Pt 1 due in 5 Hours!!! HW

Art Primary Post: 4/1/19 150 min

Time to play the screenwriter again where you take what you know and apply it in a dialogical situation. Remember that this means that you must incorporate key terms (see the introductory page of this module for a list of relevant terms).
Imagine a conversation between 3-4 artists from this chapter. The conversation can go from a recent discovery of the Laocoon, a new application of mathematics or engineering, to complaints about your patron.
The primary post will be this conversation and the two required response posts should include your critiques as the historical consultant for this film. Since this is still a formal writing assignment for this class, remember to include in-text citation where it is necessary, which includes your own paraphrases.

Art Peer Response 1: 4/3/19 100 min

Gus – mathematician

Eren – mathematician

Ray – mathematician

Roberto- artist 

Gus- Hey everyone how are you guys doing today? Anything new?

Eren- Hey Gus, Iv been doing great and Iv been thinking we need to improve our math skills and Iv been thinking of something new but its kind of complicated.

Gus- And what is it?

Ray- Well Eren and I were thinking of a way we could sum everything up by not having to add all the sides its called multiplication. It would be a great way to find the area of an art piece and instead of adding all the sides of an art piece you multiply the length and the width of the art piece

Gus- Well that sounds great ,but wouldn’t that just be with art pieces that are squared and rectangular shaped?

Eren- You do have a point we have to figure that out but for now that’s all we have.

Roberto- Yes I agree that would make my life much easier by measuring my altarpieces. I think not only would it make my life easier but also all the other artists during this 16th century.

Ray- I agree with you Roberto I think everyone can benefit from this.

Kleiner, Fred S. “Gardner’s Art Through the Ages – A Concise Global History.” Fourth Edition. Cengage. 2017. Print.

Art Peer Response 2: 4/3/19 100 min

Jan van Eyck: (comes into hipster coffee shop where Rogier and Hugo are sitting in vegan leather armchairs and sipping on locally sourced, non-GMO, farm to table, organic, gluten free, lactose free, free range, fair trade, sustainable cappuccinos). Sup dawgs? 

Rogier van der Weyden: (laughing) No one talks like that since Duccio di Buoninsegna painted Life of Jesus. 

Hugo van der Goes: Hey Jan how’s it going? How’s work?

Jan: (orders a cappuccino also because it’s just what’s done). Everything’s good, thanks for asking. You know, I still can’t believe that a little nobody artist like me landed a job working for Philip the Good.

Hugo: Come on, you’re a great artist. The Ghent Altarpiece is going to be a masterpiece!

Jan: Thanks man. I do like how it’s coming along. The poylptychs are turning out perfectly.

Rogier: Poly.. whats?

Jan: polyptychs. They’re a series of paintings on hinged panels. They’re perfect for alter pieces cuz you can fold them.

Hugo: Cool. Super cool. Can’t wait to see the finished product. 

Jan: Well that’s probably not going to happen because I die in 1441 and you’re not really around until 1441. So… that’s awkward. 

Rogier: (almost falls out of chair because he’s laughing so hard) Burn!!! He got you good, Hugo.

Hugo: (awkward laugh). Well, whether you’re dead or not my Adoration of the Shepherds is going to be a big hit with the realistic portraits on the triptych. It will be regarded as brilliant.

Jan: I don’t doubt it, my friend. And let’s not forget Rogier. Buddy, tell us about Deposition.

Rogier: For sure. It is going to look a lot like a carved shrine. I like to compress the figures in my paintings so there is the feeling of movement and action. Also, I utilize a shallow stage with simple but meaningful background and perspective. It will have great cohesion. Super duper meaningful and emotional.

Jan: Cool. Cool. (nods and sips cold overpriced espresso)

Kleiner, Fred S. “Gardner’s Art Through the Ages – A Concise Global History.” Fourth Edition. Cengage. 2017. Print.

Art Slides: 4/2/19 Well written answers***

There are three slides make sure you answer each aspect of the Prompt *see attachment*

Bio Primary Prompt: 4/3/19 250 min

An end to heart disease? Not quite. A new class of cholesterol lowering drugs called PCSK9 inhibitors (Links to an external site.)Links to an external site. is really good at lowering LDL levels, but evidence of how well it reduces the mortality of heart disease is not so clear. From this New York Times article, discuss the problems treating a complex disease like heart disease. Find information about familial hypercholesterolemia and what different treatment options would be available, considering that seven different genes are known to contribute to this disease (OMIM 143890 (Links to an external site.)Links to an external site.).  In your post, explain or summarize why the new drug Repatha is so powerful in reducing LDL cholesterol, and then pick one of the genes from OMIM (see the Phenotype-Gene Relationship table) and discuss one cause of hypercholesterolemia and possible treatment option, based on the gene you picked.

Bio Peer Response: 4/5/19 100 min

A new LDL drug was endorsed and the researchers had very high expectations and were rooting for the end of heart disease. With a following study of this new drug conducted to patients, it had simliar benefits like a statin. For patients who don’t mind or do mind the high price of this drug, it has been suggested to wait for long-term results when more and more people start to use it. The problems of this disease is that they “are not related to statins at all…[you’ll need a] doctor to determine what’s really causing [the] symptoms. And some people tolerate one statin better then another.” (Krumholz, H., 2017) This drug is so powerful in treating heart disease because typically dozes of this medication is 90 mg/dl (this is considered low) and using Repatha is 30 mg/dl. 

“Familial hypercholesterolemia is an autosomal dominant disorder characterized by elevation of serum cholesterol bound to low density lipoprotein (LDL), which promotes deeposition of cholesteral in the skin, tendons, and coronary arteries (Hobbs et al.. 1992, OMIM)” This can happen in both homozygous and heterzygous. Houlston, R. et al. 1988, all discovered that that patients coronary artery disease have a high level of LDL concentration in contrast of those who don’t have coronary artery disease. This suggests “that [LDL] measurements may help predict the risk of coronary heart disease in individuals with familial hypercholesterolemia.” Treatment for this is chaning lifestyle like exercising and consuming a “healthy low-fat diet”.

RESCOURCES:

https://www.nytimes.com/2017/03/20/health/ldl-cholesterol-heart-disease-drugs-pcsk9-inhibitors.html?rref=collection%2Fsectioncollection%2Fscience&action=click&contentCollection=science&region=stream&module=stream_unit&version=latest&contentPlacement=4&pgtype=sectionfront (Links to an external site.)Links to an external site.

https://www.omim.org/entry/143890 (Links to an external site.)Links to an external site.

https://www.mayoclinic.org/diseases-conditions/familial-hypercholesterolemia/diagnosis-treatment/drc-20353757 (Links to an external site.)

Bio Questions: 4/4/19
1. Many individuals with metabolic diseases are normal at birth but show symptoms shortly thereafter. Why?

2. List the ways in which a metabolic block can have phenotypic effects.

3. If phenylalanine was not an essential amino acid, would diet therapy (the elimination of phenylalanine from the diet) for PKU work? Do not just say yes or no. Give a short explanation.

4. Describe the quaternary structure of the blood protein hemoglobin.

5. Transcriptional regulators are proteins that bind to promoters (the 5’ flanking regions of genes) to regulate their transcription. Assume that a particular transcription regulator normally promotes transcription of gene X, a transport protein. If a mutation makes this regulator gene nonfunctional, would the resulting phenotype be similar to a mutation in the gene X itself? Why or why not?

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