Answer:
A scientist's response to the increase in food poisoning sick patients should be examining the type and source within the foods consumed.
Explanation:
Food poisoning involves the effects that decomposed or contaminated food can have on a group of people who eat it, and can cause illness in all or most individuals.
Although patients' symptoms should be treated and preventive education provided, the best course of action for a scientist is to investigate the cause.
The response of a scientist to the increase in food poisoning cases is to determine the type and source of food, as well as the nature of the alteration it has -decomposition, contamination, bacteria- in order to <u>eliminate the source and avoid new cases</u>.
- <em>The other options may be valid in the face of the appearance of food poisoning cases, but they are not the best procedure with which a scientist would respond. </em>
Glucose is converted into Pyruvate
Answer:
i want to say 6 but I am not sure
Answer:
A) parietal cells
Explanation:
Parietal cells are the epithelial cells of the stomach that have the function to secrete hydrochloric acid (HCl) and intrinsic factor. Parietal cells contain canaliculi – secretory network for the secretion of HCl via active transport.
Parietal cells are regulated via several factors such as acetylcholine, gastrin and histamine. So, if histamine receptors are blocked via antacid drugs , the secretion of the acid will be reduced.
<span>There are numerous proteins in muscle. The main two are thin actin filaments and thick myosin filaments. Thin filaments form a scaffold that thick filaments crawl up. There are many regulatory proteins such as troponin I, troponin C, and tropomyosin. There are also proteins that stabilize the cells and anchor the filaments to other cellular structures. A prime example of this is dystrophin. This protein is thought to stabilize the cell membrane during contraction and prevent it from breaking. Those who lack completely lack dystrophin have a disorder known as Duchene muscular dystrophy. This disease is characterized by muscle wasting begininng in at a young age and usually results in death by the mid 20s. The sarcomere is the repeating unit of skeletal muscle.
Muscle cells contract by interactions of myosin heads on thick filament with actin monomers on thin filament. The myosin heads bind tightly to actin monomers until ATP binds to the myosin. This causes the release of the myosin head, which subsequently swings foward and associates with an actin monomer further up the thin filament. Hydrolysis and of ATP and the release of ADP and a phosphate allows the mysosin head to pull the thick filament up the thin filament. There are roughly 500 myosin heads on each thick filament and when they repeatedly move up the thin filament, the muscle contracts. There are many regulatory proteins of this contraction. For example, troponin I, troponin C, and tropomyosin form a regulatory switch that blocks myosin heads from binding to actin monomers until a nerve impulse stimulates an influx of calcium. This causes the switch to allow the myosin to bind to the actin and allows the muscle to contract. </span><span>
</span>
