5-MeO-DALT (N,N-diallyl-5-methoxytryptamine) is a psychoactive substance, sold primarily over the Internet as a 'research chemical' or 'plant food'. Although details for the synthesis of this tryptamine have been available since 2004, its use as a hallucinogenic drug has been reported only occasionally in on-line user fora. It is controlled in only a few countries world-wide. There is little scientifically-based literature on the pharmacological, physiological, psychopharmacological, toxicological and epidemiological characteristics of 5-MeO-DALT. Here we review what is known about these aspects. We also report what we believe to be the first death involving the use of this substance. The case involved a man in his mid-20s who died in mid-2010. The coroner concluded that the deceased "died from injuries sustained after being hit by a lorry whilst under the influence of 5-MeODALT". It is critical that any other cases, including non-fatal instances, are documented so that a scientific evidence-base can be established for this drug.

Non-steroidal anti-inflammatory drugs (NSAIDs) cause peptic ulcer disease, but whether they interact with Helicobacter pylori to promote damage is controversial. Moreover, the reported induction of apoptosis in gastric cells by H. pylori lipopolysaccharide (LPS) (10(-9) g/ml) contrasts with studies showing low immunological potency of this LPS. Therefore, the effects of LPS from H. pylori NCTC 11637 and Escherichia coli O111:B4 on apoptosis in a primary culture of guinea-pig gastric mucous cells were investigated in the presence and absence of the NSAID, ibuprofen. Cell loss was estimated by a crystal violet assay, and apoptosis determined from caspase activity and from condensation and fragmentation of nuclei. Exposure to E. coli LPS for 24 h caused cell loss and enhanced apoptotic activity at concentrations >or= 10(-9) g/ml, but similar effects were only obtained with H. pylori LPS at concentrations >or= 10(-6) g/ml. Although ibuprofen (250 microM) caused cell loss and apoptosis, addition of either E. coli or H. pylori LPSs further enhanced these effects. In conclusion, LPS and ibuprofen interact to enhance gastric cell loss and apoptosis. In such interactions, E. coli LPS is more potent than that of H. pylori. The low potency of H. pylori LPS may contribute to a chronic low-grade gastritis that can be enhanced by the use of NSAIDs.

Non-steroidal anti-inflammatory drugs (NSAIDs) cause peptic ulcer disease, but whether they interact with Helicobacter pylori to promote damage is controversial. Moreover, the reported induction of apoptosis in gastric cells by H. pylori lipopolysaccharide (LPS) (10(-9) g/ml) contrasts with studies showing low immunological potency of this LPS. Therefore, the effects of LPS from H. pylori NCTC 11637 and Escherichia coli O111:B4 on apoptosis in a primary culture of guinea-pig gastric mucous cells were investigated in the presence and absence of the NSAID, ibuprofen. Cell loss was estimated by a crystal violet assay, and apoptosis determined from caspase activity and from condensation and fragmentation of nuclei. Exposure to E. coli LPS for 24 h caused cell loss and enhanced apoptotic activity at concentrations >or= 10(-9) g/ml, but similar effects were only obtained with H. pylori LPS at concentrations >or= 10(-6) g/ml. Although ibuprofen (250 microM) caused cell loss and apoptosis, addition of either E. coli or H. pylori LPSs further enhanced these effects. In conclusion, LPS and ibuprofen interact to enhance gastric cell loss and apoptosis. In such interactions, E. coli LPS is more potent than that of H. pylori. The low potency of H. pylori LPS may contribute to a chronic low-grade gastritis that can be enhanced by the use of NSAIDs.