AO, BO. cause thats makes it where the childern can have all blood types
Answer: b. Acetyl Co-A
Explanation:
Acetyl CoA produced through pyruvate, amino acids, and fatty acids are oxidized in the Krebs cycle in CO2, obtaining as products NADH, FADH2 and GTP (ATP). Parallel to this oxidation, the Krebs cycle produces compounds used as precursors for biosynthesis. As it is a cycle, an oxaloacetate molecule could, in principle, oxidize an amount indefinite of acetyl CoA. Acetyl-CoA is formed from the oxidative decarboxylation of pyruvate, sequentially performed by pyruvate dehydrogenase -PDH (complex multi enzymatic of 3 enzymes), in the mitochondrial matrix.
Answer:
The excessive alcohol consumption of the mother.
Explanation:
Alcohol consumption during pregnancy harms the developing baby, the foetus. This is because alcohol passes from the mother's blood to the baby's blood and this affects the growth of the baby's cell.
This causes severe damage to the cells of the brain and the spinal cord.
FASD - Fetal Alcohol Spectrums Disorder is characterised by growth and developmental problems and it can range from mild to severe.
Example is the baby having small head, narrow eye and behavioural problems later in life.
Answer:
A. True
Explanation:
Hemoglobin is a protein and has two distinct types of polypeptide chains. These are called the alpha and beta subunits. The gene that code for the beta chain undergoes a mutation in a single base that causes sickle cell anemia. Here, adenine base in the genetic code for glutamic acid is substituted with a thymine base.
The genetic code for glutamic acid in the beta chain gene is GAG. The "A" is replaced with "T" and the new code "GTG" codes for valine. Therefore, the mutated hemoglobin has valine in place of glutamic acid. This makes these mutated protein molecules to form aggregates resulting in a change in the shape of RBCs carrying them.
The timing of human puberty is strongly linked to genetic and dietary factors. It is also linked to historical changes, and a secular trend favoring early menarche has resulted in an ever increasing proportion of teens attaining reproductive capacity at young ages. The causes of the trend, however, have not been unequivocally ascertained. More generally, we know very little about the factors in children's proximal environments that either inhibit or accelerate the timing of pubertal maturation. But, between 1984 and 1987, it has been distributed a survey with questionnaires to over 1,000 participants who were asked about their early family experiences and their physical development. The results from this retrospective study suggest that parental absence especially the absence of the biological father-is associated with early menarche.
