bluuebunny/crossref_metadata_2025_split huggingface dataset:
OVID, TRISTIA 1.2: HIGH DRAMA ON THE HIGH SEAS
Authors: INGLEHEART JENNIFER 
Published: October 2006

In the first poem of Tristia 1, Ovid claims me mare, me uenti, me fera iactat hiems (‘the sea, the winds, the savage winter storm harass me repeatedly’, 1.1.42). This is no mere rhetorical flourish: the immediacy of the present tense becomes apparent in the second poem in the collection, which purports to be the poet's words as he faces a storm at sea. Critics tend to treat this poem as a literary exercise, focusing upon Ovid's exploitation of epic descriptions of the sea as a vast elemental force, subject to the machinations of the gods. In particular, interest has centred upon Ovid's debt to the storms which face Aeneas and Odysseus in Aeneid 1, 3, and 5 and Odyssey 5, as well as the relationship between this poem and Ovid's own version of an ‘epic’ storm in the story of Ceyx and Alcyone at Metamorphoses 11.410–748.However, this poem contains much more than the sum of its various epic models: 1.2 is programmatic for the rest of Tristia 1, not least because it can be seen as the first ‘proper’ poem of the collection, given that 1.1 is addressed to Ovid's new book of poetry as he sends it to Rome, and as such, self-consciously stands apart from the rest of the book.
Measuring Adaptability: Psychological Examinations of Jewish Detainees in Cyprus Internment Camps
Authors: Zalashik Rakefet , Davidovitch Nadav 
Published: October 2006

ArgumentTwo medical delegations, one from Palestine and one from the United States, were sent to detainment camps in Cyprus in the summer of 1947. The British Mandatory government had set up these camps in the summer of 1946 to stem the flow of Jewish immigrants into Palestine after World War II. The purpose of the medical delegations was to screen the camps' inhabitants and to propose a mental-health program for their life in Palestine. We examine the activities of these two delegations within the context of their scientific interest in the psycho-pathology of displaced persons after World War II and as part of a broader project of mental hygiene. According to the delegations, the detainees would be a potential source of strength for building a new society if they adapted to life in Palestine. However, they would become a burden if they failed to be absorbed. At the same time, the medical delegations also saw the detainee camps as a potential “living laboratory” for scientific exploration. The case of the two medical delegations in Cyprus is also a story about constructing and transgressing medical borders. Apart from the obvious fact that this case study deals with movement of people, refugees as well as health-care workers, it is also about the transmission of knowledge and professions across the ocean.
Blockade of mGluR1 receptor results in analgesia and disruption of motor and cognitive performances: effects of A‐841720, a novel non‐competitive mGluR1 receptor antagonist
Authors: El‐Kouhen O , Lehto S G , Pan J B , Chang R , Baker S J , Zhong C , Hollingsworth P R , Mikusa J P , Cronin E A , Chu K L , McGaraughty S P , Uchic M E , Miller L N , Rodell N M , Patel M , Bhatia P , Mezler M , Kolasa T , Zheng G Z , Fox G B , Stewart A O , Decker M W , Moreland R B , Brioni J D , Honore P 
Published: October 2006

Background and purpose:To further assess the clinical potential of the blockade of metabotropic glutamate receptors (mGluR1) for the treatment of pain.Experimental approach:We characterized the effects of A‐841720, a novel, potent and non‐competitive mGluR1 antagonist in models of pain and of motor and cognitive function.Key results:At recombinant human and native rat mGluR1 receptors, A‐841720 inhibited agonist‐induced calcium mobilization, with IC50 values of 10.7±3.9 and 1.0±0.2 nM, respectively, while showing selectivity over other mGluR receptors, in addition to other neurotransmitter receptors, ion channels, and transporters. Intraperitoneal injection of A‐841720 potently reduced complete Freund's adjuvant‐induced inflammatory pain (ED50=23 μmol kg−1) and monoiodoacetate‐induced joint pain (ED50=43 μmol kg−1). A‐841720 also decreased mechanical allodynia observed in both the sciatic nerve chronic constriction injury and L5‐L6 spinal nerve ligation (SNL) models of neuropathic pain (ED50=28 and 27 μmol kg−1, respectively). Electrophysiological studies demonstrated that systemic administration of A‐841720 in SNL animals significantly reduced evoked firing in spinal wide dynamic range neurons. Significant motor side effects were observed at analgesic doses and A‐841720 also impaired cognitive function in the Y‐maze and the Water Maze tests.Conclusions and implications.The analgesic effects of a selective mGluR1 receptor antagonist are associated with motor and cognitive side effects. The lack of separation between efficacy and side effects in pre‐clinical models indicates that mGluR1 antagonism may not provide an adequate therapeutic window for the development of such antagonists as novel analgesic agents in humans.British Journal of Pharmacology (2006) 149, 761–774. doi:10.1038/sj.bjp.0706877
Antidystonic effects of Kv7 (KCNQ) channel openers in thedtszmutant, an animal model of primary paroxysmal dystonia
Authors: Richter A , Sander S E , Rundfeldt C 
Published: October 2006

Background and purpose:Mutations in neuronal Kv7 (KCNQ) potassium channels can cause episodic neurological disorders. Paroxysmal dyskinesias with dystonia are a group of movement disorders which are regarded as ion channelopathies, but the role of Kv7 channels in the pathogenesis and as targets for the treatment have so far not been examined.Experimental approach:In the present study, we therefore examined the effects of the activators of neuronal Kv7.2/7.3 channels retigabine (5, 7.5, 10 mg kg−1i.p. and 10, 20 mg kg−1p.o.) and flupirtine (10, 20 mg kg−1i.p.) and of the channel blocker 10,10‐bis(4‐pyridinylmethyl)‐9(10H)‐anthracenone (XE‐991, 3 and 6 mg kg−1i.p.) in thedtszmutant hamster, a model of paroxysmal dyskinesia in which dystonic episodes occur in response to stress.Key results:Retigabine (10 mg kg−1i.p., 20 mg kg−1p.o.) and flupirtine (20 mg kg−1i.p.) significantly improved dystonia, while XE‐991 caused a significant aggravation in thedtszmutant. The antidystonic effect of retigabine (10 mg kg−1i.p.) was counteracted by XE‐991 (3 mg kg−1i.p.).Conclusions and Implications:These data indicate that dysfunctions of neuronal Kv7 channels deserve attention in dyskinesias. Since retigabine and flupirtine are well tolerated in humans, the present finding of pronounced antidystonic efficacy in thedtszmutant suggests that neuronal Kv7 channel activators are interesting candidates for the treatment of dystonia‐associated dyskinesias and probably of other types of dystonias. The established analgesic effects of Kv7 channel openers might contribute to improvement of these disorders which are often accompanied by painful muscle spasms.British Journal of Pharmacology(2006)149, 747–753. doi:10.1038/sj.bjp.0706878
Inhibition of cardiac voltage‐gated sodium channels by grape polyphenols
Authors: Wallace C H R , Baczkó I , Jones L , Fercho M , Light P E 
Published: October 2006

Background and purpose:The cardiovascular benefits of red wine consumption are often attributed to the antioxidant effects of its polyphenolic constituents, including quercetin, catechin and resveratrol. Inhibition of cardiac voltage‐gated sodium channels (VGSCs) is antiarrhythmic and cardioprotective. As polyphenols may also modulate ion channels, and possess structural similarities to several antiarrhythmic VGSC inhibitors, we hypothesised that VGSC inhibition may contribute to cardioprotection by these polyphenols.Experimental approach:The whole‐cell voltage‐clamp technique was used to record peak and late VGSC currents (INa) from recombinant human heart NaV1.5 channels expressed in tsA201 cells. Right ventricular myocytes from rat heart were isolated and single myocytes were field‐stimulated. Either calcium transients or contractility were measured using the calcium‐sensitive dye Calcium‐Green 1AM or video edge detection, respectively.Key results:The red grape polyphenols quercetin, catechin and resveratrol blocked peak INa with IC50s of 19.4 μM, 76.8 μM and 77.3 μM, respectively. In contrast to lidocaine, resveratrol did not exhibit any frequency‐dependence of peak INa block. Late INa induced by the VGSC long QT mutant R1623Q was reduced by resveratrol and quercetin. Resveratrol and quercetin also blocked late INa induced by the toxin, ATX II, with IC50s of 26.1 μM and 24.9 μM, respectively. In field‐stimulated myocytes, ATXII‐induced increases in diastolic calcium were prevented and reversed by resveratrol. ATXII‐induced contractile dysfunction was delayed and reduced by resveratrol.Conclusions and implications:Our results indicate that several red grape polyphenols inhibit cardiac VGSCs and that this effect may contribute to the documented cardioprotective efficacy of red grape products.British Journal of Pharmacology (2006) 149, 657–665. doi:10.1038/sj.bjp.0706897
Baclofen, an agonist at peripheral GABABreceptors, induces antinociceptionviaactivation of TEA‐sensitive potassium channels
Authors: Reis G M L , Duarte I D G 
Published: October 2006

Background and Purpose:Central anti‐nociceptive actions of baclofen involve activation of K+channels. Here we assessed what types of K+channel might participate in the peripheral anti‐nociception induced by baclofen.Experimental approach:Nociceptive thresholds to mechanical stimulation in rat paws treated with intraplantar prostaglandin E2.(PGE2) to induce hyperalgesia were measured 3h after PGE2injection. Other agents were also given by intraplantar injectionKey results:Baclofen elicited a dose‐dependent (15 ‐ 240 μg per paw) anti‐nociceptive effect. An intermediate dose of baclofen (60 μg) did not produce antinociception in the contralateral paw, showing its peripheral site of action. The GABABreceptor antagonist saclofen (12.5 ‐ 100 μg per paw) antagonized, in a dose‐dependent manner, peripheral antinociception induced by baclofen (60 μg), suggesting a specific effect. This antinociceptive action of baclofen was unaffected by bicuculline, GABAAreceptor antagonist (80 μg per paw), or by (1,2,5,6 tetrahydropyridin‐4‐yl) methylphosphinic acid, GABACreceptor antagonist (20 μg per paw). The peripheral antinociception induced by baclofen (60 μg) was reversed, in a dose‐dependent manner, by the voltage‐dependent K+channel blockers tetraethylammonium (7.5 ‐ 30 μg per paw) and 4‐aminopyridine (2.5 ‐ 10 μg per paw). The blockers of other K+channels, glibenclamide (160 μg), tolbutamide (320 μg), charybdotoxin (2 μg), dequalinium (50 μg) and caesium (500 μg) had no effect.Conclusions and Implications:This study provides evidence that the peripheral antinociceptive effect of the GABABreceptor agonist baclofen results from the activation of tetraethylammonium‐sensitive K+channels. Other K+channels appear not to be involved.British Journal of Pharmacology(2006)149, 733–739. doi:10.1038/sj.bjp.0706898
Inhibition of glycogen synthase kinase‐3β attenuates the development of carrageenan‐induced lung injury in mice
Authors: Cuzzocrea S , Crisafulli C , Mazzon E , Esposito E , Muià C , Abdelrahman M , Di Paola R , Thiemermann C 
Published: October 2006

Background and purpose:Glycogen synthase kinase‐3 (GSK‐3) is a ubiquitous serine‐threonine protein kinase that participates in a multitude of cellular processes and has recently been implicated in the pathophysiology of a number of diseases. The aim of this study was to investigate the effects of GSK‐3β inhibition in a model of acute inflammation. Here, we have investigated the effects of TDZD‐8, a potent and selective GSK‐3β inhibitor, in a mouse model of carrageenan‐induced pleurisy.Experimental approach:Injection of carrageenan into the pleural cavity of mice elicited an acute inflammatory response characterized by: accumulation of fluid containing a large number of neutrophils (PMNs) in the pleural cavity, infiltration of PMNs in lung tissues and subsequent lipid peroxidation, and increased production of nitrite/nitrate (NOx), prostaglandin E2(PGE2), tumour necrosis factor‐α, (TNF‐α) and interleukin‐1β (IL‐1β). Furthermore, carrageenan induced an upregulation of the adhesion molecules ICAM‐1 and P‐selectin, iNOS, COX‐2 as well as nitrotyrosine as determined by immunohistochemical analysis of lung tissues.Key results:Administration of TDZD‐8 (1, 3 or 10 mg kg−1, i.p.), 30 min prior to injection of carrageenan, caused a dose‐dependent reduction in all the parameters of inflammation measured.Conclusions and Implications:Thus, based on these findings we propose that inhibitors of the activity of GSK‐3β, such as TDZD‐8, may be useful in the treatment of various inflammatory diseases.British Journal of Pharmacology(2006)149, 687–702. doi:10.1038/sj.bjp.0706902
Inhalation of activated protein C inhibits endotoxin‐induced pulmonary inflammation in mice independent of neutrophil recruitment
Authors: Slofstra S H , Groot A P , Maris N A , Reitsma P H , Cate H ten , Spek C A 
Published: October 2006

Background and purpose:Intravenous administration of recombinant human activated protein C (rhAPC) is known to reduce lipopolysaccharide (LPS)‐induced pulmonary inflammation by attenuating neutrophil chemotaxis towards the alveolar compartment. Ideally, one would administer rhAPC in pulmonary inflammation at the site of infection to minimize the risk of systemic bleeding complications. In this study, we therefore assessed the effect of inhaled rhAPC in a murine model of acute lung injury.Experimental approach:Mice were exposed to LPS (0.5 mg kg‐1: intranasally) to induce acute lung injury. 30 minutes before and 3 hours after LPS exposure mice were subjected to vehicle or rhAPC inhalation (25 or 100 μg per mouse in each nebulization). In order to establish whether rhAPC inhalation affects neutrophil recruitment, neutrophil migration was determined in vitro using a trans‐well migration assay.Key results:rhAPC inhalation dose‐dependently decreased LPS‐induced coagulation and inflammation markers in bronchoalveolar lavage fluid (BALF), reduced protein leakage into the alveolar space and improved lung function. In contrast, rhAPC did not prevent LPS‐induced neutrophil recruitment into the alveolar space.Neutrophil migration in vitro towards FCS or interleukin (IL)‐8 was significantly inhibited by pretreatment with rhAPC (0.01‐10 μg ml‐1], whereas rhAPC (10 μg ml‐1) added to the chemoattractant (modelling for topical rhAPC administration) did not affect neutrophil migration towards FCS or IL‐8.Conclusions and Implications:rhAPC inhalation significantly diminished LPS‐induced pulmonary inflammation. The benefit of inhaled rhAPC appeared not to involve attenuation of neutrophil recruitment, in contrast to its effects after intravenous administration.British Journal of Pharmacology (2006) 149, 740–746. doi:10.1038/sj.bjp.0706915
The actions of azelnidipine, a dihydropyridine‐derivative Ca antagonist, on voltage‐dependent Ba2+ currents in guinea‐pig vascular smooth muscle
Authors: Zhu H‐L , Tomoda T , Aishima M , Ito Y , Teramoto N 
Published: October 2006

Background and purpose:Although azelnidipine is used clinically to treat hypertension its effects on its target cells, Ca2+ channels, in smooth muscle have not been elucidated. Therefore, its effects on spontaneous contractions and voltage‐dependent L‐type Ca2+ channels were investigated in guinea‐pig portal vein.Experimental approach:The inhibitory potency of azelnidipine on spontaneous contractions in guinea‐pig portal vein was compared with those of other dihydropyridine (DHP)‐derived Ca antagonists (amlodipine and nifedipine) by recording tension. Also its effects on voltage‐dependent nifedipine‐sensitive inward Ba2+ currents (I
Ba) in smooth muscle cells dispersed from guinea‐pig portal vein were investigated by use of a conventional whole‐cell patch‐clamp technique.Key results:Spontaneous contractions in guinea‐pig portal vein were reduced by all of the Ca antagonists (azelnidipine, K

i=153 nM; amlodipine, K

i=16 nM; nifedipine, K

i=7 nM). In the whole‐cell experiments, azelnidipine inhibited the peak amplitude of I
Ba in a concentration‐ and voltage‐dependent manner (‐60 mV, K

i=282 nM; −90 mV, K

i=2 μM) and shifted the steady‐state inactivation curve of I
Ba to the left at −90 mV by 16 mV. The inhibitory effects of azelnidipine on I
Ba persisted after 7 min washout at −60 mV. In contrast, I
Ba gradually recovered after being inhibited by amlodipine, but did not return to control levels. Both azelnidipine and amlodipine caused a resting block of I
Ba at ‐90 mV. Only nifedipine appeared to interact competitively with S(‐)‐Bay K 8644.Conclusions and implications:These results suggest that azelnidipine induces long‐lasting vascular relaxation by inhibiting voltage‐dependent L‐type Ca2+ channels in vascular smooth muscle.British Journal of Pharmacology (2006) 149, 786–796. doi:10.1038/sj.bjp.0706919
Prostaglandin E2receptor distribution and function in the gastrointestinal tract
Authors: Dey I , Lejeune M , Chadee K 
Published: October 2006

Prostaglandin E2(PGE2) is one of the most important biologically active prostanoids found throughout the gastrointestinal tract. Despite the fact that PGE2regulates many physiological functions of the gut including mucosal protection, gastrointestinal secretion and motility, it is implicated in the pathophysiology of inflammatory bowel diseases (IBD) and colorectal neoplasia. The varied biological functions exerted by PGE2are through the pharmacologically distinct, G‐protein coupled plasma membrane receptors termed EP receptors. Disruptions of various prostanoid receptor genes have helped in unravelling the physiological functions of these receptors. To date, all four subtypes of EP receptors have been individually knocked out in mice and various phenotypes have been reported for each subtype. Similarly,in vitroandin vivostudies using EP receptor agonists and antagonists have helped in uncoupling the diverse functions of PGE2signalling involving distinct EP receptors in the gut. In this review, we will summarize and conceptualize the salient features of EP receptor subtypes, their regional functions in the gut and how expressions of EP receptors are altered during disease states.British Journal of Pharmacology(2006)149, 611–623. doi:10.1038/sj.bjp.0706923
Effects of nitric oxide synthase inhibition with or without cyclooxygenase‐2 inhibition on resting haemodynamics and responses to exendin‐4
Authors: Gardiner S M , March J E , Kemp P A , Bennett T 
Published: October 2006

Background and purpose:Interactions between the NO system and the cyclooxygenase systems may be important in cardiovascular regulation. Here we measured the effects of acute cyclooxygenase‐2 inhibition (with parecoxib), alone and in combination with NOS inhibition (with N
G‐nitro‐L‐arginine methyl ester (L‐NAME)), on resting cardiovascular variables and on responses to the glucagon‐like peptide 1 agonist, exendin‐4, which causes regionally‐selective vasoconstriction and vasodilatation.Experimental approach:Rats were instrumented with flow probes and intravascular catheters to measure regional haemodynamics in the conscious, freely moving state. L‐NAME was administered as a primed infusion 180 min after administration of parecoxib or vehicle, and exendin‐4 was given 60 min after the onset of L‐NAME infusion.Key results:Parecoxib had no effect on resting cardiovascular variables or on responses to L‐NAME. Exendin‐4 caused a pressor response accompanied by tachycardia, mesenteric vasoconstriction and hindquarters vasodilatation. Parecoxib did not affect haemodynamic responses to exendin‐4, but L‐NAME inhibited its hindquarters vasodilator and tachycardic effects. When combined, L‐NAME and parecoxib almost abolished the hindquarters vasodilatation while enhancing the pressor response.Conclusions and implications:Cyclooxygenase‐2‐derived products do not affect basal haemodynamic status in conscious normotensive rats, or influence the NO system acutely. The inhibitory effects of L‐NAME on the hindquarters vasodilator and tachycardic effects of exendin‐4 are consistent with a previous study that showed those events to be β‐adrenoceptor mediated. The additional effect of parecoxib on responses to exendin‐4 in the presence of L‐NAME, is consistent with other evidence for enhanced involvement of vasodilator prostanoids when NO production is reduced.British Journal of Pharmacology (2006) 149, 802–809. doi:10.1038/sj.bjp.0706931
A reflection on the South African food research environment
Authors: Lues J.F.R. , Lategan L.O.K. 
Published: October 2006

PurposeThis paper seeks to cast light on the issues impacting South African food research. During the first decade of democracy the South African research and development sector has experienced many changes and although the aim of these changes was to bring about efficiency, the research and development (R&D) fraternity is still faced with various challenges in its endeavours to meet the demands from commerce and industry. As a result of continuously changing market demands the food and drink industry has become one of the main sectors that are dependant on novel technologies developed by the R&D sector.Design/methodology/approachAn overview of the broader South African research landscape is given followed by a closer look at the nature and extent of local food‐related research.FindingsIn order to meet the demand of industry a new mindset is required amongst research institutions towards providing an array of scientific services that extend intra‐ and inter‐disciplinary boundaries and where long‐term partnerships between food industries and the R&D sector are forged. However, against this backdrop South Africa's national research priorities are increasingly directed towards poverty alleviation and development. Human resources in science and technology have not been developed adequately, which in turn has resulted in an aging and declining scientific population. Thus, a balancing act is needed in order to address the scant human resources while at the same time effectively bridging the innovation chasm. This predicament extends to food researchers who find themselves amidst a well developed and technologically advanced formal industry while at the same time having to address issues relating to a relatively primitive yet lucrative informal food sector.Originality/valueThe paper presents novel information regarding South African food research and places it in context against the broader research landscape.
ELECTROLYTIC REACTIONS IN VITREOUS ENAMELS AND THEIR RELATION TO THE ADHERENCE OF ENAMELS TO STEEL*
Authors: STALEY HOMER F. 
Published: October 2006

ABSTRACTAll the metals between iron and copper in the electromotive‐force series of metals are plated out of solution during the firing of sheet‐steel ground coats by the electrolytic action of the hot iron base. Of these plates, cobalt, nickel, and antimony promote adhesion, each of the following factors probably playing a part: (1) The plates of these metals adhere tenaciously to steel while enamel does not. (2) The coefficients of thermal expansion of these metals are intermediate between those of steel and those of commercial ground‐coat and cover‐coat glasses, thus giving a gradation of coefficients found desirable by Danielson and Sweely. (3) The enamel glass is mechanically bonded to the metal plate by dendrites, aided by any jagged projections and holes. (4) These metal plates are insoluble in the molten enamel; thus any structure favorable to adhesion, once formed, remains.
THE THERMAL CONDUCTIVITY OF REFRACTORIES*
Authors: WILKES GORDON B. 
Published: October 2006

ABSTRACTThe thermal conductivity of recrystallized silicon carbide, clay‐bonded silicon carbide, and silica and fireclay brick has been determined from 200 to 2600°F. The results are compared with those of previous investigators and a possible explanation of the peculiar variation of the coefficient of thermal conductivity with temperature for certain brick is given.