Answer: 15
Explanation: since it affects only 1 out of 20, you can divide 300 by 20 which equals 15
Awareness context does the nurse determine this is closed awareness
<h3>What is pancreatic cancer ?</h3>
However, as the pancreatic cancer progresses and spreads, upper abdominal pain frequently begins to manifest, occasionally moving to the back. Following a meal or lying down, the pain might get worse. Jaundice, nauseousness, appetite loss, weight loss, exhaustion, sluggishness, and depression are some additional symptoms that could exist.
- Known risk factors for pancreatic cancer include smoking, diabetes, chronic pancreatitis, or inflammation of the pancreas, a family history of the disease, and a few genetic syndromes. Another contributing factor might be carrying extra weight that is unhealthy for your body.
Learn more about Pancreatic cancer here:
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Answer:
The answer to the question: Electrical impulses or action potentials (AP) cannot propagate across a synaptic cleft. Instead, neurotransmitters are used to communicate at the synapse, and re-restablish the AP in the post-synaptic cell, would be, true.
Explanation:
Essentially, although the CNS, PNS and ANS (Central Nervous System, Peripheral Nervous System and Autonomic Nervous System) are electrical systems, that use the electricity generated through action potentials, that in turn, are created by the exchange of electrically charged ions from within and without the neuronal cells, these electrical impulses do not pass the pre-synaptic, and post-synaptic cleft. Instead, once an AP has reached the terminal end of the pre-synaptic neuron, neurotransmitters are released by this one, into the cleft, which are then taken up by the receptors present in the post-synaptic neuron. Depending on the type of transmitter released, there will be an inhibitory or excitatory effect. Then, with the transmitter attached, the post-synaptic neuron will depolarize and a new AP will be generated in the post-synaptic neuron, which will carry on. Messages, thus are transmitted that way between neurons, and also, between the nervous system and the organs they influence.
Answer:
Okay
Explanation:
Human topoisomerase I plays an important role in removing positive DNA supercoils that accumulate ahead of replication forks. It also is the target for camptothecin-based anticancer drugs that act by increasing levels of topoisomerase I-mediated DNA scission. Evidence suggests that cleavage events most likely to generate permanent genomic damage are those that occur ahead of DNA tracking systems. Therefore, it is important to characterize the ability of topoisomerase I to cleave positively supercoiled DNA. Results confirm that the human enzyme maintains higher levels of cleavage with positively as opposed to negatively supercoiled substrates in the absence or presence of anticancer drugs. Enhanced drug efficacy on positively supercoiled DNA is due primarily to an increase in baseline levels of cleavage. Sites of topoisomerase I-mediated DNA cleavage do not appear to be affected by supercoil geometry. However, rates of ligation are slower with positively supercoiled substrates. Finally, intercalators enhance topoisomerase I-mediated cleavage of negatively supercoiled substrates but not positively supercoiled or linear DNA. We suggest that these compounds act by altering the perceived topological state of the double helix, making underwound DNA appear to be overwound to the enzyme, and propose that these compounds be referred to as ‘topological poisons of topoisomerase I’
