bluuebunny/crossref_metadata_2025_split huggingface dataset:
Roman narratives
Authors: Laurence Ray 
Published: August 2008

AbstractThe narrative structure of Roman archaeology places a particular emphasis on the acculturation of the newly conquered provinces. This ‘process’ known as Romanisation has been found wanting by many commentators on Roman archaeology. Although rejected, it can still reappear and influence the narrative structure of many studies. Reference is deliberately made to the publications of the ‘Theoretical Roman Archaeology Conference’ to highlight the revision of the usage of ‘Romanisation’ by British scholars during the 1990s. The paper identifies the cultural assumptions underpinning the revisionist views of Romanisation and the key problem of a narrative based explicitly or otherwise on textual evidence. Here, an attempt is made to account for the uniqueness of Roman archaeology as practiced in Britain – in comparison to that of prehistory or medieval archaeology. The paper suggests that there is a need to move on from Romanisation to alternative narrative forms drawing on recent revisionist agendas within the social sciences.
Crossing boundaries
Authors: Laneri Nicola 
Published: August 2008

AbstractArchaeology is not just about writing reports and interpreting ancient societies and their social structures, but it is also a process which should aim at the creation of a clear communicative message to the general public. Thus, archaeologists should be aware of every possible medium of communication – verbal, written, visual, sound – to express re-constructions of ancient pasts. In this essay I express some ideas about how archaeologists could collaborate with experts, for example theatre directors, in defining artistic way of communicating the past. Finally, I focus on the relationship between academia and fringe archaeology and I look into the political role of archaeologists in modern society.
Cultured CD4T cells and primary human lymphocytes express hOATPs: intracellular accumulation of saquinavir and lopinavir
Authors: Janneh O , Hartkoorn R C , Jones E , Owen A , Ward S A , Davey R , Back D J , Khoo S H 
Published: August 2008

Background and purpose:Drug efflux tranporters (P‐glycoprotein (P‐gp), multidrug resistance‐associated protein (MRP)) limit the cellular uptake of human immunodeficiency virus protease inhibitors but the contribution of influx transporters in cells that (over)express P‐gp or MRP is less clear. Here, we studied the expression of one influx transporter system, human organic anion‐transporting polypeptide (hOATP), in some T‐cell lines (CEM, CEMVBL, CEME1000) and in peripheral blood mononuclear cells (PBMCs) and examined the effects of manipulation of influx/efflux transporters on the uptake of saquinavir and lopinavir.Experimental approach:The expression of hOATPs was studied by PCR. We used hOATP substrate or inhibitor (estrone‐3‐sulphate (E‐3‐S) or montelukast, respectively) and inhibitors of P‐gp (XR9576) and MRP (MK571 and frusemide) to study functional interactions between influx and efflux transporters in the uptake of saquinavir and lopinavir. Lipophilicity of the drugs was measured by octanol/saline partition coefficient.Key results:CEM cells, their variants and PBMCs express various hOATP isoforms, with OATP3A1 detected in all of the cells. MK571, XR9576 and frusemide increased the uptake of saquinavir and lopinavir. E‐3‐S and montelukast reduced the uptake of saquinavir and lopinavir in some, but not all, of the cells. Pretreatment of the cells with MK571, XR9576 or frusemide, followed by E‐3‐S co‐incubation reduced the cellular accumulation of saquinavir and lopinavir. Lopinavir is much more lipophilic than saquinavir.Conclusions and implications:Human OATPs, MRP, P‐gp and lipophilicity determine the cellular uptake and retention of saquinavir and lopinavir. These data may have important implications for drug–drug interactions, drug safety and efficacy.British Journal of Pharmacology(2008)155, 875–883; doi:10.1038/bjp.2008.320; published online 18 August 2008
Pharmacology of the short QT syndrome N588K‐hERG K+channel mutation: differential impact on selected class I and class III antiarrhythmic drugs
Authors: McPate M J , Duncan R S , Hancox J C , Witchel H J 
Published: August 2008

Background and purpose:The short QT syndrome (SQTS) is associated with cardiac arrhythmias and sudden death. The SQT1 form of SQTS results from an inactivation‐attenuated, gain‐of‐function mutation (N588K) to thehuman ether‐à‐go‐go‐related gene(hERG) potassium channel. Pharmacological blockade of this mutated hERG channel may have therapeutic value. However, hERG‐blocking potencies of canonical inhibitors such as E‐4031 andD‐sotalol are significantly reduced for N588K‐hERG. Here, five hERG‐blocking drugs were compared to determine their relative potencies for inhibiting N588K channels, and two other inactivation‐attenuated mutant channels were tested to investigate the association between impaired inactivation and altered drug potency.Experimental approach:Whole‐cell patch clamp measurements of hERG current (IhERG) mediated by wild‐type and mutant (N588K, S631A and N588K/S631A) channels were made at 37 °C CHO cells.Key results:The N588K mutation attenuatedIhERGinhibition in the following order: E‐4031>amiodarone>quinidine>propafenone>disopyramide. Comparing the three inactivation mutants, the two single mutations, although occurring in different modules of the channel, attenuated inactivation to a nearly identical degree, whereas the double mutant caused considerably greater attenuation, permitting the titration of inactivation. Attenuation of channel inhibition was similar between the single mutants for each drug, and was significantly greater with the double mutant.Conclusions and implications:The degree of drug inhibition of hERG channels may vary based on the level of channel inactivation. Drugs previously identified as useful for treating SQT1 have the least dependence on hERG inactivation. In addition, our findings indicate that amiodarone may warrant further investigation as a potential treatment for SQT1.British Journal of Pharmacology(2008)155, 957–966; doi:10.1038/bjp.2008.325; published online 25 August 2008
Diabetic state, high plasma insulin and angiotensin II combine to augment endothelin‐1‐induced vasoconstriction via ETAreceptors and ERK
Authors: Kobayashi T , Nogami T , Taguchi K , Matsumoto T , Kamata K 
Published: August 2008

Background and purpose:Mechanisms associated with the enhanced contractile response to endothelin‐1 in hyperinsulinaemic diabetes have been examined using the rat aorta. Functions for angiotensin II, endothelin‐1 receptor expression and extracellular signal‐regulated kinase (ERK) have been investigated.Experimental approach:Streptozotocin‐induced diabetic rats were infused with angiotensin II or, following insulin treatment, were treated with losartan, an angiotensin II receptor antagonist. Contractions of aortic strips with or without endothelium, in response to endothelin‐1 and angiotensin II, were examinedin vitro. Aortic ETAreceptors and ERK/MEK expression were measured by western blotting.Key results:Insulin‐treated diabetic rats exhibited increases in plasma insulin, angiotensin II and endothelin‐1. The systolic blood pressure and endothelin‐1‐induced contractile responses in aortaein vitrowere enhanced in insulin‐treated diabetic rats and blunted by chronic losartan administration. LY294002 (phosphatidylinositol 3‐kinase inhibitor) and/or PD98059 (MEK inhibitor) diminished the enhanced contractile response to endothelin‐1 in aortae from insulin‐treated diabetic rats. ETAand ETBreceptors, ERK‐1/2 and MEK‐1/2 protein expression and endothelin‐1‐stimulated ERK phosphorylation were all increased in aortae from insulin‐treated diabetic rats. Such increases were blunted by chronic losartan administration. Endothelin‐1‐induced contraction was significantly higher in aortae from angiotensin II‐infused diabetic rats. angiotensin II‐infusion increased ERK phosphorylation, but the expression of endothelin receptors and ERK/MEK proteins remained unchanged.Conclusions and implications:These results suggest that the combination of high plasma angiotensin II and insulin with a diabetic state induced enhancement of endothelin‐1‐induced vasoconstriction, ETAreceptor expression and ERK expression/activity in the aorta. Losartan improved both the diabetes‐related abnormalites and the diabetic hypertension.British Journal of Pharmacology(2008)155, 974–983; doi:10.1038/bjp.2008.327; published online 18 August 2008
Treating lung inflammation with agonists of the adenosine A2Areceptor: promises, problems and potential solutions
Authors: Trevethick M A , Mantell S J , Stuart E F , Barnard A , Wright K N , Yeadon M 
Published: August 2008

Adenosine A2Areceptor agonists may be important regulators of inflammation. Such conclusions have come from studies demonstrating that, (i) adenosine A2Aagonists exhibit anti‐inflammatory propertiesin vitroandin vivo, (ii) selective A2Aantagonists enhance inflammationin vivoand, (iii) knock outs of this receptor aggravate inflammation in a wide variety ofin vivomodels. Inflammation is a hallmark of asthma and COPD and adenosine has long been suggested to be involved in disease pathology. Two recent publications, however, suggested that an inhaled adenosine A2Areceptor agonist (GW328267X) did not affect either the early and late asthmatic response or symptoms associated with allergic rhinitis suggesting that the rationale for treating inflammation with an adenosine A2Areceptor agonist may be incorrect. A barrier to fully investigating the role of adenosine A2Areceptor agonists as anti‐inflammatory agents in the lung is the side effect profile due to systemic exposure, even with inhalation. Unless strategies can be evolved to limit the systemic exposure of inhaled adenosine A2Areceptor agonists, the promise of treating lung inflammation with such agents may never be fully explored. Using strategies similar to that devised to improve the therapeutic index of inhaled corticosteroids, UK371,104 was identified as a selective agonist of the adenosine A2Areceptor that has a lung focus of pharmacological activity following delivery to the lung in a pre clinicalin vivomodel of lung function. Lung‐focussed agents such as UK371,104 may be suitable for assessing the anti‐inflammatory potential of inhaled adenosine A2Areceptor agonists.British Journal of Pharmacology(2008)155, 463–474; doi:10.1038/bjp.2008.329; published online 1 September 2008
Effects of excitatory and inhibitory neurotransmission on motor patterns of human sigmoid colonin vitro
Authors: Aulí M , Martínez E , Gallego D , Opazo A , Espín F , Martí‐Gallostra M , Jiménez M , Clavé P 
Published: August 2008

Background and purpose:To characterize thein vitromotor patterns and the neurotransmitters released by enteric motor neurons (EMNs) in the human sigmoid colon.Experimental approach:Sigmoid circular strips were studied in organ baths. EMNs were stimulated by electrical field stimulation (EFS) and through nicotinic ACh receptors.Key results:Strips developed weak spontaneous rhythmic contractions (3.67±0.49 g, 2.54±0.15 min) unaffected by the neurotoxin tetrodotoxin (TTX; 1 μM). EFS induced strong contractions during (on, 56%) or after electrical stimulus (off, 44%), both abolished by TTX. Nicotine (1–100 μM) inhibited spontaneous contractions. Latency of off‐contractions and nicotine responses were reduced byNG‐nitro‐L‐arginine (1 mM) and blocked after further addition of apamin (1 μM) or the P2Y1receptor antagonist MRS 2179 (10 μM) and were unaffected by the P2X antagonist NF279 (10 μM) or α‐chymotrypsin (10 U mL−1). Amplitude ofon‐and off‐contractions was reduced by atropine (1 μM) and the selective NK2receptor antagonist Bz‐Ala‐Ala‐D‐Trp‐Phe‐D‐Pro‐Pro‐Nle‐NH2(1 μM). MRS 2179 reduced the amplitude of EFS on‐ and off‐contractions without altering direct muscular contractions induced by ACh (1 nM–1 mM) or substance P (1 nM–10 μM).Conclusions and implications:Latency of EFS‐induced off‐contractions and inhibition of spontaneous motility by nicotine are caused by stimulation of inhibitory EMNs coreleasing NO and a purine acting at muscular P2Y1receptors through apamin‐sensitive K+channels. EFS‐induced on‐ and off‐contractions are caused by stimulation of excitatory EMNs coreleasing ACh and tachykinins acting on muscular muscarinic and NK2receptors. Prejunctional P2Y1receptors might modulate the activity of excitatory EMNs. P2Y1and NK2receptors might be therapeutic targets for colonic motor disorders.British Journal of Pharmacology(2008)155, 1043–1055; doi:10.1038/bjp.2008.332; published online 1 September 2008
Etomidate reduces glutamate uptake in rat cultured glial cells: involvement of PKA
Authors: Räth M , Föhr K J , Weigt H U , Gauss A , Engele J , Georgieff M , Köster S , Adolph O 
Published: August 2008

Background and purpose:Glutamate is the main excitatory neurotransmitter in the vertebrate CNS. Removal of the transmitter from the synaptic cleft by glial and neuronal glutamate transporters (GLTs) has an important function in terminating glutamatergic neurotransmission and neurological disorders. Five distinct excitatory amino‐acid transporters have been characterized, among which the glial transporters excitatory amino‐acid transporter 1 (EAAT1) (glutamate aspartate transporter) and EAAT2 (GLT1) are most important for the removal of extracellular glutamate. The purpose of this study was to describe the effect of the commonly used anaesthetic etomidate on glutamate uptake in cultures of glial cells.Experimental approach:The activity of the transporters was determined electrophysiologically using the whole cell configuration of the patch‐clamp recording technique.Key results:Glutamate uptake was suppressed by etomidate (3–100 μM) in a time‐ and concentration‐dependent manner with a half‐maximum effect occurring at 2.4±0.6 μM. Maximum inhibition was approximately 50% with respect to the control. Etomidate led to a significant decrease ofVmaxwhereas theKmof the transporter was unaffected. In all cases, suppression of glutamate uptake was reversible within a few minutes upon washout. Furthermore, both GF 109203X, a nonselective inhibitor of PKs, and H89, a selective blocker of PKA, completely abolished the inhibitory effect of etomidate.Conclusion and implications:Inhibition of glutamate uptake by etomidate at clinically relevant concentrations may affect glutamatergic neurotransmission by increasing the glutamate concentration in the synaptic cleft and may compromise patients suffering from acute or chronic neurological disorders such as CNS trauma or epilepsy.British Journal of Pharmacology(2008)155, 925–933; doi:10.1038/bjp.2008.336; published online 18 August 2008
The antioxidant activity of chondroitin‐4‐sulphate, in carbon tetrachloride‐induced acute hepatitis in mice, involves NF‐κB and caspase activation
Authors: Campo G M , Avenoso A , Campo S , Nastasi G , Traina P , D'Ascola A , Rugolo C A , Calatroni A 
Published: August 2008

Background and purpose:Reactive oxygen species (ROC) are the main causes of carbon tetrachloride (CCl4)‐induced acute liver injury. Chondroitin‐4‐sulphate (C4S) is known to inhibit lipid peroxidation through antioxidant mechanisms. Activation of nuclear factor (NF)‐κB and caspases may strongly intensify inflammation and cell damage, in addition to that directly exerted by ROS. We investigated whether treatment with C4S, besides exerting antioxidant activity, was able to modulate NF‐κB and apoptosis activation in CCl4‐induced liver injury in mice.Experimental approach:Acute hepatitis was induced in mice by an i.p. injection of CCl4. Varying doses of C4S were administered i.p. 1 h before, 6 and 12 h after CCl4 injection. 24 h after CCl4 injection, the mice were killed for biochemical and histological analysis.Key results:CCl4 injection produced: marked elevation of alanine aminotransferase and aspartate aminotransferase; hepatic membrane lipid peroxidation, assayed by 8‐isoprostane levels; and depletion of reduced glutathione and superoxide dismutase. CCl4 also decreased NF‐κB translocation and IkBα, and increased gene expression of mRNA and protein of metalloproteases (MMP)‐2 and ‐9, and of pro‐ and cleaved forms of caspases‐3 and ‐7. There was also increased liver polymorphonuclear infiltration, evaluated by elastase assay, and hepatic cell disruption.C4S treatment inhibited lipid peroxidation; blocked NF‐κB activation and IkBα protein loss; decreased mRNA and proteins for MMPs and caspases; restored endogenous antioxidants; limited hepatic polymorphonuclear accumulation and tissue damage.Conclusions and implications:As antioxidants may inhibit NF‐κB and caspase activation, we hypothesize that treatment with C4S was able to inhibit NF‐κB and apoptosis activation in hepatic injury.British Journal of Pharmacology (2008) 155, 945–956; doi:10.1038/bjp.2008.338; published online 25 August 2008
MDA7: a novel selective agonist for CB2receptors that prevents allodynia in rat neuropathic pain models
Authors: Naguib M , Diaz P , Xu J J , Astruc‐Diaz F , Craig S , Vivas‐Mejia P , Brown D L 
Published: August 2008

Background and purpose:There is growing interest in using cannabinoid type 2 (CB2) receptor agonists for the treatment of neuropathic pain. In this report, we describe the pharmacological characteristics of MDA7 (1‐[(3‐benzyl‐3‐methyl‐2,3‐dihydro‐1‐benzofuran‐6‐yl)carbonyl]piperidine), a novel CB2receptor agonist.Experimental approach:We characterized the pharmacological profile of MDA7 by using radioligand‐binding assays andin vitrofunctional assays at human cannabinoid type 1 (CB1) and CB2receptors.In vitrofunctional assays were performed at rat CB1and CB2receptors. The effects of MDA7 in reversing neuropathic pain were assessed in spinal nerve ligation and paclitaxel‐induced neuropathy models in rats.Key results:MDA7 exhibited selectivity and agonist affinity at human and rat CB2receptors. MDA7 treatment attenuated tactile allodynia produced by spinal nerve ligation or by paclitaxel in a dose‐related manner. These effects were selectively antagonized by a CB2receptor antagonist but not by CB1or opioid receptor antagonists. MDA7 did not affect rat locomotor activity.Conclusion and implications:MDA7, a novel selective CB2agonist, was effective in suppressing neuropathic nociception in two rat models without affecting locomotor behaviour. These results confirm the potential for CB2agonists in the treatment of neuropathic pain.British Journal of Pharmacology(2008)155, 1104–1116; doi:10.1038/bjp.2008.340; published online 1 September 2008
Pleiotropic action(s) of the bradycardic agent ivabradine: cardiovascular protection beyond heart rate reduction
Authors: Heusch G 
Published: August 2008

The bradycardic agent ivabradine has proved to be of benefit in experimental models with the end points of ischaemic myocardial blood flow and contractile function, infarct size, post‐infarct remodelling and atherosclerosis. The benefits to ischaemic myocardial blood flow and contractile function are strictly heart rate dependent; those on infarct size are partly heart rate independent. The heart rate dependency of ivabradine's benefit for atherosclerotic vascular function is contradictory, and that on post‐infarct remodelling is entirely unclear.British Journal of Pharmacology (2008) 155, 970–971; doi:10.1038/bjp.2008.347; published online 1 September 2008
Effects of Onset- and Rhyme-Related Distractors on Phonological Processing in Children With Specific Language Impairment
Authors: Seiger-Gardner Liat , Brooks Patricia J. 
Published: August 2008

Purpose
This study used the cross-modal picture–word interference task of P. J. Brooks and B. MacWhinney (2000) to compare effects of phonologically related words on lexical access in children with specific language impairment (SLI).

Method
Children (7;1 [years;months]–11;2) named pictures while ignoring auditory distractors. Three stimulus asynchrony conditions varied the timing of distractors relative to the pictures. Experiment 1 presented onset-related (bell–bed), unrelated (clown–bed), neutral (go–bed), and identical (bed–bed) distractors. Experiment 2 presented rhyme-related instead of onset-related distractors (clock–sock).

Results
Children with SLI produced longer reaction times (RTs) and more errors than their typical language development (TLD) peers. For children with SLI, onset-related distractors led to slower RTs than unrelated distractors (inhibition) when presented before the picture, and faster RTs (facilitation) when presented after the picture. Children with TLD showed facilitation from onset-related distractors when presented after the picture but no inhibition when presented before the picture. Both groups failed to show facilitation from rhyme-related distractors.

Conclusions
The priming effects from onset-related distractors and lack of effects from rhyme-related distractors in SLI supports “just-in-time” incremental processing, similar to children with TLD. However, children with SLI experience phonological interference from members of a lexical cohort while accessing words. Results are discussed with respect to observed word finding and word learning difficulties in SLI.
Toward Validation of a Minimal Competence Phonetic Core for African American Children
Authors: Stockman Ida J. 
Published: August 2008

Purpose
This study aimed to show (a) whether the minimal competence core (MCC) of consonants used by African American preschoolers in I. Stockman (2006) can be observed in a larger group of children using shorter and more controlled speech samples and (b) whether the MCC pass/fail outcomes are differentially related to performance on selected criterion measures of typical and atypical speech.

Method
Word-initial single and clustered consonants were sampled in the conversational speech of 120 Head Start students who were distributed in a northern (Lansing, Michigan) and a southern (Baton Rouge, Louisiana) regional location.

Results
The data generally corroborated the earlier preliminary report, which was based on just 7 children. More than 80% of the children met criteria for passing the core set of phonetic competencies, which included word-initial consonant clusters and 13 consonant singletons. Pass/fail outcomes were significantly related to suspected clinical delay and the overall Percentage of Consonants Correct–Revised (PCC-R).

Conclusion
The initial consonant core identified in this study is potentially useful for identifying speech delay among young African American children. Clinical and research issues related to its use for diagnostic screening are discussed.