Make a discussion of 1-2 paragraphs about atherosclerosis. Make sure to you answer the follow questions in your discussion:

What is atherosclerosis and its etiology?

In atherosclerosis, blood levels of which bad protein are high? Which protein in the blood causes atherosclerosis?

What kind of blood protein reduces the risk of atherosclerosis?

What factors can increase and decrease the risk of atherosclerosis?

Explain in detail what is the process of bacterial growth with the aid of the growth curve?

What type of research is multiple sclerosis and what type of laboratory would you do it in (e.g. cancer research lab or stem cell research lab or plant cell biology lab or some other lab)?

Compare how the inflammatory response is initiated by each of the following.

A. A Type IV hypersensitivity reaction

B. Endotoxin

C. A superantigen toxin

D. A Type III hypersensitivity response

Compare and contrast the energy consumption and pro/con of C3 carbon fixation (via Calvin cycle) vs C4 carbon fixation (via C4 pathway+Calvin cycle)

Why would some tissue cultures require different formulations of nutrients to what other would? ( i.e why would there be a higher need to be % of a particular nutrient in the media growing one particular plant to what should be in the media growing another type of plant?)

With two examples explain how you would motivate the general population to improve on their nutrition and hence health.

We spent a lot of time comparing B cell and T cell surface molecules and activation – how they’re similar and different. For each of the following, compare similarities and differences. Make sketches where indicated. Feel free to use additional sketches if they help you learn the material.

A. Compare the TH-Macrophage interaction (which activates TH cells) with the TH-B cell interaction (which activates B cells). Make a sketch of each interaction that shows the important cell surface proteins involved. Also state in words the sequence of events involved in each activation.

B. Compare T cell receptors (TCR) with B cell receptors (BCR). How do they form? What do they look like? To what do they bind? What is the difference between somatic recombination and class switching (a.k.a. “isotype switching”), and which of these happens only for BCRs?

C. Compare antigen display on MHC-I with display on MHC-II. Where do displayed antigens come from? How do they get attached to MHC-I/II? What happens when the corresponding T cell binds to each MHC? Which display is more important for your immune system to recognize viruses? To recognize bacteria?

In a pine’s life cycle, hybrid “1” pine tree the needles were found to have the
alleles Ll (heterozygous) producing long needles. In a hybrid “2” pine tree, the
needles were found to have the alleles ll (homozygous recessive) producing
short needles. If a pollen from hybrid “1” pollinated hybrid “2” to form a hybrid “3”
plant which about 50% were long needle and 50% were short needle. Give the
genotypes for the following structures found in the life cycles of these plants:
Genotype of the pollen grain’s nucleus of plant hybrid “1”?
Genotype of archegonia of plant hybrid “2”?
Genotype of megaspore mother cell of plant hybrid “2”?
Genotype of sporophyte of plant hybrid “3”?
Genotype of microspores of plant hybrid “1”?
Genotype of hypocotyl of plant hybrid “3”?
Genotype of seed coat of plant hybrid “2”?
Genotype of ovary of plant hybrid “2”?

Draw and label the parts of the entire ovule and its content’s at maturity (before
fertilization) of the two Divisions “angiosperm” and “gymnosperm (pine)”. Explain
what happens to the various parts of each ovule. Give differences between
these two ovules.

FLC is the key repressor of flowering in the process of vernalization. Methylation of Lysine 9 of histone H3 (H3K9me) is a chromatin modification associated with heterochromatin. Methylation of Lysine 4 of histone H3 (H3K4me) is a chromatin modification associated with euchromatin. Which proteins do you expect to be active on the FLC gene at specific times of year?

. You have extracted extrachromosomal DNA and genomic DNA from E. coli in the lab. What is the differentiating steps during the DNA isolation so that your target DNA is not contaminated with the other unwanted DNA (i.e. you are targeting extrachromosomal DNA, so you don’t want the genomic DNA, and vice-versa)? Why and how that step can differentiate between these groups of DNA

A mutation in the ras cellular oncogene can cause cancer when it is in the heterozygous condition, but a mutation in the RB tumor suppressor gene can cause cancer only when it is in the homozygous condition. What does this difference between dominant and recessive mutations imply about the roles that the ras and RB gene products play in normal cellular activities?