bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distributing Finite Automata Through Petri Net Synthesis
Authors: Badouel Éric , Caillaud Benoît , Darondeau P. 
Published: December 2003

Abstract.

The synthesis problem for Petri nets consists in deciding constructively the existence of a Petri net with sequential state graph isomorphic to a given graph. If events are attached to locations, one may set as an additional requirement that the synthesised net should be distributable; i.e. such that events at different locations have no common input place, whence distributed conflicts are avoided. Distributable nets are easily implemented by finite families of automata (one per location) communicating with each other by asynchronous message passing. We show that the general Petri net synthesis problem and its distributed version may both be solved in time polynomial in the size of the given graph. We report on some preliminary experiments of Petri net synthesis applied to the distribution of reactive automata using the tool

SYNET

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Editorial
Authors: COOKE JOHN 
Published: December 2003

At the time of writing this editorial, subscribers will have just received their copies of the triple issue honouring the work of Rod Burstall. Coordinating this collection was a substantial undertaking; and thanks go to all concerned, particularly to David Rydeheard and Don Sannella and the behind the scenes production staff. We (the journal editors) hope you agree that it was well worth waiting for the fascinating collection.
The production and scheduling of that set of papers, and other incidental but cumulative factors, have contributed to recent issues being late. We hope soon to be back close to our planned, evenly timed, publication timetable; however it also seems timely to mention, and to reiterate, some changes which are afoot.
As of this issue (14.1) we shall revert to our initial publication frequency of 4 issues per year, but these will be larger than in earlier volumes and will retain the large page format adopted in Volume 12. [A reminder for authors who use LaTeX to use the new class files.] We are now receiving, and publishing, long papers (but still with the option of including supplementary material on the web) and, except in special issues, strive to achieve a reasonable coverage of topics within the given constraints.
Although normally skipped over, readers of the journal front matter might notice periodic changes to the editorial board. These usually go unmentioned; our editors (who are working editors, not merely ‘names’) seek no reward or praise. Readers will also notice the recently modernised BCS-FACS logo and a declaration that the journal (although truly international in scope) was founded by (BCS-)FACS, some even to this day refer to it as ‘the FACS journal’, and we are very happy for this to continue.
Bringing these two threads together gets me to the point of this digression. Dan Simpson founded the BCS specialist group on Formal Aspects of Computing Science some 25 years ago. Without his radical suggestion that the BCS had a specialist group that actually addressed Computer Science, there would have been no FACS and no FACS journal. Dan has recently finished his spell as Dean in the Faculty of IT at Brighton University and he has also resigned as a member of our editorial board. As you can see, he was active to the very end being responsible for progressing 2 of the 3 papers in this issue. I gather he now intends to concern himself with other matters; I would counsel a less stressful life and more Bob Dylan music.
He has been a friend and colleague of many of those associated with the FACS group and its journal; on their behalf may I offer a big ‘thank you’ for all that you have done for us and offer our best wishes for whatever endeavours you are about to embark upon. Very many years ago, at a conference, I heard someone respond in debate “I didn't see who said that but it sounded like Mr Simpson from Teesside … .” – well it's no longer ‘Mr’ nor ‘Teesside’ but I can't believe that we really have seen or heard the last of this Yorkshire lad.
Thanks, goodbye and good luck.
A Mechanically Proved and Incremental Development of IEEE 1394 Tree Identify Protocol
Authors: Abrial Jean-Raymond , Cansell Dominique , Méry Dominique 
Published: December 2003

Abstract.

The IEEE 1394 tree identify protocol illustrates the adequacy of the
event-driven approach
used together with the B Method. This approach provides a complete framework for developing mathematical models of distributed algorithms. A specific development is made of a series of more and more refined models. Each model is made of a number of static properties (the invariant) and dynamic parts (the guarded events). The internal consistency of each model as well as its correctness with regard to its previous abstraction are proved with the proof engine of Atelier B, which is the tool associated with B. In the case of IEEE 1394 tree identify protocol, the initial model is very primitive: it provides the basic properties of the graph (symmetry, acyclicity, connectivity), and its dynamic parts essentially contain a single event which
elects the leader
in one shot. Further refinements introduce more events, showing how each node of the graph non-deterministically participates in the leader election. At some stage in the development, message passing is introduced. This raises a specific potential contention problem, whose solution is given. The last stage of the refinement completely localises the events by making them take decisions based on local data only.
Does angiotensin‐converting enzyme gene polymorphism affect blood pressure? Findings after 6 years of follow‐up in healthy subjects
Authors: Di Pasquale Pietro , Cannizzaro Sergio , Paterna Salvatore 
Published: December 2003

AbstractBackground:There has been an increase in research into the association between angiotensin‐converting enzyme (ACE) gene deletion polymorphism and cardiovascular disease, with conflicting results. The present prospective long‐term study was conducted to evaluate whether the DD genotype could also be associated with a higher prevalence of hypertension in healthy subjects, over 6 years of follow‐up.Methods:Population: 684 healthy volunteers (aged, 25–55 years): normotensive and free of cardiovascular diseases, with acceptable echocardiographic window. All subjects had to have a normal electrocardiogram (ECG) and echocardiogram (ECHO) at entry.Study protocol:All subjects underwent a complete physical examination, 12‐lead ECG and ECHO, and venous blood samples were drawn for DNA analysis and cholesterol. All subjects had a clinical evaluation each year for the 6 year duration of the study.Results:All 684 subjects completed 6 years of follow‐up. We identified three genetically distinct groups. The ACE‐DD group (n=225, 80F/145M, mean age 43.4±7.6 years) had 42 hypertensive subjects (18.3%), 5 heart failure (HF) subjects and 6 subjects with acute coronary syndromes (ACS). There was no association between family history, smoking habit, hypercholesterolemia and events. The ACE‐ID group (n=335, 116F/219M, mean age 43.6±7 years) had 16 hypertensive subjects (4.7%) and 3 subjects with ACS. The ACE‐II group (n=124, 45F/79M, mean age 42.5±6.9 years) had 2 hypertensive subjects (1.6%) and 1 HF subject. The incidence of hypertension and cardiovascular events was significantly higher in the ACE‐DD group (53 cases, 23%) than in the ACE‐ID and ACE‐II groups (20 and 3 cases, 5.9 and 2.4%, respectively), P=0.0001. The higher incidence of hypertension was observed in the older age groups (36–45 and 46–55 years) with ACE‐DD and ACE‐ID genotypes.Conclusion:Our data suggest that ACE‐DD polymorphism is associated with a higher incidence of hypertension in baseline healthy subjects, irrespective of other risk factors. The higher incidence of hypertension was apparent predominantly in the older age groups.
Self‐inflicted cesarean section with maternal and fetal survival
Authors: Molina‐Sosa A. , Galvan‐Espinosa H. , Gabriel‐Guzman J. , Valle R.F. 
Published: December 2003

AbstractAn unusual case of self‐inflicted cesarean section with maternal and child survival is presented. No similar event was found in an Internet literature search. Because of a lack of medical assistance and a history of fetal death in utero, a 40‐year‐old multiparous woman unable to deliver herself alone vaginally sliced her abdomen and uterus and delivered her child. She was transferred to a hospital where she underwent repair of the incisions and had to remain hospitalized. Mother and child survived the event. Unusual and extraordinary measures to preserve their offspring sometimes moves women to extreme decisions endangering their own lives. Social, educational, and health measures should be instituted all over the world, particularly in rural areas of developing countries, to avoid such extreme events.
Multiple effects of mefenamic acid on K+ currents in smooth muscle cells from pig proximal urethra
Authors: Teramoto N , Brading A F , Ito Y 
Published: December 2003

The effects of mefenamic acid on both membrane potential and K+ currents in pig urethral myocytes were investigated using patch‐clamp techniques (conventional whole‐cell, cell‐attached, outside‐out and inside‐out configuration).
In the current‐clamp mode, mefenamic acid caused a concentration‐dependent hyperpolarization, which was inhibited by preapplication of 1 μM glibenclamide. In the voltage‐clamp mode, mefenamic acid induced an outward current that was blocked by glibenclamide even in the presence of iberiotoxin (IbTX, 300 nM) at −50 mV.
ATP‐sensitive K+ channels (KATP channels) could be activated in the same patch by mefenamic acid and levcromakalim, with the same unitary amplitude and the similar opening gating at −50 mV in cell‐attached configuration.
In outside‐out recording, external application of mefenamic acid activated intracellular Ca2+‐activated IbTX‐sensitive large‐conductance K+ channels (BKCa channels).
Mefenamic acid (30 μM) activated spontaneous transient outward currents (STOCs). In contrast, mefenamic acid (100 μM) increased sustained outward currents, diminishing the activity of STOCs.
Over the whole voltage range, mefenamic acid caused opposite effects on the membrane currents in the absence and presence of 5 μM glibenclamide. In the presence of 10 mM 4‐aminopyridine (4‐AP), mefenamic acid only increased the outward currents.
These results indicate that mefenamic acid increases the channel activities of two distinct types of K+ channels (i.e. BKCa channels and KATP channels) and decreased 4‐AP‐sensitive K+ channels in pig urethral myocytes.

British Journal of Pharmacology (2003) 140, 1341–1350. doi:10.1038/sj.bjp.0705524
Thymol, a constituent of thyme essential oil, is a positive allosteric modulator of human GABAA receptors and a homo‐oligomeric GABA receptor from Drosophila melanogaster
Authors: Priestley Caroline M , Williamson Elizabeth M , Wafford Keith A , Sattelle David B 
Published: December 2003

The GABA‐modulating and GABA‐mimetic activities of the monoterpenoid thymol were explored on human GABAA and Drosophila melanogaster homomeric RDLac GABA receptors expressed in Xenopus laevis oocytes, voltage‐clamped at −60 mV. The site of action of thymol was also investigated.
Thymol, 1–100 μM, resulted in a dose‐dependent potentiation of the EC20 GABA response in oocytes injected with either α1β3γ2s GABAA subunit cDNAs or the RDLac subunit RNA. At 100 μM thymol, current amplitudes in response to GABA were 416±72 and 715±85% of controls, respectively. On both receptors, thymol, 100 μM, elicited small currents in the absence of GABA.
The EC50 for GABA at α1β3γ2s GABAA receptors was reduced by 50 μM thymol from 15±3 to 4±1 μM, and the Hill slope changed from 1.35±0.14 to 1.04±0.16; there was little effect on the maximum GABA response.
Thymol (1–100 μM) potentiation of responses to EC20 GABA for α1β1γ2s, α6β3γ2s and α1β3γ2s human GABAA receptors was almost identical, arguing against actions at benzodiazepine or loreclezole sites.
Neither flumazenil, 3‐hydroxymethyl‐β‐carboline (3‐HMC), nor 5α‐pregnane‐3α, 20α‐diol (5α‐pregnanediol) affected thymol potentiation of the GABA response at α1β3γ2s receptors, providing evidence against actions at the benzodiazepine/β‐carboline or steroid sites. Thymol stimulated the agonist actions of pentobarbital and propofol on α1β3γ2s receptors, consistent with a mode of action distinct from that of either compound. These data suggest that thymol potentiates GABAA receptors through a previously unidentified binding site.

British Journal of Pharmacology (2003) 140, 1363–1372. doi:10.1038/sj.bjp.0705542
Presynaptic group I metabotropic glutamate receptors modulate synaptic transmission in the rat superior colliculus via 4‐AP sensitive K+ channels
Authors: White Anne‐Marie , Kylänpää Risto A , Christie Louisa A , McIntosh Simon J , Irving Andrew J , Platt Bettina 
Published: December 2003

Group I metabotropic glutamate receptors (mGluRs) are thought to be important modulators of neuronal function in the superior colliculus (SC). Here, we investigated the pharmacology and signalling mechanisms underlying group I mGluR‐mediated inhibition of neuronal excitability and synaptic transmission in the rat SC slice.
The group I agonist (RS)‐3,5‐dihydroxyphenylglycine (DHPG) potently depressed synaptically evoked excitatory postsynaptic potentials (EPSPs), currents (EPSCs), and action potentials in a dose‐dependent manner (IC50: 6.3 μM). This was strongly reduced by the broad‐spectrum antagonist (+)‐alpha‐methyl‐4‐carboxyphenylglycine (MCPG, 1 mM, ∼95% reduction), by the mGluR1 antagonist LY367385 (100 μM, ∼80% reduction) but not by the mGluR5 antagonist 6‐methyl‐2‐(phenylethynyl)‐pyridine (MPEP, 1–100 μM).
The putative mGluR5‐specific agonist (RS)‐2‐chloro‐5‐hydroxyphenylglycine (CHPG, 500 μM) also inhibited EPSPs. Interestingly, CHPG's actions were not blocked by MPEP, but LY367385 (100 μM) reduced the effect of CHPG by 50%.
Inhibition induced by DHPG was independent of phospholipase C (PLC)/protein kinase C pathways, and did not require intact intracellular Ca2+ stores. It was not abolished but enhanced by the GABAA antagonist bicuculline (5 μM), suggesting that DHPG's action was not due to facilitated inhibition or changes in neuronal network activity.
The K+ channel antagonist 4‐aminopyridine (4‐AP, 50–100 μM) converted the inhibitory effect of DHPG into facilitation. Paired‐pulse depression was strongly reduced by DHPG, an effect that was also prevented by 4‐AP.
Our data indicate that group I agonists regulate transmitter release, presumably via an autoreceptor in the SC. This receptor may be involved in adaptation to repetitive stimulation via a non‐PLC mediated pathway.

British Journal of Pharmacology (2003) 140, 1421–1433. doi:10.1038/sj.bjp.0705570
The Cl− channel blocker niflumic acid releases Ca2+ from an intracellular store in rat pulmonary artery smooth muscle cells
Authors: Cruickshank Stuart F , Baxter Lynne M , Drummond Robert M 
Published: December 2003

The effect of the Cl− channel blockers niflumic acid (NFA), 5‐nitro‐2‐(3‐phenylpropylamino)‐benzoic acid (NPPB), 4,4′‐diisothiocyanatostilbene‐2,2′‐disulfonic acid (DIDS), and anthracene‐9‐carboxylic acid (A‐9‐C), on Ca2+ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca2+ concentration ([Ca2+]i) was monitored with either fura‐2 or fluo‐4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca2+ from the sarcoplasmic reticulum (SR).
NFA and NPPB significantly increased basal [Ca2+]i and attenuated the caffeine‐induced increase in [Ca2+]i. These Cl− channel blockers also increased the half‐time (t1/2) to peak for the caffeine‐induced [Ca2+]i transient, and slowed the removal of Ca2+ from the cytosol following application of caffeine. Since DIDS and A‐9‐C were found to adversely affect fura‐2 fluorescence, fluo‐4 was used to monitor intracellular Ca2+ in studies involving these Cl− channel blockers. Both DIDS and A‐9‐C increased basal fluo‐4 fluorescence, indicating an increase in intracellular Ca2+, and while DIDS had no significant effect on the t1/2 to peak for the caffeine‐induced Ca2+ transient, it was significantly increased by A‐9‐C.
In the absence of extracellular Ca2+, NFA significantly increased basal [Ca2+]i, suggesting that the release of Ca2+ from an intracellular store was responsible for the observed effect.
Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca2+]i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca2+]i induced by NFA.
These data show that Cl− channel blockers have marked effects on Ca2+ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA‐induced increase in [Ca2+]i indicates that it is likely due to Ca2+ release from an intracellular store, most probably the SR.

British Journal of Pharmacology (2003) 140, 1442–1450. doi:10.1038/sj.bjp.0705571
An optimized approach to study endocannabinoid signaling: evidence against constitutive activity of rat brain adenosine A1 and cannabinoid CB1 receptors
Authors: Savinainen Juha R , Saario Susanna M , Niemi Riku , Järvinen Tomi , Laitinen Jarmo T 
Published: December 2003

At nanomolar concentrations, SR141716 and AM251 act as specific and selective antagonists of the cannabinoid CB1 receptor. In the micromolar range, these compounds were shown to inhibit basal G‐protein activity, and this is often interpreted to implicate constitutive activity of the CB1 receptors in native tissue. We show here, using [35S]GTPγS binding techniques, that micromolar concentrations of SR141716 and AM251 inhibit basal G‐protein activity in rat cerebellar membranes, but only in conditions where tonic adenosine A1 receptor signaling is not eliminated.
Unlike lipophilic A1 receptor antagonists (potency order DPCPX≫N‐0840 ∼cirsimarin>caffeine), adenosine deaminase (ADA) was not fully capable in eliminating basal A1 receptor‐dependent G‐protein activity. Importantly, all antagonists reduced basal signal to the same extent (20%), and the response evoked by the inverse agonist DPCPX was not reversed by the neutral antagonist N‐0840. These data indicate that rat brain A1 receptors are not constitutively active, but that an ADA‐resistant adenosine pool is responsible for tonic A1 receptor activity in brain membranes.
SR141716 and AM251, at concentrations fully effective in reversing CB1‐mediated responses (10−6 M), did not reduce basal G‐protein activity, indicating that CB1 receptors are not constitutively active in these preparations.
At higher concentrations (1–2.5 × 10−5 M), both antagonists reduced basal G‐protein activity in control and ADA‐treated membranes, but had no effect when A1 receptor signaling was blocked with DPCPX. Moreover, the CB1 antagonists right‐shifted A1 agonist dose–response curves without affecting maximal responses, suggesting competitive mode of antagonist action. The CB1 antagonists did not affect muscarinic acetylcholine or GABAB receptor signaling.
When further optimizing G‐protein activation assay for the labile endocannabinoid 2‐arachidonoylglycerol (2‐AG), we show, by using HPLC, that pretreatment of cerebellar membranes with methyl arachidonoyl fluorophosphonate (MAFP) fully prevented enzymatic degradation of 2‐AG and concomitantly enhanced the potency of 2‐AG. In contrast to previous claims, MAFP exhibited no antagonist activity at the CB1 receptor.
The findings establish an optimized method with improved signal‐to‐noise ratio to assess endocannabinoid‐dependent G‐protein activity in brain membranes, under assay conditions where basal adenosinergic tone and enzymatic degradation of 2‐AG are fully eliminated.

British Journal of Pharmacology (2003) 140, 1451–1459. doi:10.1038/sj.bjp.0705577
Effect of peptidases on the ability of exogenous and endogenous neurokinins to produce neurokinin 1 receptor internalization in the rat spinal cord
Authors: Marvizón Juan Carlos G , Wang Xueren , Lao Li‐Jun , Song Bingbing 
Published: December 2003

The ability of peptidases to restrict neurokinin 1 receptor (NK1R) activation by exogenously applied or endogenously released neurokinins was investigated by measuring NK1R internalization in rat spinal cord slices.
Concentration–response curves for substance P and neurokinin A were obtained in the presence and absence of 10 μM thiorphan, an inhibitor of neutral endopeptidase (EC 3.4.24.11), plus 10 μM captopril, an inhibitor of dipeptidyl carboxypeptidase (EC 3.4.15.1). These inhibitors significantly decreased the EC50 of substance P to produce NK1R internalization from 32 to 9 nM, and the EC50 of neurokinin A from 170 to 60 nM.
Substance P was significantly more potent than neurokinin A, both with and without these peptidase inhibitors.
In the presence of peptidase inhibitors, neurokinin B was 10 times less potent than neurokinin A and 64 times less potent than substance P (EC50=573 nM).
Several aminopeptidase inhibitors (actinonin, amastatin, bacitracin, bestatin and puromycin) failed to further increase the effect of thiorphan plus captopril on the NK1R internalization produced by 10 nM substance P.
Electrical stimulation of the dorsal root produced NK1R internalization by releasing endogenous neurokinins. Thiorphan plus captopril increased NK1R internalization produced by 1 Hz stimulation, but not by 30 Hz stimulation.
Therefore, NEN and DCP restrict NK1R activation by endogenous neurokinins when they are gradually released by low‐frequency firing of primary afferents, but become saturated or inhibited when primary afferents fire at a high frequency.

British Journal of Pharmacology (2003) 140, 1389–1398. doi:10.1038/sj.bjp.0705578
Linkage and QTL mapping for Sus scrofa chromosome 13
Authors: Yue G. , Russo V. , Davoli R. , Sternstein I. , Brunsch C. , Schröffelova D. , Stratil A. , Moser G. , Bartenschlager H. , Reiner G. , Geldermann H. 
Published: December 2003

SummaryFor Sus scrofa chromosome 13 (SSC13) eleven markers were genotyped to generate linkage and QTL maps in three F2 families based on Wild Boar (W), Meishan (M) and Pietrain (P) crosses. Results of linkage maps were similar and agreed with published maps. Quantitative trait loci (QTLs) for body weights, meat conductivity and fat deposition were mapped in the M × P family to the interval S0076–S0068 (40–80 cM) and near the locus SW38 (120–150 cM). QTLs for the same traits were observed in the W × M family in different intervals explaining up to 5.3% of the F2 phenotypic variance. No significant QTLs for the traits under investigation were found in the W × P family. The effects of QTL alleles were mostly dominant. In the M × P and W × M families alleles inherited from Meishan were generally associated with high values of live weights, food consumption and fat deposition and low values of meat conductivity.
Effects of environmental variation on extinction and establishment
Authors: Drake John M. , Lodge David M. 
Published: December 2003

AbstractTheoretical models predict that increasing environmental variation increases the probability of extinction, decreases the probability of establishment, and influences the distribution of times to extinction or establishment. We conducted an experiment with 281 independent populations of Daphnia magna under controlled laboratory conditions to test these predictions. Consistent with the theory, the fraction of populations going extinct increased and the fraction of populations establishing self‐sustaining populations decreased under higher levels of environmental variation compared with controls. Time to extinction decreased under higher levels of environmental variation, but we found no effect on time to establishment. These results are consistent with theoretical predictions from models of extinction. They therefore support the use of stochastic population models to predict the fates of introductions of non‐indigenous species or native endangered species based on historic fluctuations and/or expected future conditions.