bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ultrathin SiO2 on Si. VII. Angular accuracy in XPS and an accurate attenuation length
Authors: Seah M. P. , Spencer S. J. 
Published: July 2005

AbstractFollowing an earlier study of the uncertainties for defining thicknesses by angle‐resolved XPS, one of the major instrumental uncertainties has been evaluated that limits both precision and accuracy. For analysis of the thicknesses of SiO2 on Si, certain angles of emission have been recommended, but an error of 1° in these angles leads directly to an error in the thickness of ∼1% from this contribution alone. This is significant since the total uncertainty required in the (International technology roadmap for semiconductors) ITRS is only 1%. In many instruments, to reduce sample‐stage vibration and for other reasons, the angle and other setting adjustments are engineered with backlash. This, combined with the manufacturer's tolerances, can lead to angular errors above 1°. We report here a device using a laser and reflectors, fixed to the sample mount, that allow the angle of emission to be set to a precision better than 0.1° and, furthermore, a method to set the zero angle of emission to 0.1°. Using this geometrical device as well as by measurements of intensities in XPS, it is deduced that the data in our earlier report for the CCQM (Consultative Committee for Amount of Substance) intercomparison were for angles 1.89° ± 0.15° too high. Consequently, by a re‐analysis of all of that data, we find that our recommended attenuation length data for the Si 2p photoelectrons in thermal SiO2 using Mg or Al Kα X‐rays should be increased to 2.996 nm and 3.485 nm, respectively, an increase of 1.2% on the originally calculated values. These values now have standard uncertainties of 0.54% instead of the 20% of the TPP‐2M calculations. This leads to an improved accuracy in the measurement of ultrathin thermal oxides on silicon by XPS, of better than 1% for thicknesses greater than 1.5 nm but less than 8 nm. © Crown copyright 2005. Reproduced with the permission of Her Majesty's Stationery Office. Published by John Wiley & Sons, Ltd.
Coexistence of competitive species with a stage‐structured life cycle
Authors: Mougi Akihiko , Nishimura Kinya 
Published: July 2005

AbstractEcological theory provides explanations for exclusion or coexistence of competing species. Most theoretical works on competition dynamics that have shaped current perspectives on coexistence assume a simple life cycle. This simplification, however, may omit important realities. We present a simple two‐stage structured competition model to investigate the effects of life‐history characteristics on coexistence. The achievement and the stability of coexistence depend not only on competition coefficients but also on a set of life‐history parameters that reflect the viability of an individual, namely, adult death rate, maturation rate, and birth rate. High individual viability is necessary for a species to persist, but it does not necessarily facilitate coexistence. Intense competition at the juvenile or adult stage may require higher or lower viability, respectively, for stable coexistence to be possible. The stability mechanism can be explained by the refuge effect of the less competitive stage, and the birth performance, which preserves the less competitive stage as a refuge. Coexistence might readily collapse if the life‐history characteristics, which together constitute individual viability, change, even though two species have an inherent competitive relation conducive to stable coexistence.
Developing skeletal muscle cells express functional muscarinic acetylcholine receptors coupled to different intracellular signaling systems
Authors: Furlan Ingrid , Godinho Rosely Oliveira 
Published: July 2005

This study analyzed the expression of muscarinic acetylcholine receptors (mAChRs) in the rat cultured skeletal muscle cells and their coupling to G protein, phospholipase C and adenylyl cyclase (AC).
Our results showed the presence of a homogeneous population of [3H]methyl‐quinuclidinyl benzilate‐binding sites in the membrane fraction from the rat cultured muscle (KD=0.4 nM, Bmax=8.9 fmol mg protein−1). Specific muscarinic binding sites were also detected in denervated diaphragm muscles from adult rats and in myoblasts isolated from newborn rats.
Activation of mAChRs with carbachol induced specific [35S]GTPγS binding to cultured muscle membranes and potentiated the forskolin‐dependent stimulation of AC. These effects were totally inhibited by 0.1–1 μM atropine.
In addition, mAChRs were able to stimulate generation of diacylglycerol (DAG) in response to acetylcholine, carbachol or selective mAChR agonist oxotremorine‐M.
The carbachol‐dependent increase in DAG was inhibited in a concentration‐dependent manner by mAChR antagonists atropine, pirenzepine and 4‐DAMP mustard.
Finally, activation of these receptors was correlated with increased synthesis of acetylcholinesterase, via a PKC‐dependent pathway.
Taken together, these results indicate that expression of mAChRs, coupled to G protein and distinct intracellular signaling systems, is a characteristic of noninnervated skeletal muscle cells and may be responsible for trophic influences of acetylcholine during formation of the neuromuscular synapse.

British Journal of Pharmacology (2005) 146, 389–396. doi:10.1038/sj.bjp.0706329
Effect of clopidogrel on the expression of inflammatory markers in rabbit ischemic coronary artery
Authors: Molero Laura , López‐Farré Antonio , Mateos‐Cáceres Petra J , Fernández‐Sánchez Ruth , Maestro María Luisa , Silva Jacobo , Rodríguez Enrique , Macaya Carlos 
Published: July 2005

Inflammation and platelet activation are critical phenomena in the setting of acute coronary syndromes. Platelets may contribute to increase ischemic injury by enhancing the inflammatory response of leukocytes and endothelial myocardial cells. Pharmacological inhibition of platelet activation prevents ischemic complications in patients with coronary diseases. Agents directed against the integrin glycoprotein IIb/IIIa (GP IIb/IIIa) receptor not only inhibit platelet aggregation but also have been demonstrated to limit the inflammatory response in acute coronary syndromes. The question then raised is if the inhibition of platelet activation by other mechanisms than the blockade of GP IIb/IIIa may also exert anti‐inflammatory effects. The aim of the present study was to analyze if clopidogrel may exert anti‐inflammatory effects during the acute phase of myocardial infarction.
A ligature was placed around the left anterior descending coronary artery of New Zealand White rabbits. After 15 min of ischemia, the myocardium was reperfused and the ischemic coronary artery was isolated 24 h after the ischemia. A group of ischemic rabbits was given a single oral dose of clopidogrel (20 mg kg−1) just after the arterial occlusion and the animal was recovered. Sham‐operated animals served as control.
P‐selectin expression was significantly increased in infarcted rabbits with respect to control rabbits. Clopidogrel administration reduced P‐selectin expression with respect to untreated infarcted rabbits. CD40 ligand and tissue factor expression was increased in the ischemic coronary artery and reduced after clopidogrel administration. Clopidogrel also protected endothelial nitric oxide synthase protein expression in the ischemic coronary artery, a protein that has been found downregulated under inflammatory conditions.
In conclusion, inhibition of platelet activation by clopidogrel exerted anti‐inflammatory effects on the ischemic coronary artery.

British Journal of Pharmacology (2005) 146, 419–424. doi:10.1038/sj.bjp.0706340
Comparison of the biological activities of anagrelide and its major metabolites in haematopoietic cell cultures
Authors: Wang Guosu , Franklin Richard , Hong Ying , Erusalimsky Jorge D 
Published: July 2005

The platelet‐lowering drug anagrelide inhibits bone marrow megakaryocytopoiesis by an unknown mechanism. Recently, it was found that anagrelide is bio‐transformed in humans into two major metabolites (6,7‐dichloro‐3‐hydroxy‐1,5 dihydro‐imidazo[2,1‐b]quinazolin‐2‐one (BCH24426) and 2‐amino‐5,6‐dichloro‐3,4,‐dihydroquinazoline (RL603). Whether these metabolites have biological activities that may underlie the mode of action of the parent drug is presently unclear. To clarify this question here we have compared the activities of anagrelide, BCH24426 and RL603 on the growth and differentiation of CD34+ haematopoietic progenitor cells in liquid culture and on the migration of differentiated megakaryocytes.
Incubation with either anagrelide, BCH24426 or RL603 did not affect the early expansion of CD34+ cells stimulated by thrombopoietin. In contrast, both anagrelide and BCH24426 potently inhibited the development of megakaryocytes (IC50±s.e.m.=26±4 and 44±6 nM, respectively), whereas RL603 showed no significant effect.
Anagrelide and BCH24426 did not affect erythroid or myelomonocytic differentiation stimulated by erythropoietin or granulocyte–macrophage colony‐stimulating factor, demonstrating the selectivity of these compounds against the megakaryocytic lineage.
Neither anagrelide nor its metabolites showed a significant effect on the migratory response of megakaryocytes towards stromal cell‐derived factor‐1α.
Although BCH24426 was shown to be considerably more potent than anagrelide as an inhibitor of phosphodiesterase type III (PDEIII) (IC50=0.9 vs 36 nM) this activity did not correlate with the potency of inhibition of megakaryocyte development. Furthermore, other PDEIII inhibitors of widely differing potency were shown to have negligible effects on megakaryocytopoiesis.
Taken together our results demonstrate that anagrelide and BCH24426 target a cellular event involved specifically in the megakaryocyte differentiation programme, which is independent of PDEIII inhibition.

British Journal of Pharmacology (2005) 146, 324–332. doi:10.1038/sj.bjp.0706341
Ethyl caffeate suppresses NF‐κB activation and its downstream inflammatory mediators, iNOS, COX‐2, and PGE2in vitro or in mouse skin
Authors: Chiang Yi‐Ming , Lo Chiu‐Ping , Chen Yi‐Ping , Wang Sheng‐Yang , Yang Ning‐Sun , Kuo Yueh‐Hsiung , Shyur Lie‐Fen 
Published: July 2005

Ethyl caffeate, a natural phenolic compound, was isolated from Bidens pilosa, a medicinal plant popularly used for treating certain inflammatory syndromes. The purpose of this study was to investigate the structural activity, and the anti‐inflammatory functions and mechanism(s) of ethyl caffeate.
Ethyl caffeate was found to markedly suppress the lipopolysaccharide (LPS)‐induced nitric oxide (NO) production (IC50=5.5 μg ml−1), mRNA and protein expressions of inducible nitric oxide synthase (iNOS), and prostaglandin E2 (PGE2) production in RAW 264.7 macrophages.
Transient gene expression assays using human cox‐2 promoter construct revealed that ethyl caffeate exerted an inhibitory effect on cox‐2 transcriptional activity in 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA)‐treated MCF‐7 cells.
Immunohistochemical studies of mouse skin demonstrated that TPA‐induced COX‐2 expression was significantly inhibited by ethyl caffeate with a superior effect to that of celecoxib, a nonsteroidal anti‐inflammatory drug.
The phosphorylation and degradation of inhibitor κB (IκB) and the translocation of nuclear transcription factor‐κB (NF‐κB) into the nucleus, as well as the activation of mitogen‐activated protein kinases (MAPKs) induced by LPS in macrophages, were not affected by ethyl caffeate. Ethyl caffeate, however, could inhibit NF‐κB activation by impairing the binding of NF‐κB to its cis‐acting element. These results suggest that ethyl caffeate suppresses iNOS and COX‐2 expressions partly through the inhibition of the NF‐κB·DNA complex formation.
Structure–activity relationship analyses suggested that the catechol moiety and α,β‐unsaturated ester group in ethyl caffeate are important and essential structural features for preventing NF‐κB·DNA complex formation. This study provides an insight into the probable mechanism(s) underlying the anti‐inflammatory and therapeutic properties of ethyl caffeate.

British Journal of Pharmacology (2005) 146, 352–363. doi:10.1038/sj.bjp.0706343
A comparison of the effects of unfractionated heparin, dalteparin and danaparoid on vascular endothelial growth factor‐induced tumour angiogenesis and heparanase activity
Authors: Takahashi Hidenori , Ebihara Satoru , Okazaki Tatsuma , Asada Masanori , Sasaki Hidetada , Yamaya Mutsuo 
Published: July 2005

Disseminated intravascular coagulation (DIC) is the most common complication of solid tumours. In this study, the effectiveness of three polysaccharide anticoagulants (PSAs), at therapeutic doses, at inhibiting solid tumour growth was investigated.
Mice with tumour xenografts were subcutaneously injected with either unfractionated heparin (UFH; 200 units kg−1 day−1), dalteparin (75 units kg−1 day−1) or danaparoid (50 units kg−1 day−1). At these concentrations, these PSAs are equieffective at inhibiting blood coagulation activated factor X. In mice with Lewis lung carcinoma (LLC) tumours dalteparin and, to a lesser extent, UFH inhibited both tumour growth and angiogenesis, whereas danaparoid did not. In contrast, in mice with KLN205 tumours, all the PSAs inhibited tumour growth and angiogenesis.
All the PSAs significantly inhibited proliferation, migration of endothelial cells and vessel formation in matrigel plugs containing vascular endothelial growth factor (VEGF) and there were no significant differences between these effects of the PSAs. The PSAs had no effect on endothelial cell tubular formation in vitro.
Although all the PSAs inhibited VEGF production in KLN205 tumours in vivo and cells in vitro, in LLC tumours and cells only UFH and dalteparin inhibited VEGF production, whereas danaparoid did not.
In both LLC and KLN205 tumours in vivo, heparanase activity was inhibited by UFH and dalteparin, but not by danaparoid.
Hence, UFH and dalteparin may be more effective than danaparoid at inhibiting cancer progression in DIC patients with solid tumours, due at least in part to their ability to suppress VEGF and heparanase in tumours.

British Journal of Pharmacology (2005) 146, 333–343. doi:10.1038/sj.bjp.0706344
Endogenous opioid mechanisms partially mediate P2X3/P2X2/3‐related antinociception in rat models of inflammatory and chemogenic pain but not neuropathic pain
Authors: McGaraughty Steve , Honore Prisca , Wismer Carol T , Mikusa Joseph , Zhu Chang Z , McDonald Heath A , Bianchi Bruce , Faltynek Connie R , Jarvis Michael F 
Published: July 2005

P2X3/P2X2/3 receptors have emerged as important components of nociception. However, there is limited information regarding the neurochemical systems that are affected by antagonism of the P2X3/P2X2/3 receptor and that ultimately contribute to the ensuing antinociception. In order to determine if the endogenous opioid system is involved in this antinociception, naloxone was administered just prior to the injection of a selective P2X3/P2X2/3 receptor antagonist, A‐317491, in rat models of neuropathic, chemogenic, and inflammatory pain.
Naloxone (1–10 mg kg−1, i.p.), dose‐dependently reduced the antinociceptive effects of A‐317491 (1–300 μmol kg−1, s.c.) in the CFA model of thermal hyperalgesia and the formalin model of chemogenic pain (2nd phase), but not in the L5–L6 spinal nerve ligation model of neuropathic allodynia. In comparison experiments, the same doses of naloxone blocked or attenuated the actions of morphine (2 or 8 mg kg−1, s.c.) in each of these behavioral models.
Injection of a peripheral opioid antagonist, naloxone methiodide (10 mg kg−1, i.p.), did not affect A‐317491‐induced antinociception in the CFA and formalin assays, suggesting that the opioid component of this antinociception occurred within the CNS. Furthermore, this utilization of the central opioid system could be initiated by antagonism of spinal P2X3/P2X2/3 receptors since the antinociceptive actions of intrathecally delivered A‐317491 (30 nmol) in the formalin model were reduced by both intrathecally (10–50 nmol) and systemically (10 mg kg−1, i.p.) administered naloxone.
This utilization of the opioid system was not specific to A‐317491 since suramin‐, a nonselective P2X receptor antagonist, induced antinociception was also attenuated by naloxone.
In in vitro studies, A‐317491 (3–100 μM) did not produce any agonist response at δ opioid receptors expressed in NG108‐15 cells. A‐317491 had been previously shown to be inactive at the κ and μ opioid receptors. Furthermore, naloxone, at concentrations up to 1 mM, did not compete for [3H] A‐317491 binding in 1321N1 cells expressing human P2X3 receptors.
Taken together, these results indicate that antagonism of spinal P2X3/P2X2/3 receptors results in an indirect activation of the opioid system to alleviate inflammatory hyperalgesia and chemogenic nociception.

British Journal of Pharmacology (2005) 146, 180–188. doi:10.1038/sj.bjp.0706346
Intrinsic sensory deprivation induced by neonatal capsaicin treatment induces changes in rat brain and behaviour of possible relevance to schizophrenia
Authors: Newson Penny , Lynch‐Frame Ann , Roach Rebecca , Bennett Sarah , Carr Vaughan , Chahl Loris A 
Published: July 2005

Schizophrenia is considered to be a neurodevelopmental disorder with origins in the prenatal or neonatal period. Brains from subjects with schizophrenia have enlarged ventricles, reduced cortical thickness (CT) and increased neuronal density in the prefrontal cortex compared with those from normal subjects. Subjects with schizophrenia have reduced pain sensitivity and niacin skin flare responses, suggesting that capsaicin‐sensitive primary afferent neurons might be abnormal in schizophrenia.
This study tested the hypothesis that intrinsic somatosensory deprivation, induced by neonatal capsaicin treatment, causes changes in the brains of rats similar to those found in schizophrenia. Wistar rats were treated with capsaicin, 50 mg kg−1 subcutaneously, or vehicle (control) at 24–36 h of life. At 5–7 weeks behavioural observations were made, and brains removed, fixed and sectioned.
The mean body weight of capsaicin‐treated rats was not significantly different from control, but the mean brain weight of male, but not female, rats, was significantly lower than control.
Capsaicin‐treated rats were hyperactive compared with controls. The hyperactivity was abolished by haloperidol.
Coronal brain sections of capsaicin‐treated rats had smaller cross‐sectional areas, reduced CT, larger ventricles and aqueduct, smaller hippocampal area and reduced corpus callosum thickness, than brain sections from control rats. Neuronal density was increased in several cortical areas and the caudate putamen, but not in the visual cortex.
It is concluded that neonatal capsaicin treatment of rats produces brain changes that are similar to those found in brains of subjects with schizophrenia.

British Journal of Pharmacology (2005) 146, 408–418. doi:10.1038/sj.bjp.0706349
Interactions of metoclopramide and ergotamine with human 5‐HT3A receptors and human 5‐HT reuptake carriers
Authors: Walkembach Jan , Brüss Michael , Urban Bernd W , Barann Martin 
Published: July 2005

The actions of metoclopramide and ergotamine, drugs which are used as a combined migraine medication, on human (h)5‐HT3A receptors and 5‐HT reuptake carriers, stably expressed in HEK‐293 cells, were studied with patch‐clamp‐ and ([3H]5‐HT)‐uptake techniques.
At clinical concentrations, metoclopramide inhibited peak and integrated currents through h5‐HT3A receptors concentration‐dependently (IC50=0.064 and 0.076 μM, respectively) when it was applied in equilibrium (60 s before and during 5‐HT (30 μM) exposure). The onset and offset time constants of metoclopramide action were 1.3 and 2.1 s, respectively. The potency of metoclopramide when exclusively applied during the agonist pulse decreased more than 200‐fold (IC50=19.0 μM, peak current suppression).
Metoclopramide (0.10 μM) did not alter the EC50 of 5‐HT‐induced peak currents. In contrast to the lack of competitive interaction between metoclopramide and 5‐HT in this functional assay, metoclopramide inhibited specific [3H]GR65630 binding to human h5‐HT3A receptors in a surmountable manner. This seeming discrepancy between functional studies and radioligand binding experiments may be accounted for by (1) the slow kinetics of inhibition of peak currents by metoclopramide compared with the fast onset and offset kinetics of 5‐HT‐induced currents and (2) the low efficacy of metoclopramide in inhibiting radioligand binding (e.g. only 20% binding inhibition compared to 79% peak current suppression by 200 nM metoclopramide).
At low concentrations (1–10 nM), ergotamine had no effect on 5‐HT (30 μM)‐induced peak currents. Above clinical concentrations, ergotamine (>3 μM) inhibited them.
When both drugs were applied together (0.10 μM metoclopramide+0.001 to 0.01 μM ergotamine), an inhibition of both, peak and integrated current responses was observed.
Neither metoclopramide (30 μM) nor ergotamine (30 μM) had an effect on the 5‐HT reuptake carrier as they did not alter the citalopram‐sensitive [3H]5‐HT uptake.

British Journal of Pharmacology (2005) 146, 543–552. doi:10.1038/sj.bjp.0706351
Expression and immunolocalization of aquaporin‐7 in rat gastrointestinal tract
Authors: Laforenza Umberto , Gastaldi Giulia , Grazioli Monica , Cova Emanuela , Tritto Simona , Faelli Alide , Calamita Giuseppe , Ventura Ulderico 
Published: July 2005

Background information. In the gastrointestinal tract of mammals, water can either be secreted with digestive juices or absorbed by the small and large intestine. Transcellular water movement can be mediated by the transmembrane protein family of AQPs (aquaporins), as has also been recently identified in the gastrointestinal tract. However, the localization, expression and functioning of AQPs in the gastrointestinal tract have not been completely characterized. For the present study, we investigated: (1) the expression of AQP7 in some portions of rat gastrointestinal tract by semiquantitative reverse transcriptase—PCR and by immunoblotting and (2) the cellular and subcellular localization of AQP7 by immunohistochemistry.Results. AQP7 mRNA and proteins were highly expressed in the small intestine, weakly in the caecum, colon and rectum and were absent in the stomach. Immunoblotting analysis using rat gastrointestinal tract membrane fractions showed two major bands corresponding to a molecular mass of approx. 34 and 40 kDa for the AQP7 protein. No bands were observed when the anti‐AQP7 antibody was preadsorbed with the immunizing peptide. Immunohistochemistry revealed strong AQP7 labelling in the surface epithelial cells of duodenum, jejunum, ileum, caecum, colon and rectum, whereas weak or no labelling was observed in the crypt cells. The labelling was manifest particularly in the apical membrane but intracellular staining was also observed.Conclusions. The results indicate that AQP7 is present in the small and large intestine. The higher expression of AQP7 protein at the apical pole of the superficial epithelial cells suggests its involvement in rapid fluid movement through the villus epithelium.