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Low-T3 syndrome and high-T3 syndrome: Consequences of step-up hypodeiodination, e.g. in critical illness as an example for type 1 allostasis, [20] or hyperdeiodination, as in type 2 allostasis, including posttraumatic stress disorder. [12] Resistance to thyroid hormone: Feedback loop interrupted on the level of pituitary thyroid hormone receptors.
T 3 is the more metabolically active hormone produced from T 4.T 4 is deiodinated by three deiodinase enzymes to produce the more-active triiodothyronine: . Type I present in liver, kidney, thyroid, and (to a lesser extent) pituitary; it accounts for 80% of the deiodination of T 4.
The major form of thyroid hormone in the blood is thyroxine (T 4), whose half-life of around one week [4] is longer than that of T 3. [5] In humans, the ratio of T 4 to T 3 released into the blood is approximately 14:1. [6] T 4 is converted to the active T 3 (three to four times more potent than T 4) within cells by deiodinases (5′-deiodinase).
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A complete blood type would describe each of the 45 blood groups, and an individual's blood type is one of many possible combinations of blood-group antigens. [3] Almost always, an individual has the same blood group for life, but very rarely an individual's blood type changes through addition or suppression of an antigen in infection, malignancy, or autoimmune disease.
The system is based on the expression of two codominant alleles, designated Lua and Lub. The antigens Aua and Aub, known as the Auberger antigens, were once thought to make up a separate blood group but were later shown to be Lutheran antigens arising from variations in the BCAM gene. The phenotypes Lu (a+b−) and Lu (a+b+) are found at ...
There are two major antigens in the Lewis system: Le(a) and Le(b). Individuals who are negative for Le express neither antigen and their blood type is designated as Le(a-b-). In individuals who are positive for Le, the blood type is determined by the person's secretor status.