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S. Suh

3 papers in the library · publishing 2019

Papers

Cardiotoxic effects of [3-[2-(diethylamino)ethyl]-1H-indol-4-yl] acetate and 3-[2-[ethyl(methyl)amino]ethyl]-1H-indol-4-ol: Short title: QT prolongation by 4-acetoxy-DET and 4-hydroxy-MET.

Toxicology Letters November 6, 2019 K. S. Yoon, Jin-Moo Lee, Young-Hoon Kim et al.

Two synthetic tryptamines, 4-AcO-DET and 4-HO-MET, are abused as recreational hallucinogens and may pose unknown health risks. In laboratory tests, both substances increased the proliferation of rat heart cells in a concentration-dependent manner, prolonged QT intervals in rats, and inhibited potassium channels in hamster cells, indicating potential cardiotoxicity. Expression of the PAK1 protein, involved in cardiovascular function, did not change. The findings suggest these new psychoactive substances could cause adverse cardiovascular effects, supporting evidence for their legal scheduling.

A Case Study of Imagery Rehearsal Therapy in a Nightmare Disorder Patient with Posttraumatic Stress Disorder

Journal of Sleep Medicine June 30, 2019 Soyeong Park, S. Choi, E. Joo et al.

A brief cognitive behavioral therapy for insomnia (CBT-I) delivered via a mobile app significantly improved sleep quality and reduced insomnia severity in adults with chronic insomnia. Participants using the app showed moderate to large improvements in sleep efficiency, total sleep time, and time to fall asleep compared to a control group. The app-based treatment also reduced maladaptive sleep-related beliefs. These gains were maintained at a one-month follow-up, suggesting that digital CBT-I can be an effective and accessible treatment option for chronic insomnia.

2-(2,5-Dimethoxy-4-methylphenyl)-N-(2-methoxybenzyl)ethanamine (25D-NBOMe) and N-(2-methoxybenzyl)-2,5-dimethoxy-4-chlorophenethylamine (25C-NBOMe) induce adverse cardiac effects in vitro and in vivo.

Toxicology Letters April 1, 2019 K. S. Yoon, Jaesuk Yun, Young-Hoon Kim et al.

Two emerging psychoactive substances, 25D-NBOMe and 25C-NBOMe, show potential for disrupting heart rhythm, based on laboratory and animal tests. At 100 μM, both compounds reduced cell viability in a cell-based assay. In rats, doses of 2.0 mg/kg and 0.75 mg/kg prolonged QT intervals on electrocardiography, a marker of altered cardiac repolarization. The compounds also decreased levels of PAK1, a protein linked to cardiotoxicity, and 25D-NBOMe inhibited potassium channels in a hERG assay. The findings suggest these substances may pose a risk for cardiac arrhythmias, but further research is needed to clarify the role of PAK1 down-regulation.