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It is common for contracts to include a clause that provides that on an event of default the counterparty has an unconditional right to terminate the contract or accelerate payment (an ipso facto clause). The regulation of ipso facto clauses has become a topic of debate in recent years with a number of jurisdictions introducing constraints on such clauses as part of broader restructuring reform packages. These jurisdictions include Germany in 2021 (as part of its implementation of the EU Restructuring Directive) and the United Kingdom in 2020. For jurisdictions introducing such constraints for the first time, there is much to learn from those, such as Canada, that have had constraints on ipso facto clauses in place for much longer. This article examines the experience in Canada alongside the constraints introduced in the United Kingdom, the EU Restructuring Directive and Germany, and identifies a series of steps that policymakers should follow when revising a regime on ipso facto clauses. Although there are a number of common themes that emerge, it is clear that different jurisdictions often make quite distinct policy choices regarding the rationale for any constraints on ipso facto clauses as well as on the specific nature and scope of the provisions. Different jurisdictions find different points of balance between the interests of individual creditors in upholding their freedom of contract and the rights of the debtor and creditors as a whole in preserving the business as a going concern. The range of choices is not per se problematic as long as they are implemented with clarity and transparency, so that debtors and creditors can bargain ex ante in the light of any legislative provisions.

The European Commission published a draft Directive in November 2016, with the aim of ensuring that all Member States have in place an effective mechanism for dealing with viable, but financially distressed, businesses. The draft Directive includes provisions designed to encourage financing for the debtor company, both interim financing to “keep the lights on” for a brief period while the debtor negotiates with its creditors for a resolution to its financial distress, and where possible, to finance implementation of a restructuring plan, called “new financing” in the draft Directive. Creating such a financing regime is a complex and difficult issue, as the law’s intervention in this area often involves constraints on the rights of existing creditors, requiring that a careful balance is maintained between existing creditors’ rights and the rights of the interim financier. This paper examines the underlying policy rationale and benefits of having new and interim financing available to financially distressed debtor companies, and discusses the risks involved. It examines the EU Commission’s proposals in light of the experience of jurisdictions that have already tackled these issues, notably the United States and Canada, or have developed a market-based solution to this problem, such as the UK. While the European Commission’s wish to include such measures in its restructuring proposals is laudable, the measures as drafted raise concerns, particularly regarding risks associated with priority for the grantors of such finance. The authors suggest that there are four fundamental aspects of such financing on which the Directive could give guidance to Member States, namely, effective notice to pre-filing creditors, thresholds for the debtor to qualify, a menu of relevant criteria to balance benefit and prejudice, and a role for the court in resolving disputes, ensuring fairness to stakeholders, and serving as an accountability check on interim financing arrangements, all aimed at maintaining the integrity of the insolvency process.

This paper reports on a qualitative study which has investigated female problem drug use in North Cumbria, a relatively isolated area of the UK. Cumbria is the second most sparsely populated county in England with some of the most beautiful countryside juxtaposed with areas of disadvantage, particularly in towns along the west coast. Previous research has focused on female city dwellers and less is known about the social and cultural context of drug use in non-urban settings. The reasons for women's drug use remain controversial but gender differences appear to emerge. One frequent explanation is the influence of male oppression but some studies describe women as active players in their initiation. Findings from North Cumbria challenge the conventional view of women being coerced into illicit drug use and present greater complexity. The data derived from semi-structured interviews account for the impact of curiosity and trust, motives often tempered by a range of complex personal circumstances. A known individual, usually male, was often present at initiation and this relationship appears pivotal. I discuss these factors and will call for prevention initiatives to recognise the gender-specific determinants of initiation into problem drug use.

A genetic variation in fatty acid amide hydrolase (FAAH), C385A (P129T), has been previously associated with risk for problem street drug use. FAAH is a mammalian enzyme that inactivates neuromodulatory-signaling lipids including the endogenous cannabinoid 1 receptor agonist anandamide. We investigated in adult Caucasians (N = 749) whether this FAAH variant altered the risk for trying, regular use of or dependence on cannabis, alcohol or nicotine, traditional "gateway" drugs. Consistent with our knowledge that the A/A genotype results in reduced FAAH expression and activity in humans, subjects with the A/A genotype were less likely to be THC dependent than subjects with either a C/C or C/A genotype (11% vs. 26%, P0.05). No association was observed between the A/A genotype and risk for alcohol or tobacco regular use, or DSM IV dependence. Controlling for regular use of nicotine and sedatives, both identified as confounders, those with the A/A genotype were at significantly reduced risk for being THC dependent (OR 0.25, 95% CI: 0.07-0.88) as compared with those with the C/A or C/C genotype, supporting a link between alterations in the endocannabinoid system and THC dependence. Unexpectedly, we found an increased risk for regular use of sedatives among the A/A genotype group. The relationship between the FAAH A/A genotype and risk for drug dependence in this study was drug class specific, suggesting it is not part of a more general drug abuse effect. These results, particularly the observation of altered risk for sedative drug use, should be investigated further in multiple ethnic populations.

broader. Inadvertence may qualify as a culpable mental state in circumstances when a person ought to have adverted. Treating as acting with an absent mental state a person who has acted intentionally but without adverting to a risk when he or she should have is like treating the failure to apply brakes while driving a motor vehicle as a pure omission rather than a dangerous act of driving. In a civil society there should be certain minimum duties of citizenship and every individual should have a responsibility to advert to relevant risks when actively engaging in certain conduct. Failure to live up to that can fairly be labelled culpable. This is not an objective test in the sense of ignoring the accused and asking what the reasonable person would have foreseen. The focus remains on the accused and the question is simply whether his or her mind should have been attuned to the risk. The two children in Rv G were not blameworthy because it was not reasonable to expect an eleven or twelve year old to advert to the risk that materialised. Had they instead been two drunks, it is unlikely that Rv G would have overruled Caldwell. For now, Caldwell is dead, although it lingers on as a ghost of Reid.58 A preferable course of action in Rv G would have been for the House of Lords to have endorsed an overt normative concept of recklessness by refining Glanville Williams' (an avowed subjectivist) proposed modification of Caldwell along the lines suggested here. This would allow courts to evaluate the blameworthiness of the accused's mental state according to prevailing ethical standards and distinguish between individuals who act out of 'stupidity or lack of imagination', and those who act 'outside the bounds of what humane and decent people regard as tolerable'.

Glut 5 is a member of a family of facilitative glucose transporter proteins that are involved in the transportation of glucose and/or fructose across plasma membranes. Glut 5 is one of three isoforms expressed in brain. Using immunocytochemical and immunoblotting techniques in formalin fixed tissue, we have shown that Glut 5 is exclusively expressed in microglial cells of the human and rat brain. Our data demonstrate that unlike other microglial markers, Glut 5 can be used as a microglial marker in formalin fixed tissue.

Oligodendrocytes are responsible for myelin formation in spinal cord white matter. In the mature spinal cord, the majority of white matter is localized peripherally. During early development, however, the first oligodendrocyte precursors arise in the ventral ventricular zone of the developing cord. Thus, prior to myelination, both migration and proliferation of oligodendrocyte precursors must occur. When and where these events occur is currently unclear. In the chick spinal cord, oligodendrocyte precursors express antigens recognized by the monoclonal antibody O4. Here we show that all chick spinal cord oligodendrocytes are derived from O4+ cells and all O4+ cells appear to give rise to oligodendrocytes. Analysis of the number and distribution of oligodendrocyte precursors in chick spinal cord at different stages of development suggests that relatively few cells migrate from the ventricular source which then proliferate extensively in white matter. This migration is guided by general dispersive cues. Clonal analysis of oligodendrocyte development in cultures derived from different regions of the rodent spinal cord indicated that the cells that initially populate dorsal and peripheral spinal cord retained similar clonal properties to those in ventral spinal cord, suggesting the migrating cells were immature, highly proliferative precursors. Consistent with these results, BrdU incorporation studies indicate that glial proliferation is extensive and persistent in postnatal rat spinal cord white matter. Together, these studies suggest that spinal cord white matter is initially populated by very immature precursors that then undergo extensive local proliferation prior to myelination.

In normal embryos, mRNA en- coding platelet-derived growth factorA(PDGFA) and the platelet-derived growth factor receptor a (PDGFRa) are found within and adjacent to the site of vertebral development, the sclerotome. These patterns of expression are consistent with PDGF action on the developing sclerotome and dermis. Homozygous Patch (Ph) mutant mouse embryos lack the receptor gene (Pdgfra) due to an extensive deletion at that locus. Consistent with the spatial pattern of Pdgfra expression, striking deformities are found in the spine and ribcage of Ph/Ph embryos. In particular, we show that late-gestation Ph/Ph embryos have occult spina bifida involving the entire spinal column. We have analyzed the progression of the axial defects in homozygous Patch embryos in detail. By late gestation it appears that the components of the vertebrae are present, yet the neural arches of the spine are misshapen. We propose that PDGF A is required for proper positioning of the neural arch condensation at all axial levels. Fur- thermore, since the neural tube appears to close normally, we suggest that spina bifida in the Ph homozygote is caused primarily by a somitic mesoderm abnormality rather than a neural tube defect.Dev. Dyn. 209:105-116, 1997. r 1997 Wiley-Liss, Inc.