bluuebunny/crossref_metadata_2025_split huggingface dataset:
Non‐native fishes and climate change: predicting species responses to warming temperatures in a temperate region
Authors: BRITTON J. R. , CUCHEROUSSET J. , DAVIES G. D. , GODARD M. J. , COPP G. H. 
Published: April 2010

Summary1. Temperate regions with fish communities dominated by cold‐water species (physiological optima <20 °C) are vulnerable to the effects of warming temperatures caused by climate change, including displacement by non‐native cool‐water (physiological optima 20–28 °C) and warm‐water fishes (physiological optima >28 °C) that are able to establish and invade as the thermal constraints on the expression of their life history traits diminish.2. England and Wales is a temperate region into which at least 38 freshwater fishes have been introduced, although 14 of these are no longer present. Of the remaining 24 species, some have persisted but failed to establish, some have established populations without becoming invasive and some have become invasive. The aim of the study was to predict the responses of these 24 non‐native fishes to the warming temperatures of England and Wales predicted under climate change in 2050.3. The predictive use of climate‐matching models and an air and water temperature regression model suggested that there are six non‐native fishes currently persistent but not established in England and Wales whose establishment and subsequent invasion would benefit substantially from the predicted warming temperatures. These included the common carp Cyprinus carpio and European catfish Silurus glanis, fishes that also exert a relatively high propagule pressure through stocking to support angling and whose spatial distribution is currently increasing significantly, including in open systems.4. The potential ecological impacts of the combined effects of warming temperatures, current spatial distribution and propagule pressure on the establishment and invasion of C. carpio and S. glanis were assessed. The ecological consequences of C. carpio invasion were assessed as potentially severe in England and Wales, with impacts likely to relate to habitat destruction, macrophyte loss and increased water turbidity. However, evidence of ecological impacts of S. glanis elsewhere in their introduced range was less clear and so their potential impacts in England and Wales remain uncertain.
Incidence of accessory canals in Japanese anterior maxillary teeth following root canal filling ex vivo
Authors: Adorno C. G. , Yoshioka T. , Suda H 
Published: April 2010

Adorno CG, Yoshioka T, Suda H. Incidence of accessory canals in Japanese anterior maxillary teeth following root canal filling ex vivo. International Endodontic Journal, 43, 370–376, 2010.AbstractAim  To investigate the vertical and horizontal distribution and the incidence of accessory canals in Japanese maxillary anterior teeth following root filling.Methodology  The study included maxillary teeth; 69 central incisors, 61 lateral incisors and 31 canines. After the canal systems had been dyed and root canal instrumentation had been carried out, all prepared canals were filled with gutta‐percha without using sealer. Transparent specimens were then obtained and examined with a digital microscope for horizontal and vertical distributions of accessory canals.Results  The incidence of teeth with accessory canals in the apical 3 mm was 46%, 29% and 38% for the maxillary central incisors, lateral incisors and canines, respectively. The horizontal distribution was mainly buccal for central incisors, palatal for lateral incisors and distal and palatal for canines. There was a significant difference (P < 0.05) between the apical 3 mm and the rest of the root (16%, 20% and 19% for the maxillary central incisors, lateral incisors and canines, respectively) in terms of the presence of accessory canals.Conclusions  A high percentage of accessory canals can be found in apical 3 mm of the root. The horizontal distribution of accessory canals differed amongst the tooth types studied.
Mineral trioxide aggregate and formocresol pulpotomy of primary teeth: a 2‐year follow‐up
Authors: Ansari G. , Ranjpour M. 
Published: April 2010

Ansari G, Ranjpour M. Mineral trioxide aggregate and formocresol pulpotomy of primary teeth: a 2‐year follow‐up. International Endodontic Journal, 43, 413–418, 2010.AbstractAim  To compare the clinical and radiographic response of primary teeth to vital pulpotomy using mineral trioxide aggregate (MTA) or formocresol (FC).Methodology  A group of 17 children aged 4–9 were selected from those referred to the Paedodontic Department at Shahid Beheshti University, Dental School. Cases with at least two matching teeth were selected (40 teeth), showing signs of pulp involvement. A pulpotomy procedure was carried out in all cases with FC in control teeth whilst MTA was placed in experimental teeth. Clinical and radiographic evaluations were performed at 1‐, 6‐, 12‐ and 24‐month recall. Statistical analysis using a Fischer exact test was performed on the data to determine significant differences between the groups.Results  Overall, 22 second and 18 first primary molars were included. The gender ratio was one male to three female. No significant difference was found between the clinical and radiographic outcomes of the two groups at 6‐, 12‐ and 24‐month follow‐up (P > 0.05). Internal resorption was seen significantly more often in FC cases after 12 months than MTA cases. Overall radiographic appearance of normal structures at 24th month was seen in more than 95% of the cases in MTA and 90% in the FC‐treated group (P > 0.05).Conclusion  Mineral trioxide aggregate for pulp treatment of primary teeth can be considered a replacement for FC.
Discrimination between cells of murine and human origin in xenotransplants by species specific genomic in situ hybridization
Authors: Steck Eric , Burkhardt Michaela , Ehrlich Hermann , Richter Wiltrud 
Published: April 2010

Steck E, Burkhardt M, Ehrlich H and Richter W. Discrimination between cells of murine and human origin in xenotransplants by species specific genomic in situ hybridization. Xenotransplantation 2010; 17: 153–159. © 2010 John Wiley & Sons A/S.Abstract:  Xenotransplantation of human cells into immune compromised host species is an important experimental setup to follow the faith of implanted cells and the contribution of host cells to tissue regenerates. In this context, it is of major relevance to discriminate between transplanted and host cells. Labeling techniques of donor cells frequently reach only part of the cells, have the risk of influencing their natural biological activity and may allow label transmission to host cells via vesicles or phagocytosis. To allow positive detection of donor and host cells on histological sections of a transplant, we have developed a method to identify mouse cells by in situ hybridization of murine specific genomic repetitive elements (SINE/B1, SINE/B2) which we combined with human cell detection using Alu in situ hybridization. We describe generation of mouse specific probes, hybridization and read out using biomaterial supported human chondrocyte constructs implanted subcutaneously in mice. Mouse specific genomic repeats identified attached or invaded host cells in the transplants with human specific signals confined to regions of cartilage‐like extracellular matrix. The method is suitable to discriminate specifically between cells of human and mouse origin without overlap of unspecific staining.
Neotropical birds show a humped distribution of within‐population genetic diversity along a latitudinal transect
Authors: Miller Matthew J. , Bermingham Eldredge , Klicka John , Escalante Patricia , Winker Kevin 
Published: April 2010

Ecology Letters (2010) 13: 576–586AbstractThe latitudinal gradient in species richness is a nearly universal ecological phenomenon. Similarly, conspecific genetic diversity often increases towards the equator – usually explained as the consequence of post‐glacial range expansion or due to the shared response of genetic diversity to processes that promote species richness. However, no study has yet examined the relationship between latitude and within‐population genetic diversity in exclusively tropical species. We surveyed genetic variation in nine resident bird species co‐occurring in tropical lowlands between southern Mexico and western Ecuador, where avian species richness increases with decreasing latitude. Within‐population genetic variation was always highest at mid‐range latitudes, and not in the most equatorial populations. Differences in demography and gene flow across species’ ranges may explain some of our observations; however, much of the pattern may be due simply to geometric constraints. Our findings have implications for conservation planning and for understanding how biodiversity scales from genes to communities.
Counter‐terrorism and the Politics of Aid: Civil Society Responses in Kenya
Authors: Lind Jeremy , Howell Jude 
Published: April 2010

ABSTRACTAgainst the backdrop of terrorist attacks in 1998 and 2002, Kenya has come under pressure from aid donors and diplomatic circles to co‐operate in achieving the political and military objectives of the War on Terror. The Kenyan government has received legal, technical and financial support to implement new counter‐terrorism structures. However, while these have raised concerns around human rights and the ability of people to come together and organize on shared interests, the response of civil society in Kenya has been muted. It is mainly human rights campaigners, lawyers, Muslim organizations and leaders, and some politicians that have opposed proposed anti‐terrorism legislation. Even fewer groups have spoken out against the government's participation in a regional rendition programme in the Horn of Africa supported by the United States. This weak response reflects the significant ethnic and regional fragmentation that prevails in the country. This article critically examines the impacts of counter‐terrorism in Kenya and civil society responses to these in a shifting political landscape.
Effects of highly active antiretroviral therapy on vaccine‐induced humoral immunity in HIV‐infected adults
Authors: González R , Castro P , García F , Plana M , Bayas JM , Lafuente S , Serrano B , Mora B , Argelich R , Gatell JM , Vilella A 
Published: April 2010

ObjectivesThe acquisition of adequate vaccine‐induced humoral immunity is especially important in HIV‐infected individuals, who are at increased risk of infections. The aim of the study was to assess the safety of administering a complete vaccination programme to successfully treated HIV‐infected adults and to evaluate specific humoral responses and the effect of highly active antiretroviral therapy (HAART) interruption on these responses.MethodsA placebo‐controlled, double‐blind clinical trial was designed and 26 HIV‐infected adults enrolled. Study participants were randomized to receive either a complete immunization schedule with commercial vaccines or placebo for 12 months. HAART was then discontinued for 6 months. Specific humoral responses were evaluated at baseline, at month 12 and after HAART interruption and compared between groups.ResultsThere were neither local nor systemic secondary effects related to vaccination. Specific humoral responses to vaccines were adequate, but a loss of immunoglobulin G titres was observed after HAART interruption in 12 study participants.ConclusionsHAART interruption may cause impairment of previously acquired vaccine‐induced immunity in HIV‐infected adults.
Regulatory Reform: Integrating Paradigms*
Authors: De La Torre Augusto , Ize Alain 
Published: April 2010

AbstractWhat were the market and regulatory issues that led to the subprime crisis? How should prudential regulation be fixed? The answers depend on the interpretive lenses – or ‘paradigms’– through which one sees finance. The agency paradigm, which has dominated recent regulatory policy and provides the most popular interpretation of the crisis, seems to be influencing much of the emerging reform agenda. But collective welfare failures (particularly externalities) and collective cognition failures (particularly mood swings) were as important, if not more so, in driving the crisis. These three paradigms should therefore be integrated into a more balanced policy agenda. But doing so will be difficult because they often have inconsistent policy implications.
Role of the polybasic sequence in the Doc2α C2B domain in dense‐core vesicle exocytosis in PC12 cells
Authors: Sato Mai , Mori Yasunori , Matsui Takahide , Aoki Ryo , Oya Manami , Yanagihara Yu , Fukuda Mitsunori , Tsuboi Takashi 
Published: April 2010

J. Neurochem. (2010) 114, 171–181.AbstractThe double C2 (Doc2) family is characterized by an N‐terminal Munc13‐1‐interacting domain and C‐terminal tandem C2 domains, and it comprises three isoforms, Doc2α, Doc2β, and Doc2γ, in humans and mice. Doc2α, the best‐characterized, brain‐specific isoform, exhibits Ca2+‐dependent phospholipid‐binding activity through its C2A domain, and the Ca2+‐binding activity is thought to be important for the regulation of Ca2+‐dependent exocytosis. In contrast to the C2A domain, however, nothing is known about the physiological functions of the C2B domain in regulated exocytosis. In this study, we demonstrated by a mutation analysis that the polybasic sequence in the C2B domain of Doc2α (306 KKSKHKTCVKKK 317) is required for binding of syntaxin‐1a/synaptosome‐associated protein of 25 kDa (SNAP‐25) heterodimer. We also investigated the effect of Lys‐to‐Gln (named KQ) mutations in the polybasic sequence of the C2B domain on vesicle dynamics by total internal reflection fluorescence microscopy in PC12 cells. A Doc2α(KQ) mutant, which lacks binding activity toward syntaxin‐1a/SNAP‐25 heterodimer, significantly decreased the number of plasma membrane‐docked vesicles before stimulation and strongly inhibited high‐KCl‐induced exocytosis from the plasma membrane‐docked vesicles. These results indicate that the polybasic sequence in the C2B domain functions as a binding site for syntaxin‐1a/SNAP‐25 heterodimer and controls the number of ‘readily releasable’ vesicles in neuroendocrine cells.
Nature and cause of mitochondrial dysfunction in Huntington’s disease: focusing on huntingtin and the striatum
Authors: Oliveira Jorge M. A. 
Published: April 2010

J. Neurochem. (2010) 114, 1–12.AbstractPolyglutamine expansion mutation in huntingtin causes Huntington’s disease (HD). How mutant huntingtin (mHtt) preferentially kills striatal neurons remains unknown. The link between mitochondrial dysfunction and HD pathogenesis stemmed from postmortem brain data and mitochondrial toxin models. Current evidence from genetic models, containing mHtt, supports mitochondrial dysfunction with yet uncertain nature and cause. Because mitochondria composition and function varies across tissues and cell‐types, mitochondrial dysfunction in HD vulnerable striatal neurons may have distinctive features. This review focuses on mHtt and the striatum, integrating experimental evidence from patients, mice, primary cultures and striatal cell‐lines. I address the nature (specific deficits) and cause (mechanisms linked to mHtt) of HD mitochondrial dysfunction, considering limitations of isolated vs. in situ mitochondria approaches, and the complications introduced by glia and glycolysis in brain and cell‐culture studies. Current evidence relegates respiratory chain impairment to a late secondary event. Upstream events include defective mitochondrial calcium handling, ATP production and trafficking. Also, transcription abnormalities affecting mitochondria composition, reduced mitochondria trafficking to synapses, and direct interference with mitochondrial structures enriched in striatal neurons, are possible mechanisms by which mHtt amplifies striatal vulnerability. Insights from common neurodegenerative disorders with selective vulnerability and mitochondrial dysfunction (Alzheimer’s and Parkinson’s diseases) are also addressed.
Signaling pathways controlling the phosphorylation state of WAVE1, a regulator of actin polymerization
Authors: Ceglia Ilaria , Kim Yong , Nairn Angus C. , Greengard Paul 
Published: April 2010

J. Neurochem. (2010) 114, 182–190.AbstractThe Wiskott‐Aldrich syndrome protein (WASP)‐family verprolin homologous protein 1 (WAVE1) is a key regulator of Arp (actin‐related protein) 2/3 complex‐mediated actin polymerization. We have established previously that the state of phosphorylation of WAVE1 at three distinct residues controls its ability to regulate actin polymerization and spine morphology. Cyclin‐dependent kinase 5 phosphorylates WAVE1 at Ser310, Ser397 and Ser441 to a high basal stoichiometry, resulting in inhibition of WAVE1 activity. Our previous and current studies show that WAVE1 can be dephosphorylated at all three sites and thereby activated upon stimulation of the D1 subclass of dopamine receptors and of the NMDA subclass of glutamate receptors, acting through cAMP and Ca2+ signaling pathways, respectively. Specifically, we have identified protein phosphatase‐2A and protein phosphatase‐2B as the effectors for these second messengers. These phosphatases act on different sites to mediate receptor‐induced signaling pathways, which would lead to activation of WAVE1.
β‐Chemokine production by neural and glial progenitor cells is enhanced by HIV‐1 Tat: effects on microglial migration
Authors: Hahn Yun Kyung , Vo Phu , Fitting Sylvia , Block Michelle L. , Hauser Kurt F. , Knapp Pamela E. 
Published: April 2010

J. Neurochem.(2010)114, 97–109.AbstractHuman immunodeficiency virus (HIV)‐1 neuropathology results from collective effects of viral proteins and inflammatory mediators on several cell types. Significant damage is mediated indirectly through inflammatory conditions promulgated by glial cells, including microglia that are productively infected by HIV‐1, and astroglia. Neural and glial progenitors exist in both developing and adult brains. To determine whether progenitors are targets of HIV‐1, a multi‐plex assay was performed to assess chemokine/cytokine expression after treatment with viral proteins transactivator of transcription (Tat) or glycoprotein 120 (gp120). In the initial screen, ten analytes were basally released by murine striatal progenitors. The beta‐chemokines CCL5/regulated upon activation, normal T cell expressed and secreted, CCL3/macrophage inflammatory protein‐1α, and CCL4/macrophage inflammatory protein‐1β were increased by 12‐h exposure to HIV‐1 Tat. Secreted factors from Tat‐treated progenitors were chemoattractive towards microglia, an effect blocked by 2D7 anti‐CCR5 antibody pre‐treatment. Tat and opiates have interactive effects on astroglial chemokine secretion, but this interaction did not occur in progenitors. gp120 did not affect chemokine/cytokine release, although both CCR5 and CXCR4, which serve as gp120 co‐receptors, were detected in progenitors. We postulate that chemokine production by progenitors may be a normal, adaptive process that encourages immune inspection of newly generated cells. Pathogens such as HIV might usurp this function to create a maladaptive state, especially during development or regeneration, when progenitors are numerous.
Reduced blockade by extracellular Mg2+ is permissive to NMDA receptor activation in cerebellar granule neurons that model a migratory phenotype
Authors: Gerber Adam M. , Beaman‐Hall Carol M. , Mathur Anjili , Vallano Mary Lou 
Published: April 2010

J. Neurochem. (2010) 114, 191–202.AbstractNMDA receptors (NMDAR) contribute to neuronal development throughout the CNS. However, their mode(s) of activation preceding synaptic maturation is unclear, as they are not co‐localized with alpha‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate receptors (AMPARs) which normally provide sufficient depolarization to relieve voltage‐dependent blockade by Mg2+. We used cerebellar granule neurons (CGNs) cultured at a near‐physiological KCl concentration to examine maturation‐dependent changes in NMDAR responses. In contrast, most studies use KCl‐supplemented medium to promote survival. At 2–4 days in vitro CGNs: (i) express developmental markers resembling the in vivo migratory phenotype; (ii) maintain a basal amount of calcium responsive element‐binding protein phosphorylation that requires NMDARs and calcium/calmodulin‐dependent kinases, but not AMPARs; (iii) exhibit NMDA‐mediated Ca2+ influx not effectively blocked by ambient Mg2+ (0.75 mM) or AMPARs; (iv) maintain a more depolarized resting membrane potential and increased resistance compared to synaptically‐connected CGNs. Moreover, migrating CGNs in explant cultures demonstrate NMDA‐mediated Ca2+ influx not effectively blocked by 0.75 mM Mg2+, and NMDAR but not AMPAR antagonists slow migration. These data suggest the biophysical properties of immature CGNs render NMDARs less sensitive to Mg2+ blockade, enhancing the likelihood of activation in the absence of AMPAR depolarization.
Inhibition of extracellular signal‐regulated kinases 1/2 provides neuroprotection in spinal cord ischemia/reperfusion injury in rats: relationship with the nuclear factor‐κB‐regulated anti‐apoptotic mechanisms
Authors: Lu Kang , Liang Cheng‐Loong , Liliang Po‐Chou , Yang Chih‐Hui , Cho Chung‐Lung , Weng Hui‐Ching , Tsai Yu‐Duan , Wang Kuo‐Wei , Chen Han‐Jung 
Published: April 2010

J. Neurochem. (2010) 114, 237–246.AbstractPreviously we demonstrated benefits of inhibiting the extracellular signal‐regulated kinases 1/2 (ERK1/2) signaling pathway in spinal cord ischemia/reperfusion (I/R) injury. To further identify the underlying mechanisms, we investigated the impact of ERK inhibition on apoptosis and cellular protective mechanisms against cell death. Spinal cord I/R injury induced ERK1/2 phosphorylation, followed by neuronal loss through caspase 3‐mediated apoptosis. Pre‐treatment with U0126, a specific inhibitor of MAPK/ERK kinases 1/2 (MEK1/2), inhibited ERK1/2 phosphorylation, and significantly attenuated apoptosis and increased neuronal survival. MEK/ERK inhibition also induced I‐κB phosphorylation and enhanced nuclear factor (NF)‐κB/DNA binding activity, leading to expression of cellular inhibitors of apoptosis protein 2 (c‐IAP2), a known nuclear factor‐κB (NF‐κB)‐regulated endogenous anti‐apoptotic molecule. Pyrrolidine dithiocarbamate, an NF‐κB inhibitor, by blocking I‐κB phosphorylation, NF‐κB activation, and c‐IAP2 synthesis, abolished the protective effects of U0126. The MEK/ERK pathway appears to mediate cellular death following I/R injury. The U0126 neuroprotection appears related to NF‐κB‐regulated transcriptional control of c‐IAP2. MEK/ERK inhibition at the initial stage of I/R injury may cause changes in c‐IAP2 gene expression or c‐IAP2/caspase 3 interactions, resulting in long lasting therapeutic effects. Future research should focus on the possible cross‐talk between the MEK/ERK pathway and the NF‐κB transcriptional cascade.
Eating disorders and psychoeducation – patients’ experiences of healing processes
Authors: Pettersen Gunn , Rosenvinge Jan H. , Wynn Rolf 
Published: April 2010

Scand J Caring Sci; 2011; 25; 12–18

Eating disorders and psychoeducation – patients’ experiences of healing processes In the treatment of eating disorders, little is known about the role and impact of psychoeducative programmes and whether patients experience such programmes as helpful in their healing processes. Examining these questions is the purpose of this study, using an explorative and descriptive design based on content analysis. Thirteen female patients participated in qualitative interviews. The analysis of healing processes experienced during the programme participation resulted in six main categories, i.e. ‘Self‐awareness’, ‘Setting boundaries’, ‘Feelings and self‐mobilization’, ‘Self‐regulation’, ‘Self‐reflexivity’ and ‘Motivation and Self‐improvement’. Our study clearly indicates that according to the patients’ experiences, a psychoeducative programme may facilitate healing processes. The study also supports a possible indirect impact on healing processes in terms of more readiness to seek treatment. There is a need for more knowledge about how to bring about an effective interplay between treatment and psychoeducative programmes.