Answer:
Your car/transportation is named "Friday"
Explanation:
I'm not too sure
Answer:
D. Decreasing vessel diameter
Explanation:
Cardiac output is the amount of blood pumped per unit time by heart. Increased cardiac output corresponds to increased blood pressure which will result in increased blood flow. In vasodilation the smooth muscles within the blood vessels relax making them wide hence decreasing vascular resistance leading to more blood flow. Decreased blood viscosity will also decrease the resistance to blood flow.
Decreasing vessel diameter will not increase the blood flow, it will rather restrict it because there will be more resistance to passage of blood due to small space.
Answer: Parietal pericardium
Explanation: The Parietal pericardium - very thick fibrous serous membrane that forms a loose fitting sac around the heart & lines the wall of the pericardial cavity.
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’
