Guide: How to cite a Conference proceedings in Ecological Entomology style

Guide: How to cite a Conference proceedings in Ecological Entomology style

Cite A Conference proceedings in Ecological Entomology style

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Use the following template to cite a conference proceedings using the Ecological Entomology 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 Ecological Entomology 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. In Publication Title. Publisher, City, p. Pages Used.

Example:

Pacher, P. & Mechoulam, R. (2011) Is lipid signaling through cannabinoid 2 receptors part of a protective system?. Progress in Lipid Research, 50, 193-211.

In-text citation

Place this part right after the quote or reference to the source in your assignment.

Template

(Author Surname, Year Published)

Example

Overwhelming evidence has established an important role for endocannabinoid-CB2 receptor signaling in a large number of the major pathologies affecting humans. The broad spectrum of actions that can be attributed to CB2 receptor signaling in inflammatory, autoimmune, cardiovascular, gastrointestinal, liver, kidney, neuro-degenerative, psychiatric and many other diseases have been reviewed here in some detail (Fig. 1 and Table 2). Most likely, the primary cellular targets and executors of the CB2 receptor-mediated effects of endocannabinoids or synthetic agonists are the immune and immune-derived cells (e.g. leukocytes, various populations of T and B lymphocytes, monocytes/macrophages, dendritic cells, mast cells, microglia in the brain, Kupffer cells in the liver, etc.), however the number of other potential cellular targets is also expanding, including now endothelial and smooth muscle cells, fibroblasts of various origin, cardiomyocytes, and certain neuronal elements of the peripheral or central nervous systems (Fig. 2). Interestingly, it appears that in many of the above mentioned pathological conditions the inflammation/tissue injury not only triggers rapid elevation in local endocannabinoid level, which in turn initiates fast signaling processes in immune and perhaps other cell types modulating their critical functions, but may also lead to marked increases in CB2 receptor expressions both in inflammatory, as well as in some parenchymal cells. However, the drastic elevation in CB2 receptor expressions recently reported in various diseased tissues calls for some cautious note until these studies are confirmed using more rigorous positive and negative controls and supported by functional evidence. The latter is extremely important given the known, but often ignored limitations of the recently available CB2 antibodies and knockout mouse models.

In immune or immune derived cells CB2 activation generally mediates immunosuppressive effects comprising inhibition of proliferation, induction of apoptosis, suppression of cytokine and chemokine production and migration of stimulated immune cells, and induction of T regulatory cells, with consequent attenuation of autoimmune inflammatory response. These effects limit the tissue injury in large number of the above mentioned pathological conditions, particularly in those associated with sterile inflammatory response. However, in other disease states these immunosuppressive effects of the CB2 receptor activation may enhance or even inflict tissue damage as discussed in previous parts (e.g. in infections with various live pathogens, certain types of cancers in which the protective role of the immune system is critical to control the cancer growth, etc.). It is also important to keep in mind that even the relatively selective CB2 agonists may activate CB1 receptors in target tissues, particularly at higher doses (often resulting in opposite cellular and functional consequences on the disease progression as it became evident in many pathological conditions recently) and when the relative expression of CB1 over CB2 is high in the diseased tissue. This can also be one explanation for the bell-shaped dose response often seen with recently available CB2 agonists in various disease models. Furthermore, in many disease models the CB2 agonists appear to be most effective if given before the initiation of the insult, and may lose their effect or even promote inflammation when given at later time points. Thorough knowledge of CB2 receptor signaling in key target immune and/or other cell types is still largely enigmatic; hence understanding of the precise course of the disease and the exact sequel of pathological events behind these changes is extremely important in order to devise meaningful therapeutic approaches based on targeted modulation of CB2 receptor signaling.

Collectively, multiple lines of evidence discussed above support the view that lipid endocannabinoid signaling through CB2 receptors represents an aspect of the mammalian protective armamentarium, and its modulation by either selective CB2 receptor agonists or inverse agonists/antagonists (depending on the disease and its stage) holds unique therapeutic potential in huge number of diseases (the main targets of CB2 receptor modulation in inflammation and tissue injury are summarized in Fig. 3). Excitingly, large number of novel synthetic [64–69] and natural [285,286] CB2 receptor ligands has also been intensively investigated, giving hope that some of the above discussed preclinical results could also be translated into clinical treatments in the near future to ease human sufferings. (Pacher & Mechoulam, 2011)

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