The sequence of a polypeptide X is as follows:
THCARKEDSGYPEWANVRDECW

1. The Optical Density (O.D.) at 280 nm of a solution of the above polypeptide X is 0.51 at the standard experimental conditions (i.e. optical length L = 1.0 cm) . What is the concentration of the polypeptide X in this solution (in mM)? (The molar absorptivity (e) for tyrosine and tryptophan residues at 280 nm are 1,400 M^(-1)cm^(-1) and 5,500 M^(-1)cm^(-1), respectively).

2. Estimate the molecular weight of this peptide.

3. Draw side-chain structures and peptide bonds for the first five amino acid residues of the polypeptide X.

Hydrogen ions and carbon dioxide promote the release of oxygen from hemoglobin. This regulation of oxygen binding by hydrogen ions and carbon dioxide is called the ________ effect.

Fetal hemoglobin binds oxygen more tightly than does adult hemoglobin owing to weaker ____________ binding, stabilizing the T state and lowering the oxygen affinity of hemoglobin. This allows oxygen transfer from maternal to fetal blood.

Sickle-cell anemia is caused by the substitution of a single specific amino acid in one hemoglobin chain. ____________, the other prevalent inherited disorder of hemoglobin, is caused by the loss or substantial reduction of a single hemoglobin chain.

There are as many as 200 common variations in the MC1R gene that are associated with differences in skin and hair color and several others associated with pathological conditions associated with a lack of (albinism) or loss of (vitiligo) pigmentation.

9a) Red hair and fair skin is associated with a variant located in the second intracellular loop of the receptor (depicted as a red star on the light side of figure 2). Compare the most common, wildtype, mRNA sequence for the MC1R gene with that of the redhead variant. (5 marks)  

1. Translate the mRNAs below to identify the mutation and its effect. Clearly identify the difference by circling the affected amino acid(s). Answer the subsequent questions to identify how this might result in a change in pigmentation.

Wildtype mRNA             478 – GCG  CGG  CGA  GCC  GUU – 493

                                           N’ ____   ____   ____   ____   ____    C’  

Redhead mRNA         478 – GCG UGG CGA GCC GUU - 493

                                      N’ ____   ____   ____   ____   ____    C’  

2. Does the mutation in part (i) affect the chemistry of the amino acid(s)? If so, how?

3. How could the mutation in part (i) result in a change in pigmentation in affected individuals? *Hint - think about the mechanism of action of this receptor.

9b) You are studying the genome of a family that experiences albinism (lack of pigmentation). You do not observe any of the known mutations that cause albinism but identify a tRNA gene that has undergone a mutation such that its anticodon now recognizes the stop codon of the MC1R gene. Describe the impact this would have on the MC1R protein produced and why this might lead to an absence of pigmentation. (2 marks)

This is my review study guide for my biology final can someone please answer them so i can study. Thank you

1. Assuming only full-chromosome separations in meiosis, how many different genetic combinations are there for Kate and Jon’s offspring? Show an equation for calculating this and explain the math.
2. The phenotype for cheater-gene expression is recessive. Kate was homozygous for the cheater gene mutation, and thus was very promiscuous with partners outside her relationship. Jon was homozygous too, but lacked the cheater-gene mutation. What are the chances that their child will express the trait of the cheater gene (i.e. - what are the chances that their child will have the cheater-gene phenotype)? Draw a Punnett square to illustrate this concept.
3. What if Jon and Kate have two children, a boy and a girl, and those two children have children (yuck!). Genetically speaking, what are the chances that their offspring (the F2 cross) will be homozygous for the cheater gene mutation? Draw a Punnett square to illustrate this concept.
4. The DNA sequence containing the Cheater Gene is given below.
   Transcribe the DNA into mRNA (as if RNA polymerase was using the gene below as a template).
   T C A G T A C A C A G T A C T C C G A T G A C T T G C A A C T T C A G
5. Translate the mRNA sequence you created in question 11 into an amino acid sequence. Use the single letter abbreviations given for each amino acid given in the table below (example: use A for Ala, M for Met, etc.)

Use the information above to answer the following questions.

5’…TAC ACC GAT GGA TAA GTC…3’ DNA Coding strand

3’…ATG TGG CTA CCT ATT CAG…5’ DNA template strand

A. Write the sequences of the two double-stranded daughter DNAs which will be replicated from the sequence above. Indicate which sequences are directly from the parent. Show accurate direction of each sequence. 0.5 points

​​​​​​​B. Write the sequence of the mRNA strand that will be transcribed from the above DNA sequence. Show accurate direction of the sequence 0.5 points

C. Write the sequence of the tRNA strand carrying the anticodons which will hydrogen bond with the mRNA sequence complimentarily. Show accurate direction of the sequence 0.5 points

​​​​​​D. Using the mRNA codons table from your transcription/translation slides, predict and write out the amino acid sequence which will be translated from the mRNA transcript. Be sure to use the accurate open reading frame. Be careful you do not miss a step/nucleotide. 0.5 points.

​​​​​​​E. What will the amino acid sequence be If there was a point mutation in the original DNA sequence which changed the ‘second A’ to T in the DNA template strand? 0.5 points

F. ​​​​​​​Will the mutation in E affect the function of the peptide/protein? Why or why not? Note that it’s either Yes or No. You receive points for the reasoning only if you chose the right answer. 0.5 points.

ONLY answer E and F please!!

For this discussion post, I want you to search primates and tool use: How did tool use begin? do all primates use tools? Why is this so important for non-human primates? In your post-I want you to tell us about the tool use you found and the primates who use it. Then, I want you to hyperlink the article, so we can see it. And then...do you think this tool use is similar to our human ancestors?

To summarize: 1. Look up primates and tool use; 2. Find an article you like, and want to share; 3. Summarize the article for us, and give us the article / webpage your found in a hyperlink; 4. Do you think this skill set is similar to those developed by our "not quite human yet" ancestors? Why or why not?

Artificial intelligence (AI) and data science are hailed as society’s answer to human bias in decision-making. Why not let the computer algorithms take over, make the decision-making process free of human interaction, and supposedly, free from human bias. Isn’t this rational decision-making? What could go wrong?

• Apple new credit cards (issued by Goldman Sachs) reveal bias against women (lower limits to women, than men)
• 2016 investigation by ProPublica revealed that data-driven AI used by judges to decide whether a convicted criminal will commit future crimes is biased against minorities and people of color.
• Face recognition software make more mistakes in identifying women and people of color
• Automated financial underwriting reveals gender and ethnic biases.

Why is this happening?

What is decision making going to look like in the future?

Question 3:

A) Why is education level such a strong variable in a typical worker’s human capital earnings function and the age–earnings profile? How might the human capital investment (the dominant) view contrast to the screening, signaling and ability hypotheses (to explain the connection of education to earnings)?

B) What is the "college/high school earnings premium"? How has this altered the human capital investment decision of individuals who are weighing the potential, long-run benefits vs. costs of higher education? How might it alter a college student's choice to work (or not) at a paid job WHILE they are enrolled in college (classes)?

C) Which side has more incentive to make the often costly, up-front investments in firm-specific vs. industry-specific vs. general training? Why? Provide a concrete example of each type of training.

1. Explain, in your own words, what Thomson means when she claims that “Being a good K is being good qua K.”

2. According to Thomson, what is a “goodness-fixing kind”?

3. According to Thomson, what is a “function kind”? Are function kinds “goodness-fixing kinds”? Why or why not?

4. According to Thomson, what is a “natural kind” (i.e. a “non-function kind” like “beefsteak tomato” and “tiger”)? Are natural kinds “goodness-fixing kinds?” Why or why not?

5. According to Thomson, why is being physically fit sufficient to call a tiger a “good tiger”?

6. According to Thomson, why is being physically fit not sufficient to call a human being a “good human being”?

7. According to Aristotle, what is the characteristic activity of good human persons? Explain, in detail, how he reaches this conclusion and how his argument resembles Thomson’s.

The first video below contains some famous claims and comments stemming from Elon Musk, the CEO of Tesla and SpaceX (and one of the founders of PayPal, some time ago) -- and Stephen Hawking, and others. What do these observations have to do with ethics? The question is how we address the impact of technology on jobs, on human behavior, and even the meaning of human life. Be sure to check these out! Then make comments on your responses with regard to how human beings should respond, adapt, or prepare for these changes. It's probably that we can't go 'backwards'; how do we come to terms with what... 'we' have wrought!

https://www.youtube.com/watch?v=xs_HhZrCBdg&t=15s

Nick Bostrom, "What Happens When our Computers get Smarter than We Are?"

https://www.ted.com/talks/nick_bostrom_what_happens_when_our_computers_get_smarter_than_we_are?referrer=playlist-talks_on_artificial_intelligen#t-612076