How Do You Spell ACTIVATED FACTOR XI?

Pronunciation: [ˈaktɪvˌe͡ɪtɪd fˈaktə ɹˌə͡ʊmən ɪlˈɛvən] (IPA)

Activated Factor XI is a clotting protein that plays a crucial role in maintaining haemostasis. The spelling of this term can be challenging, but the International Phonetic Alphabet (IPA) can help explain it. The pronunciation of "Activated" is /ˈæktəˌveɪtɪd/. For "Factor", it is /ˈfæktər/. Finally, for "XI", it is /ɛks aɪ/. Therefore, the correct spelling for this term can be pronounced as /ˈæktəˌveɪtɪd ˈfæktər ɛks aɪ/. This spelling is used widely in medical research and practice to ensure clarity and accuracy.

ACTIVATED FACTOR XI Meaning and Definition

1. Activated Factor XI (FXIa) is a crucial component of the coagulation cascade, a series of enzymatic reactions that lead to blood clot formation. It is an activated form of Factor XI, a glycoprotein zymogen found in the blood plasma and synthesized in the liver. FXIa plays a vital role in amplifying and enhancing the coagulation process.

   Upon activation, FXIa converts Factor IX into its active form, Factor IXa, thereby initiating the intrinsic pathway of coagulation. This pathway primarily contributes to clot formation in response to tissue injury or surface contact with foreign substances. Activation of FXIa occurs either through intrinsic activation, involving contact with negatively charged surfaces such as collagen or platelets, or through extrinsic activation by coagulation factors including Factor XII and thrombin.

   Once activated, FXIa cleaves multiple molecules of Factor IX, effectively increasing the quantity of active Factor IXa present. The subsequent activation of Factor IXa triggers a chain reaction leading to the conversion of Factor X into Factor Xa. Factor Xa plays a central role in the final steps of coagulation, ultimately resulting in the formation of a fibrin clot.

   The dysregulation or deficiency of activated Factor XI can contribute to bleeding disorders, such as hemophilia C, where individuals experience prolonged bleeding due to insufficient clot formation. Research into the mechanisms and regulation of FXIa is essential for understanding and developing treatments for hematologic disorders related to blood clotting.

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