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Clinical effects of cannabis compared to synthetic cannabinoid receptor agonists (SCRAs): a retrospective cohort study of presentations with acute toxicity to European hospitals between 2013 and 2020.
No full textINTRODUCTION: Cannabis is the most common recreational drug worldwide and synthetic cannabinoid receptor agonists are currently the largest group of new psychoactive substances. The aim of this study was to compare the clinical features and outcomes of lone acute cannabis toxicity with lone acute synthetic cannabinoid receptor agonist toxicity in a large series of presentations to European emergency departments between 2013-2020.
METHODS: Self-reported drug exposure, clinical, and outcome data were extracted from the European Drug Emergencies Network Plus which is a surveillance network that records data on drug-related emergency department presentations to 36 centres in 24 European countries. Cannabis exposure was considered the control in all analyses. To compare the lone cannabis and lone synthetic cannabinoid receptor agonist groups, univariate analysis using chi squared testing was used for categorical variables and non-parametric Mann-Whitney U- testing for continuous variables. Statistical significance was defined as a P value of <0.05.
RESULTS: Between 2013-2020 there were 54,314 drug related presentations of which 2,657 were lone cannabis exposures and 503 lone synthetic cannabinoid receptor agonist exposures. Synthetic cannabinoid receptor agonist presentations had statistically significantly higher rates of drowsiness, coma, agitation, seizures and bradycardia at the time of presentation. Cannabis presentations were significantly more likely to have palpitations, chest pain, hypertension, tachycardia, anxiety, vomiting and headache.
DISCUSSION: Emergency department presentations involving lone synthetic cannabinoid receptor agonist exposures were more likely to have neuropsychiatric features and be admitted to a psychiatric ward, and lone cannabis exposures were more likely to have cardiovascular features. Previous studies have shown variability in the acute toxicity of synthetic cannabinoid receptor agonists compared with cannabis but there is little comparative data available on lone exposures. There is limited direct comparison in the current literature between lone synthetic cannabinoid receptor agonist and lone cannabis exposure, with only two previous poison centre series and two clinical series. Whilst this study is limited by self-report being used to identify the drug(s) involved in the presentations, previous studies have demonstrated that self-report is reliable in emergency department presentations with acute drug toxicity.
CONCLUSION: This study directly compares presentations with acute drug toxicity related to the lone use of cannabis or synthetic cannabinoid receptor agonists. It supports previous findings of increased neuropsychiatric toxicity from synthetic cannabinoid receptor agonists compared to cannabis and provides further data on cardiovascular toxicity in lone cannabis use
About the International Asteroid Warning Network (IAWN) and the Space Mission Planning Advisory Group (SMPAG)
No full textQuantitative Antioxidant Profiling Throughout Beer Brewing Followed by Discovery and Isolation of Precursors from Barley (<i>Hordeum vulgare</i> L.)
No full textThe application of high-performance liquid chromatography-mass spectrometry (HPLC-MS/MS) revealed the origin and evolution of antioxidants during the brewing process of hopped and unhopped reference beer. As tachioside (3-methoxy-4-hydroxyphenyl-β-d-glucopyranoside), arbutin (4-hydroxyphenyl-β-d-glucopyranoside), and hordatines clearly increased during the fermentation step, the raw material barley was investigated as a source of the corresponding precursors. Therefore, 4-hydroxyphenyl-β-d-glucopyranosyl-(1 → 6)-β-d-glucopyranosyl-(1 → 6)-β-d-glucopyranoside, 4-hydroxy-3-methoxyphenyl-β-d-glucopyranosyl-(1 → 6)-β-d-glucopyranoside, 4-hydroxy-3-methoxyphenyl-β-d-glucopyranosyl-(1 → 6)-β-d-glucopyranosyl-(1 → 6)-β-d-glucopyranoside, and 4-hydroxy-2-methoxyphenyl-β-d-glucopyranosyl-(1 → 6)-β-d-glucopyranosyl-(1 → 6)-β-d-glucopyranoside were isolated from barley for the first time, and identified using liquid chromatography-mass spectrometry (LC-MS) and one-dimensional/two-dimensional-nuclear magnetic resonance (1D/2D-NMR) experiments. Moreover, hordatine glucosides A, B, and C were isolated and identified from barley, and hordatine C glucoside was characterized for the first time. A fermentation model followed by HPLC-MS/MS analysis substantiated the release of tachioside from 4-hydroxy-3-methoxyphenyl-β-d-glucopyranosyl-(1 → 6)-β-d-glucopyranoside by Saccharomyces cerevisiae. Quantitation experiments monitoring the content in wheat, barley, and different barley malt types demonstrated a wide range of concentrations, providing a basis for further comprehensive investigations to optimize the antioxidant yield in beer to contribute to improved flavor stability
A Highly Flexible and Elastic Low-Cost Stencil-Printed Coplanar Waveguide on Rough Airbag Nylon 66 Textile
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Stellenwert der Bewegungsdiagnostik zur Förderung früher körperlicher und sportlicher Aktivität bei Kinderrheuma
No full textGender and geography as inequality dimensions in forest research: insights from a multi-method study
No full textMutual regulation of CD4+ T cells and intravascular fibrin in infections.
No full textInnate myeloid cells especially neutrophils and their extracellular traps are known to promote intravascular coagulation and thrombosis formation in infections and various other conditions. Innate myeloid cell-dependent fibrin formation can support systemic immunity while its dysregulation enhances the severity of infectious diseases. Less is known about the immune mechanisms preventing dysregulation of fibrin homeostasis in infection. During experimental systemic infections local fibrin deposits in the liver microcirculation cause rapid arrest of CD4+ T cells. Arrested T-helper cells mostly represent Th17 cells that partially originate from the small intestine. Intravascular fibrin deposits activate mouse and human CD4+ T cells which can be mediated by direct fibrin-CD4+ T-cell interactions. Activated CD4+ T cells suppress fibrin deposition and microvascular thrombosis by directly counteracting coagulation activation by neutrophils and classical monocytes. T-cell activation, which is initially triggered by IL-12p40- and MHC-II-dependent mechanisms, enhances intravascular fibrinolysis via LFA-1. Moreover, CD4+ T cells disfavor the association of the thrombin-activatable fibrinolysis inhibitor (TAFI) with fibrin whereby fibrin deposition is increased by TAFI in the absence but not in the presence of T cells. In human infections thrombosis development is inversely related to microvascular levels of CD4+ T cells. Thus, fibrin promotes LFA-1-dependent T-helper cell activation in infections which drives a negative feedback cycle that rapidly restricts intravascular fibrin and thrombosis development