Biology

Due Friday by 3:00 pm

The Thalidomide Tragedy
As we learned in chapter four, atoms and functional groups can have a powerful effect on how molecules function and react. Watch the following video and read the PDF article attached.
Post a minimum of 350 words discussing; what caused the thalidomide tragedy, what role did the FDA have in protecting US citizens, what are the harmful side effects of thalidomide, how and why does thalidomide cause birth defects, and finally, do you agree with thalidomide being approved for sale again? Explain your argument in detail.
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The Shadow of the Thalidomide Tragedy | Retro Report | The New York Times (Links to an external site.)

ThalidomideChiralDrug.pdf

Carbohydrates
Copy, paste and complete the chart below into your assignment submission. Populate the following examples in the correct place in the chart and provide information in the third column. (Starch, sucrose, glucose, cellulose, fructose, ribose, lactose, glycogen and maltose)

Type of Carbohydrate Examples Info/Properties/functional groups
monosaccharide

disaccharride

polysaccharide

Lipids

Use chapter 5, section 3 (5.3) to complete this chart. Copy and paste your chart or add a table just below the “B” for bold in the content editor about your text submission box.

Type of Lipid Examples/where found Properties/functional groups
fats

steroids

phospholipids

One of My Heroes
1. Read the background essay below.
2. Watch the video.
https://www.pbslearningmedia.org/resource/drey07.sci.phys.matter.cortisone/making-cortisone-from-plants/ (Links to an external site.)
3. Submit answers to the following questions.
• Why was cortisone initially so scarce?
• How are plant steroids similar to our steroids?
• Explain the importance of Julian’s Compound S. How did it ultimately make cortisone more readily available?
• Have you or someone you know ever had to be treated with cortisone? Hydrocortisone? If so, what was the outcome?
Background Reading
Cortisone is a naturally occurring hormone made by the human body’s adrenal glands, located just above the kidneys. It is also present in the bile of cattle. In 1948, recognizing cortisone’s remarkable effectiveness in shutting down pain receptors, doctors began using cortisone produced from animal bile to treat patients suffering from a debilitating condition called rheumatoid arthritis.
Although some cortisone circulates naturally through the body, large doses of it are needed to treat the symptoms of rheumatoid arthritis. Because millions of people suffered from the condition—and because animal bile yielded precious little cortisone at a very high cost—cortisone was in high demand but short supply. The challenge for scientists was to somehow make a far greater quantity of it at a much lower cost.
The process of making a natural substance in the lab from simple building blocks is called synthesis. In order to synthesize a hormone like cortisone, chemists have to first understand how the natural molecule is put together. Based on its chemical structure, cortisone is classified as a steroid hormone. Although different steroids produce different physiological effects, all steroid molecules have a similar chemical structure: a nucleus composed of three six-sided carbon rings fused to each other, and one five-sided ring. In 1948, the procedure used to synthesize cortisone using animal bile involved 38 steps.
In 1949, the African American chemist Percy Julian pioneered a much simpler approach, one that used a cheap and abundant source—soybeans—in place of animal bile. Working from knowledge established during the 1920s and 1930s, when chemists had discovered that certain plant compounds contained a structural and functional similarity to animal compounds, Julian set out to create a plant-derived compound that would produce the same physiological response in humans as animal-derived cortisone.
Julian succeeded in synthesizing a molecule that, though it wasn’t exactly cortisone, was very similar in its chemical framework. It varied from cortisone by one single oxygen atom. Julian’s molecule, known as “Compound S,” was also present in the human body. In fact, the body used it to produce natural cortisone in one simple step. Likewise, to make synthetic cortisone from Compound S, one had only to deliver the missing oxygen atom to a precise location on the molecule. Scientists found a way to do this within two years, and cortisone that had previously cost hundreds of dollars a gram could be made for pennies.

Protein
Use chapter 5, section 4 (5.4) to define 14 bold words from pages 75-83.

The Skinny on Sweeteners
Read the following article and write a 250 word minimum discussion post that includes answers to
Why do you choose or not choose to ingest artificial sweeteners?

How artificial sweeteners work?

Why don’t they have any calories (or low in calories)?

Are they better than sugar?

Are they healthy for humans?

In your discussion, include three examples of artificial sweeteners.

chemmatters-oct2011-sweeteners-brownlee.pdf

Fad or Fab??
Read the following article and write a 250 word minimum discussion post that covers the following topics.
How do low-carb diets work?
What is ketosis?
Are you in favor of low-carb diets? Why or why not?

22-3 Carb Crazy.pdf

Personal DNA

Watch the following video and write 200 word minimum discussion posting on whether you would provide your DNA sample to the Personal Genome Project (PGP). In your discussion include SNPs, what SNPs reveal, the goals of the PGP, the benefits of the PGP and the dangers of the PGP.
https://www.pbslearningmedia.org/resource/biot09.biotech.concpt.prsnldna/personal-dna-testing/ (Links to an external site.)

DNA vs RNA
Read chapter 5, section 5 (5.5).
Complete the chart on DNA and RNA. Copy and paste this chart or create your own using the table insert selection below the “B” for bold.
DNA RNA
Full Name
Sugar involved
Nitrogen Bases in structure
location in the cell
role or job in the cell
Using the following sequence and base pairing rules of A-T and T-A and G-C and C-G, complete the chart.
AAT CCG AGC TTA GTC GGA
Complementary strand mRNA complement
Typically how many strands?
Shape

Sickle Cell Disease

A change in the primary sequence of amino acids in a hemoglobin protein causes a folding and function problem in the secondary, tertiary, and quaternary structures in the cell.
1.Read/reread pages 79-83 in the text. Focus on the four levels of protein structure.
2. Read the following background essay below.
3. Watch the following video.
https://www.pbslearningmedia.org/resource/tdc02.sci.life.gen.mutationstory/a-mutation-story/ (Links to an external site.)
4. Submit your answers the following questions.
• How can a genetic mutation be harmful in one environment and helpful in another?
• Why do you think certain mutations persist if they can be lethal?
• Why are there more people with sickle cell disease in one part of the world than in other parts?

Background Reading
A gene known as HbS was the center of a medical and evolutionary detective story that began in the middle 1940s in Africa. Doctors noticed that patients who had sickle cell anemia, a serious hereditary blood disease, were more likely to survive malaria, a disease which kills some 1.2 million people every year. What was puzzling was why sickle cell anemia was so prevalent in some African populations.
How could a “bad” gene—the mutation that causes the sometimes lethal sickle cell disease—also be beneficial? On the other hand, if it didn’t provide some survival advantage, why had the sickle gene persisted in such a high frequency in the populations that had it?
The sickle cell mutation is a like a typographical error in the DNA code of the gene that tells the body how to make a form of hemoglobin (Hb), the oxygen-carrying molecule in our blood. Every person has two copies of the hemoglobin gene. Usually, both genes make a normal hemoglobin protein. When someone inherits two mutant copies of the hemoglobin gene, the abnormal form of the hemoglobin protein causes the red blood cells to lose oxygen and warp into a sickle shape during periods of high activity. These sickled cells become stuck in small blood vessels, causing a “crisis” of pain, fever, swelling, and tissue damage that can lead to death. This is sickle cell anemia.
But it takes two copies of the mutant gene, one from each parent, to give someone the full-blown disease. Many people have just one copy, the other being normal. Those who carry the sickle cell trait do not suffer nearly as severely from the disease.
Researchers found that the sickle cell gene is especially prevalent in areas of Africa hard-hit by malaria. In some regions, as much as 40 percent of the population carries at least one HbS gene. It turns out that, in these areas, HbS carriers have been naturally selected, because the trait confers some resistance to malaria. Their red blood cells, containing some abnormal hemoglobin, tend to sickle when they are infected by the malaria parasite. Those infected cells flow through the spleen, which culls them out because of their sickle shape—and the parasite is eliminated along with them.
Scientists believe the sickle cell gene appeared and disappeared in the population several times, but became permanently established after a particularly vicious form of malaria jumped from animals to humans in Asia, the Middle East, and Africa. In areas where the sickle cell gene is common, the immunity conferred has become a selective advantage. Unfortunately, it is also a disadvantage because the chances of being born with sickle cell anemia are relatively high.
For parents who each carry the sickle cell trait, the chance that their child will also have the trait—and be immune to malaria—is 50 percent. There is a 25 percent chance that the child will have neither sickle cell anemia nor the trait which enables immunity to malaria. Finally, the chances that their child will have two copies of the gene, and therefore sickle cell anemia, is also 25 percent. This situation is a stark example of genetic compromise, or an evolutionary “trade-off.”