bluuebunny/crossref_metadata_2025_split huggingface dataset:
Grain legume–cereal intercropping: The practical application of diversity, competition and facilitation in arable and organic cropping systems
Authors: Hauggaard-Nielsen Henrik , Jørnsgaard Bjarne , Kinane Julia , Jensen Erik Steen 
Published: February 2008

AbstractIntercropping is the simultaneous cultivation of more than one crop species on the same piece of land and is regarded as the practical application of basic ecological principles such as diversity, competition and facilitation. Field experiments were carried out on a sandy loam soil and a sandy soil in Denmark over three consecutive cropping seasons including dual grain legume (pea, faba bean and lupin)–barley intercropping as compared to the respective sole crops (SC). Yield stability of intercrops (IC) was not greater than that of grain legume SC, with the exception of the IC containing faba bean. Faba bean and lupin had lower yield stability than pea and fertilized barley. However, the different IC used environmental resources for plant growth up to 50% (LER=0.91–1.51) more effectively as compared to the respective SC, but with considerable variation over location, years and crops. The SC performance supported the interspecific interactions within the IC stand. On the sandy loam 13% greater grain yield of pea cv. Agadir (520 g m−2) was observed as compared to cv. Bohatyr. Faba bean and lupin yielded similarly (340 g m−2) in the sandy loam soil, with decreasing yields on the sandy soil (320–270 g m−2). Nitrogen fixation was very constant in grain legume SC over species and location, varying from 13.2 to 15.8 g N m−2, being lowest in peas and highest in faba bean and lupin. The intercropped grain legumes increased the proportion of plant N derived from N2-fixation by on average 10–15% compared to the corresponding SC. However, especially lupin was suppressed when intercropping, with a reduced N2-fixation from 15 to 5–6 g N m−2. The IC were particularly effective at suppressing weeds, capturing a greater share of available resources than SC. Weed infestation in the different crops was comparable; however, it tended to be the highest in sole cropped faba bean, lupin and unfertilized barley, where the application of urea to barley reduced the weed infestation by around 50%. Reduction in disease was observed in all IC systems compared to the corresponding SC, with a general disease reduction in the range of 20–40%. For one disease in particular (brown spot on lupin) disease reduction was almost 80% in the IC. Intercropping practices offer many advantages but improved understanding of the ecological mechanisms associated with planned spatial diversity, including additional benefits with associated diversity, is needed to enhance the benefits achieved.
The antiarrhythmic effect of centrally administered rilmenidine involves muscarinic receptors, protein kinase C and mitochondrial signalling pathways
Authors: Iwasaki M , Hayashi Y , Kamibayashi T , Yamatodani A , Mashimo T 
Published: February 2008

Background and purpose:We have previously demonstrated that stimulation of imidazoline receptors in the CNS prevented halothane–adrenaline arrhythmias during halothane anaesthesia and that stimulation of the vagus nerve may be critical to this effect. However, details of the mechanism(s) involved are not yet available. The present study was designed to examine the role of muscarinic receptors, protein kinase C (PKC), ATP‐sensitive potassium channels (KATP) and the mitochondrial permeability transition pore (MPTP) in the antiarrhythmic effect of rilmenidine, an imidazoline receptor agonist.Experimental approach:Rats were anaesthetized with halothane and monitored continuously for arterial blood pressure and premature ventricular contractions. The arrhythmogenic dose of adrenaline was defined as the lowest dose producing three or more premature ventricular contractions within a 15‐s period. We confirmed that centrally administered rilmenidine prevented halothane–adrenaline arrhythmias and then examined the antiarrhythmic effect of rilmenidine in the presence of atropine methylnitrate, a muscarinic receptor antagonist, calphostin C, a PKC inhibitor, HMR‐1098, a sarcolemmal KATPinhibitor, 5‐hydroxydecanoic acid, a mitochondrial KATPinhibitor or atractyloside, an MPTP opener.Key results:The antiarrhythmic effect of rilmenidine was significantly inhibited by atropine methylnitrate, calphostin C, 5‐hydroxydecanoic acid and atractyloside, but the effects of HMR‐1098 in our model were not clear.Conclusions and implications:The present results suggest that muscarinic receptors, PKC, mitochondrial KATPchannels and MPTP may be crucial components of the mechanism involved in the antiarrhythmic effect of rilmenidine given into the CNS.British Journal of Pharmacology(2008)153, 1623–1630; doi:10.1038/bjp.2008.35; published online 25 February 2008
Indomethacin promotes nitric oxide function in the ductus arteriosus in the mouse
Authors: Sodini D , Baragatti B , Barogi S , Laubach V E , Coceani F 
Published: February 2008

Background and purpose:Prenatal patency of ductus arteriosus is maintained by prostaglandin (PG) E2in concert with nitric oxide (NO) and carbon monoxide (CO). Accordingly, we have previously found that NO activity increases upon deletion of either COX. Here, we have examined whether COX inhibition by indomethacin mimics COX deletion in promoting NO.Experimental approach:Experiments were performedin vitroandin vivowith wild‐type (WT) and eNOS−/−, near‐term mouse foetuses. Indomethacin was given p.o. to the mother as single (acute treatment) or repeated (daily for 3 days; chronic treatment) doses within a therapeutic range (2 mg kg−1).Key results:Indomethacin promoted eNOS mRNA expression in the WT ductus. Coincidentally, the drug enhanced the contraction of the isolated ductus to the NOS inhibitor,NG‐nitro‐L‐arginine methyl ester, and its effect augmented with the length of treatment. No such enhancement was seen with the eNOS−/− ductus. Chronic indomethacin also increased, albeit marginally, the contraction of the WT ductus to the CO synthesis inhibitor, zinc protoporphyrin. Whether given acutely or chronically, indomethacin induced a little narrowing of the ductus antenatally and had no effect on postnatal closure of the vessel.Conclusions and implications:We conclude that activation of NO and, to a much lesser degree, CO mechanisms is an integral part of the indomethacin effect on the ductus. This relaxing influence may oppose the contraction from PGE2suppression and could explain the failures of indomethacin therapy in premature infants with persistent duct.British Journal of Pharmacology(2008)153, 1631–1640; doi:10.1038/bjp.2008.36; published online 25 February 2008
A nitric oxide/Ca2+/calmodulin/ERK1/2 mitogen‐activated protein kinase pathway is involved in the mitogenic effect of IL‐1β in human astrocytoma cells
Authors: Meini A , Sticozzi C , Massai L , Palmi M 
Published: February 2008

Background and purpose:Evidence is accumulating to support a role for interleukin‐1β (IL‐1β) in astrocyte proliferation. However, the mechanism by which this cytokine modulates this process is not fully elucidated.Experimental approach:In this study we used human astrocytoma U‐373MG cells to investigate the role of nitric oxide (NO), intracellular Ca2+ concentration ([Ca2+]i), and extracellular signal‐regulated protein kinase (ERK) in the signalling pathway mediating IL‐1β‐induced astrocyte proliferation.Key results:Low IL‐1β concentrations induced dose‐dependent ERK activation which paralleled upregulation of cell division, whereas higher concentrations gradually reversed both these responses by promoting apoptosis. Pretreatment with the nonspecific NOS inhibitor, N‐ω‐nitro‐l‐arginine methyl ester (L‐NAME) or the selective iNOS inhibitor, N‐[[3‐(aminomethyl)phenyl]methyl]‐ethanimidamide dihydrochloride (1400W), antagonized ERK activation and cell proliferation induced by IL‐1β. Inhibition of cGMP formation by the guanylate cyclase inhibitor, 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ), partially inhibited ERK activation and cell division. Functionally blocking Ca2+ release from endoplasmic reticulum with ryanodine or 2‐aminoethoxydiphenylborane (2‐APB), inhibiting calmodulin (CaM) activity with N‐(6‐aminohexyl)‐5‐chloro‐1‐naphthalenesulphonamide hydrochloride (W7) or MAPK kinase activity with 1,4‐diamino‐2,3‐dicyano‐1,4‐bis[2‐aminophenylthiol]butadiene (U0126) downregulated IL‐1β‐induced ERK activation as well as cell proliferation. The cytokine induced a transient and time‐dependent increase in intracellular NO levels which preceded elevation in [Ca2+]i.Conclusions and implications:These data identified the NO/Ca2+/CaM/ERK signalling pathway as a novel mechanism mediating the mitogenic effect of IL‐1β in human astrocytes. As astrocyte proliferation is a hallmark of reactive astrogliosis, our results reveal a new potential target for therapeutic intervention in neuroinflammatory disorders.British Journal of Pharmacology (2008) 153, 1706–1717; doi:10.1038/bjp.2008.40; published online 25 February 2008
A physiological role for endocannabinoid‐derived products of cyclooxygenase‐2‐mediated oxidative metabolism
Authors: Guindon J , Hohmann A G 
Published: February 2008

The endocannabinoid lipid 2‐arachidonoylglycerol (2‐AG) is deactivated by intracellular hydrolysis catalyzed by monoacylglycerol lipase. 2‐AG also serves as a substrate for oxidative metabolism catalyzed by cyclooxygenase 2 (COX‐2). However, products of COX‐2‐mediated metabolism of endocannabinoids have not been identifiedin vivo. Hu and colleagues in this issue of theBJPdemonstrate that COX‐2 converts 2‐AG into a biologically active, pro‐nociceptive compound, prostaglandin E2glycerol ester (PGE2‐G). PGE2‐G produces hyperalgesiain vivoand activates a rapidly acting transcription factor, nuclear factor kappa‐Bin vitro. These biological actions may be attributed to a unique receptor. This report of pro‐nociceptive actions of an endogenous COX‐2 metabolite of 2‐AG that are largely opposite to known anti‐nociceptive and anti‐inflammatory actions of endocannabinoids has physiological relevance. These discoveries place renewed emphasis on the importance of understanding the highly interactive nature of lipid signalling pathways in the nervous system and the physiological roles of these lipid mediators in controlling homeostasis.British Journal of Pharmacology(2008)153, 1341–1343; doi:10.1038/bjp.2008.41; published online 25 February 2008
Structural requirements for the cytoprotective actions of mono‐unsaturated fatty acids in the pancreatic β‐cell line, BRIN‐BD11
Authors: Dhayal S , Welters H J , Morgan N G 
Published: February 2008

Background and purpose: Exposure of pancreatic β‐cells to long‐chain free fatty acids leads to differential responses according to the chain length and degree of unsaturation. In particular, long‐chain saturated molecules such as palmitate (C16:0) cause apoptosis, whereas equivalent mono‐unsaturated species (for example, palmitoleate (C16:1)) are not overtly toxic. Moreover, mono‐unsaturates exert a powerful cytoprotective response against a range of proapoptotic stimuli. However, the structural requirements that determine cytoprotection have not been determined and form the basis of the present study.Experimental approach: BRIN‐BD11 and INS‐1 β‐cells were exposed either to the saturated fatty acid palmitate, or to serum withdrawal, to mediate cytotoxicity. The protective effects of a wide range of mono‐unsaturated fatty acid derivatives were tested in cytotoxicity assays. Effector caspase activity was also measured and correlated with viability.Key results: The cytotoxic actions of palmitate were inhibited dose‐dependently by long‐chain mono‐unsaturated fatty acids with a defined potency order C18:1>C16:1≫C14:1. The configuration of the double bond was also important with cis forms being more potent than trans forms. Alkylated mono‐unsaturated fatty‐acid derivates were also cytoprotective, although their efficacy declined as the alkyl chain length increased. Cytoprotection was achieved rapidly on addition of mono‐unsaturates and correlated with a rapid and dramatic inhibition of caspase‐3/7 activity in palmitate‐treated cells.Conclusions and implications: The data reveal the structural requirements that dictate the cytoprotective actions of mono‐unsaturated fatty acids in pancreatic β‐cells. Metabolic activation is not required and the data point at the potential involvement of a fatty acid receptor in mediating cytoprotection.British Journal of Pharmacology (2008) 153, 1718–1727; doi:10.1038/bjp.2008.43; published online 25 February 2008
Role of CCK and potential utility of CCK1 receptor antagonism in the treatment of pancreatitis induced by biliary tract obstruction
Authors: Barrett T D , Yan W , Freedman J M , Lagaud G J , Breitenbucher J G , Shankley N P 
Published: February 2008

Background and purpose: Cholecystokinin (CCK) stimulates the release of amylase and lipase from the normal pancreas. However, it is not clear to what extent this occurs in the early stages of pancreatitis induced by biliary tract obstruction in the rat and whether CCK initiates an inflammatory cascade in this condition.Experimental approach: Selective CCK1 receptor antagonists, JNJ‐17156516 ((S)‐(3‐[5‐(3,4‐dichloro‐phenyl)‐1‐(4‐methoxy‐phenyl)‐1H‐pyrazol‐3‐yl]‐2‐m‐tolyl‐propionic acid) and dexloxiglumide, were used to assess the response of plasma amylase and lipase to a CCK analogue, CCK8S, in normal rats and in rats with bile duct ligation.Key results: Both antagonists suppressed CCK8S‐induced elevation of plasma amylase activity in normal rats. JNJ‐17156516 was more potent than dexloxiglumide (ED50=8.2 vs >30 μmol kg−1 p.o.) and produced a longer lived inhibition (6 vs 2 h). Plasma amylase and lipase activity were elevated in parallel to CCK plasma concentrations after bile duct ligation and both activities were suppressed in a dose‐dependent manner by JNJ‐17156516 and dexloxiglumide. JNJ‐17156516 was ∼5‐ to 10‐fold more potent than dexloxiglumide. Infusion of CCK8S to naïve rats to achieve levels similar to those observed after bile duct ligation (20 pM) increased plasma amylase activity and activated nuclear factor‐κB in the pancreas. These effects were prevented by pretreatment with JNJ‐17156516.Conclusions and implications: The elevation of plasma amylase and lipase activity in the early stages of obstruction‐induced pancreatitis is largely driven by elevation of plasma CCK concentration and activation of CCK1 receptors. These data show that CCK is an initiating factor in acute pancreatitis in the rat.British Journal of Pharmacology (2008) 153, 1650–1658; doi:10.1038/bjp.2008.44; published online 25 February 2008
Cardiovascular effects of activation of central α7 and α4β2 nAChRs: a role for vasopressin in anaesthetized rats
Authors: Moore C , Wang Y , Ramage A G 
Published: February 2008

Background and purpose: Central application of nicotine causes the release of vasopressin and affects blood pressure. Involvement of the 5 neuronal nicotinic receptor groups, α2*–α7* in these effects is unknown. The availability of selective agonists for α7 (PSAB‐OFP) and α4β2 (TC‐2559) nACh receptors allowed their role to be investigated.Experimental approach: Recordings were made of arterial blood pressure, heart rate and renal sympathetic nerve activity in anaesthetized male rats with neuromuscular blockade and artificial respiration. Effects of the agonists, PSAB‐OFP (1–10 μmol kg−1) and TC‐2559 (1–10 μmol kg−1) on these variables given intracerebroventricularly (i.c.v.) and intracisternally (i.c.) in the presence or absence of the antagonists, DhβE (10 μmol kg−1) and MLA (0.5 μmol kg−1), for the appropriate nicotinic receptor subtypes, respectively, and a V1 receptor antagonist, given i.v. or centrally, were investigated.Key results: Both agonists given i.c.v. caused a delayed rise in blood pressure and renal nerve activity which could be blocked only with the appropriate antagonist. The agonists had an earlier onset of action when given i.c., favouring the brainstem as the major site of action. The effects of these agonists were also attenuated by the V1 receptor antagonist given i.v. and blocked when this antagonist was given centrally. Antagonists had no effect on baseline variables.Conclusions and implications: Activation of α4β2 and α7 receptors in the brainstem is mainly responsible for the cardiovascular effects of activating these receptors, which have a similar profile of action. These actions, although independent, are mediated by the central release of vasopressin.British Journal of Pharmacology (2008) 153, 1728–1738; doi:10.1038/bjp.2008.47; published online 25 February 2008
Phytophthora infestans: the plant (and R gene) destroyer
Authors: FRY WILLIAM 
Published: February 2008

SUMMARY Phytophthora infestans remains a problem to production agriculture. Historically there have been many controversies concerning its biology and pathogenicity, some of which remain today. Advances in molecular biology and genomics promise to reveal fascinating insight into its pathogenicity and biology. However, the plasticity of its genome as revealed in population diversity and in the abundance of putative effectors means that this oomycete remains a formidable foe.
Expression of transcription factors NF‐κB and AP‐1 in nasal polyposis
Authors: Valera F. C. P. , Queiroz R. , Scrideli C. , Tone L. G. , Anselmo‐Lima W. T. 
Published: February 2008

SummaryBackground
The treatment and prognosis of nasal polyposis (NP) may be influenced by transcription factors, but their expression is poorly understood.Objective
To determine the expression of transcription factors [(nuclear factor‐κB) NF‐κB and (activator protein) AP‐1], cytokines [IL‐1β, TNF‐α and (granulocytes and macrophage colony‐stimulating factor) GM‐CSF], growth factor (b‐FGF), chemokine (eotaxin‐2) and adhesion molecule (ICAM‐1) in NP in comparison with nasal mucosa controls.Methods
Cross‐sectional study. Twenty biopsies of nasal polyps were compared with eight middle turbinate biopsies. p65, c‐Fos, IL‐1β, TNF‐α, ICAM‐1, b‐FGF, eotaxin‐2 and GM‐CSF were analysed through RQ‐PCR, and p65 and c‐Fos were also analysed through Western blotting.Results
NF‐κB expression was increased in patients with NP when compared with control mucosa (P<0.05), whereas AP‐1 expression did not differ significantly between groups. Expressions of IL‐1β, eotaxin‐2 and b‐FGF were also increased in patients with NP compared with controls (P<0.05).Conclusions
The transcription factor NF‐κB is more expressed in NP than in control mucosa. This is important in NP because NF‐κB can induce the transcription of cytokines, chemokines and adhesion molecules, which play an important role in the inflammatory process. Moreover, transcription factors influence the response to corticosteroids, which are the basis of NP treatment. Transcription factor AP‐1 does not seem to have a significant role in the pathological process.
Detecting dispersal of Nuphar lutea in river corridors using microsatellite markers
Authors: FÉR TOMÁŠ , HROUDOVÁ ZDENKA 
Published: February 2008

Summary1. River corridors are well‐known for their role in plant dispersal. The buoyancy of seeds, the possibility of dispersal by vegetative fragments, and the frequency and efficiency of dispersal among different river catchments determine linear distribution patterns. Little is known about the relative importance of these factors to observed patterns of genetic variation.2. One hundred and fifty‐six Nuphar lutea individuals from forty‐four sampling sites in the river catchments of the Cidlina River, the Mrlina River and the Labe River (Czech Republic) were studied using ten microsatellite markers. Interpretation of patterns in genetic variation allowed several conclusions about dispersal mechanisms.3. Vegetative long‐distance dispersal is probably very limited in this species. Only one multilocus genotype was found in more than one sampling site. The distance between the sites was about 75 km.4. To explain the distribution of Bayesian based clusters of related multilocus genotypes, both along‐river and inter‐river long‐distance dispersals have to be invoked.5. A marginally significant tendency for higher genetic diversity in the lower part of the river Cidlina was detected. Continuous downstream dispersal of seeds by water currents could be a valid explanation.6. Significant positive autocorrelation was found among individuals at within‐river distances of up to 25 km. Repeated dispersal of seeds over distances in the range of tens of kilometers is common.
Down‐regulation of ATBF1 is a major inactivating mechanism in hepatocellular carcinoma
Authors: Kim C J , Song J H , Cho Y G , Cao Z , Lee Y S , Nam S W , Lee J Y , Park W S 
Published: February 2008

Aims:  α‐Fetoprotein (AFP) is frequently detected in hepatocellular carcinomas (HCCs) and AT motif binding factor 1 (ATBF1) down‐regulates AFP gene expression in hepatic cells. The ATBF1 gene also inhibits cell growth and differentiation, and altered gene expression is associated with malignant transformation. The aim was to investigate the potential role of the ATBF1 gene in HCCs.Methods and results:  Somatic mutations, allelic loss and hypermethylation of the ATBF1 gene were analysed in 76 sporadic HCCs. The level of ATBF‐1 mRNA expression was analysed using quantitative real‐time reverse transcriptase‐polymerase chain reaction. Genetic studies of the ATBF1 gene revealed absence of somatic mutation in the hotspot region and 15 (25%) of 60 informative cases showed allelic loss at the ATBF1 locus. Hypermethylation in the intron 1 region of the ATBF1 gene was detected in only one case. Interestingly, ATBF1 mRNA expression in HCCs was significantly reduced in 55 (72.4%) samples compared with the corresponding surrounding liver tissues. Reduced expression was not statistically associated with clinicopathological parameters including stage, histological grade, infective virus type, and serum α‐fetoprotein level.Conclusions:  The ATBF1 gene may contribute to the development of HCCs via transcriptional down‐regulation of mRNA expression, but not by genetic or epigenetic alterations.
The effect of maintaining apical patency on canal transportation
Authors: Tsesis I. , Amdor B. , Tamse A. , Kfir A. 
Published: February 2008

AbstractAim  To evaluate, ex vivo, the effect of maintaining apical patency on the original canal shape during preparation of curved roots by two different techniques.Methodology  Forty extracted human maxillary and mandibular molars were evaluated. Occlusal surfaces were ground and roots sectioned to the level of the cemento‐enamel junction to allow only one root to remain for evaluation in each tooth. Specimens were divided into four experimental groups (10 canals each): Group 1 – root canals prepared using the balanced force technique with stainless steel K‐files, and patency established with size 10 K‐files between each instrument; Group 2 – same as Group 1 but without the use of a patency file; Group 3 – canals instrumented with LightSpeed® instruments and patency established with size 10 K‐files between each instrument; and Group 4 – same as Group 3 but without the use of a patency file. Specimens were mounted and a series of radiographs taken. Initial and post‐preparation digital images were superimposed and the distance between two central axes at 1, 2 and 4 mm from the working length (WL) was measured to obtain an indication of the degree of apical transportation. Results were subjected to statistical analysis using two‐way analysis of variance (anova).Results  No significant differences were found in degree of apical transportation at different levels of the root canal (P > 0.05) nor in loss of WL between groups (P > 0.05).Conclusion  In this laboratory study, maintaining apical patency did not influence canal transportation in the apical 4 mm.