The beneficial uses of bacterial toxins in medicine are more and more used lately. For example, Botulinum toxin is a toxic protein produced by the bacterium Clostridium botulinum which has paralytic effects (injection of this toxin into muscle relax specific muscles). Botulinum toxin accomplishes his effects on the neuromuscular junction where he prevents the release of the neurotransmitter acetylcholine (Ach). Utilization of this toxin is in the treatment of various muscle spasms. It is also used in the treatment of migraines. Diphtheria toxin is also one of the toxins used for medical purposes for the treatment of cutaneous and non-Hodgkin T-cell lymphomas. <span>Some bacterial toxins can be used in the treatment of tumours. For example, immunotoxin, which is protein made by fusion of modified antibody and toxin.The antibody binds to an antigen on the target cell, the toxin then enters via endocytosis and kills the cell. Commonly used bacterial toxins in immunotoxins are Diphtheria toxin and the Pseudomonas exotoxin.</span>
<h3><u>Answer;</u></h3>
The above statement is <u>False </u>
<h3><u>Explanation;</u></h3>
- Speciation is an evolutionary process in which new species arise. There are three types of speciation, namely; sympatric, parapatric and allopatric speciation.
- <em><u>Sympatric speciation is a pattern in which speciation occurs in the absence of a physical barrier to gene flow; ex. polyploidy arising in flowers.</u></em>
- In an Allopatric speciation on the other hand, a physical barrier arises and separates two populations, ending gene flow between them and allowing reproductive isolating mechanisms to evolve so that later if the two groups come back into contact they will no longer be able to reproduce together, therefore making them different species.
An agonist exhibit a positive biological effect similar to the receptor it stimulates. For instance, beta agonists (i.e. Salbutamol) stimulate the beta receptors in the bronchial system therefore leading to bronchodialtion. A competitive antagonist negates the function of the specific receptor by binding to the receptor binding site before the biological ligand. A non-competitive agonist negates the function of the specific receptor by binding to an allosteric site leading to a conformational change of the receptor site.
