What I Know

Ever since I have been in this class, my view on the body has been very different. When people move, I think of ways on how we classify the movements. I really enjoyed the movement lab because through that, I was able to my knowledge of movements and apply them. At first, I was really slow with all the planes and the directional movements, but I can now name most of the movements with confidence because of the lab. Some of the things that we are covering in the class is a review from my previous classes. We are now covering landmarks of the bones, I remember the bone names, but I am having difficulty remembering the landmarks of the bones because there is so many to remember! That is the only problem that I have so far.

Last Blog of the Year

What was your favorite topic this semester? Why? - My favorite topic of this semester was the invertebrates and vertebrates chapters. I really like learning about the different animals. The fun part was the dissections, I feel that they really do help with realizing where each body part is. From there we begin to learn it's function and how the part works. What was your least favorite? -My least favorite topic of the semester was probably genetics with finding if genes were sex-linked or autosomal. I'm not great with looking at pedigrees and determining how genes were inherited. For the most part, I feel that if I did more practice problems on these I would understand the concept. As of right now, it is still my least favorite as well as the Mendelian numbers. What would you change about this class if you could? -I would change the amount of in-class tests/quizzes that you give us. I feel like it really is not enough. It's the in class tests/quizzes that prove to you whether or not we've been reviewing over the material and I feel that those should be more frequent for your next year students. What do you feel is your biggest accomplishment in biology this year? - I feel that my biggest accomplishment this year was reading and covering all the chapters that we went through. This was the first time in any science class that I covered so much content. I learned a lot from this class and I hope to carry on this knowledge later on in life~

Entry #10: Chromsome 19: Prevention

In this chapter, we discuss about a family of genes called the apolipoprotein genes, or APO genes. They come in four basic varieties, called A,B,C and E. There is various different versions of each oh different chromosomes. The one that we discuss about is APOE which lies on chromosome 19. To understand APOE's job requires a digression into the habits of cholesterol and triglyceride fats. The job of APOE's protein is to effect an introduction between VLDL and a receptor on a cell that needs some triglycerides, APOB's job is to do the same for the cholesterol drop-off. If these two are not working, the cholesterol and fat stay in the bloodstream and can build up on the walls of arteries as atherosclerosis. We did not just want to talk about heart disease, but we also can see how this genes comes to play in the Alzheimer's disease. It is said that if you carry two E4 genes your chances of eventually getting Alzheimer's disease are much greater than those of the population at large.

Entry # 9: Chromsome 17: Death

In this chapter, the author focuses on cancer and talks about cells and how they sometimes reproduce themselves when they are not supposed. As a result, we have cancer. A gene called TP53, which is located on the short arm of chromosome 17 is responsible for suppressing rogue cancer cells. this gene was first discovered by David lane, he recognized this as a tumor suppressor. Mutation in the TP53 gene is almost the defining feature of a lethal cancer; in fifty-five percent of all human cancers, TP53 is broken. People with one faulty version of TP53 out of two they inherit have a ninety-five percent chance of cancer at a usually an early age. the story of P53 and the oncogenes challenges the argument that genetic research is necessarily dangerous and should be curtailed. The author also explains that in various types of cancers, TP53 is mutated very early which explains why chemotherapy and radiation therapy is not always effective. Apoptosis can also be useful in preventing other kinds of mutiny than cancer, such as genetic distortion of the kind induced by transposons.

Entry #8: Chromosome 14: Immortality

In this chapter, Matt Ridley talks about how people have been wondering about immortality for quite some time and whether or not it exists. The question is answered on chromosome 14, in the shape of a gene called TEP1. The product of TEP1 is a protein which forms part of the most unusual little biochemical machine called telomerase. Lack of telomerase causes senescence and addition of telomerase turns certain cells immortal. The story begins with the discovery James Watson discovered. He noticed that the biochemical machines that copy DNA called polymerases cannot start at the very tip of a DNA strand. rather the start several letters into the text. therefore the text gets a little shorter every time it is duplicated. everytime the chromosome is copied, a little bit of the telomere is left off. After a few hundred copies, the chromosome is getting so short at the end that meaningful genes are in danger of being left off. In your body, the telomeres are shortening and the result is aging. This is why that people realize now that telomerase could be the result of immorality.

Entry #7: Chromosomes X and Y: Conflict

In this chapter, the author discusses how the body is the victim, plaything, battleground and vehicle for the ambitions of genes. The X and Y chromosome are always in conflict with each other. The sex chromosomes X and Y determine the sex of the body. Each chromosome attracts genes that are beneficial to that sex. Men have no 'spare' chromosome and because of this they are much more likely to suffer from recessive problems like colorblindness and hemophilia. This outbreak of antagonism between genes is a dangerous situation. It is said from scientists that later on in the years, the X chromosome will dominate over the Y chromosome. Not that the male species will be extinct because if that was the case, then that would mean that there would be no human beings on Earth. What that basically means is that later on in the future, male species will be more feminine than they are in the past because of the dominance in the X chromosome. The conflict has almost been shown to be the attributor for a heritability of homosexuality

Genome Entry #6: Chromosome 11 Personality

In this chapter, we learn that the gene D4DR is located on the short arm of the chromosome. D4DR codes for dopamine is a neurotransmitter that motivates us to have action. It is the recipe for dopamine receptor protein and it is switched on in cells of certain parts of the brain but not in others. Dean Hamer shows in a study that D4DR correlates with “novelty-seeking” behavior, but only accounts for four percent of such behavior. It is shown that in the book it shows that too little and the person lacks initiative and motivation. Too much and the person is easily bored and frequently seeks new adventures. A long D4DR gene implies a low responsiveness to dopamine in certain parts of the brain, whereas a short D4DR gene implies a high responsiveness. People with long D4DR genes have low responsiveness to dopamine, so they need to take a more adventurous approach to life to get the same dopamine buzz that short-gened people get from simple things. 36 percent of this gene is heritable, and the rest is environmental. There could be over 500 heritable genes to control behavior. Other factors including diet, like cholesterol intake could also affect one's personality.