Tutor profile: Elizabeth E.
How does the speed of action potential propagation depend on the physical dimensions of the neural axon?
An action potential propagating along an axon can be modeled as charges flowing along a pipe. As the diameter of the pipe is increased the resistance to the flow of charges is reduced (by Bernoulli's equation) and therefore the action potential will be able to spread down the axon more quickly. Increased diameter of an axon allows for a greater velocity of action potential propagation as it increases the ratio of cross-sectional area to membrane surface area which allows for greater flow of charges. Additionally, myelination increases the rate of action potential propagation because it allows for saltatory (jumping) conduction as membrane capacitance is low. Action potentials travel quickly along myelinated stretches of axon and then are regenerated at nodes of Ranvier or unmyelinated areas of axon. The two primary ways to increase speed of action potential propagation are to myelinate an axon or to increase the axon diameter.
What is allosteric inhibition of an enzyme?
Allosteric modulation of enzymatic activity is key to both physiologic and pharmacologic manipulation of enzyme activity. Allosteric ligands bind the enzyme at a site different from the active site but by causing conformational changes in the protein affect the enzyme's affinity for substrate or catalytic efficiency. When an allosteric or noncompetitive inhibitor is present in can modify both the Vmax (maximum velocity) and Km (substrate binding affinity) of an enzyme. There are many allosteric regulators of enzymatic activity in the body, from other proteins that can alter the activity of another protein complex or small molecules that can bind to inhibit or optimize an enzyme's activity. However, allosteric inhibitors are also an important avenue of drug development as they allow for all regions of the protein to be targeted, not just the active site. Additionally, allosteric inhibitors are advantageous compared to competitive (active-site) inhibitors because they cannot be out competed by increasing the concentration of substrate and therefore are more likely to have an effect in a greater range of conditions.
How do cancers develop?
Cancerous cell masses (tumors) arise out of a series of mutations that accumulate in a population of cells. This can include hereditary mutations and mutations that are acquired sporadically or because of environmental damage. As a cell develops more mutations, it becomes less controlled in its division and begins to grow in an unregulated manner. This excessive cell growth may eventually lead to the development of cancer in which a subset of cells does not respond to the body's normal signals and can cause harmful effects to the rest of the body. The accumulation of mutations is a process shared by many types of cancers and explains why many cancers take decades to develop and become clinically detectable. Understanding how these mutations arise and what mutations are present in specific cancers is important to screening for and treating cancer.
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