Part 2: The Making of the Mutation Story.

 Some questions that I had before making the mutation story:

1. How rare is progeria in the world?
2. Is there a cure for this disease?
3. Is it life threatening? If so, how?
4. What age group or gender does it affect?
5. How does the disease affect normal life?
6. What are the symptoms of progeria?
7. How does it affect the genes of the person?

What new or familiar digital tools did you try to use as you worked through this project?

In this project, I used the the online Webpath search engine on the school’s library site to search up facts and information about progeria from school approved websites that match my curriculum in depth and in language. I also typed in the word progeria into Google and into Youtube to find some videos explaining progeria.

 What was the process you used to investigate the topic?

I followed the steps of information fluency learned in class and applied it to study this topic. The steps of information fluency were: Ask, Acquire, Analyze, Apply, Assess.

How did you verify and cite the information you found?

First of all, I used school approved websites from official medical institutions around the world (not from a forum or individual blog) and checked multiple different websites to compare and contrast if the facts were any different. Then, every time I decided to use a bit of the information on the website, I would copy down the URL for the website and paste it into my “sources used” list.

How did the process of completing this challenge go? What could you have done better?

Overall, I thought that completing this project wasn’t too hard as the facts and information out on the internet all had very clear details and explanations. I thought that the only challenging part was coming up with a story that would contain all the necessary information and not be boring to read like a research paper. I think I could’ve done better on the ending of the story because I feel that it is a little sudden.

Images of progeria

 

Sources for the Mutation Story

From the Riverside School Library Webpath Express Search Engine:

https://ghr.nlm.nih.gov/condition/hutchinson-gilford-progeria-syndrome#genes

http://www.progeriaresearch.org/about_progeria.html

From Google:

http://www.mayoclinic.org/diseases-conditions/progeria/basics/causes/con-20029424

https://en.wikipedia.org/wiki/Progeria

From Youtube:

https://www.youtube.com/watch?v=rs5-a8-fwtk

https://www.youtube.com/watch?v=DunGu7Re8vA

Image Sources (from Google Images):

In order from left to right (the pictures)

https://en.wikipedia.org/wiki/Progeria#/media/File:Hutchinson-Gilford_Progeria_Syndrome.png

https://prezi.com/zecyztr5h5n4/progeria/

https://www.emaze.com/@AOWWCTCR/Progeria

 

 

Part 1: Mutation Story    Progeria

Hi there, my name is Paul, I am a gene in my host’s Tom’s body. However, I am not like any other gene. In fact, I am extremely special and rare. One in four million newborn babies in the world today would have me as their gene. In the beginning, I was just a gene a normal gene, known as lamin A which makes a protein necessary for holding nucleus of a cell together. But I had a defect, this defect made the cell I was in unstable, which leaded to my young host to rapidly age. When my host was first born, the effects weren’t at all that noticeable on the outside of him. As eighteen to twenty-four months passed, my hosts parents slowly started to notice that Tom was beginning to look abnormal. His facial appearance included prominent eyes, a thin nose with a beaked tip, thin lips, small chin, and protruding ears. Moreover, he also had thin hair and aged-looking skin, joint abnormalities, and a loss of fat under the skin. In other words, he was beginning to look like an old man. Immediately, he was taken to the hospital where the doctors found out that he had progeria or Hutchinson–Gilford progeria syndrome. When Tom reached fourteen, his health began to deteriorate drastically so he had to go to the hospital constantly for checkups and treatments.  Now how did his health worsen? I will explain. As a defective gene, I cause my host to experience severe hardening of the arteries which greatly increases the chances of having a heart attack or stroke at a young age. Unfortunately, this means that Tom didn’t get to play sports or eat whatever he wants like all the other kids. That year, Tom suffered many strokes and heart attacks and eventually died in a hospital. Almost all hosts of the defective lamin A gene die at an age of fourteen as there isn’t a cure for it presently. Despite the severity and rarity of me, I am not inheritable. So if even if Tom ever got to have kids, the chances of them hosting me again isn’t at all that great.