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Search Results: 1 - 10 of 211723 matches for " Stephen P Hunt "
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Lamina I NK1 expressing projection neurones are functional in early postnatal rats and contribute to the setting up of adult mechanical sensory thresholds
Sharon HW Man, Sandrine M Geranton, Stephen P Hunt
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-35
Abstract: At P3, a subset of lamina I neurons were found to express the neurokinin 1 (NK1) receptor. Using fluorogold retrograde tracing, we found that the NK1 positive neurons projected upon the parabrachial nucleus (PB) within the hindbrain. Using c-fos immunohistochemistry, we showed that lamina I and PB neurons in P3 rats responded to noxious stimulation of the periphery. Finally, ablation of lamina I neurons with substance-P saporin conjugates at P3 resulted in increased mechanical sensitivity from P45 onwards compared to control animals of the same age.These results suggest that the lamina I pathway is present and functional at least from P3 and required for establishing and fine-tuning mechanical sensitivity in adult rats.
Review of Melissa M. Wilcox, Queer Women and Religious Individualism, Bloomington, IN: Indiana University Press 2009
Stephen Hunt
Religion and Gender , 2011,
Review of Susannah Cornwall, Sex and Uncertainty in the Body of Christ: Intersex Conditions and Christian Theology (Gender, Theology and Spirituality Series), London/Oakville: Equinox 2011
Stephen Hunt
Religion and Gender , 2012,
Review of Stefan Horlacher (ed.), Constructions of Masculinity in British Literature from the Middle Ages to the Present
Stephen Hunt
Journal of Men, Masculinities and Spirituality , 2012,
Effect of screw position on bone tissue differentiation within a fixed femoral fracture  [PDF]
Saghar Nasr, Stephen Hunt, Neil A. Duncan
Journal of Biomedical Science and Engineering (JBiSE) , 2013, DOI: 10.4236/jbise.2013.612A009

Plate and screw constructs are routinely used in the treatment of long bone fractures. Despite considerable advancements in technology and techniques, there can still be complications in the healing of long bone fractures. Non-unions, delayed unions, and hardware failures are common complications observed in clinical practice following open reduction and internal fixation of fractures [1]. Potential causes of these adverse clinical effects may be disruptive to the periosteal and endosteal blood supply, stress shielding effects, and inadequate mechanical stability. The goal of the present study was to explore the effect of screw position on the fracture healing and formation of new bone tissue with mechanoregulatory algorithms in a computational model. An idealized poroelastic 3D finite element (FE) model of a femur with a 5 mm fracture gap, including a plate-screw construct was developed. Nineteen different plate-screw combinations, created by varying the number and position of screws within the plate, were created to identify a construct with the most favourable attributes for fracture healing. The first phase of the study evaluated constructs through mechanical stress analyses to identify those constructs with high loadsupport capability. The second phase of the study evaluated healing and bone formation with a biphasic mechanoregulatory algorithm to simulate tissue differentiation for fixation within selected constructs. The results of our analysis demonstrated a 4-screw symmetrical construct with the largest distance between screws to provide the most favourable balance of stability and optimized conditions to promote fracture healing.


The differential contribution of tumour necrosis factor to thermal and mechanical hyperalgesia during chronic inflammation
Julia J Inglis, Ahuva Nissim, Delphine M Lees, Stephen P Hunt, Yuti Chernajovsky, Bruce L Kidd
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1743
Abstract: Pain and disability are the principal clinical features associated with chronic arthritis. Inflammation is associated with sensitisation of specialised sensory neurons that comprise the nociceptive (pain) pathway, leading to enhanced pain sensations in response to both noxious and non-noxious stimuli (termed hyperalgesia and allodynia, respectively) [1]. Neural sensitisation is thought to arise in response to the actions of mediators on both peripheral and central nociceptive neurons. Whereas acute inflammatory mediators such as prostaglandins and bradykinin have been shown to exert important effects on neuronal sensitisation in the short term, the longer-term influences of these and other mediators on nociceptive neurons remain less clear.Therapies directed against tumour necrosis factor (TNF) have proved highly effective in treating rheumatoid arthritis. In addition to exerting an anti-inflammatory effect and slowing the progression of rheumatoid arthritis, anti-TNF therapy produces a profound and rapid analgesia [2]. The mechanism of this latter action remains uncertain, but the action suggests an important role for TNF in persistent inflammatory (neuroplastic) pain.In acute situations, TNF has been reported to sensitize nociceptive neurons indirectly via the induction of a proinflammatory cytokine cascade involving IL-1β, IL-6, and IL-8, resulting in the release of prostaglandins and other mediators from immune cells [3-5]. Evidence for more direct TNF actions comes from electrophysiological studies showing that low-dose subcutaneous injections of TNF-α induce ectopic activity in nociceptive neurons within 2 minutes, with higher doses producing significant mechanical and thermal hyperalgesia by 15 minutes [6-8]. Furthermore, application of TNF-α enhances calcium currents and increases neuron sensitivity to the neurotoxin capsaicin in cultures of sensory neurons [9-11].TNF acts via two receptors, including the p55 TNF receptor type 1 (TNFR1) and the p75 TNF recep
Injury induced activation of extracellular signal-regulated kinase (ERK) in the rat rostral ventromedial medulla (RVM) is age dependant and requires the lamina I projection pathway
Sandrine M Géranton, Keri K Tochiki, Winnie WY Chiu, Sarah A Stuart, Stephen P Hunt
Molecular Pain , 2010, DOI: 10.1186/1744-8069-6-54
Abstract: The rostral ventromedial medulla (RVM) plays an essential role in the regulation of spinal cord nociceptive activity and pain transmission [1-5]. The RVM, inclusive of the nucleus raphe magnus, nucleus reticularis gigantocellularis and ventral nucleus reticularis gigantocellularis, receives projections from the periaqueductal grey and, in the adult rat, [5,6] activation of separate populations of RVM neurons generates either descending inhibition or facilitation [7-10]. It has been shown that high intensity stimulation within the RVM inhibited spinal nociception while low intensity stimulation was facilitatory [6,11]. Finally, inactivation of the RVM with lidocaine or excitatory block with the glutamate receptor antagonist kynurenate lead to attenuation of mechanical allodynia caused by inflammation or peripheral nerve ligation respectively [12,13].The Mitogen Activated Protein (MAP) kinases are known to play an essential role in the regulation of neuronal plasticity via post-translational and transcriptional modifications. An increase in spinal extracellular signal-related kinase (ERK) activity has been implicated in the induction and/or maintenance of pain states following noxious stimulation of the periphery [14-16]. Phospho-ERK (pERK) was also up-regulated in the RVM following peripheral inflammation induced by Complete Freund's Adjuvant (CFA)injected into the hind paw [17] and inhibition of ERK signaling within the RVM somewhat reduced thermal hyperalgesia at 24 h (but not 7 h) after inflammation [17,18].Although up-regulation of pERK after digit amputation has been described in the anterior cingulate cortex [19], the link between ERK activity in the RVM and increased pain sensitivity in models of neuropathic pain remains to be elucidated.Descending controls from the RVM are indirectly modulated by activity in ascending pathways originating in lamina I/III projection neurons of the dorsal horn. Selective ablation of these ascending projections leads to signific
The expression of spinal methyl-CpG-binding protein 2, DNA methyltransferases and histone deacetylases is modulated in persistent pain states
Keri K Tochiki, Joel Cunningham, Stephen P Hunt, Sandrine M Géranton
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-14
Abstract: Using immunohistochemistry, we found that neurones, oligodendrocytes and astrocytes expressed MeCP2. Microglia, oligodendrocyte precursor cells and Schwann cells never showed any positive stain for MeCP2. Quantitative analyses showed that MeCP2 expression was increased in the superficial dorsal horn 7 days following CFA injection in the ankle joint but decreased 7 days following spared nerve injury. Overall, the expression of DNA methyltransferases and a subset of histone deacetylases followed the same pattern of expression. However, there were no significant changes in the expression of the MeCP2 targets that we had previously shown are regulated in the early time points following CFA injection in the ankle joint. Finally, the expression of MeCP2 was also down regulated in damaged dorsal root ganglion neurones following spared nerve injury.Our results strongly suggest that changes in chromatin compaction, regulated by the binding of MeCP2 complexes to methylated DNA, are involved in the modulation of gene expression in the superficial dorsal horn and dorsal root ganglia during the maintenance of persistent pain states.The induction and maintenance of persistent pain states, whether inflammatory or neuropathic, involve a number of changes in gene expression both in the dorsal root ganglia (DRGs) [1-4] and in the spinal cord [5-7]. Regulation of gene expression can be achieved through DNA CpG methylation, a process implemented by DNA methyltransferases (DNMTs). DNA methylation induces chromatin remodeling and gene silencing through a transcriptional repressor complex comprising the Methyl-CpG-binding protein 2 (MeCP2) and a subset of histone deacetylases (HDACs) [8]. Recently, we have found that MeCP2 activity had a crucial role in the pattern of gene expression seen in the superficial dorsal horn following injection of Complete Freund's Adjuvant (CFA) into the rat ankle joint [5]. A rapid increase in expression of a family of genes under the transcriptional control
Descending serotonergic controls regulate inflammation-induced mechanical sensitivity and methyl-CpG-binding protein 2 phosphorylation in the rat superficial dorsal horn
Sandrine M Géranton, Vincenza Fratto, Keri K Tochiki, Stephen P Hunt
Molecular Pain , 2008, DOI: 10.1186/1744-8069-4-35
Abstract: Here, we describe how descending controls regulate MeCP2 phosphorylation (P-MeCP2), known to relieve transcriptional repression by MeCP2, and Zif268 and Fos expression in the rat superficial dorsal horn, after CFA injection into the hind paw. First, we report that CFA significantly increased P-MeCP2 in Lamina I and II, from 30 min post injection, with a maximum reached after 1 h. The increase in P-MeCP2 paralleled that of Zif268 and Fos, and P-MeCP2 was expressed in large sub-populations of Zif268 and Fos expressing neurones. Serotonergic depletion of the lumbar spinal cord with 5,7 di-hydroxytryptamine creatinine sulphate (5,7-DHT) reduced the inflammation evoked P-MeCP2 in the superficial dorsal horn by 57%, and that of Zif268 and Fos by 37.5% and 30% respectively. Although 5,7-DHT did not change primary thermal hyperalgesia, it significantly attenuated mechanical sensitivity seen in the first 24 h after CFA.We conclude that descending serotonergic pathways play a crucial role in regulating gene expression in the dorsal horn and mechanical sensitivity associated with an inflammatory pain state.The development and maintenance of pain states are dependant upon plastic changes in neurones of the superficial dorsal horn that are thought to be under the control of descending pathways originating in the brainstem [1,2]. The transcription factors Fos, Zif268 and Methyl-CpG-binding protein 2 (MeCP2) have been implicated in dorsal horn plasticity yet their dependence on descending controls for their full activation has not been explored.MeCP2 is a transcriptional repressor that regulates activity-dependent gene transcription and is critical for normal neurological function. Mutations in human MeCP2 result in the neurodevelopmental disorder Rett syndrome [3,4]. However, we know very little about the physiological role of MeCP2 in the central nervous system. MeCP2 regulates gene transcription by binding to methylated CpG dinucleotides and recruiting co-repressors such as his
Masculinity, Homosexuality and the Defence of Islam: A Case Study of Yusuf al-Qaradawi’s Media Fatwa
Scott Kugle,Stephen Hunt
Religion and Gender , 2012,
Abstract: This paper analyses how Islamic Neo-traditionalists perceive gender constructs through a distorted view of religious texts and cultural conventions. It explores the ramifications of these constructs for attitudes towards same-sex orientations and relationships. These themes are discussed with reference to a case study of a TV talk show on 5 June 2006 by one conservative scholar-activist, Shaykh Yusuf al-Qaradawi, whose teachings have an impact in the Middle-East and on Muslim minorities in the West. The paper will demonstrate how al-Qaradawi articulates his views of homophobia as part of an agenda to reinforce perceived threats to Muslim masculinity.
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