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Introduction: 25B-NBOH is a synthetic hallucinogen closely related to the "NBOMe" family of N-substituted 2C phenethylamine derivatives. There have been no published reports documenting the clinical toxicity of NBOH derivatives., Case Series: Five patients presented to the Emergency Department (ED) with altered conscious state following exposure to powder sold as "powdered LSD" at a party. A 24-year-old male who ingested the powder developed mydriasis, tachycardia, hypertension, and severe agitation requiring parenteral sedation. A 22-year-old male who insufflated the powder developed status epilepticus requiring intubation. Both patients developed acute kidney injury and one had rhabdomyolysis. In both cases, blood analysis detected 25-NBOH and no other illicit/licit drugs. Three other patients developed mild hallucinations. Hyperthermia was not documented in any case., Discussion: Exposure to 25B-NBOH in a powdered form produced sympathomimetic toxicity, including hallucinations. Insufflation of 25B-NBOH led to rapid onset of status epilepticus in one case. Toxicity in all cases resolved within 12 h. Despite in vitro evidence of 5-HT 2A receptor agonism, hyperthermia was not observed. Potent hallucinogens are often delivered via blotter paper to avoid excessive dosing. The severe clinical toxicity documented in these cases highlights the potential for development of adverse health effects with exposure to apparent small volumes of potent sympathomimetics.

A number of different strategies have been used to identify genes for which genetic variation contributes to type 1 diabetes (T1D) pathogenesis. Genetic studies in humans have identified >40 loci that affect the risk for developing T1D, but the underlying causative alleles are often difficult to pinpoint or have subtle biological effects. A complementary strategy to identifying "natural" alleles in the human population is to engineer "artificial" alleles within inbred mouse strains and determine their effect on T1D incidence. We describe the use of the Sleeping Beauty (SB) transposon mutagenesis system in the nonobese diabetic (NOD) mouse strain, which harbors a genetic background predisposed to developing T1D. Mutagenesis in this system is random, but a green fluorescent protein (GFP)-polyA gene trap within the SB transposon enables early detection of mice harboring transposon-disrupted genes. The SB transposon also acts as a molecular tag to, without additional breeding, efficiently identify mutated genes and prioritize mutant mice for further characterization. We show here that the SB transposon is functional in NOD mice and can produce a null allele in a novel candidate gene that increases diabetes incidence. We propose that SB transposon mutagenesis could be used as a complementary strategy to traditional methods to help identify genes that, when disrupted, affect T1D pathogenesis., (Copyright © 2015 Elso et al.)