Approved White Paper Topics and their Proud Owners

Hooray!  Once you are arrive here you are about 20% of the way there.

Don’t celebrate too soon though.  There’s a lot of work to be done still.

Yes it IS possible to wait to long after picking a topic to build your argument and strengthen the individuality of your claim.  Sadly enough sometimes the lowest grades we give out are to students who pick their topics early in the semester and then go into quiet mode :(  Everyday involvement is required to make this work.

Dr. Wilk and I ALWAYS love helping you guys and we will be arguing against you with data to get a reaction out of you (we are moms – tough love is sometimes the best medicine).  But desperate, last-minute bloggers beware, we are busy and don’t have time to save you the week before.  By that point, it will be way to late anyways :)

Hope to see all of you here soon.  Who’s going to beat the crowd here and get the class rolling?

Writing The Final Paper

Amazingly, Huffington Post came up with customized advice how to write that knockout final paper.

And here is something to cheer you up

Calling Dr. Love

Let’s move 20 years into the not-so-bright future where genetic testing is an affordable reality  but type 2 diabetes still cannot be fixed with pills.
Your patient has 3 genes that increase the chance of type 2 diabetes. He/she was not given any advice throughout their childhood and now comes to you with symptoms of glucose intolerance. What advice are you going to give him/her? Remember he/she is an intelligent person and will ask why every step of the way. You can talk in general terms or pick a susceptibility gene of your choice.

Have fun!

Claiming your prize: the genetic predisposition of type 2 diabetes

Post by Phebe

Genes. So, you spun the wheel of fate, lucked out, and claimed your (not so wonderful) prize. Time to see what you’ve won! This section will focus on the case of genetic predisposition in type 2 diabetes (T2D). What genes are involved and how? The risk is estimated at 30-70% for T2D from genetics. Since T2D is described as polygenic and heterogeneous, there are many genetic factors to look at. Are you an unfortunate victim of bad genes? Will you be lying on your death bed, blaming your family?

Table 3 from the review paper (Doria et al) lists “common variety” T2D gene loci. Let’s make the genes we focus on from this table. In terms of jobs, there are 19 listed on this table. Some people will have to pick two (but no more than 2 per person). Please include general information about the gene (what is it and what does it do) along with what happens when the protein is deformed (specifically, in reference to T2D). Remember that the claim is not just the genes but, how the genes are having an effect on T2D!

Table 3. Genetic Loci Implicated in “Common Variety” Type 2 Diabetes

Chromosome Location Gene Symbol Common/Other name Cellular Function OMIM Number OR Frequency of Risk Allele
1p12 NOTCH2 Notch 2 preproprotein Regulator of cell differentiation 600275 1.13 0.11
2p21 THADA Thyroid adenoma-associated gene Unknown 611800 1.15 0.90
3p14 ADAMTS9 Disintegrin-like and metalloproteinase with thrombospondin type 1 motif Proteolytic enzyme regulating extracellular matrix 605421 1.09 0.76
3p25 PPARG Peroxisome proliferator activating receptor gamma (PPARγ) Transcription factor receptor for TZDs and prostaglandins 601487 1.17 0.85
3q28 IGF2BP2 IMP2 IGF2 mRNA-binding protein 2 608289 1.14 0.29
6p22.3 CDKAL1 CDK5 regulatory subunit associated protein 1-like 1 Presumed regulator of cyclin kinase 611259 1.0-1.20 0.31
7p15 JAZF1 Juxtaposed with another zinc finger gene 1 Zinc-finger protein of unknown function 606246 1.10 0.50
8q24.11 SLC30A8 ZNT8 Zinc transporter 8 611145 1.18 0.65
9p21 CDKN2A CDKN2B p16 (INK4a) p14(ARF)p15 (INK4b) Cyclin-dependent kinase inhibitor 2A and 2B 600431 1.20 0.83
10p13-p14 CDC123 Cell division cycle protein 123 homolog Required for S phase entry of the cell cycle - 1.11 0.18
CAMK1D Calcium/calmodulin-dependent protein kinase i-delta Mediator of chemokine signal transduction in granulocytes 607957
10q23-q25 IDE Insulin degrading enzyme Neutral metallo-peptidase that can degrade many peptides 146680 1.13 0.53
HHEX Hematopoietically expressed homeobox; PRHX Homeobox transcription factor 604420
KIF11 Kinesin family member 11; Homologue of Xenopus EG-5 Kinesin related motor in microtubule & spindle function 148760
10q25.3 TCF7L2 TCF4 High mobility group transcription factor 602228 1.31-1.71 0.26
11p15.1 KCNJ11 Kir6.2 Inwardly rectifying potassium channel 600937 1.14 0.47
12q21 TSPAN8 Tetraspanin 8 Cell surface glycoprotein 600769 1.09 0.27
LGR5 Leucine-rich repeat-containing G protein-coupled Orphan G protein-receptor 606667
16q12.2 FTO Fat Mass- and Obesity-Associated Gene 58kD protein with nuclear localization signal 610966 1.27 0.38

OR = Odss ratio of type 2 diabetes per risk allele.

Doria, A., Patti, M., & Kahn, C. R. (2008). The Emerging Genetic Architecture of Type 2 Diabetes. Cell Metabolism, 8(3), 186-200.

Exercising the demon of type 2 diabetes

Post by Eric, the workout guru

Ah, exercise. Seems to be the cure for everything, doesn’t it? Everyone’s in on working out and staying active, with thousands of people spending thousands of dollars nationwide on gym memberships, home exercise equipment, workout DVDs (P90x or Insanity, anyone?), and the like. But can pumping iron make you pump type II diabetes out of your life?

In class, we came to a consensus that a constant positive energy balance is a major culprit in causing type II diabetes. As such, it makes sense that we would want to achieve a negative energy balance, or at the very least, a net balance of zero, in order to not get type II diabetes. So we want to find the body processes that can help achieve negative energy balance. It has been suggested that exercise is one of these processes, and is able to make a dent, that is, clear some extra room in your bank, so to speak. Think of what cash is spent in terms of the bank model that we used today (whether on food, clothes, credit, or investment) when we exercise.

Here are just a couple things to think about as you research. These are not necessarily topics for you to pick and choose from, they are merely sparks to spur the elevator talk of your choice. Whatever you find, you will talk about, and post in the blog for me to confirm. I want to hear from everyone.

-Differentiate between types of exercise in regards to type II diabetes. Low-intensity, high-intensity, etc. Does it activate the stress response? Ex: running a marathon vs. strength training session

-Is exercise catabolic, anabolic, or both?
-Which stores does exercise dip into?

Think about it this way. You are a doctor who has a patient named Nigel that has type II diabetes. He tells you that he is willing to go on whatever workout regimen you recommend (assuming they don’t question your authority, haha). Our job is to tell him when to work out, how long, what type of exercise, etc. OR we tell them exercise does NOT help with type II diabetes at all and we provide an alternative to exercise that will put them in negative energy balance. C’mon guys, let’s cure poor Nigel.

To arms!

T2D, does it matter what we eat?

Matt”s topic continued
Which puts you at higher risk for diabetes type 2? 500 Hamburgers or 500 packets of sugar? In the spirit of the November elections, as well as the last blog entry, we are going to have a very strong debate on whether or not type 2 diabetes is the result of carbohydrate intake or if it is the amount of food taken in (protein, carbohydrate, lipids, minerals, styrofoam in McNuggets, etc). Unlike the November elections, we will be stern in our stance, will be able to use strong words, much lewder vulgarities, and most important, will have actual evidence supporting our claims! So, don’t just agree with what your peers say, debate the hell out of it! Call them ‘asshats’ or ‘equivocal Machiavellian pricks’, disprove and dispute their claims, their papers, their evidences. Just think like a politician, but back it like a scientist (be vocal, but not full of crap…this isn’t a popularity contest but a contest for who is right and who is wrong).

By the way, you all are wrong. May the dietary lifestyle debate commence!

Hope this will spur on everyone for a healthy debate!

Type 2 Diabetes or How I Stopped Worrying and Loved the Disease

Post by Matt
Type 2 diabetes sucks. It is non-insulin dependent diabetes mellitus (NIDDM, for those who love acronyms), and occurs in people in many shapes and sizes. Now, there is a huge debate as to what actually causes type 2, and some of them range from reasonable (carbohydrate induced), to insane (government plot to control us all, I kid you not), to Oprah (??). We are going to draw a few lines in the sand and get this debate all fired up. So pick a side, grab a helmet, and get your hands dirty!

Case 1: Carbohydrates. In many different forms, from good, complex carbs (brown rice, vegetables) to bad, simple/stupid carbs (honey, white rice, soda) to tastily evil carbs (cupcakes and Snickers), this high influx of sugar in your blood causes a manifestation of type 2 diabetes as well as vampires sweetening their tea with your blood (just in time for Halloween).

Case 2: Positive energy balance. You just put your KFC meal into your body’s savings account and you hardly touch it (contrary to actual money). Therefore, the body is stuck in a positive energy balance and type 2 manifests as a result of this, regardless of carbohydrate/protein/fat/additive/cardboard intake after eating the value meal.

Case 3: Genetics. You spun the wheel of fate and lost big time. Congratulations, your parents gave you type 2 diabetes disposition! Collect your prize at a random time and enjoy the potential heart failure and amputations!

Case 4: Obesity. Face it, you are fat (big boned people exempt). Thanks to this, nature decided to reward you with type 2 diabetes! Collect your prize along with the people with bad genetics! So here is how we shall break down the debate:

Job #1: Give us the lowdown on the pathways of glucose metabolism. Focal question: How is glucose absorbed, used and stored in the body?
Job #2:At least ten conditions that stimulate insulin secretion. Hint: high blood glucose level is just one of them.
Job #3: Blood/insulin/glucagon levels in response to a meal (mixed meal, protein only, veggie diet, vegan diet). Focal question: Does your diet really impact your levels of hormone and sugar levels in blood?
Job #4: Energy balance. Give me some proof that working out (negative energy balance) helps prevent diabetes, and sitting on ass (positive energy balance) increases incidence of diabetes. Focal question: Does working out help to decrease or prevent diabetes?
Job #5: Diabetes mellitus type 2. Focal question: What is it exactly, what are signs, symptoms, risk factors, etc.?
Job #6: Genetic predisposition of diabetes. Focal question: What are genetic markers, and what do they code for/regulate (statistics if diabetes incidence also needed)?
Job #7, Job #8, Job #9: TBA

To Hell With Sunblock

Post by Kendall
We’ve all heard it.. our parents reminding us to put on sunscreen before a summer day at the pool, beach, or the lake. Those of us that have heeded our parents warnings had a pleasant experience. Those who decided to build sand castles out under the sun for 6 hours with no sunscreen, won’t forget it either. When I was 7 years old I remember the situation vividly. That’s the type of sunburn you never forget. Everyone has jumped on the bandwagon of skin protection with ads promoting wrinkle free skin, retaining youthful looking skin, as well as the bombardment of sunscreen and their advances. It’s true skin cancer is possible, and maybe to some extent, inevitable for people with excessive, unprotected sun exposure. Should skin cancer be a concern?

In 2007 there were 60,000 cases of melanoma (the most serious form of skin cancer) in the US. That cancer contributed to 8,000 deaths that year. The 5 year localized survival rate is 99%, while the 5 year overall survival rate is 91%. In my opinion the odds are not bad. This is for the serious skin cancer guys, this isn’t even recognizing the more mild forms of skin cancer.

Let’s contrast that to prostate cancer where 217,000 cases will be diagnosed in US men this year, and 32,000 men will die. It is the second leading cause of death in men, behind only lung cancer.
Statistics courtesy of the American Cancer Society at

Although not as well known as the relationship between sun exposure and skin cancer, there is another relationship with sun exposure and other types of cancer, specifically, breast, prostate, and colon cancer. It is an inverse relationship. The more sun exposure, the less risk for incidence of cancer. So why are we throwing on all this sunblock that is constantly being improved to the point that no UV light is reaching our skin anymore? Why is this awareness of decreased sun exposure and increased risk of other cancers not receiving public attention? It has been known since the 1930s!

Is the benefit of sunblock worth the risk of developing other cancers?
Shoot me your ideas and let’s solve this!

* Solar UV Spectrum
o Types
o Which one is important for Vitamin D
o Is direct exposure required?
+ Can UV penetrate through glass (driving in a car), clothing?
* Vitamin D
o Textbook information
+ structure, storage, function
o Renal Vitamin D vs. Extra-renal Vitamin D
o Studies that connect vitamin D deficiency to breast cancer (girls look up), prostate cancer (boys look up), colon cancer (everyone look up)
o Active vs. Inactive Vitamin D
o Will supplements of vitamin D have same effect as vitamin D formed in skin from the sun?
o How much vitamin D do we need?
o How much sunlight exposure do we need?
* Melanin and Skin Tones, cancer rates related to skin tone
* Breast, prostate, colon basic info
o Do studies of these cancer rates in specific races/ethnicities to see if skin tone is a culprit
*Skin cancer (to provide contrasting view and argument for sunblock)
+ Types, Causes
+ Are there increased risk groups?
* Finally! Non-skin Cancer Rates and Connection to Vitamin D
o Is there a correlation?
o Does correlation equal causation? (No, but what can we infer from it)
* With new found knowledge, make decision if sunblock is causing a greater risk in your life in the form of other cancers than protection from skin cancer

Since you are getting screwed with cancer either way, which one would you rather have?
Which has a greater survival rate?
Which cancer has an advanced treatment plan?

Osteoporosis, are we chasing the wrong culprit?

Dr. Wilk likes Clayton’s organization of topics but you as presenters need to make sure that during your elevator talks you don’t just review the assigned topic but select information as it pertains to the question and claim. In this case, the question would be IS OSTEOPOROSIS A CALCIUM DEFICIENCY DISEASE OR PHYSIOLOGICAL ADAPTATION OF OUR BONES TO LIFESTYLE WE LEAD?
You should all study the topics and possess comprehensive knowledge of them in order to answer any questions that might come up from your assigned area. We’ve been having a little trouble with getting students to get the “elevator” to move past the first floor :)  As leader, Clayton is charged with making sure the presenters follow the line of HIS reasoning, not talk about everything they know. For example, to define the disease he might want the comparison between healthy and osteoporotic bone in as many biochemical markers as possible, not just composition of healthy bone. Dr. Wilk will cut you off if Clayton doesn’t! 

Remember about additional research like demographics of high risk groups, dietary calcium levels, vitamin D levels and so on, so our class discussions presents a variety of scientific evidence that helps us analyze the topic and LEADS US TO AN ANSWER.

We want layers of information from a bunch of sources and explanations of WHY? Look for information where you normally wouldn’t (aka outside of textbooks and medical websites).  Your bones can tell a lot about your life story and will remain on this planet long after we’re gone.

I’ve just given you all PLENTY of questions that I generated in my head while I was working in the yard this afternoon.  Help Clayton fill out the outline so our next class meeting is informative, interesting and incendiary.

Male hormonal contraceptive part 2

I have enjoyed our class discussion today and I am looking forward to Wednesday class. Please use this post to continue examining the intricacies of male reproductive physiology that make the development of male hormonal contraceptive difficult or even impossible.

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