international importance of the UK wine market, plus the increasing incorporation of wine into regular consumption behaviour, it is remarkable how few academic studies have been undertaken into the consumption behaviour of moderate, social UK wine consumers. This paper aims to start developing that knowledge, thus adding to our understanding of consumer behaviour in general. The results show that consumers use wine in very sophisticated ways via purchasing, gifting and consumption. The findings also show that social interaction with wine varies significantly, dependant upon occasion and environment. Behaviour also varies if the purchase, as gift and/or for consumption, is perceived as a private or public activity. This paper places UK wine consumer behaviour within a social context, and is able to show that all consumers display a range of behaviours in relation to wine which are situation and occasion dependant.
Individualism and the ‘new tourism’: a perspective on emulation, personal control and choice
Authors: Voase Richard 
Published: August 2007

AbstractChanges can be identified in patterns of Western tourism over recent decades. The changes are linked with the theorized cultural shift from modern to postmodern. The discourse of change points to a shift in emphasis from the designated resort environment to a proliferation of individuated experiences. Analysts are apt to link these changes to a growth in individualism and individualistic expression. This study argues that the new tourists' real needs are to discover a new form of the collective. The argument is constructed drawing on the work of Veblen and Bourdieu. The final diagnosis draws on the work of Foucault.
The binding and phosphorylation of Thr231 is critical for Tau’s hyperphosphorylation and functional regulation by glycogen synthase kinase 3β
Authors: Lin Yuh‐Te , Cheng Jiin‐Tsuey , Liang Li‐Ching , Ko Chiung‐Yuan , Lo Yuk‐Keung , Lu Pei‐Jung 
Published: August 2007

AbstractNeuropathological hallmarks of Alzheimer’s disease are extracellular senile plaques and intracellular neurofibrillary lesions. The neurofibrillary lesions mainly consist of the hyperphosphorylated microtubule‐associated protein Tau predominantly expressed in the axon of CNS neurons. Hyperphosphorylation of Tau negatively affects its binding to tubulin and decreases the capacity to promote microtubule assembly. Among a number of proline‐directed kinases capable of phosphorylating paired helical filament‐Tau, glycogen synthase kinase 3β (GSK3β) was first identified as a Tau protein kinase I and has been demonstrated to phosphorylate Tau both in vivo and in vitro. However, the phosphorylation mechanism of Tau by GSK3β remained unclear. In this study, we show that the T231 is the primary phosphorylation site for GSK3β and the Tau227–237 (AVVRTPPKSPS) derived from Tau containing T231P232 motif is identified as the GSK3β binding site with high affinity of a Kd value 0.82 ± 0.16 μmol/L. Our results suggest that direct binding and phosphorylation of T231P232 motif by GSK3β induces conformational change of Tau and consequentially alters the inhibitory activity of its N‐terminus that allows the phosphorylation of C‐terminus of Tau by GSK3β. Furthermore, hyperphosphorylation reduces Tau’s ability to promote tubulin assembly and to form bundles in N18 cells. T231A mutant completely abolishes Tau phosphorylation by GSK3β and retains the ability to promote tubulin polymerization and bundle formation. Taken together, these results suggest that phosphorylation of T231 by GSK3β may play an important role in Tau’s hyperphosphorylation and functional regulation.
Functional and immunocytochemical evidence for the expression and localization of the secretory pathway Ca2+‐ATPase isoform 1 (SPCA1) in cerebellum relative to other Ca2+ pumps
Authors: Sepúlveda M. Rosario , Berrocal María , Marcos Daniel , Wuytack Frank , Mata Ana M. 
Published: August 2007

AbstractMembrane fractions of pig cerebellum show Ca2+‐ATPase activdity and Ca2+ transport due to the presence of the secretory pathway Ca2+‐ATPase (SPCA). The SPCA1 isoform shows a wide distribution in the neurons of pig cerebellum, where it is found in the Golgi complex of the soma of Purkinje, stellate, basket and granule cells, and also in more distal components of the secretory pathway associated with a synaptic localization such as in cerebellar glomeruli. The SPCA1 may be involved in loading the Golgi complex and the secretory vesicles of these specific neuronal cell types with Ca2+ and also Mn2+. This study of the cellular and subcellular localization of SPCA1 pumps relative to the sarco(endo) plasmic reticulum Ca2+‐ATPase and plasma membrane Ca2+‐ATPase pumps hints to a possible specific role of SPCA1 in controlling the luminal secretory pathway Ca2+ (or Mn2+) levels as well as the local cytosolic Ca2+ levels. In addition, it helps to specify the zones that are most vulnerable to Ca2+ and/or Mn2+ dyshomeostasis, a condition that is held responsible of an increasing number of neurological disorders.
Peroxisome proliferator‐activated receptor‐alpha is required for the neurotrophic effect of oleic acid in neurons
Authors: Bento‐Abreu André , Tabernero Arantxa , Medina José M. 
Published: August 2007

AbstractOleic acid synthesized by astrocytes behaves as a neurotrophic factor for neurons, up‐regulating the molecular markers of axonal and dendritic outgrowth, growth‐associated protein 43 and microtubule‐associated protein 2. In this work, the nature of the receptor involved in this neurotrophic effect was investigated. As oleic acid has been reported to be a ligand and activator of the peroxisome proliferator‐activated receptor (PPAR), we focus on this family of receptors. Our results show that PPARα, β/δ, and γ are expressed in neurons in culture. However, only the agonists of PPARα, Wy14643, GW7647 and oleoylethanolamide, promoted neuronal differentiation, while PPAR β/δ and γ agonists did not modify neuronal differentiation. Consequently, we investigated the involvement of PPARα (Nr1c1) in oleic acid‐induced neuronal differentiation. Our results indicate that oleic acid activates PPARα in neurons. In addition, the effect of oleic acid on neuronal morphology, growth‐associated protein 43 and microtubule‐associated protein 2 expression decreases in neurons after PPARα has been silenced by small interfering RNA. Taken together, our results suggest that PPARα could be the receptor for oleic acid in neurons, further broadening the range of functions attributed to this family of transcription factors. Although several works have reported that PPARα could be involved in neuroprotection, the present work provides the first evidence suggesting a role of PPARα in neuronal differentiation.
Pituitary adenylate cyclase‐activating polypeptide induces translocation of its G‐protein‐coupled receptor into caveolin‐enriched membrane microdomains, leading to enhanced cyclic AMP generation and neurite outgrowth in PC12 cells
Authors: Zhang Weishi , Duan Wei , Cheung Nam Sang , Huang Zhili , Shao Ke , Li Qiu‐Tian 
Published: August 2007

AbstractPituitary adenylate cyclase‐activating polypeptide (PACAP), a member of the secretin/glucagon/vasoactive intestinal peptide family expressed throughout the nervous system, binds to the PACAP‐specific G‐protein‐coupled receptor family members to promote both neuronal differentiation and survival. Although the PACAP receptor is known to activate its effector protein, adenylate cyclase (AC), and thus enhance cAMP generation, the molecular mechanism utilized by the receptor to activate AC is lacking. Here, we show that PACAP induces neurite outgrowth in PC12 cells by induction of translocation of the PACAP type 1 receptor (PAC1R) into caveolin‐enriched Triton X‐100‐insoluble microdomains, leading to stronger PAC1R‐AC interaction and elevated cAMP production. Moreover, we demonstrate that translocation of PAC1R is blocked by various treatments that selectively disrupt caveolae. As a result, intracellular cAMP level is decreased and consequently the PACAP‐induced neurite outgrowth retarded. In contrast, addition of exogenous ganglioside GM1 to the cells shows the opposite effects. These results therefore identify the PACAP‐induced translocation of its G‐protein‐coupled receptor into caveolae, where both AC and the regulating G‐proteins reside, as the key molecular event in activating AC and inducing cAMP‐mediated differentiation of PC12 cells.
The expression of L‐type voltage‐gated calcium channels in retinal photoreceptors is under circadian control
Authors: Ko Michael L. , Liu Yilin , Dryer Stuart E. , Ko Gladys Y.‐P. 
Published: August 2007

AbstractPhotoreceptors are non‐spiking neurons, and their synapses mediate the continuous release of neurotransmitters under the control of L‐type voltage‐gated calcium channels (VGCCs). Photoreceptors express endogenous circadian oscillators that play important roles in regulating photoreceptor physiology and function. Here, we report that the L‐type VGCCs in chick cone photoreceptors are under circadian control. The L‐type VGCC currents are greater when measured during the subjective night than during the subjective day. Using antibodies against the VGCCα1C and VGCCα1D subunits, we found that the immunofluorescence intensities of both VGCCα1C and VGCCα1D in photoreceptors are higher during the subjective night. However, the mRNA levels of VGCCα1D, but not VGCCα1C, are rhythmic. Nocturnal increases in L‐type VGCCs are blocked by manumycin A, PD98059, and KN93, which suggest that the circadian output pathway includes Ras, Erk, and calcium‐calmodulin dependent kinase II. In summary, four independent lines of evidence show that the L‐VGCCs in cone photoreceptors are under circadian control.
Collapsin response mediator protein‐2 hyperphosphorylation is an early event in Alzheimer’s disease progression
Authors: Cole Adam R. , Noble Wendy , Aalten Lidy van , Plattner Florian , Meimaridou Rena , Hogan Dale , Taylor Margaret , LaFrancois John , Gunn‐Moore Frank , Verkhratsky Alex , Oddo Salvatore , LaFerla Frank , Giese K. Peter , Dineley Kelly T. , Duff Karen , Richardson Jill C. , Yan Shi Du , Hanger Diane P. , Allan Stuart M. , Sutherland Calum 
Published: August 2007

AbstractCollapsin response mediator protein 2 (CRMP2) is an abundant brain‐enriched protein that can regulate microtubule assembly in neurons. This function of CRMP2 is regulated by phosphorylation by glycogen synthase kinase 3 (GSK3) and cyclin‐dependent kinase 5 (Cdk5). Here, using novel phosphospecific antibodies, we demonstrate that phosphorylation of CRMP2 at Ser522 (Cdk5‐mediated) is increased in Alzheimer’s disease (AD) brain, while CRMP2 expression and phosphorylation of the closely related isoform CRMP4 are not altered. In addition, CRMP2 phosphorylation at the Cdk5 and GSK3 sites is increased in cortex and hippocampus of the triple transgenic mouse [presenilin‐1 (PS1)M146VKI; Thy1.2‐amyloid precursor protein (APP)swe; Thy1.2tauP301L] that develops AD‐like plaques and tangles, as well as the double (PS1M146VKI; Thy1.2‐APPswe) transgenic mouse. The hyperphosphorylation is similar in magnitude to that in human AD and is evident by 2 months of age, ahead of plaque or tangle formation. Meanwhile, there is no change in CRMP2 phosphorylation in two other transgenic mouse lines that display elevated amyloid β peptide levels (Tg2576 and APP/amyloid β‐binding alcohol dehydrogenase). Similarly, CRMP2 phosphorylation is normal in hippocampus and cortex of Tau(P301L) mice that develop tangles but not plaques. These observations implicate hyperphosphorylation of CRMP2 as an early event in the development of AD and suggest that it can be induced by a severe APP over‐expression and/or processing defect.
A rapid oxidation and persistent decrease in the vesicular monoamine transporter 2 after methamphetamine
Authors: Eyerman David J. , Yamamoto Bryan K. 
Published: August 2007

AbstractMethamphetamine (METH) produces long‐term decreases in markers of dopamine (DA) terminals in animals and humans. A decrease in the function of the vesicular monoamine transporter 2 (VMAT2) has been associated with damage to striatal DA terminals caused by METH; however, a possible mechanism for this decrease in VMAT2 function has not been defined. The current study showed that METH caused a rapid decrease to 68% of controls in VMAT2 protein immunoreactivity of the vesicular fraction from striatal synaptosomes within 1 h after a repeated high‐dose administration regimen of METH. This decrease was associated with a 75% increase in nitrosylation of VMAT2 protein in the synaptosomal fraction as measured by nitrosocysteine immunoreactivity of VMAT2 protein. The rapid decreases in VMAT2 persisted when evaluated 7 days later and were illustrated by decreases in VMAT2 immunoreactivity and DA content of the vesicular fraction to 34% and 51% of control values, respectively. The decreases were blocked or attenuated by prior injections of the neuronal nitric oxide synthase inhibitor,S‐methyl‐l‐thiocitrulline. These studies demonstrate that METH causes a rapid neuronal nitric oxide synthase‐dependent oxidation of VMAT2 and long‐term decreases in VMAT2 protein and function. The results also suggest that surviving DA terminals after METH exposure may have a compromised capacity to buffer cytosolic DA concentrations and DA‐derived oxidative stress.
NO‐induced neuroprotection in ischemic preconditioning stimulates mitochondrial Mn‐SOD activity and expression via RAS/ERK1/2 pathway
Authors: Scorziello A. , Santillo M. , Adornetto A. , Dell’Aversano C. , Sirabella R. , Damiano S. , Canzoniero L.M.T. , Renzo G.F. Di , Annunziato L. 
Published: August 2007

AbstractTo identify the transductional mechanisms responsible for the neuroprotective effect of nitric oxide (NO) during ischemic preconditioning (IPC), we investigated the effects of this gaseous mediator on mitochondrial Mn‐superoxide dismutase (Mn‐SOD) expression and activity. In addition, the possible involvement of Ras/extracellular‐regulated kinase (ERK) ERK1/2 pathway in preserving cortical neurons exposed to oxygen and glucose deprivation (OGD) followed by reoxygenation was also examined. Ischemic preconditioning was obtained by exposing neurons to a 30‐min sublethal OGD (95% N2 and 5% CO2). Then, after a 24‐h interval, neurons were exposed to 3 h of OGD followed by 24 h of reoxygenation (OGD/Rx). Our results revealed that IPC reduced cytochrome c (cyt c) release into the cytosol, improved mitochondrial function, and decreased free radical production. Moreover, it induced an increase in nNOS expression and NO production and promoted ERK1/2 activation. These effects were paralleled by an increase in Mn‐SOD expression and activity that persisted throughout the following OGD phase. When the neurons were treated with L‐NAME, a well known NOS inhibitor, the increase in Mn‐SOD expression occurring during IPC was reduced and, as a result, IPC‐induced neuroprotection was prevented. Similarly, when ERK1/2 was inhibited by its selective inhibitor PD98059, the increase in Mn‐SOD expression observed during IPC was almost completely abolished. As a result, its neuroprotective effect on cellular survival was thwarted. The present findings indicate that during IPC the increase in Mn‐SOD expression and activity are paralleled by NO production. This suggests that NO neuroprotective role occurs through the stimulation of Mn‐SOD expression and activity. In particular, NO via Ras activation stimulates downstream ERK1/2 cascade. This pathway, in turn, post‐transcriptionally activates Mn‐SOD expression and activity, thus promoting neuroprotection during preconditioning.
Activation of phospholipase C pathways by a synthetic chondroitin sulfate‐E tetrasaccharide promotes neurite outgrowth of dopaminergic neurons
Authors: Sotogaku Naoki , Tully Sarah E. , Gama Cristal I. , Higashi Hideho , Tanaka Masatoshi , Hsieh‐Wilson Linda C. , Nishi Akinori 
Published: August 2007

AbstractIn dopaminergic neurons, chondroitin sulfate (CS) proteoglycans play important roles in neuronal development and regeneration. However, due to the complexity and heterogeneity of CS, the precise structure of CS with biological activity and the molecular mechanisms underlying its influence on dopaminergic neurons are poorly understood. In this study, we investigated the ability of synthetic CS oligosaccharides and natural polysaccharides to promote the neurite outgrowth of mesencephalic dopaminergic neurons and the signaling pathways activated by CS. CS‐E polysaccharide, but not CS‐A, ‐C or ‐D polysaccharide, facilitated the neurite outgrowth of dopaminergic neurons at CS concentrations within the physiological range. The stimulatory effect of CS‐E polysaccharide on neurite outgrowth was completely abolished by its digestion into disaccharide units with chondroitinase ABC. Similarly to CS‐E polysaccharide, a synthetic tetrasaccharide displaying only the CS‐E sulfation motif stimulated the neurite outgrowth of dopaminergic neurons, whereas a CS‐E disaccharide or unsulfated tetrasaccharide had no effect. Analysis of the molecular mechanisms revealed that the action of the CS‐E tetrasaccharide was mediated through midkine‐pleiotrophin/protein tyrosine phosphatase ζ and brain‐derived neurotrophic factor/tyrosine kinase B receptor pathways, followed by activation of the two intracellular phospholipase C (PLC) signaling cascades: PLC/protein kinase C and PLC/inositol 1,4,5‐triphosphate/inositol 1,4,5‐triphosphate receptor signaling leading to intracellular Ca2+ concentration‐dependent activation of Ca2+/calmodulin‐dependent kinase II and calcineurin. These results indicate that a specific sulfation motif, in particular the CS‐E tetrasaccharide unit, represents a key structural determinant for activation of midkine, pleiotrophin and brain‐derived neurotrophic factor‐mediated signaling, and is required for the neuritogenic activity of CS in dopaminergic neurons.
Exopolymeric substances of sulfate‐reducing bacteria: Interactions with calcium at alkaline pH and implication for formation of carbonate minerals
Authors: BRAISSANT O. , DECHO A. W. , DUPRAZ C. , GLUNK C. , PRZEKOP K. M. , VISSCHER P. T. 
Published: August 2007

ABSTRACTSulfate‐reducing bacteria (SRB) have been recognized as key players in the precipitation of calcium carbonate in lithifying microbial communities. These bacteria increase the alkalinity by reducing sulfate ions, and consuming organic acids. SRB also produce copious amounts of exopolymeric substances (EPS). All of these processes influence the morphology and mineralogy of the carbonate minerals. Interactions of EPS with metals, calcium in particular, are believed to be the main processes through which the extracellular matrix controls the precipitation of the carbonate minerals. SRB exopolymers were purified from lithifying mat and type cultures, and their potential role in CaCO3 precipitation was determined from acid‐base titrations and calcium‐binding experiments. Major EPS characteristics were established using infrared spectroscopy and gas chromatography to characterize the chemical functional groups and the sugar monomers composition. Our results demonstrate that all of the three SRB strains tested were able to produce large amounts of EPS. This EPS exhibited three main buffering capacities, which correspond to carboxylic acids (pKa = 3.0), sulfur‐containing groups (thiols, sulfonic and sulfinic acids – pKa = 7.0–7.1) and amino groups (pKa = 8.4–9.2). The calcium‐binding capacity of these exopolymers in solution at pH 9.0 ranged from 0.12gCa gEPS−1–0.15 gCa gEPS−1. These results suggest that SRB could play a critical role in the formation of CaCO3 in lithifying microbial mats. The unusually high sulfur content, which has not been reported for EPS before, indicates a possible strong interaction with iron. In addition to changing the saturation index through metabolic activity, our results imply that SRB affect the rock record through EPS production and its effect on the CaCO3 precipitation. Furthermore, EPS produced by SRB may account for the incorporation of metals (e.g. Sr, Fe, Mg) associated with carbonate minerals in the rock record.