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Book: Stroke genomics

Read, Simon J.

methods and reviews

(Methods in molecular medicine ; 104)

2005

Author's details	ed. by Simon J. Read
Series title	Methods in molecular medicine ; 104
Collection
Keywords	Cerebrovascular Accident / genetics
Language	English
Size	X, 351 S. : Ill., graph. Darst.
Publisher	Humana Press
Publishing place	Totowa, NJ
Publishing country	United States
Document type	Book
HBZ-ID	HT014040946
ISBN	1-58829-333-5 ; 978-1-58829-333-6
Database	Catalogue ZB MED Medicine, Health

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2005 A 4136	order for loan	Magazin

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Book: Stroke genomics

Read, Simon J / Virley, David

methods and reviews

(Methods in molecular medicine, ; 104)

2005

Author's details	edited by Simon J. Read, David Virley
Series title	Methods in molecular medicine, ; 104
MeSH term(s)	Stroke/genetics
Language	English
Size	x, 351 p. :, ill.
Publisher	Humana Press
Publishing place	Totowa, N.J
Document type	Book
ISBN	9781588293336 ; 1588293335 ; 9781592598366 ; 1592598366
Database	Catalogue of the US National Library of Medicine (NLM)

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Article ; Online: Osteoarthritic pain: a review of current, theoretical and emerging therapeutics.

Read, Simon J / Dray, Andy

Expert opinion on investigational drugs

2008 Volume 17, Issue 5, Page(s) 619–640

Abstract: Background: Despite exciting progress and growth in the understanding of molecular and cellular mechanisms of chronic pain, osteoarthritis (OA) pain remains a challenging clinical entity to treat. There is an emerging diversity of algogenic mechanisms ... ...

Abstract	Background: Despite exciting progress and growth in the understanding of molecular and cellular mechanisms of chronic pain, osteoarthritis (OA) pain remains a challenging clinical entity to treat. There is an emerging diversity of algogenic mechanisms suggesting heterogeneity in pain aetiology in the OA patient population. Objective/methods: This review article summarises key issues in existing therapies for OA pain and highlights the emerging compounds in early and late development. It also highlights where tolerability may be a concern, especially in the older populations in which treatment interactions for co-morbid conditions may further narrow therapeutic index. Importantly, the authors also examine the diversity of biology that underpins OA pain and highlight the opportunities for the future. Results/conclusions: Many emerging therapies are presently in proof-of-concept clinical testing for treatment of OA. A growing understanding of the heterogeneity in the OA patient population, will challenge the ability to accurately understand observed efficacy or safety signals in these relatively small trials and how they may titrate to a broader patient population. We may need to wait several more years to understand whether the need for a differentiated therapy demanded by patients, payors and physicians alike, will be met.
MeSH term(s)	Analgesics, Opioid/administration & dosage ; Analgesics, Opioid/therapeutic use ; Anti-Inflammatory Agents, Non-Steroidal/administration & dosage ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Bone and Bones/drug effects ; Bone and Bones/metabolism ; Bone and Bones/pathology ; Cannabinoids/administration & dosage ; Cannabinoids/therapeutic use ; Clinical Trials as Topic ; Glucosamine/administration & dosage ; Glucosamine/therapeutic use ; Humans ; Joints/drug effects ; Joints/metabolism ; Joints/pathology ; Osteoarthritis/complications ; Osteoarthritis/drug therapy ; Osteoarthritis/metabolism ; Osteoarthritis/pathology ; Pain/drug therapy ; Pain/etiology ; Pain/metabolism ; Pain/pathology
Chemical Substances	Analgesics, Opioid ; Anti-Inflammatory Agents, Non-Steroidal ; Cannabinoids ; Glucosamine (N08U5BOQ1K)
Language	English
Publishing date	2008-04-22
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1182884-5
ISSN	1744-7658 ; 0967-8298 ; 1354-3784
ISSN (online)	1744-7658
ISSN	0967-8298 ; 1354-3784
DOI	10.1517/13543784.17.5.619
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Article ; Online: Arthritis and pain. Future targets to control osteoarthritis pain.

Dray, Andy / Read, Simon J

Arthritis research & therapy

2007 Volume 9, Issue 3, Page(s) 212

Abstract: Clinical presentation of osteoarthritis (OA) is dominated by pain during joint use and at rest. OA pain is caused by aberrant functioning of a pathologically altered nervous system with key mechanistic drivers from peripheral nerves and central pain ... ...

Abstract	Clinical presentation of osteoarthritis (OA) is dominated by pain during joint use and at rest. OA pain is caused by aberrant functioning of a pathologically altered nervous system with key mechanistic drivers from peripheral nerves and central pain pathways. This review focuses on symptomatic pain therapy exemplified by molecular targets that alter sensitization and hyperexcitability of the nervous system, for example, opioids and cannabinoids. We highlight opportunities for targeting inflammatory mediators and their key receptors (for example, prostanoids, kinins, cytokines and chemokines), ion channels (for example, NaV1.8, NaV1.7 and CaV2.2) and neurotrophins (for example, nerve growth factor), noting evidence that relates to their participation in OA etiology and treatment. Future neurological treatments of pain appear optimistic but will require the systematic evaluation of emerging opportunities.
MeSH term(s)	Animals ; Arthralgia/drug therapy ; Arthralgia/etiology ; Humans ; Osteoarthritis/complications ; Osteoarthritis/physiopathology
Language	English
Publishing date	2007-06-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/ar2178
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Zs.A 5490: Show issues

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Article: Introduction to stroke genomics.

Read, Simon J / Barone, Frank C

Methods in molecular medicine

2003 Volume 104, Page(s) 3–16

Abstract: Translation of the explosion in knowledge of acute ischemic stroke into satisfactory treatment regimens has yet to happen. At present tPA, intra-arterial prourokinase and low-molecular-weight heparin form the vanguard for therapeutic intervention, yet ... ...

Abstract	Translation of the explosion in knowledge of acute ischemic stroke into satisfactory treatment regimens has yet to happen. At present tPA, intra-arterial prourokinase and low-molecular-weight heparin form the vanguard for therapeutic intervention, yet these treatments have a limited therapeutic window. Part of this expansion in understanding has been driven by the contribution of stroke genetics and genomics. However, despite the enormous preclinical and clinical information of receptors, enzymes, second messenger systems, and so forth, that are implicated in stroke pathophysiology, delivery of novel drug treatment has been slow. This introductory chapter discusses the multiple sources of clinical and preclinical genetic information. It will describe the importance of integrating expression information into multiple preclinical models with temporal and spatial roles in lesion pathology and, furthermore developing an understanding of function in the clinic before claiming a role in ischemic stroke. The goal of such a holistic integration of information is to increase the yield from current datasets of gene expression and ultimately to help expand the choice of treatment available to the physician and patient.
MeSH term(s)	Animals ; Disease Models, Animal ; Gene Expression ; Genomics ; Humans ; Proteins/genetics ; Rats ; Risk Factors ; Stroke/genetics ; Twin Studies as Topic
Chemical Substances	Proteins
Language	English
Publishing date	2003-06-09
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1543-1894
ISSN	1543-1894
DOI	10.1385/1-59259-836-6:003
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Effect of baseline rheumatoid factor and anticitrullinated peptide antibody serotype on rituximab clinical response: a meta-analysis.

Isaacs, John D / Cohen, Stanley B / Emery, Paul / Tak, Paul P / Wang, Jianmei / Lei, Guiyuan / Williams, Sarah / Lal, Preeti / Read, Simon J

Annals of the rheumatic diseases

2012 Volume 72, Issue 3, Page(s) 329–336

Abstract: Background: Studies examining the relationship between serological status (rheumatoid factor and/or anticitrullinated antibody) and rituximab treatment outcome in rheumatoid arthritis (RA) have been hampered by limited numbers of seronegative patients.!# ...

Abstract	Background: Studies examining the relationship between serological status (rheumatoid factor and/or anticitrullinated antibody) and rituximab treatment outcome in rheumatoid arthritis (RA) have been hampered by limited numbers of seronegative patients. Objective: To carry out a meta-analysis of trials from the rituximab RA clinical programme to investigate this relationship further. Methods: This was a meta-analysis of four placebo-controlled, phase II or III clinical trials. The efficacy end point in all analyses was change from baseline in Disease Activity Score in 28 joints-erythrocyte sedimentation rate (DAS28-ESR) at 24 weeks. Assay of serotype and missing data imputation methods were consistent across all studies. Results: The population analysed comprised 2177 patients (rituximab, n=1416; placebo, n=761). Demographics and baseline disease characteristics were well balanced. When a fixed-effects meta-analysis approach was used, the overall-effect model indicated evidence of additional treatment benefit with rituximab in seropositive patients: reduction in DAS28-ESR at week 24 was on average 0.35 units (95% CI 0.12 to 0.84; n=1394) greater than in seronegative patients; this effect was not seen in placebo patients. Heterogeneity indices indicated significant uncertainty in the overall-effect model (Q=8.8, I=0.77; p=0.03 (χ(2) test)). Baseline Health Assessment Questionnaire score, pain visual analogue scale, swollen joint counts of 28 joints and race were significant contributors to this heterogeneity, with additional analysis indicating that these effects may predominate in early RA (methotrexate-naïve) populations. A dominant effect was seen in patients for whom one or more tumour necrosis factor inhibitors had failed. Conclusion: Although the difference was modest, the overall-effect model indicates that seropositive patients respond better to rituximab than seronegative patients.
MeSH term(s)	Antibodies, Monoclonal, Murine-Derived/therapeutic use ; Antirheumatic Agents/therapeutic use ; Arthritis, Rheumatoid/blood ; Arthritis, Rheumatoid/drug therapy ; Arthritis, Rheumatoid/immunology ; Autoantibodies/blood ; Double-Blind Method ; Humans ; Multicenter Studies as Topic ; Randomized Controlled Trials as Topic ; Rheumatoid Factor/blood ; Rituximab ; Treatment Outcome
Chemical Substances	Antibodies, Monoclonal, Murine-Derived ; Antirheumatic Agents ; Autoantibodies ; Rituximab (4F4X42SYQ6) ; Rheumatoid Factor (9009-79-4)
Language	English
Publishing date	2012-06-11
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/annrheumdis-2011-201117
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Article ; Online: Structural pathology in a rodent model of osteoarthritis is associated with neuropathic pain: increased expression of ATF-3 and pharmacological characterisation.

Ivanavicius, Stefan P / Ball, Adrian D / Heapy, Chris G / Westwood, Russell F / Murray, Fraser / Read, Simon J

Pain

2007 Volume 128, Issue 3, Page(s) 272–282

Abstract: Intra-articular injection of mono-iodoacetate (MIA) in the rat knee joint induces a histopathology with similarities to osteoarthritis (OA). Typically, a synovitis (days 1-3) is observed followed by thinning of articular cartilage and subsequent lesion ... ...

Abstract	Intra-articular injection of mono-iodoacetate (MIA) in the rat knee joint induces a histopathology with similarities to osteoarthritis (OA). Typically, a synovitis (days 1-3) is observed followed by thinning of articular cartilage and subsequent lesion of subchondral bone at days 8-14 onwards. Behaviourally, weight-bearing asymmetry is observed, which is sensitive to anti-inflammatory pharmacology at early but not later (days 14+) time points. As subchondral bone is densely innervated, an intriguing possibility is that focal bone pathology may cause neuropathy in this model. In male Wistar rats, activating transcription factor (ATF)-3-immunofluorescence was used as a marker of nerve injury in lumber (L)4 and L5 dorsal root ganglia of the ipsilateral knee. Significantly increased ATF-3-immunoreactivity following MIA treatment was measured in L5 on days 8 and 14 (P<0.05, Kruskal-Wallis and Mann-Whitney U-test), compared to saline controls. Furthermore, in an additional study animals were orally dosed vehicle (5 ml/kg), naproxen (0.3-10 mg/kg), celecoxib (1-10 mg/kg), amitriptyline (3-30 mg/kg) and gabapentin (10-100mg/kg) and evaluated for weight-bearing asymmetry on days 14, 21 and 28 post-MIA. Significant resolution of weight-bearing was observed at high and intermediate doses of amitriptyline and gabapentin at all time points (P<0.05, ANOVA, post-hoc Bonferroni's, vs pre-dose measurements). Transient and weak effects were observed with naproxen (10mg/kg) on days 14 and 28, whereas celecoxib showed no significant effects. Collectively, these data suggest that this putative model of OA is associated with an early phase neuropathy in the L5 innervation territory of the knee.
MeSH term(s)	Activating Transcription Factor 3/metabolism ; Animals ; Disease Models, Animal ; Gene Expression/drug effects ; Humans ; Hyperalgesia/chemically induced ; Hyperalgesia/metabolism ; Hyperalgesia/pathology ; Iodoacetic Acid ; Male ; Neuralgia/chemically induced ; Neuralgia/metabolism ; Neuralgia/pathology ; Osteoarthritis, Knee/chemically induced ; Osteoarthritis, Knee/metabolism ; Osteoarthritis, Knee/pathology ; Rats ; Rats, Wistar
Chemical Substances	ATF3 protein, human ; Activating Transcription Factor 3 ; Iodoacetic Acid (WF5188V710)
Language	English
Publishing date	2007-02-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	193153-2
ISSN	1872-6623 ; 0304-3959
ISSN (online)	1872-6623
ISSN	0304-3959
DOI	10.1016/j.pain.2006.12.022
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Article: Programmable microchip monitoring of post-stroke pyrexia: effects of aspirin and paracetamol on temperature and infarct size in the rat.

Legos, Jeffrey J / Mangoni, Arduino A / Read, Simon J / Campbell, Colin A / Irving, Elaine A / Roberts, Jenny / Barone, Frank C / Parsons, Andrew A

Journal of neuroscience methods

2001 Volume 113, Issue 2, Page(s) 159–166

Abstract: Background: Recent studies have demonstrated spontaneous and prolonged hyperthermia following stroke in both humans and rodents. However, a full characterization of these pyretic changes and the effects of anti-pyretic drugs on outcome is not available.! ...

Abstract	Background: Recent studies have demonstrated spontaneous and prolonged hyperthermia following stroke in both humans and rodents. However, a full characterization of these pyretic changes and the effects of anti-pyretic drugs on outcome is not available. Methods: The aims of this study were to monitor conscious body temperature (n=10 per group) using programmable microchips for up to 24 h in rats following either permanent (p) or 90 min transient (t) middle cerebral artery occlusion (MCAO) or sham surgery, and to evaluate the relationship to hypothalamic damage. Also, the effects of anti-pyretic drug therapy on body temperature and infarct volume were evaluated in animals treated with vehicle, optimal doses of either aspirin or paracetamol (250 mg/kg i.p.) following pMCAO (n=10 per group). Results: At 1 h, body temperature significantly (P<0.01) increased to 38.6+/-0.2 degrees C following tMCAO and 38.9+/-0.1 degrees C following pMCAO compared with sham-operated animals (37.1+/-0.1 degrees C). Sustained hyperthermia (> or =38.1 degrees C) was observed for up to 24 h following pMCAO but approached baseline within 30 min (37.6+/-0.2 degrees C) following tMCAO with reperfusion. The post-stroke pyrexia was related to the degree of ischemia where hypothalamic damage was observed in (80%) of the animals undergoing pMCAO and (0%) in the tMCAO group (P<0.05). Treatment with paracetamol (250 mg/kg i.p.) significantly attenuated (P<0.05) but did not normalize core body temperature up to 2 h (38.2+/-0.4 degrees C) compared with vehicle treated animals (39.3+/-0.1 degrees C). Aspirin had no effect on temperature under these conditions. Hypothalamic damage and lesion volume were not different between animals treated with paracetamol (253.3+/-8.5 mm(3)), aspirin (264.0+/-11.6 mm(3)) or vehicle (274.4+/-8.2 mm(3)). Conclusions: This study is the first to demonstrate the utility of programmable microchips to monitor serial changes in post-stroke hyperthermia. The sustained post-stroke pyrexia and negative effects of antipyretic treatment may be attributed to the extensive hypothalamic injury suggesting that better pharmacologic approaches to reduce body temperature should be identified and evaluated for brain protection in severe experimental stroke.
MeSH term(s)	Acetaminophen/pharmacology ; Analgesics, Non-Narcotic/pharmacology ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Aspirin/pharmacology ; Body Temperature/drug effects ; Fever/drug therapy ; Fever/pathology ; Fever/physiopathology ; Hypothalamus/pathology ; Hypothalamus/physiopathology ; Infarction, Middle Cerebral Artery/drug therapy ; Infarction, Middle Cerebral Artery/pathology ; Infarction, Middle Cerebral Artery/physiopathology ; Male ; Rats ; Rats, Sprague-Dawley ; Software ; Telemetry/instrumentation
Chemical Substances	Analgesics, Non-Narcotic ; Anti-Inflammatory Agents, Non-Steroidal ; Acetaminophen (362O9ITL9D) ; Aspirin (R16CO5Y76E)
Language	English
Publishing date	2001-12-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	282721-9
ISSN	1872-678X ; 0165-0270
ISSN (online)	1872-678X
ISSN	0165-0270
DOI	10.1016/s0165-0270(01)00488-5
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