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Migraine Disorders: HELP
Articles from Merseyside
Based on 12 articles published since 2008
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These are the 12 published articles about Migraine Disorders that originated from Merseyside during 2008-2019.
 
+ Citations + Abstracts
1 Review Cortical spreading depression and calcitonin gene-related peptide: a brief review of current progress. 2013

Wang, Minyan. ·Department of Biological Sciences, Xi'an Jiaotong-Liverpool University, Suzhou 215123, PR China. Electronic address: minyan.wang@xjtlu.edu.cn. ·Neuropeptides · Pubmed #24220568.

ABSTRACT: Although detailed disease mechanisms of migraine remain poorly understood, migraine is known to have a complex pathophysiology with both vascular and neuronal mechanisms. The neuronal mechanisms of migraine may be attributed to cortical spreading depression (CSD); consequently, CSD has been widely studied for understanding the pathophysiology of migraine. Well validated CSD models have been developed for evaluating anti-migraine drugs. Neuropeptides, mainly, calcitonin gene-related peptide (CGRP), have been proposed as an emerging class of effective drugs against migraine headache. The central role of this neuropeptide has led to research into CSD for understanding disease mechanisms of migraine. This review briefly summarizes our current understanding of CSD and CGRP involvement in CSD. Although CSD can also worsen strokes, this brief paper has excluded the possible connection between the neuropeptide and CSD associated with them. Instead it has focused solely on CGRP in CSD associated with migraine.

2 Review Migraine and restless legs syndrome: is there an association? 2011

Cannon, Paul R / Larner, Andrew J. ·Walton Centre for Neurology and Neurosurgery, Lower Lane, Fazakerley, Liverpool L9 7LJ, UK. ·J Headache Pain · Pubmed #21660429.

ABSTRACT: Occasional clinical reports have suggested a link between migraine and restless legs syndrome. We undertook a systematic review of the evidence, which supports this association, and consider possible shared pathogenic mechanisms and the implications for current clinical practice.

3 Article ROS/TRPA1/CGRP signaling mediates cortical spreading depression. 2019

Jiang, Liwen / Ma, Dongqing / Grubb, Blair D / Wang, Minyan. ·Centre for Neuroscience, Xi'an Jiaotong-Liverpool University, Suzhou, China. · Department of Biological Sciences, Xi'an Jiaotong-Liverpool University, 111 Renái Road, Suzhou, 215123, People's Republic of China. · Institute of Translational Medicine, University of Liverpool, Crown Street, Liverpool, UK. · Centre for Neuroscience, Xi'an Jiaotong-Liverpool University, Suzhou, China. Minyan.wang@xjtlu.edu.cn. · Department of Biological Sciences, Xi'an Jiaotong-Liverpool University, 111 Renái Road, Suzhou, 215123, People's Republic of China. Minyan.wang@xjtlu.edu.cn. ·J Headache Pain · Pubmed #30841847.

ABSTRACT: OBJECTIVES: The transient receptor potential ankyrin A 1 (TRPA1) channel and calcitonin gene-related peptide (CGRP) are targets for migraine prophylaxis. This study aimed to understand their mechanisms in migraine by investigating the role of TRPA1 in cortical spreading depression (CSD) in vivo and exploring how reactive oxygen species (ROS)/TRPA1/CGRP interplay in regulating cortical susceptibility to CSD. METHODS: Immunohistochemistry was used for detecting TRPA1 expression. CSD was induced by K RESULTS: TRPA1 was expressed in cortical neurons and astrocytes of rats and mice. TRPA1 deactivation by an anti-TRPA1 antibody reduced cortical susceptibility to CSD in rats and decreased ipsilateral MDA level induced by CSD. In mouse brain slices, H CONCLUSIONS: ROS/TRPA1/CGRP signaling plays a critical role in regulating cortical susceptibility to CSD. Inhibition ROS and deactivation of TRPA1 channels may have therapeutic benefits in preventing stress-triggered migraine via CGRP.

4 Article The Transient Receptor Potential Ankyrin Type 1 Plays a Critical Role in Cortical Spreading Depression. 2018

Jiang, Liwen / Wang, Yan / Xu, Yuewei / Ma, Dongqing / Wang, Minyan. ·Centre for Neuroscience, Xi'an Jiaotong-Liverpool University, Suzhou 215123, China; Department of Biological Sciences, Xi'an Jiaotong-Liverpool University, Suzhou 215123, China. · Centre for Neuroscience, Xi'an Jiaotong-Liverpool University, Suzhou 215123, China. · Department of Biological Sciences, Xi'an Jiaotong-Liverpool University, Suzhou 215123, China. · Centre for Neuroscience, Xi'an Jiaotong-Liverpool University, Suzhou 215123, China; Department of Biological Sciences, Xi'an Jiaotong-Liverpool University, Suzhou 215123, China. Electronic address: Minyan.wang@xjtlu.edu.cn. ·Neuroscience · Pubmed #29719223.

ABSTRACT: The transient receptor potential ankyrin type-1 (TRPA1) channels have been proposed as a potential target for migraine therapy. Yet the role of cortical TRPA1 channels in migraine mechanism has not been fully understood. Cortical spreading depression (CSD) is known as an underlying cause of migraine aura. The aim of this study is to investigate if cortical TRPA1 activity is required for CSD genesis and propagation. A mouse brain slice CSD model with intrinsic optical imaging was applied for TRPA1 signaling pharmacology. The results showed that the TRPA1 agonist, umbellulone, facilitated the propagation of submaximal CSD. Correspondingly, an anti-TRPA1 antibody and two selective TRPA1 antagonists, A967079 and HC-030031, prolonged the CSD latency and reduced magnitude, indicating a reduced cortical susceptibility to CSD under TRPA1 deactivation. Furthermore, the TRPA1 agonist, allyl-isothiocyanate (AITC), reversed the suppression of CSD by HC-030031, but not by A967079. Interestingly, the inhibitory action of A967079 on CSD was reversed by exogenous calcitonin-gene-related peptide (CGRP). Consistent to TRPA1 deactivation, the prolonged CSD latency was observed by an anti-CGRP antibody in the mouse brain slice, which was reversed by exogenous CGRP. We conclude that cortical TRPA1 is critical in regulating cortical susceptibility to CSD, which involves CGRP. The data strongly suggest that deactivation of TRPA1 channels and blockade of CGRP would have therapeutic benefits in preventing migraine with aura.

5 Article Independent prescriber physiotherapist led balance clinic: the Southport and Ormskirk pathway. 2017

Burrows, L / Lesser, T H / Kasbekar, A V / Roland, N / Billing, M. ·Department of Physiotherapy,Southport and Ormskirk NHS Trust,Southport,UK. · Department of Otolaryngology,Head and Neck Surgery,Aintree University Hospital,Liverpool,UK. · Department of Otology and Hearing Implantation,Cambridge University Hospitals,UK. · Department of Audiology,Southport and Ormskirk NHS Trust,Southport,UK. ·J Laryngol Otol · Pubmed #28202097.

ABSTRACT: OBJECTIVE: To report the introduction and impact of non-medical prescribing, initiated to improve patient pathways for those presenting with dizziness and balance disorders. METHODS: The Southport and Ormskirk physiotherapy-led vestibular clinic sees and treats all patients with dizziness and balance disorders referred to the ENT department. Letters are triaged by an audiologist, who also performs an otological examination and hearing test; this is followed by an assessment with the independent prescriber physiotherapist. An ENT consultant is nearby if joint consultation is needed. Diagnoses, treatments and patient satisfaction were studied, with an analysis of the impact of medication management (stopping or starting medicines) on patients and service. RESULTS: In 12 months, 413 new patients with dizziness and balance disorders had appointments. The most common diagnoses were benign paroxysmal positional vertigo and vestibular migraine. Eighty-four per cent of patients required self-management strategies, 50 per cent exercise therapy, 48 per cent medication management and 24 per cent a particle repositioning manoeuvre. Patient satisfaction was high (99 per cent). CONCLUSION: Having an independent prescriber physiotherapist leading the balance clinic has reduced the number of hospital visits and onward referrals. Nearly half of all patients required medication management as part of their dizziness or balance treatment.

6 Article Involvement of CGRP receptors in retinal spreading depression. 2016

Wang, Yan / Li, Yanli / Wang, Minyan. ·Centre for Neuroscience, Xi'an Jiaotong-Liverpool University, Suzhou, PR China. · Centre for Neuroscience, Xi'an Jiaotong-Liverpool University, Suzhou, PR China; Department of Biological Sciences, Xi'an Jiaotong-Liverpool University, Suzhou, PR China. Electronic address: minyan.wang@xjtlu.edu.cn. ·Pharmacol Rep · Pubmed #27362770.

ABSTRACT: BACKGROUND: Cortical spreading depression (CSD) is a transient propagating excitation of synaptic activity followed by depression, which is implicated in migraine with aura and is regarded as the underlying cause of migraine. Calcitonin-gene related peptide (CGRP) receptors play a crucial role in mediating the magnitude of CSD in rat cortical slice. This study aimed to examine whether CGRP receptors are involved in retinal spreading depression (RSD) in chicks. METHODS: Western blot was used for detection of calcitonin-receptor like receptor (CALCRL) and intrinsic optical imaging was used for pharmacological investigation. RESULTS: We found that the key component of CGRP receptor, CALCRL, is expressed in the chick retina. Using an in vitro migraine RSD model, we demonstrated that BIBN4096, a potent antagonist for CGRP receptors, markedly reduced the magnitude of RSD induced by K(+), but also the propagation rate. CONCLUSIONS: The data suggest that CGRP receptors mediate RSD propagation involving neuronal mechanism and approve that RSD is an efficient in vitro approach for assessing anti-migraine drugs targeting CGRP receptors.

7 Article Meta-analysis of 375,000 individuals identifies 38 susceptibility loci for migraine. 2016

Gormley, Padhraig / Anttila, Verneri / Winsvold, Bendik S / Palta, Priit / Esko, Tonu / Pers, Tune H / Farh, Kai-How / Cuenca-Leon, Ester / Muona, Mikko / Furlotte, Nicholas A / Kurth, Tobias / Ingason, Andres / McMahon, George / Ligthart, Lannie / Terwindt, Gisela M / Kallela, Mikko / Freilinger, Tobias M / Ran, Caroline / Gordon, Scott G / Stam, Anine H / Steinberg, Stacy / Borck, Guntram / Koiranen, Markku / Quaye, Lydia / Adams, Hieab H H / Lehtimäki, Terho / Sarin, Antti-Pekka / Wedenoja, Juho / Hinds, David A / Buring, Julie E / Schürks, Markus / Ridker, Paul M / Hrafnsdottir, Maria Gudlaug / Stefansson, Hreinn / Ring, Susan M / Hottenga, Jouke-Jan / Penninx, Brenda W J H / Färkkilä, Markus / Artto, Ville / Kaunisto, Mari / Vepsäläinen, Salli / Malik, Rainer / Heath, Andrew C / Madden, Pamela A F / Martin, Nicholas G / Montgomery, Grant W / Kurki, Mitja I / Kals, Mart / Mägi, Reedik / Pärn, Kalle / Hämäläinen, Eija / Huang, Hailiang / Byrnes, Andrea E / Franke, Lude / Huang, Jie / Stergiakouli, Evie / Lee, Phil H / Sandor, Cynthia / Webber, Caleb / Cader, Zameel / Muller-Myhsok, Bertram / Schreiber, Stefan / Meitinger, Thomas / Eriksson, Johan G / Salomaa, Veikko / Heikkilä, Kauko / Loehrer, Elizabeth / Uitterlinden, Andre G / Hofman, Albert / van Duijn, Cornelia M / Cherkas, Lynn / Pedersen, Linda M / Stubhaug, Audun / Nielsen, Christopher S / Männikkö, Minna / Mihailov, Evelin / Milani, Lili / Göbel, Hartmut / Esserlind, Ann-Louise / Christensen, Anne Francke / Hansen, Thomas Folkmann / Werge, Thomas / Anonymous5370872 / Kaprio, Jaakko / Aromaa, Arpo J / Raitakari, Olli / Ikram, M Arfan / Spector, Tim / Järvelin, Marjo-Riitta / Metspalu, Andres / Kubisch, Christian / Strachan, David P / Ferrari, Michel D / Belin, Andrea C / Dichgans, Martin / Wessman, Maija / van den Maagdenberg, Arn M J M / Zwart, John-Anker / Boomsma, Dorret I / Smith, George Davey / Stefansson, Kari / Eriksson, Nicholas / Daly, Mark J / Neale, Benjamin M / Olesen, Jes / Chasman, Daniel I / Nyholt, Dale R / Palotie, Aarno. ·Psychiatric and Neurodevelopmental Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. · Medical and Population Genetics Program, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA. · Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA. · Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, UK. · Analytic and Translational Genetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. · FORMI, Oslo University Hospital, Oslo, Norway. · Department of Neurology, Oslo University Hospital, Oslo, Norway. · Institute of Clinical Medicine, University of Oslo, Oslo, Norway. · Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland. · Estonian Genome Center, University of Tartu, Tartu, Estonia. · Division of Endocrinology, Boston Children's Hospital, Boston, Massachusetts, USA. · Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. · Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark. · Illumina, San Diego, California, USA. · Pediatric Neurology, Vall d'Hebron Research Institute, Barcelona, Spain. · Folkhälsan Institute of Genetics, Helsinki, Finland. · Neuroscience Center, University of Helsinki, Helsinki, Finland. · Molecular Neurology Research Program, Research Programs Unit, University of Helsinki, Helsinki, Finland. · 23andMe, Inc., Mountain View, California, USA. · Institute of Public Health, Charité-Universitätsmedizin Berlin, Berlin, Germany. · Division of Preventive Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA. · deCODE Genetics, Reykjavik, Iceland. · Medical Research Council (MRC) Integrative Epidemiology Unit, University of Bristol, Bristol, UK. · Department of Biological Psychology, Vrije Universiteit, Amsterdam, the Netherlands. · Department of Neurology, Leiden University Medical Centre, Leiden, the Netherlands. · Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland. · Department of Neurology and Epileptology, Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. · Institute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilians-Universität München, Munich, Germany. · Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. · Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. · Institute of Human Genetics, Ulm University, Ulm, Germany. · Center for Life Course Epidemiology and Systems Medicine, University of Oulu, Oulu, Finland. · Department of Twin Research and Genetic Epidemiology, King's College London, London, UK. · Department of Epidemiology, Erasmus University Medical Center, Rotterdam, the Netherlands. · Department of Radiology, Erasmus University Medical Center, Rotterdam, the Netherlands. · Department of Clinical Chemistry, Fimlab Laboratories, School of Medicine, University of Tampere, Tampere, Finland. · Department of Public Health, University of Helsinki, Helsinki, Finland. · Harvard Medical School, Boston, Massachusetts, USA. · Department of Neurology, University Duisburg-Essen, Essen, Germany. · Landspitali University Hospital, Reykjavik, Iceland. · Department of Psychiatry, VU University Medical Centre, Amsterdam, the Netherlands. · Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri, USA. · Department of Neurosurgery, NeuroCenter, Kuopio University Hospital, Kuopio, Finland. · Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. · MRC Functional Genomics Unit, Department of Physiology, Anatomy &Genetics, Oxford University, Oxford, UK. · Nuffield Department of Clinical Neuroscience, University of Oxford, Oxford, UK. · Oxford Headache Centre, John Radcliffe Hospital, Oxford, UK. · Max Planck Institute of Psychiatry, Munich, Germany. · Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. · Institute of Translational Medicine, University of Liverpool, Liverpool, UK. · Institute of Clinical Molecular Biology, Christian Albrechts University, Kiel, Germany. · Institute of Human Genetics, Helmholtz Zentrum München, Neuherberg, Germany. · Institute of Human Genetics, Technische Universität München, Munich, Germany. · Department of General Practice and Primary Health Care, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. · National Institute for Health and Welfare, Helsinki, Finland. · Institute of Clinical Medicine, University of Helsinki, Helsinki, Finland. · Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA. · Department of Internal Medicine, Erasmus University Medical Center, Rotterdam, the Netherlands. · Department of Pain Management and Research, Oslo University Hospital, Oslo, Norway. · Medical Faculty, University of Oslo, Oslo, Norway. · Department of Ageing and Health, Norwegian Institute of Public Health, Oslo, Norway. · Kiel Pain and Headache Center, Kiel, Germany. · Danish Headache Center, Department of Neurology, Rigshospitalet, Glostrup Hospital, University of Copenhagen, Copenhagen, Denmark. · Institute of Biological Psychiatry, Mental Health Center Sct. Hans, University of Copenhagen, Roskilde, Denmark. · Institute of Biological Psychiatry, MHC Sct. Hans, Mental Health Services Copenhagen, Copenhagen, Denmark. · Institute of Clinical Sciences, Faculty of Medicine and Health Sciences, University of Copenhagen, Copenhagen, Denmark. · iPSYCH-The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Copenhagen, Denmark. · Department of Health, National Institute for Health and Welfare, Helsinki, Finland. · Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland. · Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Turku, Finland. · Department of Neurology, Erasmus University Medical Center, Rotterdam, the Netherlands. · Department of Epidemiology and Biostatistics, MRC Health Protection Agency (HPE) Centre for Environment and Health, School of Public Health, Imperial College London, London, UK. · Biocenter Oulu, University of Oulu, Oulu, Finland. · Unit of Primary Care, Oulu University Hospital, Oulu, Finland. · Institute of Human Genetics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. · Population Health Research Institute, St George's, University of London, London, UK. · Department of Human Genetics, Leiden University Medical Centre, Leiden, the Netherlands. · Faculty of Medicine, University of Iceland, Reykjavik, Iceland. · Statistical and Genomic Epidemiology Laboratory, Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, Queensland, Australia. · Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA. ·Nat Genet · Pubmed #27322543.

ABSTRACT: Migraine is a debilitating neurological disorder affecting around one in seven people worldwide, but its molecular mechanisms remain poorly understood. There is some debate about whether migraine is a disease of vascular dysfunction or a result of neuronal dysfunction with secondary vascular changes. Genome-wide association (GWA) studies have thus far identified 13 independent loci associated with migraine. To identify new susceptibility loci, we carried out a genetic study of migraine on 59,674 affected subjects and 316,078 controls from 22 GWA studies. We identified 44 independent single-nucleotide polymorphisms (SNPs) significantly associated with migraine risk (P < 5 × 10(-8)) that mapped to 38 distinct genomic loci, including 28 loci not previously reported and a locus that to our knowledge is the first to be identified on chromosome X. In subsequent computational analyses, the identified loci showed enrichment for genes expressed in vascular and smooth muscle tissues, consistent with a predominant theory of migraine that highlights vascular etiologies.

8 Article A Pilot Study of Obesogenic Eating Behaviors in Children With Migraine. 2016

Ray, Stephen / Singh, Shashi Bhushan / Halford, Jason C G / Harrold, Joanne A / Kumar, Ram. ·Department of Neurology, Alder Hey Children's NHS Foundation Trust, Liverpool, United Kingdom Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom dr.stj.ray@gmail.com. · Manchester Royal Infirmary Hospital, Manchester, United Kingdom. · Department of Experimental Psychology, University of Liverpool, Liverpool, United Kingdom. · Department of Neurology, Alder Hey Children's NHS Foundation Trust, Liverpool, United Kingdom. ·J Child Neurol · Pubmed #26863998.

ABSTRACT: We studied associations between migraine severity and obesogenic eating behaviors in children with a prospective cross-sectional, clinic-based study. Migraine severity was quantified using the PedMIDAS tool and attack frequency. Eating behaviors were assessed using the Dutch Eating Behaviour Questionnaire and the Child Eating Behaviour Questionnaire. Food intake was assessed using a Food Intake Questionnaire. Statistical tests of association between eating behavior, food intake, and adiposity with migraine severity were performed. Sixty children (mean age = 10.9 years, standard deviation = 3.1; 26 males) were recruited. There was a positive correlation between the Child Eating Behaviour Questionnaire desire to drink subscale and PedMIDAS scores (r = 0.41, P = .01). Attack frequency was associated with higher intake of high fat or sugar content food and drink (r = 0.27, P = .04). No association between migraine severity and adiposity was found. Suggestion that migraine severity in children is associated with certain obesogenic eating behaviors requires further large study investigation.

9 Article A pilot study of cognitive behavioural therapy and relaxation for migraine headache: a randomised controlled trial. 2015

Cousins, S / Ridsdale, L / Goldstein, L H / Noble, A J / Moorey, S / Seed, P. ·Kings College London, Denmark Hill Campus, PO57, SE5 8AF, London, UK. · Kings College London, Denmark Hill Campus, PO57, SE5 8AF, London, UK. leone.ridsdale@kcl.ac.uk. · University of Liverpool, Merseyside, UK. ·J Neurol · Pubmed #26477023.

ABSTRACT: Headache is being viewed more commonly in a biopsychosocial framework, which introduces the possible utilisation of psychological treatment options, such as cognitive behavioural therapy and relaxation. No such treatments have been trialled in the UK. We conducted a randomised controlled pilot trial, comparing a brief guided self-help CBT and relaxation treatment with standard medical care (SMC), in a UK NHS setting. Participants were recruited from specialist headache clinics across London. Participants were randomised to receive either treatment or standard medical care. Our objective was to provide design information necessary for a future definitive trial of the SHE treatment, including, recruitment/retention rates, acceptability of randomisation, treatment fidelity and estimations of mean and variances of outcome measures. From the initial 275 patients identified, 73 were randomised. There was no difference in drop-out rates between SMC and treatment groups. Of the 36 participants randomised to receive treatment, 72% attended all sessions. Findings show that a future definitive trial of the SHE treatment is feasible, with small modifications of protocol, within a UK NHS context.

10 Article Charles Féré (1852-1907). 2011

Larner, A J. ·Cognitive Function Clinic, Walton Centre for Neurology and Neurosurgery, Lower Lane, Fazakerley, Liverpool L9 7LJ, UK. a.larner@thewaltoncentre.nhs.uk ·J Neurol · Pubmed #20978905.

ABSTRACT: -- No abstract --

11 Article Tailor treatment to the patient with migraine. 2008

Krishnan, Anita / Silver, Nicholas. ·Walton Centre for Neurology & Neurosurgery. Liverpool. ·Practitioner · Pubmed #18575386.

ABSTRACT: -- No abstract --

12 Minor Acute confusional migraine and transient global amnesia: variants of cognitive migraine? 2013

Larner, A J. ·Cognitive Function Clinic, Walton Centre for Neurology and Neurosurgery, Liverpool, UK. a.larner@thewaltoncentre.nhs.uk. ·Int J Clin Pract · Pubmed #24073981.

ABSTRACT: -- No abstract --