The origin of congenital adrenal hyperplasia occurs when circulating cortisol levels are low.
Congenital adrenal hyperplasia (CAH) is an autosomal recessive disease which results from mutations of genes for enzymes involved in the biochemical steps of production of mineralocorticoids, glucocorticoids or sex steroids from cholesterol by the adrenal glands (steroidogenesis). <span>Low cortisol production results in rising levels of ACTH (adrenocorticotropic hormone) because cortisol usually inhibits ACTH production. This increased ACTH production induces overgrowth (hyperplasia) and overactivity of the steroid-producing cells of the adrenal cortex.</span>
The kingdom is Animals.
The genus is Haliaeetus.
The species is leucocephalus are the statements which Julio can make about the bald eagle.
The option C is the correct answer.
Explanation:
Given that Bald eagle has binomial name as Haliaeetus leucocephalus.
Modern classification of binomial nomenclature is given by Carl Linnaeus.
From the modern system of classification the sequence is as kingdom, phylum, class, order, family, genus and species. The classification of bald eagle is:
Kingdom - Animalia
Phylum - chordata
class - Aves
Order- Accipitriformes
family - Accipitridae
Genus - Haliaeetus
species - leucocephalus.
The two word name of the species having genus first followed by species is binomial nomenclature which Julio has used for bald eagle as Haliaeetus leucocephalus.
Answer:
1) intake of glucose molecules from the blood by specific transporters
2) high amount of glucose in the blood, sending signals toward the pancreas
3) binding of hormones with receptors on the liver
4) release of hormones from the receptors
5) synthesis of hormones by beta cells
Explanation:
During ingestion of the meal, insulin is produced in response to high blood glucose levels (concentration of glucose increases after digestion of food). Like other hormones, insulin performed its action through binding specific signals to specific receptors e.g, liver, muscle cells. The high glucose level in the blood send signals through hormones to liver, fat, and muscle cell receptors. These receptors release specific hormones to beta cells of the pancreas. In response to the signals from receptors, beta cells synthesize insulin to minimize glucose levels in the bloodstream.
Adenosine triphosphate
ATP
Answer:
One of the common genetic disorders is sickle cell anemia, in which 2 recessive alleles must meet to allow for destruction and alteration in the morphology of red blood cells. This usually leads to loss of proper binding of oxygen to hemoglobin and curved, sickle-shaped erythrocytes. The mutation causing this disease occurs in the 6th codon of the HBB gene encoding the hemoglobin subunit β (β-globin), a protein, serving as an integral part of the adult hemoglobin A (HbA), which is a heterotetramer of 2 α chains and 2 β chains that is responsible for binding to the oxygen in the blood. This mutation changes a charged glutamic acid to a hydrophobic valine residue and disrupts the tertiary structure and stability of the hemoglobin molecule. Since in the field of protein intrinsic disorder, charged and polar residues are typically considered as disorder promoting, in opposite to the order-promoting non-polar hydrophobic residues, in this study we attempted to answer a question if intrinsic disorder might have a role in the pathogenesis of sickle cell anemia. To this end, several disorder predictors were utilized to evaluate the presence of intrinsically disordered regions in all subunits of human hemoglobin: α, β, δ, ε, ζ, γ1, and γ2. Then, structural analysis was completed by using the SWISS-MODEL Repository to visualize the outputs of the disorder predictors. Finally, Uniprot STRING and D2P2 were used to determine biochemical interactome and protein partners for each hemoglobin subunit along with analyzing their posttranslational modifications. All these properties were used to determine any differences between the 6 different types of subunits of hemoglobin and to correlate the mutation leading to sickle cell anemia with intrinsic disorder propensity.
Explanation: