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The field of psychedelics is in an important era, with a significant focus on the potential role of psychedelic compounds in the treatment of mental health and substance use disorders. In 2022, a scientific research conference was held in Toronto to bring together stakeholders from a variety of disciplines and to promote dialogue and collaboration. This Special Issue includes 8 papers based on presentations from the conference, which showcase the breadth of topics that were brought forward. Included are both quantitative and qualitative works, as well as two letters to the editors which further advance these important conversations. These articles not only present the current state of research into psychedelics, but also present viewpoints about their impacts on underrepresented communities, the need to recognize the history of these compounds that extends beyond this new Western "renaissance," and the complexities of integrating psychedelics into mainstream medicine. This Special Issue serves as both an exploration of a much-discussed topic and a reminder that collaboration can advance the field in order to harness its potential impact. [ABSTRACT FROM AUTHOR]

Background and Objectives: Buprenorphine/naloxone has been shown to be effective in the treatment of opioid use disorder. Due to its pharmacological properties, induction can be challenging, time-consuming, and result in sudden onset of withdrawal symptoms.Methods: Retrospective case series (n = 2).Results: Two patients with opioid use disorder were successfully started on buprenorphine/naloxone using a rapid micro-induction technique that did not cause precipitated withdrawal or require preceding cessation of other opioids.Discussion and Conclusions: These cases provide an alternative method for starting buprenorphine/naloxone that offers unique benefits compared to protocols previously described in the literature.Scientific Significance: This method can be used to minimize barriers to opioid agonist therapy. (Am J Addict 2019;28:262-265). [ABSTRACT FROM AUTHOR]

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Background: Diets rich in the n-3 fatty acid alpha-linolenic acid (ALA) have been shown to reduce breast tumor growth, enhance the effectiveness of the HER2-targeted drug trastuzumab (TRAS) and reduce HER2 signaling in mouse models. It is unclear whether this is due to direct effects of ALA or due to its long-chain n-3 fatty acids metabolites including docosahexaenoic acid (DHA). Methods: The ability of HER2-overexpressing BT-474 human breast cancer cells to convert ALA to long-chain n-3 fatty acids was determined by measurement of phospholipid fatty acids by gas chromatography following treatment with 100 μM ALA. The effects of 96 h treatment with ALA or DHA, at serum levels seen in mice (50-100 μM), alone and combined with TRAS (10 μg/ml), on BT-474 cell growth measured by trypan blue exclusion, apoptosis measured by flow cytometric analysis of Annexin-V/7-AAD stained cells (ALA and TRAS treatment only) and protein biomarkers HER2 signaling measured by western blot were determined. Results: ALA-treated BT-474 cells had higher phospholipid ALA but no increase in downstream n-3 metabolites including DHA. Both ALA and DHA reduced cell growth with and without TRAS. ALA had no effect on apoptosis. ALA and DHA showed opposite effects on Akt and MAPK phosphorylation; ALA increased and DHA decreased phosphorylation. Conclusions: Together these data suggest that, while both ALA and its DHA metabolite can reduce HER2- overexpressing breast cancer growth with and without TRAS, they demonstrate for the first time that DHA is responsible for the effects of ALA-rich diets on HER2 signaling pathways. [ABSTRACT FROM AUTHOR]

Background: Diets rich in the n-3 fatty acid alpha-linolenic acid (ALA) have been shown to reduce breast tumor growth, enhance the effectiveness of the HER2-targeted drug trastuzumab (TRAS) and reduce HER2 signaling in mouse models. It is unclear whether this is due to direct effects of ALA or due to its long-chain n-3 fatty acids metabolites including docosahexaenoic acid (DHA). Methods: The ability of HER2-overexpressing BT-474 human breast cancer cells to convert ALA to long-chain n-3 fatty acids was determined by measurement of phospholipid fatty acids by gas chromatography following treatment with 100 μM ALA. The effects of 96 h treatment with ALA or DHA, at serum levels seen in mice (50–100 μM), alone and combined with TRAS (10 μg/ml), on BT-474 cell growth measured by trypan blue exclusion, apoptosis measured by flow cytometric analysis of Annexin-V/7-AAD stained cells (ALA and TRAS treatment only) and protein biomarkers HER2 signaling measured by western blot were determined. Results: ALA-treated BT-474 cells had higher phospholipid ALA but no increase in downstream n-3 metabolites including DHA. Both ALA and DHA reduced cell growth with and without TRAS. ALA had no effect on apoptosis. ALA and DHA showed opposite effects on Akt and MAPK phosphorylation; ALA increased and DHA decreased phosphorylation. Conclusions: Together these data suggest that, while both ALA and its DHA metabolite can reduce HER2- overexpressing breast cancer growth with and without TRAS, they demonstrate for the first time that DHA is responsible for the effects of ALA-rich diets on HER2 signaling pathways. [ABSTRACT FROM AUTHOR]