Dilemmas:
Lack of communication, because doctors may not always know the same language as their patients.
Cultural limits on medicine, such as Jehovah’s Witnesses not accepting blood transfusions even though it might save them.
Skills Required:
Patience
Communication of complex concepts
Understanding of different cultures
Do you have those skills?
Yes/No
Do to Acquire:
Research another culture and maybe even learn the language if possible
Answer:
Explanation:
could we get a multiple choice or ?
You didn’t list any options for us to answer the question jsut ssyinf 1
Retinopathy develops in patients with diabetes mellitus because of Retinal ischemia and red blood cell aggregation occurrence.
Anyone with diabetes can develop diabetic retinopathy.
Diabetes Retinopathy is caused by high blood sugar due to diabetes, having too much of sugar can damage retina.
At start of this, it might cause no symptoms or only mild vision problems. but longer can cause blindness.
as the time passes, too much sugar in blood leads to the blockage of the tiny blood vessels that nourish the retina and cuts off its blood supply.
and the eye attempts to grow new blood vessels. but they don't grow properly and can cause leakage.
Complications of retinopathy include blindness and also vitreous hemorrhage, Retinal detachment. and Glaucoma.
To prevent the risk, one should Manage your diabetes, monitor your blood sugar level and also keep BP and cholesterol under control.
To know more about diabetes retinopathy,
brainly.com/question/28871921
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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’
