Guide: How to cite a Podcast in Freshwater Biology style
Cite A Podcast in Freshwater Biology style
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Use the following template to cite a podcast using the Freshwater Biology citation style. For help with other source types, like books, PDFs, or websites, check out our other guides. To have your reference list or bibliography automatically made for you, try our free citation generator.
Key:
Pink text = information that you will need to find from the source.
Black text = text required by the Freshwater Biology style.
Reference list
Place this part in your bibliography or reference list at the end of your assignment.
Template:
Author Surname Author Initial. (Year Published) Title. Publication Title.
Example:
Russo E. (2004) Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel sy... - PubMed - NCBI. Ncbi.nlm.nih.gov.
In-text citation
Place this part right after the quote or reference to the source in your assignment.
Template
(Author Surname Year Published)
Example
The preceding material has pertained to conjectural and experimental evidence of a conceptual alternative biochemical explanation for certain disease manifestations, but one must ask how these would obtain? Baker et al. have described how endocannabinoids may demonstrate an impairment threshold if too high, and a range of normal function below which a deficit threshold may be crossed [112]. Syndromes of CECD may be congenital or acquired. In the former case, one could posit that genetically-susceptible individuals might produce inadequate endocannabinoids, or that their degradation is too rapid. The same conditions might be acquired in injury or infection. Unfortunately, the regulation of endocannabinoid synthesis and degradation are far from fully elucidated (reviewed [116]). While a single enzyme, anandamide synthase, catalyzes AEA production, its degradation by fatty acid amidohydrolase (FAAH), is shared with many substrates. To complicate matters, an endocannabinoid with antagonistic properties at CB1 called virodhamine (virodha, Sanskrit for “opposition”) has recently been discovered [117]. Further research may shed light on these relationships. In the meantime, a clinical agent that modifies endocannabinoid function will soon be clinically available in the form of cannabidiol. Recent research has demonstrated that although THC does not share VR1 agonistic activity with AEA, CBD does so to a similar degree as capsaicin [78]. What is more, CBD inhibits uptake of the endocannabinoid anandamide (AEA), and weakly inhibits its hydrolysis. The presence of this component in available cannabis based medicine extracts portends to vastly extend the clinical applications and therapeutic efficacy of this re-emerging modality [118–120]. It is highly likely that additional regulatory roles for endocannabinoids will be discovered for this neuroand immunomodulatory system. Some simple human experiments may be valuable, such as cerebrospinal fluid assay of AEA and 2-AG before and after ECT treatment. It is likely in the future that positron emission tomography (PET) or functional magnetic resonance imaging (fMRI) for cannabinoid ligands may clarify these concepts. This article has examined the inter-relationships of three clinical syndromes and biochemical basis in endocannabinoid function, as well as reflecting on other conditions that may display similar correlations. Only time and the scientific method will ascertain whether a new paradigm is applicable to human physiology and treatment of its derangements. Our insight into these possibilities is dependent on the contribution of one unique healing plant; for clinical cannabis has become a therapeutic compass to what modern medicine fails to cure. (Russo 2004)
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