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While the opioid crisis has justifiably occupied news headlines, emergency rooms are seeing many thousands of visits for another cause: cannabinoid toxicity. This is partly due to the spread of cheap and extremely potent synthetic cannabinoids that can cause serious neurological and cardiovascular complications—and deaths—every year. While an opioid overdose can be reversed by naloxone, there is no analogous treatment for cannabis toxicity. Without an antidote, doctors rely on sedatives, with their own risks, or 'waiting it out' to treat these patients. We have shown that the canonical synthetic 'designer' cannabinoids are highly potent CB1 receptor agonists and, as a result, competitive antagonists may struggle to rapidly reverse an overdose due to synthetic cannabinoids. Negative allosteric modulators (NAMs) have the potential to attenuate the effects of synthetic cannabinoids without having to directly compete for binding. We tested a group of CB1 NAMs for their ability to reverse the effects of the canonical synthetic designer cannabinoid JWH018 in vitro in a neuronal model of endogenous cannabinoid signaling and also in vivo. We tested ABD1085, RTICBM189, and PSNCBAM1 in autaptic hippocampal neurons that endogenously express a retrograde CB1-dependent circuit that inhibits neurotransmission. We found that all of these compounds blocked/reversed JWH018, though some proved more potent than others. We then tested whether these compounds could block the effects of JWH018 in vivo, using a test of nociception in mice. We found that only two of these compounds—RTICBM189 and PSNCBAM1—blocked JWH018 when applied in advance. The in vitro potency of a compound did not predict its in vivo potency. PSNCBAM1 proved to be the more potent of the compounds and also reversed the effects of JWH018 when applied afterward, a condition that more closely mimics an overdose situation. Lastly, we found that PSNCBAM1 did not elicit withdrawal after chronic JWH018 treatment. In summary, CB1 NAMs can, in principle, reverse the effects of the canonical synthetic designer cannabinoid JWH018 both in vitro and in vivo, without inducing withdrawal. These findings suggest a novel pharmacological approach to at last provide a tool to counter cannabinoid toxicity. [ABSTRACT FROM AUTHOR]

The outbreak of COVID-19 caused by the novel coronavirus SARS-CoV-2 is a global public health threat. As high-risk environments for transmission, hospitals require effective methods to inactivate the virus on surfaces and in the air to prevent further spread among hospitals. The aim of this systematic review was to evaluate the use of ozone gas to inactivate surface and airborne SARS-CoV-2 in hospital settings. A systematic literature search was performed in databases including PubMed, Scopus and Web of Science from 2019 to 2024. Studies that assessed the use of ozone gas to inactivate SARS-CoV-2 in hospital settings were included. The quality assessment of the studies was done using the Critical Appraisal Skills Program (CASP) tool. A total of 10 studies met the inclusion criteria and were included in the review. Studies have reported that ozone effectively inactivates SARS-CoV-2 on surfaces and air in hospital environments. However, there were variations in ozone concentration, exposure time, and relative humidity (RH) used in each study. Ozone demonstrates promise as an effective disinfectant for inactivating SARS-CoV-2 on surfaces and air in hospital environments. It should be focused on determining the optimal conditions for maximum efficiency and establishing relevant protocols in terms of human health. [ABSTRACT FROM AUTHOR]