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SAGLIK ALANINDA KENEVIR

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There is a growing body of evidence that cannabis may be effective as an analgesic with potential to reduce opioid usage in chronic pain. This review synthesizes the available literature to elucidate the possible role that cannabis might play in reducing opioid use in gynecological disorders that may potentially lead to a recommendation of substituting opioids with cannabis. With reports of a decrease in opioid use after cannabis initiation, an opioid-sparing effect has been seen in gynecologic malignancies such as ovarian, uterine, endometrial, and cervical cancers in addition to chronic pelvic pain. Though many studies have found an association between cannabis and various adverse maternal and neonatal outcomes, there is a lack of randomized-controlled trials making it difficult to claim a directly causal relationship between cannabis and these adverse outcomes. Additionally, with increased use of cannabis during pregnancy, evidence of possible benefits and risks to mothers and fetuses is examined.
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Synthetic cannabinoids (SC) are the most common type of new psychoactive substances used predominantly as a replacement for cannabis. There is a wealth of literature on the negative effects experienced by users of SC. However, there is a paucity of research on the experience of addiction to SC from the users' perspectives. The present study qualitatively explored the experience of addiction to SC. Online blog entries detailing the experience of SC addiction were analyzed using thematic analysis. Users reported being stuck in a cycle of addiction which was composed of addiction hallmarks. They also experienced a range of significant physical, mental health and psychosocial problems. Suicidal ideation was also reported, with potential for its occurrence during withdrawal, due to shame of being addicted, and as the only way to stop the addiction cycle. Additionally, both psychotic and cognitive symptoms were reported to persist following cessation, enhancing current understanding of long-term SC effects. Therefore, users require both clinical and psychosocial support for these issues, most notably suicidal ideation.
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Palmitoylethanolamide (PEA) and oleamide are two fatty acid amides which 1) share some cannabimimetic actions with L.9-tetrahydrocanna­ binol, anandamide and 2-arachidonoylglycerol, and 2) may interact with proteins involved in the biosynthesis, action and inactivation of endocannabinoids. Palmitoylethanolamide (PEA) and oleamide are two fatty acid amides which 1) share some cannabimimetic actions with L.9-tetrahydrocanna­ binol, anandamide and 2-arachidonoylglycerol, and 2) may interact with proteins involved in the biosynthesis, action and inactivation of endocannabinoids. Due to its pharmacological actions and its accumulation in damaged cells, PEA may have a physio-pathological role as an analgesic, anti-oxidant and anti-inflammatory mediator. However, its mechanism of action is puzzling. In fact, PEA does not bind to CB1 and CB2 receptors transfected into host cells, but might be a ligand for a putative CBn receptor present in the RBL-2H3 cell line. On the other hand, the analgesic effect of PEA is reversed by SR144528, a CB2 antagonist. PEA may act as an "entourage" compound for endocannabinoids, i.e. it may enhance their action for example by inhibiting their inactivation. Oleamide is a sleep inducing lipid whose mechanism of action is far from being understood. Although it does not bind with high affinity to CB1 or CB2 receptors, it exhibits some cannabimimetic actions which could be explained at least in part by 'entourage' effects. It is likely that oleamide and anandamide have common as well as distinct pathways of action. The 5-HT2A receptor appears to be a target for oleamide but the possibility of the existence of specific receptors for this compound is open. The biosynthesis and tissue distribution of oleamide remain to be assessed in order to both substantiate its role as a sleep-inducing factor and investigate its participation in other physiopathological situations.
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Introduction: Ovarian folliculogenesis requires a fine balance between extra- and intra-ovarian factors. Endocannabinoids are found in the female reproductive system and are essential for a normal follicular growing process and ovulation. First, our study aimed to analyze levels of the endocannabinoid-2-arachidonoylglycerol (2-AG)-in patients with polycystic ovary syndrome (PCOS) and to compare with healthy controls. In addition, the study aimed to explore the association of 2-AG with hormonal and metabolic alterations, ovulatory dysfunction, and the presence of polycystic ovarian morphology (PCOM) across the classical PCOS phenotypes. Methods: Fifty-four women with PCOS were compared with 26 healthy controls. PCOS patients were diagnosed and phenotyped according to the Rotterdam criteria. Further analyses were performed with the classical PCOS phenotypes A and B comprising hyperandrogenism with oligo-anovulation with or without PCOM, respectively. Full medical history, clinical investigations, anthropometric measurements, laboratory tests, and ultrasound investigations were carried out in the follicular phase. Serum levels of 2-AG were measured by enzyme-linked immunosorbent assay. Results: PCOS patients (n=54) and healthy controls (n=26) showed similar metabolic parameters and anthropometric characteristics. PCOS patients were more hirsute than healthy women (p=0.001). Luteinizing hormone/follicle-stimulating hormone ratio and serum levels of androgens were significantly higher in the patient than in the control group (p=0.035, p<0.001, respectively). Free androgen index was also higher in the patient group (p=0.002). Serum levels of 2-AG did not significantly differ when comparing all PCOS patients versus healthy controls; however, further analysis of individual phenotype groups revealed that 2-AG levels in PCOS patients with phenotyope A (n=30) were significantly lower when compared with PCOS patients with phenotype B (n=20) and healthy controls (n=26). Conclusion: Serum levels of 2-AG were similar between PCOS patients and healthy controls. Nevertheless, phenotype A PCOS patients had significantly lower levels of the endocannabinoid compared with phenotype B patients and healthy controls. Collectively, these results suggest that overall serum levels of 2-AG are not a diagnostic marker for PCOS; however, their altered secretion or activity may influence normal follicular processes.