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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 2.46 μM under the same conditions. The neuroprotection ratio of CBD against H2O2 ([H2O2]=10 μM) was 2.40 with 5 μM of CBD, increasing the cell viability to 57% from 24%. The CLSM analysis suggested that the cell-death mechanisms were different for CBD and H2O2, and CBD did not completely rescue the morphological alterations of primary hippocampal neurons caused by H2O2, such as neurite degeneration, at least in the in vitro neuron culture. Conclusion Although CBD showed both neurotoxic and neuroprotective effects on hippocampal neurons in the in vitro setting, the use of low-concentrated (i.e., 5 μM) CBD, not causing toxic effects on the neurons, significantly rescued the neurons from the oxidative stress (H2O2), confirming its neuroprotection capability.Introduction Cannabidiol (CBD), the nonintoxicating constituent of cannabis, is largely employed for pharmaceutical and cosmetic purposes. CBD can be extracted from the plant or chemically synthesized. Impurities of psychotropic cannabinoids Δ9-tetrahydrocannabinol (Δ9-THC) and Δ8-THC have been found in extracted CBD, thus hypothesizing a possible contamination from the plant. Materials and Methods In this study, synthetic and extracted CBD samples were analyzed by ultrahigh-performance liquid chromatography coupled to high-resolution mass spectrometry and the parameters that can be responsible of the conversion of CBD into THC were evaluated by an accelerated stability test. Results In synthetic and extracted CBD no trace of THC species was detected. In contrast, CBD samples stored in the dark at room temperature on the benchtop for 3 months showed the presence of such impurities. Experiments carried out under inert atmosphere in the absence of humidity or carbon dioxide led to no trace of THC over time even at high temperature. Conclusions The results suggested that the copresence of carbon dioxide and water from the air could be the key for creating the acidic environment responsible for the cyclization of CBD. These findings suggest that it might be appropriate to review the storage conditions indicated on the label of commercially available CBD.The term "hemp" refers to Cannabis sativa cultivars grown for industrial purposes that are characterized by lower levels of tetrahydrocannabinol (THC), the active principle responsible for Cannabis psychotropic effects. Hemp is an extraordinary crop, with enormous social and economic value, since it can be used to produce food, textiles, clothing, biodegradable plastics, paper, paint, biofuel, and animal feed, as well as lighting oil. find more Various parts of the hemp plant represent a valuable source of food and ingredients for nutritional supplements. While hemp inflorescence is rich in nonpsychoactive, yet biologically active cannabinoids, such as cannabidiol (CBD), which exerts potent anxiolytic, spasmolytic, as well as anticonvulsant effects, hempseed has a pleasant nutty taste and represents a valuable source of essential amino acids and fatty acids, minerals, vitamins, and fibers. In addition, hempseed oil is a source of healthy polyunsaturated fatty acids, and hemp sprouts are rich in antioxidants. This review article aims to provide a comprehensive outlook from a multidisciplinary perspective on the scientific evidence supporting hemp beneficial properties when consumed as food or supplement. Marketing of hemp-derived products is subjected to diversified and complex regulations worldwide for several reasons, including the fact that CBD is also the active principal of pharmaceutical agents and that regulatory bodies in some cases ban Cannabis inflorescence regardless of its THC content. Some key regulatory aspects of such a complex scenario are also analyzed and discussed in this review article.Coronavirus disease-19 (COVID-19)-related anxiety and post-traumatic stress symptoms (PTSS) or post-traumatic stress disorder (PTSD) are likely to be a significant long-term issue emerging from the current pandemic. We hypothesize that cannabidiol (CBD), a chemical isolated from Cannabis sativa with reported anxiolytic properties, could be a therapeutic option for the treatment of COVID-19-related anxiety disorders. In the global over-the-counter CBD market, anxiety, stress, depression, and sleep disorders are consistently the top reasons people use CBD. In small randomized controlled clinical trials, CBD (300-800 mg) reduces anxiety in healthy volunteers, patients with social anxiety disorder, those at clinical high risk of psychosis, in patients with Parkinson's disease, and in individuals with heroin use disorder. Observational studies and case reports support these findings, extending to patients with anxiety and sleep disorders, Crohn's disease, depression, and in PTSD. Larger ongoing trials in this area continue to add to this evidence base with relevant patient cohorts, sample sizes, and clinical end-points. Pre-clinical studies reveal the molecular targets of CBD in these indications as the cannabinoid receptor type 1 and cannabinoid receptor type 2 (mainly in fear memory processing), serotonin 1A receptor (mainly in anxiolysis) and peroxisome proliferator-activated receptor gamma (mainly in the underpinning anti-inflammatory/antioxidant effects). Observational and pre-clinical data also support CBD's therapeutic value in improving sleep (increased sleep duration/quality and reduction in nightmares) and depression, which are often comorbid with anxiety. Together these features of CBD make it an attractive novel therapeutic option in COVID-related PTSS that merits investigation and testing through appropriately designed randomized controlled trials.In the evolving field of medicinal cannabis, there are many questions and concerns broached by patients to which health care providers cannot respond with anything other than anecdotal evidence. Many simple knowledge gaps persist due to barriers to high-quality research at the institutional and state levels barriers that, in turn, stem from the federal designation of cannabis as an illegal substance. These perspectives of a California-based pain physician on the approach to the cannabis-curious pain patient highlight the necessity of a change in the classification of cannabis to streamline research as to the benefits and risks of this now ubiquitous substance.Mankind has long utilized Cannabis for diverse purposes. However, it has only been since the late 19th century that its individual cannabinoids began to be isolated, analyzed, and synthesized. By the mid-20th century it was discovered that many cannabinoids were asymmetric, with chirality often controlling their pharmacology. Increasingly accurate measurement and understanding of cannabinoid chirality will facilitate their synthesis and accelerate their medicinal applications.Benign thyroid nodules (BTNs) are commonly found in the general population. They are usually asymptomatic and their incidence has increased as a result of wide-spread use of ultrasound. Benign nodules are typically monitored clinically until they increase in size, resulting in compressive symptoms warranting surgery. However, although surgery is generally well-tolerated and of low-risk, it is associated with a small risk for several complications including hypothyroidism, nerve injury, hematoma, injury to other structures and wound infection. Recently, newer image-guided ablation techniques including radiofrequency ablation (RFA) have been introduced. RFA has a similar safety profile when compared to surgery and has shown promising results in challenging surgical candidates. Though several studies have been published in Asian and European countries on the efficacy of RFA, limited data is available on the North American population. The aim of the study is to review the current literature establishing the clinical outcomes and safety of RFA for benign nodules.
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To determine differences in incidence and duration of postoperative symptomatic hypocalcemia between those taking and those not taking proton pump inhibitors (PPIs) at the time of total or completion thyroidectomy.
A retrospective chart review of adult patients who underwent total or completion thyroidectomy at a tertiary medical center between January 2013 and January 2018 was performed. Development of symptomatic hypocalcemia, duration of symptoms, postoperative parathyroid hormone levels, PPI usage and emergency department (ED) visits were recorded.
Data from 371 patients were analyzed. Sixty of 371 (16.2%) patients developed symptomatic hypocalcemia. Sixteen of 89 (18.0%) patients on a PPI developed symptomatic hypocalcemia compared to 44 of 282 (15.6%) not on a PPI (
= .63). The overall average duration of symptoms was 4.3 days (SD [SD] 3.77 days). The average duration of symptoms in those on a PPI was 4.8 days (SD 2.8 days) compared to 4.2 days (SD 4.1 days) in those not on a PPI (
= 0.16). Six of 282 patients (2.1%) not taking a PPI had a postoperative ED visit, compared to two of the 89 patients (2.3%) taking a PPI (
= 1.00).
There was no clinically significant difference in incidence and duration of symptomatic hypocalcemia or ED visits after total or completion thyroidectomy between patients that were and were not taking PPIs perioperatively. While the decision to continue PPI should be made on an individual basis, these data suggest that patients may be counseled to continue their PPI perioperatively without increased risk of symptomatic hypocalcemia.
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