a.
- everyone now goes on about sea levels rising which means that polar animals habitats are being destroyed etc etc.
Answer:
B. It was passed to the individual by a gamete from the father.
Explanation:
<u>DNA is transferred</u> to the next generation <u>via gametes</u>, which are produced during <u>meiosis</u>. During meiosis, <u>half of the genetic material</u> is <u>transferred</u> from parent cell to their gametes. Therefore, among the given options, only <u>B is correct</u>.
Option A is not correct because it talks about <u>somatic cells;</u> whereas, in somatic cells, <u>genetic material is not transferred half</u> rather duplicate first and then a complete duplicated set of genetic material is transferred.
Option C is also not correct because only <u>one gamete (sperm)</u> fertilizes the egg. Hence, not half of his cells descend from father gamete. Similarly, option D is also incorrect because it is not possible to descend half of the nuclei from the father to the offspring.
Answer:
A: Many genes can affect a trait
B: A single gene can influenced many traits
C:Traits can be influence many environments
D: Patterns of dominance are not influenced by genes
Explanation:
its C Traits can be influence many environments
This is because of the location at which the Peyer's patches develop or are formed. These patches are excessive multiplication of lymphoid nodules within the lower portions of the small intestines.The occurrence of this abnormal cell division may prevent the linings of the intestines to perform its normal functions.
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®).
