Answer:
C-able to relieve haemophilia
Explanation:
Factor V111 is a blood clotting factor;produced in the liver and body endothelial cells. It is usually exist as inactive form beacuse it is binded to glycoprotein (glycogen +protein) called Von Willebrand factor when released into the blood stream.
If absent in the gene of certain individuals due to mutations, it result in a sex-linked conndtion called haemophilia, where blood failed to clot when blood vessels are damaged leading to profuse bleeding/ hemorrhage.
Ideally in a normal individuals the inactive from of factor VIII are continuously circulated in inactive forms in the blood stream, until a damaged blood vessels occurs. At the injured site they are converted to active from called coagulating factor VIIIa,,by separation from Willebrand factor, react with coagulating factor IX to initiate clotting. The factor VIII is a co- factor for factor IX, and together with calcium ion,phospholipids converts t to factor IXa,
The latter converts prothrombin to thrombin. The thrombin convert fibrinogen to fibrin, which form a stable fibrin clot at the injured site to arrest bleeding.<u> </u><u>The cascade of events is lacking individual without factor VIII. Therefore bleeding occurs.
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Consequently, symptoms of hemophilia can be relieved by a functional factor VIII, because it will prevent the deficiency in factor VIII in the affected individuals by acting as co-factors for the conversion of factor IX to IXa, to initiate clotting.
<h2>Sodium channels </h2>
Explanation:
Depolarization is a result of sodium channels opening as a result of chemical or pressure-based stimuli
- Depolarization starts when a threshold stimulus applied on a neuron via Na+ mechanically operated channels that trigger action potential
- Action potential is an efficient signaling process by which distantly located cells communicate to each other
- Depolarization of membrane potential is due to influx of Na+ via voltage gated Na+ channels
- Fast opening of voltage gated Na+ channel shifts membrane potential from -70mV to + 50mV at which voltage gated Na+ channels become inactive thus influx of Na+ abruptly stops
