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History

Swedish physiologist Ulf von Euler and British physiologist M.G. Goldblatt, first discovered prostaglandins independently in 1935. Prostaglandins were noted for having blood pressure reducing effects and smooth muscle regulation effects. Prostaglandin E2 itself was identified in 1962 by Swedish biochemist Sune Bergström in the seminal fluid of sheep. Prostaglandins were discovered to be products of arachidonic acid and with the ability to radio label arachidonic acid in the early 1960s, American chemist E.J. Corey was able to synthesize PGE2 in the lab in the 1970. Prostaglandin E2 was approved for medical use in the United States in 1977 and it is on the World Health Organization's List of Essential Medicines. PGE2 was approved by the FDA in 1977

Neurological effects

In response to physiologic and psychologic stress, Prostaglandin E2 is involved in several inflammation and immunity pathways. It regulates these responses through binding to G coupled protein PGE2 receptors (EP1, EP2, EP3, and EP4). The activation of these different EP receptors is dependent on the type of triggering stress stimuli and results in the corresponding stress response. Activation of EP1 vis PGE2 results in the suppression of impulse behaviors in response to psychological stress. Prostaglandin E2 is involved in regulating illness induced memory impairment via activation of EP2. Prostaglandin E2 activation of EP3 results in regulation of illness induced fever. EP4 is functionally similar to EP2 and has also been shown in studies to have a role in hypothermia and anorexia.

A common side effect of prostaglandin E2 is its effect on gastrointestinal smooth muscle resulting in nausea, vomiting and diarrhea. The suppository form of prostaglandin E2 is associated with increased severity of these symptoms. Fever is also a common side effect with use of prostaglandin E2. The insert and gel forms have been shown to have minimal gastrointestinal effects, but are more associated with increase stimulation of the uterus. Uterine hyperstimulation is effectively treated by stopping use of prostaglandin E2

Heaf test

Issues with this article are that there are a lot of claims without citations. The history of the test could be separated into its own section. The interpretation of the test needs to be clarified so it is less confusing. There is a section on equivalent the Mantoux tests which could use more context. These changes will support the work of people currently editing the article as they have the same goals for improving it (Make it less confusing and cite more sources).