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Drugs Act (drug + act)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Analyses of second-generation ,legal highs' in the UK: Initial findings

DRUG TESTING AND ANALYSIS, Issue 8 2010
Simon D. Brandt
Abstract In the UK, mephedrone and other so-called ,legal high' derivatives have recently been classified as Class B, Schedule I under the Misuse of Drugs Act 1971. Since then, alternative products have been advertised on a number of websites. In order to obtain an immediate snapshot of the situation, 24 products were purchased online from 18 UK-based websites over a period of 6 weeks following the ban in April 2010. Qualitative analyses were carried out by gas chromatography ion trap mass spectrometry using electron- and chemical ionization modes, nuclear magnetic resonance spectroscopy, and comparison with reference standards. Overall, the purchased products consisted of single cathinones or cathinone mixtures including mephedrone, butylone, 4-methyl- N -ethylcathinone, flephedrone (4-fluoromethcathinone) and MDPV (3,4-methylenedioxypyrovalerone), respectively. Benzocaine, caffeine, lidocaine, and procaine were also detected. The emphasis was placed on ,Energy 1' (NRG-1), a product advertised as a legal replacement for mephedrone-type derivatives usually claiming to contain naphyrone (naphthylpyrovalerone, O-2482). It was found that 70% of NRG-1 and NRG-2 products appeared to contain a mixture of cathinones banned in April 2010 and rebranded as ,new' legal highs, rather than legal chemicals such as naphyrone as claimed by the retailers. Only one out of 13 NRG-1 samples appeared to show analytical data consistent with naphyrone. These findings also suggest that both consumers and online sellers (unlike manufacturers and wholesalers) are, most likely unknowingly, confronted with the risk of criminalization and potential harm. Copyright © 2010 John Wiley & Sons, Ltd. [source]

How ideology shapes the evidence and the policy: what do we know about cannabis use and what should we do?

ADDICTION, Issue 8 2010
John Macleod
ABSTRACT In the United Kingdom, as in many places, cannabis use is considered substantially within a criminal justice rather than a public health paradigm with prevention policy embodied in the Misuse of Drugs Act. In 2002 the maximum custodial sentence tariff for cannabis possession under the Act was reduced from 5 to 2 years. Vigorous and vociferous public debate followed this decision, centred principally on the question of whether cannabis use caused schizophrenia. It was suggested that new and compelling evidence supporting this hypothesis had emerged since the re-classification decision was made, meaning that the decision should be reconsidered. The re-classification decision was reversed in 2008. We consider whether the strength of evidence on the psychological harms of cannabis has changed substantially and discuss the factors that may have influenced recent public discourse and policy decisions. We also consider evidence for other harms of cannabis use and public health implications of preventing cannabis use. We conclude that the strongest evidence of a possible causal relation between cannabis use and schizophrenia emerged more than 20 years ago and that the strength of more recent evidence may have been overstated,for a number of possible reasons. We also conclude that cannabis use is almost certainly harmful, mainly because of its intimate relation to tobacco use. The most rational policy on cannabis from a public health perspective would seem to be one able to achieve the benefit of reduced use in the population while minimizing social and other costs of the policy itself. Prohibition, whatever the sentence tariff associated with it, seems unlikely to fulfil these criteria. [source]

Anticonvulsant Efficacy of Topiramate in Phenytoin-Resistant Kindled Rats

EPILEPSIA, Issue 4 2000
Elke Reissmüller
Summary: Purpose: We evaluated the anticonvulsant efficacy of topiramate (TPM), a structurally novel antiepileptic drug (AED), in amygdala kindled rats that had been preselected with respect to their response to phenytoin (PHT). Methods: Anticonvulsant response was tested by determining the afterdischarge threshold (ADT;i.e., a sensitive measure for drug effects on focal seizure activity). By repeated testing with the PHT prodrug fosphenytoin (FOS) three groups of kindled rats were separated: rats in which consistent anticonvulsant effects were obtained (PHT responders), rats that showed no anticonvulsant response (PHT nonresponders), and rats with variable responses (variable PHT responders). The latter, largest group was used to evaluate at which doses and pretreatment times TPM exerted significant anticonvulsant effects on ADT. For this purpose, TPM was tested at four doses (20, 40, 80, 160 mg/kg i.p.) and two pretreatment times (1 and 4 h). The most effective treatment protocol was then used for TPM testing in PHT responders and nonresponders. Results: TPM proved to be an effective AED in the kindling model. At 40 mg/kg, significant ADT increases were obtained after both 1 and 4 h after administration. In addition to the effect on focal seizure threshold, seizure severity and duration recorded at ADT were decreased by TPM, indicating that this drug acts on both seizure threshold and seizure spread. In PHT nonresponders, TPM significantly increased ADT, which is in line with its proven efficacy in patients with refractory partial epilepsy in whom phenytoin has failed. However, TPM was more efficacious in increasing ADT in PHT responders than in nonresponders, substantiating that the difference between these groups of kindled rats extends to other AEDs. Repeated testing of kindled rats with TPM indicated that, similar to PHT, there are individual kindled rats without anticonvulsant response to TPM (i.e., TPM nonresponders). Conclusions: The data of this study substantiate that PHT nonresponders are a unique model for the search of new AEDs with improved efficacy in refractory partial epilepsy. [source]

Brain Imaging in Migraine Research

HEADACHE, Issue 9 2010
David Borsook MD
Understanding the pathophysiology and pharmacology of migraine has been driven by astute clinical observations, elegant experimental medicine studies, and importantly by studying highly effective anti-migraine agents in the laboratory and the clinic. Significant progress has been made in the use of functional brain imaging to compliment observational studies of migraine phenotypes by highlighting pathways within the brain that may be involved in predisposition to migraine, modulating migraine pain or that could be sensitive to pharmacological or behavioral therapeutic intervention (Fig. 1). In drug discovery, molecular imaging approaches compliment functional neuroimaging by visualizing migraine drug targets within the brain. Molecular imaging enables the selection and evaluation of drug candidates by confirming that they engage their targets sufficiently at well tolerated doses to test our therapeutic hypotheses. Figure 1.,. Imaging and defining the migraine brain disease state: from anatomy to chemical entities (targets) to functional systems (function and pathways) (from Borsook et al31 with permission, Nature Publishing Group). Migraine is a progressive disorder. Developing our knowledge of where drugs act in the brain and of how the brain is altered in both episodic migraine (interictal state and ictal state) and chronic migraine are important steps to understanding why there is such differential responsiveness to therapeutics among migraine patients and to improving how they are evaluated and treated. [source]