bluuebunny/crossref_metadata_2025 huggingface dataset:
The heritability of P300 amplitude in 18‐year‐olds is robust to adolescent alcohol use
Authors: Perlman Greg , Johnson Wendy , Iacono William G.
Published: June 2009

P3 amplitude reduction (P3AR) is associated with adolescent alcohol use (AAU) and highly heritable, suggesting that P3AR may index a genetic predisposition (e.g., an endophenotype) for AAU. However, because P3AR and AAU covary naturally in the population, these observations are also consistent with P3AR reflecting neurotoxic effects of AAU on the developing adolescent brain. In this report, we describe the use of recent advancements in biometric modeling to examine changes in the genetic and environmental contributions to variability in P3 amplitude related to cumulative AAU by late adolescence in a large community‐based twin sample. We found that the genetic and environmental contributions to variability in P3 amplitude were unaffected by AAU. This suggests that P3AR indexes risk for alcoholism independent of any deleterious effect of AAU on adolescent brain development.
Aging effects on early‐stage face perception: An ERP study
Authors: Gao Lei , Xu Jing , Zhang Bingwei , Zhao Lun , Harel Assaf , Bentin Shlomo
Published: June 2009

We compared early stages of face processing in young and older participants as indexed by ERPs elicited by faces and non‐face stimuli presented in upright and inverted orientations. The P1 and N170 components were larger in older than in young participants. However, the early distinction between stimulus categories as reflected by N170 face was similar across groups. Face inversion increased and delayed the N170 peak in the younger group while in older participants inversion delayed the N170 peak but had no effect on amplitude. The N170 amplitude was right‐lateralized in the young, but not in the older group. Yet, the difference between the N170 elicited by faces and non‐face stimuli was similarly right‐lateralized in both groups. These data suggest that detection of faces and their streaming to face‐characteristic structural encoding is not altered by age. In contrast, the absence of face‐inversion effects on N170 amplitudes in the elderly suggest that face individuation, which is probably the default strategy in younger people, might not be attempted by default in older people, at least when they look at young faces.
Cuban Labour at 50: What About the Workers?
Authors: LUDLAM STEVE
Published: June 2009

Cuba is reforming its employment relations as it emerges from the economic crisis and restructuring of the 1990s. Employment relations are one key indicator of the state of Cuba's socialist ambition as it celebrates the 50th anniversary of the Revolution. Several key aspects of recent employment law and salary reform are discussed. It is argued that, within a state‐dominated economy, Cuba's workers and trade unions continue to exercise real influence, both in national policy‐making and in workplaces.
Tomás Gutiérrez Alea and the Art of Revolutionary Cinema
Authors: WOOD DAVID
Published: June 2009

Tomás Gutiérrez Alea has been widely acclaimed for his cinematic production and for his role as a key figure in the elaboration of a distinctively Cuban aesthetic. Drawing on notions such as Martín‐Barbero's mediations, Billig's banal nationalism, and Gutiérrez Alea's own viewer's dialectic, consideration is given here to the mutual influences of the Revolution's cultural policies on cinema, and of cinema on the Revolution. Analysis will focus on the films Memorias del subdesarrollo (1968), Hasta cierto punto (1983), Fresa y chocolate (1993) and Guantanamera (1995), which will allow for discussion of some of the director's key themes, including gender issues, the place and role of intellectuals and artists in relation to the Revolution, and the defence of a critical space in which to explore such issues.
An information behaviour investigation of the community pharmacists in Greece for developing library and information services
Authors: Kostagiolas P. A. , Bairaktaris K. D. , Niakas D.
Published: June 2009

Background and objectives:  Community pharmacists require a constant provision of high quality information for updating their knowledge and improving their practices and skills. The development of library and information services for the pharmacists in a meaningful way should take into consideration their information behaviour and needs. This study is an investigation of the information behaviour of community pharmacists in Greece, as well as their perceptions regarding the contribution of library and information services in their future professional development. This is the only empirical investigation which has been made available regarding the information behaviour of the community pharmacists in Greece.

Methods:  An empirical investigation has been conducted between March and April of 2008 through the development and the distribution of a semi‐structured questionnaire. The sample of the respondents consists of 92 community pharmacists from 22 pharmacy associations in Greece.

Results:  The community pharmacists have access to the Internet, with limited access to specialized information resources, and they are increasingly utilizing information services in their everyday practices. The pharmaceutical associations (national and local) could play a significant role as information providers and specialized hybrid libraries and information services are required in order to satisfy the current information needs of the community pharmacists.

Conclusions:  Meaningful library and information services depend on setting specifications relevant to the community pharmacists’ information behaviour. Indeed, in the near future, structured information services may come to rescue the role of the community pharmacists and empower their irreplaceable position in serving the local communities.
F‐spondin plays a critical role in murine neuroblastoma survival by maintaining IL‐6 expression
Authors: Cheng Yung‐Chih , Liang Chi‐Ming , Chen Yen‐Po , Tsai Inn‐Ho , Kuo Cheng‐Chin , Liang Shu‐Mei
Published: June 2009

F‐spondin is associated with the regulation of axonal growth and the development of the nervous system. Its mechanism of action, however, is not clearly understood. In this study, we found that murine neuroblastoma Neuro‐2a cells expressed a significant level of IL‐6, but only trace amounts of IL‐12, tumor necrosis factor α and nitric oxide. Knock‐down of F‐spondin mRNA in murine neuroblastoma NB41A3 and Neuro‐2a cells using small interfering RNAs led to decreased IL‐6 levels along with lower resistance to serum starvation and cytotoxic amyloid β1–42 (Aβ1–42) peptide. Restoring decline of F‐spondin or IL‐6 induced by F‐spondin knock‐down through adding exogenous F‐spondin, IL‐6 or over‐expressing F‐spondin reversed the cell death induced by Aβ1–42 peptide or serum starvation. The decrease of IL‐6 level was positively correlated with decrease of NF‐κB and inhibition of p38 mitogen‐activated protein kinase (MAPK). Over‐expressing MEKK, a kinase activator of the p38 MAPK pathway, increased IL‐6 production, restored the decrease of p38 induced by F‐spondin knock‐down, and rescued the cells from death caused by Aβ1–42 peptide. Taken together, these results suggest that F‐spondin may play a critical role in murine neuroblastoma survival under adverse conditions by maintaining IL‐6 level via a MEKK/p38 MAPK/NF‐κB‐dependent pathway.
l‐Aspartate as an amino acid neurotransmitter: mechanisms of the depolarization‐induced release from cerebrocortical synaptosomes
Authors: Cavallero Anna , Marte Antonella , Fedele Ernesto
Published: June 2009

The role ofl‐aspartate as a classical neurotransmitter of the CNS has been a matter of great debate. In this study, we have characterized the main mechanisms of its depolarization‐induced release from rat purified cerebrocortical synaptosomes in superfusion and compared them with those of the well‐known excitatory neurotransmitterl‐glutamate. High KCl and 4‐aminopyridine were used as depolarizing agents. At 15 mM KCl, the overflows of both transmitters were almost completely dependent on external Ca2+. At 35 and 50 mM KCl, the overflows ofl‐aspartate, but not those ofl‐glutamate, became sensitive todl‐threo‐β‐benzyloxyaspartic acid (dl‐TBOA), an excitatory amino acid transporter inhibitor. In the presence ofdl‐TBOA, the 50 mM KCl‐evoked release ofl‐aspartate was still largely external Ca2+‐dependent. Thedl‐TBOA insensitive, external Ca2+‐independent component of the 50 mM KCl‐evoked overflows ofl‐aspartate andl‐glutamate was significantly decreased by the mitochondrial Na+/Ca2+exchanger blocker CGP 37157. The Ca2+‐dependent, KCl‐evoked overflows ofl‐aspartate andl‐glutamate were diminished by botulinum neurotoxin C, although to a significantly different extent. The 4‐aminopyridine‐inducedl‐aspartate andl‐glutamate release was completely external Ca2+‐dependent and never affected bydl‐TBOA. Superimposable results have been obtained by pre‐labeling synaptosomes with [3H]d‐aspartate and [3H]l‐glutamate. Therefore, our data showing thatl‐aspartate is released from nerve terminals by calcium‐dependent, exocytotic mechanisms support the neurotransmitter role of this amino acid.
A highly conserved tryptophan residue in the fourth transmembrane domain of the A1 adenosine receptor is essential for ligand binding but not receptor homodimerization
Authors: Suzuki Tokiko , Namba Kazunori , Yamagishi Ryosuke , Kaneko Hiroki , Haga Tatsuya , Nakata Hiroyasu
Published: June 2009

Dimerization between G protein‐coupled receptors (GPCRs) is a clearly established phenomenon. However, limited information is currently available on the interface essential for this process. Based on structural comparisons and sequence homology between rhodopsin and A1 adenosine receptor (A1R), we initially hypothesized that four residues in transmembrane (TM) 4 and TM5 are involved in A1R homodimerization. Accordingly, these residues were substituted with Ala by site‐directed mutagenesis. Interestingly, the mutant protein displayed no significant decrease in homodimer formation compared with wild‐type A1R, as evident from coimmunoprecipitation and BRET2 analyses (improved bioluminescence resonance energy transfer system offered by Perkin‐Elmer Life Sciences), but lost ligand binding activity almost completely. Further studies disclosed that this effect was derived from the mutation of one particular residue, Trp132, which is highly conserved among many GPCRs. Confocal immunofluorescence and cell‐surface biotinylation studies revealed that the mutant receptors localized normally at transfected cell membranes, signifying that loss of ligand binding was not because of defective cellular trafficking. Molecular modeling of the A1R‐ligand complex disclosed that Trp132 interacted with several residues located in TM3 and TM5 that stabilized agonist binding. Thus, loss of interactions of Trp with these residues may, in turn, disrupt binding to agonists. Our study provides strong evidence of the essential role of the highly conserved Trp132 in TM4 of adenosine receptors.
The SIRT1 activator resveratrol protects SK‐N‐BE cells from oxidative stress and against toxicity caused by α‐synuclein or amyloid‐β (1‐42) peptide
Authors: Albani Diego , Polito Letizia , Batelli Sara , De Mauro Stefania , Fracasso Claudia , Martelli Giuliana , Colombo Laura , Manzoni Claudia , Salmona Mario , Caccia Silvio , Negro Alessandro , Forloni Gianluigi
Published: June 2009

Human sirtuins are a family of seven conserved proteins (SIRT1‐7). The most investigated is the silent mating type information regulation‐2 homolog (SIRT1, NM_012238), which was associated with neuroprotection in models of polyglutamine toxicity or Alzheimer’s disease (AD) and whose activation by the phytocompound resveratrol (RES) has been described. We have examined the neuroprotective role of RES in a cellular model of oxidative stress, a common feature of neurodegeneration. RES prevented toxicity triggered by hydrogen peroxide or 6‐hydroxydopamine (6‐OHDA). This action was likely mediated by SIRT1 activation, as the protection was lost in the presence of the SIRT1 inhibitor sirtinol and when SIRT1 expression was down‐regulated by siRNA approach. RES was also able to protect SK‐N‐BE from the toxicity arising from two aggregation‐prone proteins, the AD‐involved amyloid‐β (1‐42) peptide (Aβ42) and the familiar Parkinson’s disease linked α‐synuclein(A30P) [α‐syn(A30P)]. Alpha‐syn(A30P) toxicity was restored by sirtinol addition, while a partial RES protective effect against Aβ42 was found even in presence of sirtinol, thus suggesting a direct RES effect on Aβ42 fibrils. We conclude that SIRT1 activation by RES can prevent in our neuroblastoma model the deleterious effects triggered by oxidative stress or α‐syn(A30P) aggregation, while RES displayed a SIRT1‐independent protective action against Aβ42.
Subcellular compartment‐specific molecular diversity of pre‐ and post‐synaptic GABAB‐activated GIRK channels in Purkinje cells
Authors: Fernández‐Alacid Laura , Aguado Carolina , Ciruela Francisco , Martín Ricardo , Colón José , Cabañero María José , Gassmann Martin , Watanabe Masahiko , Shigemoto Ryuichi , Wickman Kevin , Bettler Bernhard , Sánchez‐Prieto José , Luján Rafael
Published: June 2009

Activation of G protein‐gated inwardly‐rectifying K+ (GIRK or Kir3) channels by metabotropic gamma‐aminobutyric acid (B) (GABAB) receptors is an essential signalling pathway controlling neuronal excitability and synaptic transmission in the brain. To investigate the relationship between GIRK channel subunits and GABAB receptors in cerebellar Purkinje cells at post‐ and pre‐synaptic sites, we used biochemical, functional and immunohistochemical techniques. Co‐immunoprecipitation analysis demonstrated that GIRK subunits are co‐assembled with GABAB receptors in the cerebellum. Immunoelectron microscopy showed that the subunit composition of GIRK channels in Purkinje cell spines is compartment‐dependent. Thus, at extrasynaptic sites GIRK channels are formed by GIRK1/GIRK2/GIRK3, post‐synaptic densities contain GIRK2/GIRK3 and dendritic shafts contain GIRK1/GIRK3. The post‐synaptic association of GIRK subunits with GABAB receptors in Purkinje cells is supported by the subcellular regulation of the ion channel and the receptor in mutant mice. At pre‐synaptic sites, GIRK channels localized to parallel fibre terminals are formed by GIRK1/GIRK2/GIRK3 and co‐localize with GABAB receptors. Consistent with this morphological evidence we demonstrate their functional interaction at axon terminals in the cerebellum by showing that GIRK channels play a role in the inhibition of glutamate release by GABAB receptors. The association of GIRK channels and GABAB receptors with excitatory synapses at both post‐ and pre‐synaptic sites indicates their intimate involvement in the modulation of glutamatergic neurotransmission in the cerebellum.
Oxidized phosphatidylcholine formation and action in oligodendrocytes
Authors: Qin Jingdong , Testai Fernando D , Dawson Sylvia , Kilkus John , Dawson Glyn
Published: June 2009

Reactive oxygen species play a major role in neurodegeneration. Increasing concentrations of peroxide induce neural cell death through activation of pro‐apoptotic pathways. We now report that hydrogen peroxide generated sn‐2 oxidized phosphatidylcholine (OxPC) in neonatal rat oligodendrocytes and that synthetic OxPC [1‐palmitoyl‐2‐(5′‐oxo)valeryl‐sn‐glycero‐3 phosphorylcholine, POVPC] also induced apoptosis in neonatal rat oligodendrocytes. POVPC activated caspases 3 and 8, and neutral sphingomyelinase (NSMase) but not acid sphingomyelinase. Downstream pro‐apoptotic pathways activated by POVPC treatment included the Jun N‐terminal kinase proapoptotic cascade and the degradation of phospho‐Akt. Activation of NSMase occurred within 1 h, was blocked by inhibitors of caspase 8, increased mainly C18 and C24:1 ceramides, and appeared to be concentrated in detergent‐resistant microdomains (Rafts). We concluded that OxPC initially activated NSMase and converted sphingomyelin into ceramide to mediate a series of downstream pro‐apoptotic events in oligodendrocytes.
Stress hormones collaborate to induce lymphocyte apoptosis after high level spinal cord injury
Authors: Lucin Kurt M. , Sanders Virginia M. , Popovich Phillip G.
Published: June 2009

Post‐traumatic immune suppression renders individuals with spinal cord injury (SCI) susceptible to infection. Normally, proper immune function is regulated by collaboration between the sympathetic nervous system (SNS) and hypothalamic–pituitary–adrenal (HPA) axis and involves the controlled release of glucocorticoids (GCs) and norepinephrine (NE). Recently, we showed that after high thoracic (T3) SCI, aberrant levels of GCs and NE accumulate in the blood and spleen, respectively. These changes are associated with splenic atrophy, splenic leucopenia, increased intrasplenic caspase 3 levels, and suppressed B lymphocyte function. As GCs boost SNS function, in part by increasing the expression and affinity of β2 adrenergic receptors (β2ARs) while simultaneously preventing β2AR down‐regulation, we predicted that surges in stress hormones (i.e., GCs and NE) in the blood and spleen of mice with high‐level SCI would act concurrently to adversely affect lymphocyte function and survival. Here, we show that post‐SCI concentrations of GCs enhance the sensitivity of lymphocytes to β2AR stimulation causing an increase in intracellular Bcl‐2 interacting mediator of cell death (Bim) and subsequent apoptosis.In vivo, the combined antagonism of GC receptors and β2ARs significantly diminished lymphocyte Bim levels and SCI‐induced splenic lymphopenia. Together, these data suggest that pharmacological antagonists of the HPA/SNS axes should be considered as adjunct therapies for ameliorating post‐traumatic immune suppression in quadriplegics and high paraplegics.
Morphine withdrawal regulates phosphorylation of cAMP response element binding protein (CREB) through PKC in the nucleus tractus solitarius‐A2catecholaminergic neurons
Authors: Martín Fátima , Laorden M. Luisa , Milanés M. Victoria
Published: June 2009

The transcription factor cAMP response element binding protein (CREB) has been implicated in the actions of drugs of abuse in several brain areas. However, little is known about CREB regulation in the nucleus tractus solitarius (NTS)‐A2catecholaminergic cell group, one of the key regions of the brain stress system. Morphine withdrawal modulates gene expression in the NTS through various second‐messenger signal transduction systems including activation of extracellular signal‐regulated kinases 1/2 (ERK1/2) and protein kinase C (PKC). In the current study we used immunoblotting and immunohistochemistry to investigate changes in CREB phosphorylation in the NTS and kinases that may mediate the morphine withdrawal‐triggered activation of CREB and hypothalamo‐pituitary‐adrenocortical (HPA) axis (another stress system circuit) response after naloxone‐induced morphine withdrawal. We found an increased phosphorylation of CREB (pCREB) selectively within tyrosine hydroxylase (TH) immunoreactive neurons in the NTS from morphine‐withdrawn rats, which parallel elevated corticosterone levels. We also measured expression levels of TH and phosphorylated ERK1/2(pERK1/2), and found that both are up‐regulated following morphine withdrawal. SL327, an inhibitor of ERK activation, at doses which reduced the hyperactive pERK1/2levels, did not attenuated the rise in pCREB and TH immunoreactivity or plasma corticosterone secretion during morphine withdrawal, indicating that ERK kinase/ERK pathway was not directly needed for either activation of CREB and TH expression in the NTS or HPA axis hyperactivity. In contrast, PKC inhibitor calphostin C reduced the withdrawal‐triggered rise in pCREB, pERK1/2, TH expression and corticosterone secretion. The results indicate that PKC mediates both CREB activation and HPA response by morphine withdrawal and might suggest that CREB activation in the NTS is related to TH expression associated with morphine withdrawal.
Leucine‐rich repeat kinase 2 phosphorylates brain tubulin‐beta isoforms and modulates microtubule stability – a point of convergence in Parkinsonian neurodegeneration?
Authors: Gillardon Frank
Published: June 2009

Autosomal dominant mutations in leucine‐rich repeat kinase 2 (LRRK2) are the most common genetic cause of late‐onset Parkinson’s disease. The most prevalent LRRK2(G2019S) mutation has repeatedly been shown to enhance kinase activity and neurotoxicity, however, the molecular mechanisms leading to neurodegeneration remain poorly defined. Here we show that recombinant human LRRK2 preferentially phosphorylates tubulin‐beta purified from bovine brain and that phosphorylation is three‐fold enhanced by the LRRK2(G2019S) mutation. By tandem mass spectrometry, Thr107 was identified as phosphorylation site which is highly conserved between tubulin‐beta family members and also between tubulin‐beta genes of different species. LRRK2 was co‐immunoprecipitated with tubulin‐beta both from wild‐type mouse brain and from LRRK2 over‐expressing, non‐neuronal human embryonic kidney 293 cells. However, an effect of LRRK2 on tubulin phosphorylation and assembly was only detectable in mouse brain samples. In vitro co‐incubation of bovine brain tubulins with LRRK2 increased microtubule stability in the presence of microtubule‐associated proteins which may explain the reduction in neurite length in LRRK2‐deficient neurons in culture. These findings suggest that LRRK2(G2019S)‐induced neurodegeneration in Parkinsonian brains may be partly mediated by increased phosphorylation of tubulin‐beta and constraining of microtubule dynamics.
Activation of the histaminergic H3receptor induces phosphorylation of the Akt/GSK‐3β pathway in cultured cortical neurons and protects against neurotoxic insults
Authors: Mariottini Chiara , Scartabelli Tania , Bongers Gerold , Arrigucci Silvia , Nosi Daniele , Leurs Rob , Chiarugi Alberto , Blandina Patrizio , Pellegrini‐Giampietro Domenico E. , Beatrice Passani Maria
Published: June 2009

Stimulation of histamine H3receptors (H3R) activates Gi/o‐proteins that inhibit adenylyl cyclase and triggers MAPK and phospholipase A2. In a previous study, we showed that H3R‐mediated phosphorylation of Akt at Ser473 occurs in primary cultures of rat cortical neurons, but neither the downstream targets nor the function of such activation were explored. In this report we address these questions. Western blotting experiments showed that H3R‐mediated activation of Akt in cultured rat cortical neurons was inhibited by LY 294004 and U0126, suggesting that it depends on phosphoinositide‐3‐kinase and mitogen‐activated protein kinase kinase. H3R activation phosphorylated, hence inactivated, the Akt downstream effector glycogen synthase kinase‐3β, increased the expression of the antiapoptotic protein Bcl‐2 and protected cultured rat and mouse cortical neurons from neurotoxic insults in a dose‐dependent manner. All these effects were inhibited by the H3R antagonist inverse/agonist thioperamide. Mouse cortical cells expressed H3R as revealed by immunostaining experiments, and stimulation of H3R phoshorylated Akt and decreased caspase 3 activity. Hence, we uncovered a yet unexplored action of the H3R that may help understand the impact of H3R signaling in the CNS.
Functional dissection of the α‐synuclein promoter: transcriptional regulation by ZSCAN21 and ZNF219
Authors: Clough Richard Lee , Dermentzaki Georgia , Stefanis Leonidas
Published: June 2009

Alpha‐Synuclein (SNCA) is an abundant neuronal protein involved in synaptic neurotransmission. SNCA expression levels have been strongly implicated in Parkinson’s disease pathogenesis. We have previously demonstrated that in the PC12 cell line elements in intron 1 may mediate SNCA transcriptional regulation in response to neurotrophins. We have now identified transcription factor (TF) binding sites in intron 1 and the 5′‐promoter of SNCA. A binding site for the TF zinc finger and SCAN domain containing (ZSCAN)21 in the 5′‐region of intron 1 is required for intron 1 transcriptional activity. Small interfering RNA against ZSCAN21 inhibits activation in the luciferase assay and diminishes SNCA protein levels in naïve and neurotrophin‐treated PC12 cells and in primary cultured cortical neurons, demonstrating that ZSCAN21 is a novel transcriptional regulator of SNCA in neuronal cells. The 5′‐promoter of SNCA has a complex architecture, including multiple binding sites for the TF zinc finger protein (ZNF)219, which functions as both an activator and a repressor. Targeting ZSCAN21 or other TFs controlling SNCA transcriptional activity may provide novel therapeutic avenues not only for Parkinson’s disease but also for other synucleopathies.
Transformation of vivianite by anaerobic nitrate‐reducing iron‐oxidizing bacteria
Authors: MIOT J. , BENZERARA K. , MORIN G. , BERNARD S. , BEYSSAC O. , LARQUET E. , KAPPLER A. , GUYOT F.
Published: June 2009

In phosphate‐rich environments, vivianite (FeII3(PO4)2, 8H2O) is an important sink for dissolved Fe(II) and is considered as a very stable mineral due to its low solubility at neutral pH. In the present study, we report the mineralogical transformation of vivianite in cultures of the nitrate‐reducing iron‐oxidizing bacterial strain BoFeN1 in the presence of dissolved Fe(II). Vivianite was first transformed into a greenish phase consisting mostly of an amorphous mixed valence Fe‐phosphate. This precipitate became progressively orange and the final product of iron oxidation consisted of an amorphous Fe(III)‐phosphate. The sub‐micrometer analysis by scanning transmission X‐ray microscopy of the iron redox state in samples collected at different stages of the culture indicated that iron was progressively oxidized at the contact of the bacteria and at a distance from the cells in extracellular minerals. Iron oxidation in the extracellular minerals was delayed by a few days compared with cell‐associated Fe‐minerals. This led to strong differences of Fe redox in between these two types of minerals and finally to local heterogeneities of redox within the sample. In the absence of dissolved Fe(II), vivianite was not significantly transformed by BoFeN1. Whereas Fe(II) oxidation at the cell contact is most probably directly catalyzed by the bacteria, vivianite transformation at a distance from the cells might result from oxidation by nitrite. In addition, processes leading to the export of Fe(III) from bacterial oxidation sites to extracellular minerals are discussed including some involving colloids observed by cryo‐transmission electron microscopy in the culture medium.
Clinical supervision: an appropriate term for physiotherapists?
Authors: Hall Toni , Cox Diane
Published: June 2009

The aim of this study was to investigate the experiences of physiotherapists engaged in clinical supervision. It aimed to indicate whether physiotherapists understood the purpose of clinical supervision and whether the term affected their understanding and use of the process. The study is set in a physiotherapy department in an acute District General Hospital. Sixteen potential participants were contacted, eight qualified physiotherapists consented to take part. The study adopted a qualitative approach using semi‐structured audio‐taped interviews which were transcribed prior to content analysis.

A key finding was that the physiotherapists did not have a clear understanding of the purpose of clinical supervision in relation to other support available, for example annual appraisal and rotational reviews. Tensions arose for those who associated clinical supervision with line management and appraisal. Clinical supervision was most effective for physiotherapists who had selected their own supervisor, who were clear about its purpose and who were able to make the link between clinical supervision, continuing professional development and reflective practice.

The study concludes that the purpose of clinical supervision in relation to other support needs to be clarified to help physiotherapists use the process more effectively and that clinical supervisors should receive support and training in this important role. Clinical supervision is used for different purposes at different stages of a career and can enhance the development of confident practitioners. The term ‘clinical supervision’ is inappropriate for physiotherapists due to its lack of clarity. ‘Peer Support and Development’ is an example of an alternative title that may better describe the purpose of the activity.
Adventitia removal does not modify the α1D‐adrenoceptors response in aorta during hypertension and ageing
Authors: Gómez‐Zamudio J. H. , Villalobos‐Molina R.
Published: June 2009

1The aim of the current study was to characterize the α1‐adrenergic receptors (α1‐ARs) present in the isolated tunica media of aorta, in normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats during the course of ageing and hypertension (rats of 1, 3, 6 and 12 months of age). In all vessels, endothelium was removed.

2In isolated aortic rings, phenylephrine increased contraction in a concentration‐ and age‐dependent manner and was impaired in old SHR compared with WKY rats.

3The α1‐AR selective antagonist prazosin showed high affinity (pA2) in vessels from both rat strains.

4The potency of the α1A‐AR selective antagonists, RS 100329 (5‐methyl‐3‐[3‐[4‐[2‐(2,2,2,‐trifluoroethoxy) phenyl]‐1‐piperazinyl] propyl]‐2,4‐(1H)‐pyrimidinedione) and 5‐methylurapidil in antagonizing aortic phenylephrine‐responses was low.

5The α1D‐AR selective antagonist, BMY 7378 (8‐[2‐[4‐(2‐methoxyphenyl)‐1 piperazynil] ethyl]‐8‐azaspiro [4.5] decane‐7,9‐dione) potently blocked phenylephrine‐induced responses in aorta from both strains and at all ages.

6Adventitia removal decreasedEmaxin older rats and modified the relative affinity (pD2), but did not affect the affinity of the selective antagonists.

7The results suggest that aorta tunica α1D‐AR is the main subtype involved in phenylephrine‐induced contraction of rat aorta, while α1A‐AR plays only a minor role.

8Ageing and hypertension did not modify α1‐ARs in the blood vessel and the tunica adventitia does not seem to participate in contraction, even though α1‐ARs are expressed.
Mast cells, peptides and cardioprotection – an unlikely marriage?
Authors: Walsh S. K. , Kane K. A. , Wainwright C. L.
Published: June 2009

1 Mast cells have classically been regarded as the ‘bad guys’ in the setting of acute myocardial ischaemia, where their released contents are believed to contribute both to tissue injury and electrical disturbances resulting from ischaemia. Recent evidence suggests, however, that if mast cell degranulation occurs in advance of ischaemia onset, this may be cardioprotective by virtue of the depletion of mast cell contents that can no longer act as instruments of injury when the tissue becomes ischaemic.

2 Many peptides, such as ET‐1, adrenomedullin, relaxin and atrial natriuretic peptide, have been demonstrated to be cardioprotective when given prior to the onset of myocardial ischaemia, although their physiological functions are varied and the mechanisms of their cardioprotective actions appear to be diverse and often ill defined. However, one common denominator that is emerging is the ability of these peptides to modulate mast cell degranulation, raising the possibility that peptide‐induced mast cell degranulation or stabilization may hold the key to a common mechanism of their cardioprotection.

3 The aim of this review was to consolidate the evidence implying that mast cell degranulation could play both a detrimental and protective role in myocardial ischaemia, depending upon when it occurs, and that this may underlie the cardioprotective effects of a range of diverse peptides that exerts physiological effects within the cardiovascular system.
Long‐term changes in dynamic cerebral autoregulation: a 10 years follow up study
Authors: Brodie Fiona G. , Panerai Ronney B. , Foster Stephanie , Evans David H. , Robinson Thompson G.
Published: June 2009

This study takes a novel approach to describing time‐related changes in dynamic cerebral autoregulation (dCA). It is well‐recognized that dCA exhibits both intra‐ and inter‐ subject variability, and this study seeks to characterize the extent to which intra‐subject variability occurs after a significant period of time by studying the same subjects 10 years apart, thus eliminating inter‐subject variability as a source of error. Ten healthy subjects were identified in 1998 and followed up in 2008. On each visit they underwent simultaneous recordings of right middle cerebral artery cerebral blood flow velocity (RMCA CBFV), blood pressure and heart rate. Data were analysed in the frequency domain using transfer function analysis and in the time domain using CBFV step response, from which the autoregulatory index (ARI) was calculated. Ten subjects of mean age 35·5 (range 24–51) years in 1998 (seven male) were studied. There was a significant fall in ARI from 1998–2008 (ΔARI = 1·1, P = 0·021), along with a significant rise in coherence in 2008 (at 0·05 Hz, P = 0·018). Difference in mean step response between 1998 and 2008 was also significant (P = 0·045). This is the first study to assess dCA in the same subjects 10 years apart, providing a novel opportunity to assess intra‐subject variation in dCA after a long time period has elapsed. A fall in frequency and time domain parameters was observed. This is important, and needs to be considered in future studies assessing long‐term changes in dCA, particularly given the body evidence which suggests that dCA is unaffected by ageing.
Evaluation of endothelial function using finger plethysmography
Authors: Faizi A. K. , Kornmo D. W. , Agewall S.
Published: June 2009

Background:  The aims of this study were to establish the optimum duration of blood flow occlusion to obtain maximal response and to compare the response after lower‐arm and upper‐arm occlusion.

Methods:  Pulse wave amplitude was analysed using a novel finger plethysmograph (EndoPat; Itamar). For measuring reactive hyperaemic index (RHI) induced by forearm cuff occlusion, 30 healthy subjects were examined at different days in a random order of four cuff occlusion times (1·5, 3, 5 and 8 min). RHI induced by 5 min upper‐arm cuff occlusion was also measured in 20 subjects.

Results:  Average RHI was lower with 1·5 and 3 min forearm occlusion compared with 8 min forearm occlusion (P = 0·002 and P = 0·024). There was no significant difference between values of 5 min and 8 min forearm occlusion and between 5 min forearm and 5 min upper‐arm occlusion (P = 0·1). All subjects reported less discomfort after forearm occlusion compared with upper‐arm occlusion.

Conclusion:  Maximum response was reached after 5 min of blood flow occlusion and therefore this occlusion time is recommended. The response after forearm and upper‐arm occlusion did not differ significantly. Forearm occlusion might be preferred as this caused less discomfort.
Influence of humic acid on water retention and nutrient acquisition in simulated golf putting greens
Authors: Van Dyke A. , Johnson P. G. , Grossl P. R.
Published: June 2009

Humic substances are frequently applied to creeping bentgrass (Agrostis palustris Huds.) on golf putting greens to improve turf health and are marketed to enhance nutrient acquisition and possibly aid in retaining water in drought prone environments, but information on the role of humic substances in increasing soil water retention is limited. Additionally, it is difficult to separate the beneficial effects of nutrients and other ingredients added to commercial humic formulations from the effects of the pure humic substance. In our study, pure humic acid, tannic and citric acids were added to simulated creeping bentgrass putting greens. The organic acids were applied at normalized carbon rates of 250 mg C per litre by watering solutions through an automated irrigation system. Volumetric water content (VWC) and irrigation frequency, shoot and root growth, and tissue nutrient concentration of the turf were measured. None of the organic acid treatments improved water retention in the simulated greens. The humic acid‐treated greens required more frequent irrigation than the untreated greens indicating that they were drying out more quickly. In addition, the addition of humic acid did not result in an increased tissue concentration of nutrients in the creeping bentgrass, top growth or dry shoot mass compared with the other treatments. However, creeping bentgrass root length was greater in the greens treated with humic acid compared with the untreated control.
Aggregate stability in organically and conventionally farmed soils
Authors: Williams N. D. , Petticrew E. L.
Published: June 2009

A range of factors that influence aggregate stability and soil erodibility were analysed for soils sampled from land managed under contrasting agricultural methods. These included: an organic farm; a conventional farm that incorporated organic fertilizers; a conventional farm that only used inorganic fertilizers; and a non‐cultivated control site. The stability of aggregates that compose the bulk soil structure (macroaggregates), and aggregates that were mobilized from the soil by simulated rainfall and surface runoff (microaggregates), were evaluated in terms of the soil fragmentation fractal dimension, organic carbon content and ATP (adenosine 5′‐triphosphate; a signature of live biomass) concentration. The results were used to interpret the existing physical condition of the soils, the (microbial) processes that contribute to that physical structure, and how both pedogenic processes and existing soil quality are influenced by agricultural methods. The soils sampled for this study were demonstrated to be multi‐fractal in nature: soils with greater bulk density were composed of more stable macro‐aggregates, which, in turn, fragmented into larger, more stable micro‐aggregates, rendering the entire soil structure less erodible. Soil erodibility and sustainable soil management should therefore be approached at multiple scales. The primary control on both macro‐ and micro‐aggregate stability was determined to be the organic matter input to the soil, as represented by measurements of organic carbon and ATP. Organic content was greatest for the non‐cultivated soil, which reflects the degradation of organic reserves in cultivated soils. For cultivated soils, it was not possible to differentiate aggregate stability for soils managed under organic or conventional (i.e. using biological and inorganic fertilizers) farming practices, but aggregates of soils that only received artificial fertilizers consistently exhibited less stability.
Integer linear programming for a cutting problem in the wood‐processing industry: a case study
Authors: Koch Sören , König Sebastian , Wäscher Gerhard
Published: June 2009

In this paper, the authors present a case study from the wood‐processing industry. It focuses on a cutting process in which material from stock is cut down in order to provide the items required by the customers in the desired qualities, sizes, and quantities. In particular, two aspects make this cutting process special. Firstly, the cutting process is strongly interdependent, with a preceding handling process, which, consequently, cannot be planned independently. Secondly, if the trim loss is of a certain minimum size, it can be returned into stock and used as input to subsequent cutting processes. In order to reduce the cost of the cutting process, a decision support tool has been developed that incorporates an integer linear programming model as a central feature. The model is described in detail, and experience from the application of the tool is reported.
The nature of publishing and assessment in Geography and Environmental Studies: evidence from the Research Assessment Exercise 2008
Authors: Richards Keith , Batty Mike , Edwards Kevin , Findlay Allan , Foody Giles , Frostick Lynne , Jones Kelvyn , Lee Roger , Livingstone David , Marsden Terry , Petts Judith , Philo Chris , Simon David , Smith Susan , Thomas David
Published: June 2009

We present a summary of the kinds of outputs submitted to the Geography and Environmental Studies sub‐panel (H‐32) for the 2008 Research Assessment Exercise (RAE), and examine the relationships between the peer assessment of research quality that the RAE process has typified, and alternative modes of assessment based on bibliometrics. This comparison is effected using (in aggregate form) some of the results from the RAE, together with citation data gathered after completion of the RAE assessment, specifically for the purpose of this paper. We conclude that, if it continues to be necessary and desirable to assess, in some measure and however imprecisely, research quality, then peer assessment cannot be replaced by bibliometrics. Bibliometrics permit measurement of something that may be linked to quality but is essentially a different phenomenon – a measure of ‘impact’, for example.
THE AFFINITIES OF THE ENIGMATIC DINOSAUR ESHANOSAURUS DEGUCHIIANUS FROM THE EARLY JURASSIC OF YUNNAN PROVINCE, PEOPLE’S REPUBLIC OF CHINA
Authors: BARRETT PAUL M.
Published: June 2009

Abstract:  Eshanosaurus deguchiianus is based on a single left dentary from the Lower Lufeng Formation (Lower Jurassic) of Yunnan Province, China. It was originally identified as the earliest known member of Therizinosauroidea (Theropoda: Coelurosauria), a conclusion that results in a significant downward range extension for this clade (>65 million years) and for many other major lineages within Coelurosauria. However, this interpretation has been questioned and several authors have proposed that the anatomical features used to refer Eshanosaurus to Therizinosauroidea are more consistent with attribution to a basal sauropodomorph dinosaur. Detailed consideration of the holotype specimen suggests that several features of the dentary and dentition exclude Eshanosaurus from Sauropodomorpha and support its inclusion within Therizinosauroidea. If accepted as an Early Jurassic coelurosaur, Eshanosaurus has important implications for understanding the timing and tempo of early theropod diversification. Moreover, its provenance also suggests that substantial portions of the coelurosaur fossil record may be missing or unsampled. However, the Early Jurassic age of Eshanosaurus requires confirmation if this taxon is to be fully incorporated into broader evolutionary studies.
MEASURING THE ECONOMIC PERFORMANCE OF TRANSITION ECONOMIES: SOME LESSONS FROM CHINESE EXPERIENCE
Authors: Maddison Angus
Published: June 2009

This article quantifies the comparative performance of China in several dimensions. Firstly, it shows that China's move from a command to a market economy was less abrupt and more successful than that of 29 other economies making a similar transition. Secondly, while official estimates show annual GDP growth of 9.6 percent in 1978–2003, this is reduced to 7.9 percent after adjustment for exaggeration of industrial performance and growth in non‐material services. Thirdly, as the exchange rate understates China's achievement, a purchasing power parity (PPP) converter is necessary to measure comparativelevelof performance. Our PPP converter shows that China in 2005 was the world's second largest economy, with a GDP about 80 percent of the U.S. It is assumed that China will have overtaken the U.S. as the world's biggest economy before 2015. Until recently, the World Bank estimate of the PPP for China was close to that of Maddison, but the Bank's new estimate for 2005 shows Chinese GDP about half this level. The Bank's new estimates for China and other Asian countries are not plausible, and this paper advances several reasons for rejecting them. Finally, energy use per head of population is a good deal smaller than that of the U.S., and its total energy use for a much bigger population is likely to be somewhat smaller than that of the U.S. in 2030. However, heavy dependence on dirty coal means that it will have bigger carbon emissions than the U.S. This is a major problem as Beijing and other big cities already have severe pollution problems.
INDUSTRIAL AND AGGREGATE MEASURES OF PRODUCTIVITY GROWTH IN CHINA, 1982–2000
Authors: Cao Jing , Ho Mun S. , Jorgenson Dale W. , Ren Ruoen , Sun Linlin , Yue Ximing
Published: June 2009

We estimate productivity growth for 33 industries covering the entire Chinese economy using a time series of input–output tables covering 1982–2000. Capital input is measured using detailed investment data by asset and labor input uses demographic information from household surveys. We find a wide range of productivity performance at the industry level. We then show how these industry growth accounts may be consistently aggregated to deliver a decomposition of aggregate GDP growth. For the 1982–2000 period aggregate TFP growth was 2.5 percent per year; decelerating from a rapid rate in the early 1980s to negative growth during 1994–2000. The main source of growth during the 1982–2000 period was capital accumulation, with a small negative contribution from the reallocation of factors across industries.
TEMPORARY AND PERSISTENT POVERTY AMONG ETHNIC MINORITIES AND THE MAJORITY IN RURAL CHINA
Authors: Gustafsson Björn , Sai Ding
Published: June 2009

Poverty among ethnic minorities and the majority in rural China for the years 2000, 2001 and 2002 is investigated, taking a dynamic view and using a large sample covering 22 provinces. Based on the National Bureau of Statistics' low income line, almost one‐third of the ethnic minorities experienced poverty during the three years studied while the corresponding proportion among the ethnic majority was only about half as high. Still, by far most of the poor in rural China belong to the ethnic majority. The relatively high poverty rates for ethnic minorities in rural China are found to be due to higher rates of entry than for the majority, while differences in exit rates across ethnicities are few. To a large extent, ethnic poverty differences can be attributed to differences in location, together with temporary and persistent poverty in rural China having a very clear spatial character. Poverty is concentrated in the western region and villages with low average income. Determinants of persistent and temporary poverty in rural China differ due to location as well as household characteristics.
The long‐term development of organised business and its implications for corporatism: A cross‐national comparison of membership, activities and governing capacities of business interest associations, 1980–2003
Authors: TRAXLER FRANZ
Published: June 2009

Internationalisation of markets and the demise of Keynesianism have made business more independent of associational action. Membership density and ‘corporatist’ involvement in wage bargaining and public policy have declined only modestly, while the capacity to govern members has dwindled significantly. This development is driven by the way in which large firms and the state relate to business associations. Large firms still have a vital interest not only in associational action, but also in integrating their smaller counterparts. Stated‐based support for multi‐employer bargaining, as established in most countries, buttresses business associations. By equipping the associations with an encompassing grip on the labour market, this support prompts governments to involve them in public policy. Since encompassing labour market regulation enables the associations to impose negative externalities on unaffiliated businesses, it provides them with a strong selective incentive for membership. The significant decline of the associations' governing capacity emanates from pressures of their large members to reduce costs of association. The implications of this development for interest intermediation are twofold. Given the strong decay of union power, the resilience of corporatism strongly hinges on the continued strength of organised business and on its state‐sponsored engagement in bargaining. At the same time, leeway for compromising has been restrained by the significant decline in the governing capacity of organised business. This decline echoes an ever‐growing predominance of large firms in business associations, while economic internationalisation exacerbates interest conflicts between larger and smaller firms. To the extent that this configuration of interest and power weakens the ability of business associations to integrate the mass of small firms, it develops into the new Achilles heel of corporatism.