bluuebunny/crossref_metadata_2025_split huggingface dataset:
A trophic cascade in a macrophyte‐based food web at the land–water ecotone
Authors: Schlacher Thomas A. , Cronin Greg 
Published: December 2006

AbstractTrophic cascades may purportedly be more common in aquatic than terrestrial food webs, but herbivory on freshwater vascular plants has historically been considered low. Water lilies are an exception, suffering severe grazing damage by leaf beetles. To test whether a central prediction of cascade models—that predator effects propagate downwards to plants—operates in a macrophyte‐based food web, we experimentally manipulated predation pressure on a key herbivore of water lilies in the littoral zone of a lake in Michigan, USA. Field experiments comprised combinations of caging treatments to alter the number of predators (larvae of the ladybird beetleColeomegilla maculata) that hunt the grazers of the macrophytes (larvae of the leaf beetlesGalerucella nymphaeae) on the leaves of the water lilyNuphar advena. Predatory larvae of the ladybird beetles significantly reduced grazing damage to water‐lily leaves by 35–43%. The predators reduced plant damage chiefly via density‐mediated effects, when lower densities of grazers translated to significant declines in plant damage. Plant damage caused by the surviving herbivores was less than predicted from individual grazing rates under predator‐free conditions. This suggests that trait‐mediated effects may possibly also operate in this cascade. The observed strong effect of predators on a non‐adjacent trophic level concurs with an essential component of the trophic cascade model, and the cascade occurred at the ecotone between aquatic and terrestrial habitats:Nupharis an aquatic macrophyte with emergent and floating leaves, whereas both beetle species are semi‐terrestrial and use the dry, emergent and floating leaves of the water lily as habitat. Also, the cascade is underpinned by freshwater macrophytes—a group for which trophic processes have often been underappreciated in the past.
Correlations of relative rate constants for sulfonation of alkylbenzenes with molecular structure
Authors: Roberts David W. , Ward Robert S. , Hughes Paul J. 
Published: December 2006

AbstractRelative sulfonation rates of a series of linear alkylbenzenes are correlated with carbon numbers of the linear branches from which the alkyl groups are constituted. The trends are interpreted in terms of a composite steric parameter which reflects the degrees of freedom lost in forming the transition state. The results lend support to the argument that the entropy of activation is the main factor determining the relative reactivities of the different homologs and isomers in this reaction.
Synergistic solubilization of decafluorobiphenyl by micelles of fluorocarbon surfactants
Authors: Asakawa Tsuyoshi , Kitaguchi Takashi , Miyagishi Shigeyoshi 
Published: December 2006

AbstractSolubilization of decafluorobiphenyl (FBIP) by surfactants in aqueous solution was examined to investigate the properties of micelles composed of surfactants having a per‐fluorocarbon chain. Fluorocarbon surfactants solubilize FBIP better than hydrocarbon surfactants. Significant solubilization by fluorocarbon surfactants was observed upon addition of salt. Highly synergistic solubilization of FBIP using surfactant mixtures was also observed for fluorocarbon and hydrocarbon surfactants in the presence of salt. The high solubilization ability of surfactants can be attributed to micelle growth. A simple geometrical consideration of molecular packing in micelles revealed that the characteristic micelle is composed of bulky fluorocarbon chains. The solubilization behavior accompanied by micelle growth would be closely associated with a change in interfacial contact area between the micelle core and bulk water. The behavior of fluorescence intensity of micelle‐solubilized FBIP also indicated a change in micropolarity of fluorocarbon micelles accompanied by micelle growth.
Safety to human skin of cocamidopropyl betaine: A mild surfactant for personal‐care products
Authors: Hunter J. Edward , Fowler Joseph F. 
Published: December 2006

AbstractCocamidopropyl betaine (CAPB) is a mild surfactant used in shampoos, conditioners, body washes, and other personal‐care products. Several recently published case reports have suggested that CAPB may be a skin sensitizer. A 6‐wk product‐use study was conducted to determine whether subjects with previous positive patch tests to CAPB could use personal‐care products (prototype hair shampoo, liquid handsoap, and body wash) with this surfactant without problems. Post‐study patch testing suggested that amidoamine, a material used in the synthesis of CAPB and a contaminant of CAPB preparations, is a likely sensitizer. However, patch testing did not rule out the possibility that CAPB itself may be an allergen to a small number of presensitized individuals. It is recommended that CAPB with minimal levels of contamination be used for the formulation of personal‐care products.
Molecular characterization of three peroxisome proliferator‐activated receptors from the sea bass (Dicentrarchus labrax)
Authors: Boukouvala Evridiki , Antonopoulou Efthimia , Favre‐Krey Laurence , Diez Amalia , Bautista José M. , Leaver Michael J. , Tocher Douglas R. , Krey Grigorios 
Published: December 2006

AbstractPeroxisome proliferator‐activated receptors (PPAR) are nuclear hormone receptors that control the expression of genes involved in lipid homeostasis in mammals. We searched for PPAR in sea bass, a marine fish of particular interest to aquaculture, after hypothesizing that the physiological and molecular processes that regulate lipid metabolism in fish are similar to those in mammals. Here, we report the identification of complementary DNA and corresponding genomic sequences that encode three distinct PPAR from sea bass. The sea bass PPAR are the structural homologs of the mammalian PPARα, β/δ and γ isotypes. As revealed by RNase protection, the tissue expression profile of the fish PPAR appears to be very similar to that of the mammalian PPAR homologs. Thus, PPARα is mainly expressed in the liver, PPARγ in adipose tissue, and PPARβ in all tissues tested, with its highest levels in the liver, where it is also the dominant isotype expressed. Like mammalian PPAR, the sea bass isotypes recognize and bind to PPAR response elements of both mammalian and piscine origin, as heterodimers with the 9‐cis retinoic acid receptor. Through the coactivator‐dependent receptor ligand assay, we also demonstrated that natural FA and synthetic hypolipidemic compounds can act as ligands of the sea bass PPARα and β isotypes. This suggests that the sea bass PPAR act through similar mechanisms and perform the same critical lipid metabolism functions as mammalian PPAR.
Role of p38 mitogen‐activated protein kinase in cardiac remodelling
Authors: Frantz S , Behr T , Hu K , Fraccarollo D , Strotmann J , Goldberg E , Ertl G , Angermann C E , Bauersachs J 
Published: December 2006

Background and purpose:Mitogen‐activated protein kinases (MAPK) are centrally involved in several mechanisms important for heart failure such as apoptosis, activation of inflammatory responses and cell proliferation. We therefore evaluated the effect of the selective p38 MAPK inhibitor SB 239063 on progression of left ventricular remodelling after myocardial infarction (MI) in rats.Experimental approach:Rats were treated for 9 weeks with placebo or SB 239063 by gavage (15mg kg‐1) twice daily starting 7 days after ligation of the left anterior descending artery. Serial transthoracic echocardiography was performed at days 7, 36 and 70.Key results:Over the 9 weeks, mortality was not different between the groups. On echocardiography, animals after myocardial infarction exhibited significant left ventricular dilatation as expected (week 10, end‐systolic diameter, placebo sham 5.21± 0.34 vs. placebo MI 8.44± 0.57 mm). However, there was no difference between placebo and SB 239063‐treated rats (week 10, end‐systolic diameter, SB MI 7.76± 0.74mm, not significantly different from placebo MI). Haemodynamics changed accordingly. Moreover, SB 239063 had no effect on left ventricular hypertrophy. Treatment with SB 239063 significantly reduced cytokine expression of tumour necrosis factor and interleukin‐1β after myocardial infarction. However, collagen content was not influenced by the treatment.Conclusion:Despite a reduction of inflammation, treatment with the p38 inhibitor SB 239063 does not affect cardiac remodelling and cardiac function when treatment is started 7 days after myocardial infarction.British Journal of Pharmacology(2007)150, 130–135. doi:10.1038/sj.bjp.0706963
Protease‐activated receptor‐4: a novel mechanism of inflammatory pain modulation
Authors: Asfaha S , Cenac N , Houle S , Altier C , Papez M D , Nguyen C , Steinhoff M , Chapman K , Zamponi G W , Vergnolle N 
Published: December 2006

Background and purpose:Protease‐activated receptor‐4 (PAR4), the most recently discovered member of the PARs family, is activated by thrombin, trypsin and cathepsin G, but can also be selectively activated by small synthetic peptides (PAR4‐activating peptide, PAR4‐AP). PAR4is considered a potent mediator of platelet activation and inflammation. As both PAR1and PAR2have been implicated in the modulation of nociceptive mechanisms, we investigated the expression of PAR4in sensory neurons and the effects of its selective activation on nociception.Experimental approach and key results:We demonstrated the expression of PAR4in sensory neurons isolated from rat dorsal root ganglia by reverse transcription‐polymerase chain reaction and immunofluorescence. We found that PAR4colocalized with calcitonin gene‐related peptide and substance P. We also showed that a selective PAR4‐AP was able to inhibit calcium mobilization evoked by KCl and capsaicin in rat sensory neurons. Moreover, the intraplantar injection of a PAR4‐AP significantly increased nociceptive threshold in response to thermal and mechanical noxious stimuli, while a PAR4inactive control peptide had no effect. The anti‐nociceptive effects of the PAR4‐AP were dose‐dependent and occurred at doses below the threshold needed to cause inflammation. Finally, co‐injection of the PAR4‐AP with carrageenan significantly reduced the carrageenan‐induced inflammatory hyperalgesia and allodynia, but had no effect on inflammatory parameters such as oedema and granulocyte infiltration.Conclusions and implications:Taken together, these results identified PAR4as a novel potential endogenous analgesic factor, which can modulate nociceptive responses in normal and inflammatory conditions.British Journal of Pharmacology(2007)150, 176–185. doi:10.1038/sj.bjp.0706975
Characterization of kinin receptors in human cultured detrusor smooth muscle cells
Authors: Bellucci F , Cucchi P , Santicioli P , Lazzeri M , Turini D , Meini S 
Published: December 2006

Background and purpose:Kinins have an important role in inflammatory cystitis and in animal pathophysiological models, by acting on epithelium, fibroblasts, sensory innervation and smooth muscle. The aim of this study was to characterize the receptors responsible for direct motor responses induced by kinins on human detrusor.Experimental approach:Human detrusor cells from biopsies were isolated and mantained in culture. B1and B2kinin receptors were characterized by means of radioligand and functional experiments (PI accumulation and PGE2release).Key results:[3H]‐[desArg9]‐Lys‐BK and [3H]‐BK saturation studies indicated receptor density (Bmax) andKdvalues of 19 or 113 fmol mg−1, and 0.16 or 0.11 nM for the B1or B2receptors, respectively. Inhibition binding studies indicated the selectivity of the B1receptor antagonist [desArg9Leu8]‐Lys‐BK and of the B2receptor antagonists Icatibant and MEN16132. [DesArg9]‐Lys‐BK and BK induced PI accumulation with an EC50of 1.6 and 1.4 nM and different maximal responses (Emaxof [desArg9]‐Lys‐BK was 10% of BK). BK also induced prostaglandin E2release (EC502.3 nM), whereas no response was detected with the B1receptor agonist. The incubation of detrusor smooth muscle cells with interleukin 1β (IL‐1β) or tumour necrosis factor‐α(TNF‐α) (10 ng ml−1) induced a time‐dependent increase in radioligand‐specific binding, which was greater for the B1than for the B2receptor.Conclusions and Implications:Human detrusor smooth muscle cells in culture retain kinin receptors, and represent a suitable model to investigate the mechanisms and changes that occur under chronic inflammatory conditions.British Journal of Pharmacology(2007)150, 192–199. doi:10.1038/sj.bjp.0706976
The function of α‐ and β‐adrenoceptors of the saphenous artery in caveolin‐1 knockout and wild‐type mice
Authors: Neidhold S , Eichhorn B , Kasper M , Ravens U , Kaumann A J 
Published: December 2006

Background and purpose:Adrenoceptors can associate with cardiac caveolae. To investigate the function of vascular caveolae, adrenoceptor‐mediated effects were compared in the saphenous artery of caveolin‐1 knockout (cav‐1KO) and wild‐type (WT) mice.Experimental approach:Electronmicroscopy was used to detect caveolae. Real‐Time quantitative PCR was used for adrenoceptor subtypes. Catecholamine‐evoked contractions and relaxations were studied in arterial segments.Key results:Caveolae were found in arterial smooth muscle from WT but not from cav‐1KO mice. Arterial mRNA levels for the adrenoceptors α1A, α1B, α1D, β1, β2and β3were similar in cav‐1KO and WT. (‐)‐Noradrenaline contracted cav‐1KO (‐log EC50M=7.1) and WT (‐log EC50M=7.3) arteries through prazosin‐sensitive receptors. Maximum (‐)‐noradrenaline‐evoked contractions were greater in cav‐1KO than WT arteries. (‐)‐Isoprenaline relaxed WT arteries (‐log EC50M=7.3) more potently than cav‐1KO arteries (‐log EC50M=6.8); the effects were antagonized partially and similarly by the β2‐selective antagonist ICI118551 (50 nM). The (‐)‐isoprenaline‐evoked relaxation was partially antagonized by the β1‐adrenoceptor‐selective antagonist CGP20712 (300 nM) in WT but not cav‐1KO arteries. The β3‐adrenoceptor‐selective antagonist L748337 (100nM) partially antagonized the relaxant effects of (‐)‐isoprenaline in cav‐1KO but not in WT arteries. BRL37344 partially relaxed arteries through β3‐adrenoceptors in cav‐1KO but not WT. The relaxant effects of BRL37344 were decreased by the NO synthase inhibitor ΩL‐nitroarginine.Conclusions and implications:The function of arterial α1‐ and β2‐adrenoceptors is similar in cav‐1KO and WT mice. β1‐adrenoceptor‐mediated relaxation in WT is lost in cav‐1KO and replaced by the appearance of β3‐adrenoceptors.British Journal of Pharmacology(2007)150, 261–270. doi:10.1038/sj.bjp.0706980
Antagonist, partial agonist and antiproliferative actions of B‐9870 (CU201) as a function of the expression and density of the bradykinin B1and B2receptors
Authors: Morissette G , Houle S , Gera L , Stewart J M , Marceau F 
Published: December 2006

Background and purpose:A bradykinin (BK) B2receptor (B2R) antagonist, B‐9870 (CU201), has been proposed to behave as a ‘biased agonist’ at B2Rs and to exert anti‐neoplasic effects. It was unclear whether these effects were determined by the activation of B2Rs by the drug. B‐9870 was evaluated for antagonism or stimulation of several responses mediated by the rabbit B2R or B1receptor (B1R); its anti‐proliferative activity was also characterized.Experimental approach and key results:B‐9870 was an insurmountable B2R antagonist in the rabbit jugular vein contractility assay, but a partial agonist in HEK 293 cells expressing the rabbit B2R or a green fluorescent protein (GFP) conjugate of the latter (ERK1/2 phosphorylation, [Ca2+]i, [3H]‐arachidonate release, endocytosis). The agonist‐like effects of B‐9870 were inhibited by the B2R antagonist LF 16.0687 and absent in untransfected cells. In addition, B‐9870 was a surmontable antagonist of the rabbit B1R in the aorta contractility assay, and blocked Lys‐des‐Arg9‐BK‐induced ERK1/2 phosphorylation in HEK 293 cells expressing a fluorescent B1R conjugate. B‐9870 inhibited the growth of MDA‐MB‐231 cells. The latter effect was not influenced by B1R or B2R antagonists and was not apoptotic. MDA‐MB‐231 cells expressed a small population of B2Rs but no B1Rs; they responded to BK (small calcium transients) and B‐9870 behaved as an antagonist.Conclusion and implications:B‐9870 is a dual B1R and B2R antagonist with confirmed stimulating effects at the B2R in high expression systems only. Its cell type‐specific anti‐proliferative effect occurs at a high concentration, independently from kinin receptors and apoptosis.British Journal of Pharmacology(2007)150, 369–379. doi:10.1038/sj.bjp.0706982
Identification of an antagonist that selectively blocks the activity of prostamides (prostaglandin‐ethanolamides) in the feline iris
Authors: Woodward D F , Krauss A H , Wang J W , Protzman C E , Nieves A L , Liang Y , Donde Y , Burk R M , Landsverk K , Struble C 
Published: December 2006

Background and Purpose:The prostamides (prostaglandin‐ethanolamides) and prostaglandin (PG) glyceryl esters are biosynthesized by COX‐2 from the respective endocannabinoids anandamide and 2‐arachidonyl glycerol. Agonist studies suggest that their pharmacologies are unique and unrelated to prostanoid receptors. This concept was further investigated using antagonists.Experimental Approach:The isolated feline iris was used as a key preparation, where prostanoid FP receptors and prostamide activity co‐exist. Activity at human recombinant FP and other prostanoid receptors was determined using stable transfectants.Key Results:In the feline iris, AGN 204396 produced a rightward shift of the dose‐response curves for prostamide F2αand the prostamide F2αanalog bimatoprost but did not block the effects of PGF2αand synthetic FP receptor agonists. Studies on human recombinant prostanoid receptors confirmed that AGN 204396 did not behave as a prostanoid FP receptor antagonist. AGN 204396 exhibited no antagonism at DP and EP1‐4, but was a highly effective TP receptor antagonist. Contrary to expectation, the FP receptor antagonist AL‐8810 efficaciously contracted the cat iris. AGN 204396 did not affect AL‐8810 induced contractions, demonstrating that AL‐8810 and AGN 204396 are pharmacologically distinct. Unlike AL‐8810, the ethylamide derivate of AL‐8810 was not an agonist. Al‐8810 did not block prostamide F2αactivity. Finally, AGN 204396 did not block PGE2‐glyceryl ester activity.Conclusions and Implications:The ability of AGN 204396 to selectively block prostamide responses suggests the existence of prostamide sensitive receptors as entities distinct from receptors recognizing PGF2αand PGE2‐glyceryl ester.British Journal of Pharmacology(2007)150, 342–352. doi:10.1038/sj.bjp.0706989
Effects of budesonide on P‐glycoprotein expression in intestinal cell lines
Authors: Maier A , Zimmermann C , Beglinger C , Drewe J , Gutmann H 
Published: December 2006

Background and purpose:P‐glycoprotein (P‐gp) is an important efflux transporter that supports the barrier function of the gut against invading antigens and against administered drugs. Since glucocorticoids, such as budesonide, are frequently used during inflammatory bowel disease we investigated how budesonide influences P‐gp expression in different intestinal cell lines.Experimental approach:LS180 and Caco‐2 cells were incubated with budesonide and changes in P‐gp expression were determined on mRNA, protein and functional level. The mRNA expression levels of glucocorticoid receptor (GR) and pregnane X receptor (PXR) were determined in these cell lines. PXR receptor was transiently transfected into Caco‐2 cells.Key results:Budesonide showed an induction of P‐gp in LS180 cells and a down‐regulation in Caco‐2 cells. Expression levels of nuclear receptors revealed high expression ofPXRonly in LS180 cells and exclusive expression ofGRin Caco‐2 cells. Mifepristone, an anti‐glucocorticoid, could not reverse the down‐regulation of P‐gp by budesonide in Caco‐2 cells. InPXR‐transfected Caco‐2 cells the budesonide‐mediated down‐regulation of P‐gp was abolished. Furthermore the expression of cytochrome P450 3A4 (CYP3A4), another PXR target gene, was induced inPXR‐transfected Caco‐2 cells after budesonide treatment.Conclusions and Implications:Budesonide has the potential to influenceMDR1expressionin vitro. In LS180 cells, the induction ofMDR1by budesonide probably is mediated via PXR. The mechanism of the down‐regulation in Caco‐2 cells still remains unclear, but GR does not seem to be involved. Further studies are required to evaluate how budesonide alters P‐gp expressionin vivo.British Journal of Pharmacology(2007)150, 361–368. doi:10.1038/sj.bjp.0706992
Comparative antagonist pharmacology at the native mouse bradykinin B2receptor: radioligand binding and smooth muscle contractility studies
Authors: Meini S , Cucchi P , Bellucci F , Catalani C , Giuliani S , Santicioli P , Maggi C A 
Published: December 2006

Background and purpose:The aim was to characterize the recently discovered non‐peptide antagonist MEN16132 at the mouse B2receptor, relative to other antagonists.Experimental approach:[3H]‐BK binding experiments used mouse lung and ileum tissue membranes and antagonist potency was measured in the isolated ileum contractility assay.Key results:Two BK binding sites resulted from saturation and homologous competition experiments. A role for the B1receptor was excluded because of the poor affinity of B1receptor ligands (pIC50<5). MEN16132, and the other reference antagonists, inhibited only one portion of BK specific binding, and the rank order of potency was (pIC50): Icatibant (lung 10.7; ileum 10.2)=MEN11270 (lung 10.4; ileum 9.9)=MEN16132 (lung 10.5; ileum 9.9). > LF16‐0687 (lung 8.9; ileum 8.8) > FR173657 (lung 8.6; ileum 8.2). BK homologous curves performed with lung membranes after treatment with the antagonist MEN16132 or Icatibant (10 nM) displayed only the low affinity site. The functional antagonism by MEN16132 (pA29.4) and Icatibant (pA29.1), towards BK (control EC506.1 nM) induced ileum contractions, was concentration‐dependent and surmountable, but the Schild plot slope was less than unity.Conclusions and Implications:In mouse tissue, radiolabelled BK recognizes two binding sites and B2receptor antagonists can compete only for the higher affinity one. The pharmacological profile of the novel non‐peptide antagonist MEN16132 indicates that it exhibits subnanomolar affinity and potency for the mouse B2receptor and is suitable for further characterization inin vivopathophysiological models.British Journal of Pharmacology(2007)150, 313–320. doi:10.1038/sj.bjp.0706995