Guide: How to cite a Interview in The American Naturalist style

Guide: How to cite a Interview in The American Naturalist style

Cite A Interview in The American Naturalist style

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Use the following template to cite a interview using the The American Naturalist 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 The American Naturalist 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. Location.

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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