Answer:
Height
Explanation:
Height is polygenic trait which means that is controlled by more than one gene. This is different than Mendelian genetics in which one gene controls one trait-monogenic trait (e.g. flower color). Expressed phenotype of polygenic trairs is mix of all genes that control it (each gene has the same influence on phenotype) and it can express range of possible phenotypes (not only tall ad short but alos something in between).
This type of inheritance is known as polygenic inheritance or quantitative inheritance.
Traits that are also polygenic are skin and hair color, intelligence etc.
A larger overall leave size is the answer.
NOTE: Marking this answer as brainliest would be much appreciated! :)
Answer:
Thanks for you question. Your hypothesis suggests a linear relationship between serum Cholesterol levels and MI. This hypothesis seems to ignore the difference in the prevalence and effectiveness of LDL receptors in the FH patient.
FH patients who have inherited the mutation from both parents have very few LDL receptors in their blood and therefore almost no ability to pass the unused Cholesterol through the liver. FH patients who are heterozygous will have more LDL receptors although both will find Cholesterol removal problematic without the addition of a PCSK9 inhibitor.
In short, your hypothesis need to account for other factors that are in play.
Explanation:
Consider my case. I am a 64 year old male who has Heterozygous Familial Hypercholesterolemia. Before treatment at age 12 my Total cholesterol was 510 mg/dl. My genetic testing shows two mutations to the LDL Receptor gene with only one mutation being pathogenic. My first heart attack was at 47 and first stroke at 62. My current LDL is too low to detect with the use of a PCSK9 inhibitor (Repatha®).
Answer:
atoms
Explanation:
everything is made from atoms
