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0 before cannabis use to 6±2.1 after introduction of cannabis (p=0.0002). Discussion In children and young adults with FASD, cannabis, mostly cannabidiol (CBD), has been associated with a marked and statistically significant improvement in serious disruptive behavior. These cases suggest that the efficacy and safety of CBD should be tested in well-controlled studies.Introduction Over the last few years, a growth in research and interest in medical cannabis (most often referred to as medical marijuana) use have occurred nationally. Medical cannabis has become a treatment option for disease conditions, such as epilepsy, wasting syndrome associated with AIDs, and post-traumatic stress disorder, when traditional medication is ineffective. Objectives The objectives were to identify knowledge deficits of the medical cannabis program (MCP) in Connecticut among Connecticut pharmacists and the impact of MCP on Connecticut pharmacy practice and concerns Connecticut pharmacists have regarding medical cannabis use. Methods A cross-sectional survey through an online platform, Google forms, was administered for 2 months (October 15, 2017-December 15, 2017). An e-mail containing the link to the survey was e-mailed to all pharmacists whose e-mail addresses were available from the State of Connecticut's Commission of Pharmacy database (n = 6182). Of those with available e-mail addresses,enough about the side effects of medical cannabis to provide appropriate counseling to patients. Conclusion Overall, the results of our survey found that Connecticut licensed pharmacists had lack of complete and accurate knowledge regarding the state's MCP. As more states legalize medical cannabis, it will be imperative that education of pharmacists and other health care professionals about the MCP and the clinical use of cannabis occur.Context Medical cannabis use has increased in recent years despite being a federally illegal drug in the United States. States with medical cannabis use laws require patients to be certified by physicians. However, little is known about the education, knowledge, and practice characteristics of physicians who recommend and supervise patients' use of medical cannabis. Objective This study assessed how U.S. physicians who practice cannabis medicine are educated, self-assess their knowledge, and describe their practice. Methods In fall 2017, a 57-item, electronic survey was sent to all members of the Society of Cannabis Clinicians. Because California has had legalized medical cannabis for longer than any other state, we analyzed responses for 14 items between California and non-California physicians. Results Of 282 surveyed, 133 were eligible and 45 completed the survey. Of those, multiple medical specialties were represented. Only one physician received education during medical school about cannabis medicine, buquire a physician's recommendation, yet few states require specific clinical training. Findings of this study suggest the need for more formal education and training of physicians in medical school and residency, more opportunities for cannabis-related continuing medical education for practicing physicians, and clinical and basic science research that will inform best practices in cannabis medicine.Introduction Treatment of traumatic brain injury (TBI) with granulocyte colony-stimulating factor (G-CSF) has been shown to enhance brain repair by direct neurotrophic actions on neural cells and by modulating the inflammatory response. Administration of cannabinoids after TBI has also been reported to enhance brain repair by similar mechanisms. Objectives The primary objective of this study was to test the hypothesis that G-CSF mediates brain repair by interacting with the endocannabinoid system. Methods and Results (i) Mice that underwent controlled cortical impact (CCI) were treated with G-CSF for 3 days either alone or in the presence of selective cannabinoid receptor 1 (CB1-R) or cannabinoid receptor 2 (CB2-R) agonists and antagonists. The trauma resulted in decreased expression of CB1-R and increased expression of CB2-R in the cortex, striatum, and hippocampus. Cortical and striatal levels of the major endocannabinoid ligand, 2-arachidonoyl-glycerol, were also increased by the CCI. Administration of the hematopoietic cytokine, G-CSF, following TBI, resulted in mitigation or reversal of trauma-induced CB1-R downregulation and CB2-R upregulation in the three brain regions. Nimbolide Treatment with CB1-R agonist (WIN55) or CB2-R agonist (HU308) mimicked the effects of G-CSF. (ii) Pharmacological blockade of CB1-R or CB2-R was not effective in preventing G-CSF's mitigation or reversal of trauma-induced alterations in these receptors. Conclusions These results suggest that cellular and molecular mechanisms that mediate subacute effects of G-CSF do not depend on activation of CB1 or CB2 receptors. Failure of selective CB receptor antagonists to prevent the effects of G-CSF in this model has to be accepted with caution. CB receptor antagonists can interact with other CB and non-CB receptors. Investigation of the role of CB receptors in this TBI model will require studies with CB1-R and in CB2-R knockout mice to avoid nonspecific interaction of CB receptor agents with other receptors.Introduction Reports on the neurotoxic and neuroprotective effects of cannabidiol (CBD) have not been in complete accord, showing different and somewhat contradictory results depending upon the brain cell types and experimental conditions employed. This work systematically examines the neuroprotective capability of CBD against oxidative stress (i.e., hydrogen peroxide [H2O2]) as well as its toxicity profile in the in vitro culture platform of primary hippocampal neurons. Materials and Methods The low cell-density (100 neurons per mm2) culture was used for analyzing the viability and morphology of neurons at a single-cell level with a confocal laser-scanning microscope (CLSM). Primary neurons were obtained from the hippocampal tissues of embryonic day-18 (E18) Sprague-Dawley rat pups and treated with CBD (0.1-100 μM) and/or H2O2 (0.1-50 μM) at 1 DIV (days in vitro). Results The lethal concentration 50 (LC50) value (the concentration causing 50% cell death) of CBD was calculated to be 9.85 μM after 24 h of incubation, and that of H2O2 was 2.