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            ‐Butylacetylene

Campbell, Kenneth N.; Campbell, Barbara K.

doi:10.1002/0471264180.os030.06

Cited by 9 publications

(15 citation statements)

References 4 publications

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“…Though this may seem unpalatable, it does not breach his right to be presumed innocent. 101 He may regard his reputation and professional standing as having been compromised by virtue of the contentions in court that his behaviour constituted bribery or facilitation; that is beside the point as neither domestic nor ECHR jurisprudence precludes this, as he is not being tried, convicted or punished. Accordingly, I conclude that there are no due process objections to extension of the failure to prevent approach.…”

Section: A Due Process Rightsmentioning

confidence: 99%

Corporate Liability and the Criminalisation of Failure

Campbell

2018

Law and Financial Markets Review

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Defining and prosecuting corporate criminality has long been fraught with difficulty. As a result, the UK legislature is turning to an indirect form of omissions liability, by criminalising failure to prevent certain crimes like bribery and the facilitation of tax evasion. This article charts the development of indirect omissions corporate liability in the UK, and examines its rationales and benefits. Existing commentary has not explicated the implications of extension to other offences; I consider possible objections, regarding due process rights; reliance on omissions liability; effectiveness; and the use of the measures to date. Though its likely impact is less than clear, I conclude that, on balance, corporate liability for failure to prevent crime is justifiable and warrants being extended to economic offences and beyond. A. Introduction Under common law, the imposition of criminal liability on corporate entities 2 has long been fraught with difficulty. Corporate offending, like crimes involving individuals, runs the gamut *Professor of criminal law, Durham University.

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Section: A Due Process Rightsmentioning

confidence: 99%

Corporate Liability and the Criminalisation of Failure

Campbell

2018

Law and Financial Markets Review

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“…A theory which recognises that the interests of children could be of such crucial signifi cance that they need to be protected by rights is therefore much sounder in terms of contributing to the protection of the needs of this vulnerable social group. 27…”

Section: Theoretical Backgroundmentioning

confidence: 99%

The Twofold Approach to Children’s Freedom of Movement Rights Under European Law: Can ‘Children’s Equilibrium’ Guide the Interpretation of the Post-Brexit Rights of UK Children Residing in the EU?

Petrova¹

2018

CYELP

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“…For example, in neuropathic pain induced by chemotherapeutic drugs damage of the neurons caused by toxicity of the cytostatic drugs is characteristic [50,51]. Thus, depending on the cause of neuropathic pain, the underlying mechanisms leading to neuropathic pain can be highly divers [42,52,53]. Nevertheless, in this work the focus will be on the mechanisms underlying nerveinjury induced neuropathic pain.…”

Section: Neuropathic Painmentioning

confidence: 99%

“…Nerve damage is known to result in macrophage infiltration, T cell activation and increased expression of proinflammatory cytokines [53]. Therefore, tissues regarding the pain transmission pathway, sciatic nerve (SN) (Fig.…”

Section: Distribution Of Immune Cells At the Site Of Injurymentioning

confidence: 99%

“…or nerve growth factor (NGF), which are known to be increased during neuropathic pain, did not show any difference in their concentration between the genotypes (Fig. 17D and E) [6,8,53,[167][168][169]. Since NGF is the downstream target of the proinflammatory cytokine IL-1β it is not surprising that there was no difference observed in the concentration of IL-1β either [6,53] (Fig.…”

Section: Changes Along the Pain Transmission Pathway After Sni Surgerymentioning

confidence: 99%

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Oxidized lipids and signaling pathways of G2A receptor involved in nerve injury induced neuropathic pain

Osthues¹

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Neuropathic pain, a form of chronic pain, is a steadily rising health problem due to health costs and increasing numbers of patients. Neuropathic pain conditions arise upon metabolic disorders, infections, chemotherapeutic treatment, trauma or nerve injury. Especially nerve injury induced neuropathic pain is characterized by spontaneous or ongoing pain due to neuroimmune interactions. Thereby, inflammatory mediators, released by the injured nerve, recruit to and activate immune cells at the site of injury. Those mediators further activate transient receptor potential vanilloid 1 (TRPV1), a known channel involved in pain perception, or bind to G-protein coupled receptors (GPCR) in peripheral nerve endings. The following activated second messenger signaling pathways lead to sensitization of TRPV1. One of those GPCRs is G2A. The overall aim of this thesis was to investigate the role of G2A in nerve-injury induced neuropathic pain. For this, the common mouse model of nerve-injury induced neuropathic pain, the spared-nerve injury, was used. As measurements with dynamic plantar aesthesiometer showed, G2A-deficiency leads to reduced mechanical hypersensitivity. Upon analysis with FACS, ELISA and Luminex a reduced number of macrophages and neutrophils at the injured nerve, as well as less inflammatory mediators (TNFα, IL-6, VEGF) in G2A-deficient animals was observed. In dorsal root ganglia (DRGs) there was only a reduced number of macrophages and less IL-12 observed in G2A-deficient animals. Additionally, in wild-type mice, G2A agonist 9-HODE was elevated at the injured nerve, as a LC-MS/MS analysis showed. To investigate the underlying pathways of G2A-9-HODE signaling, a proteom screen was performed. This screen revealed upregulation of multiple proteins involved in migration in wild-type macrophages. Additionally, Ca-Imaging and transwell migration assays showed that the G2A antagonist G2A11, had desensitizing effects on DRG neurons and inhibited macrophage migration. Overall, the results suggest that loss of G2A has dual effects. On the one hand loss of G2A is antinociceptive. On the other hand, G2A-deficiency leads to reduced inflammation, suggesting G2A as promising target in treatment of neuropathic pain. Here, an antagonist had inhibitory effects on the migration and the sensitization.

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n ‐Butylacetylene

Abstract: n ‐butylacetylene product: n ‐butylacetylene product: n ‐propylacetylene product: n ‐Amylacetylene produc… Show more

Cited by 9 publications

References 4 publications

Corporate Liability and the Criminalisation of Failure

Corporate Liability and the Criminalisation of Failure

The Twofold Approach to Children’s Freedom of Movement Rights Under European Law: Can ‘Children’s Equilibrium’ Guide the Interpretation of the Post-Brexit Rights of UK Children Residing in the EU?

Oxidized lipids and signaling pathways of G2A receptor involved in nerve injury induced neuropathic pain

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