By: Jordan Gaines Lewis, 4th year PhD candidate in the Neuroscience Graduate Program
“Perhaps it had something to do with living in a dark cupboard, but Harry had always been small and skinny for his age…[he] had a thin face, knobbly knees…and wore round glasses held together with a lot of Scotch tape because of all the times Dudley had punched him on the nose.”
And so we are introduced to The Boy Who Lived, the Chosen One—the famous Harry Potter. His seven books have been translated into 73 different languages and sold over 450 million copies worldwide.
But readers wouldn’t guess, after author J.K. Rowling’s introduction of Harry in Chapter 2, that the orphaned boy would be the one to defeat the powerful and devastating Dark Lord Voldemort. Snubbed by his only remaining family, bullied by his cousin and classmates, and residing in the cupboard under the stairs, Harry is short, skinny, and totally non-threatening.
And it’s clear to us why. His Uncle Vernon, Aunt Petunia, and cousin Dudley Dursley—to whom he was passed as an infant after the death of his parents— ensure that he’s properly malnourished at all times. After spending a day cleaning the Dursleys’ entire house and doing yardwork in the blazing July heat (on his 12th birthday, no less), Aunt Petunia prepares for Harry “two slices of bread and a lump of cheese” before sending him off to hide during their dinner party with the Masons. It’s no wonder he’s so small for his age.
But perhaps something other than the physical abuse held back his growth, too. Beyond the malnourishment, it’s possible that Harry Potter suffered from what is known as psychosocial short stature.
The judges’ scores have been tabulated, and we’re thrilled to announce the winners of our inaugural blog award!
Thanks to everyone for participating. We’ll be back with a shiny new prompt next year!
We’d like to extend a huge thanks to Dr. Michael Verderame, Dr. Kirsteen Browning, Amanda White, and Jordan Gaines Lewis for judging the competition this year.
The following post is the third in our series of entries submitted for the 1st Annual Lions Talk Science Blog Award. This piece is by Sang-Min Lee, a 5th year PhD candidate in Pharmacology.
Image credit: Bill Branson (Wikimedia Commons)
The concept of receptor-drug interaction has been the main mechanism for how drugs develop their clinical benefits. Drugs generally have target molecules and regulate their activity to make significant changes originated in cells.
My research field is the dopamine D1 receptor, and it has been a promising drug target because its activation has shown to improve the symptoms of at least two neurodisorders: motor symptoms of Parkinson’s disease and verbal working memory in schizotypal personality patients.
Nonetheless, more desirable D1 receptor activators are still required to maximize clinical efficacy and applications because the current D1 activators have several side effects and pharmacokinetic issues.
The following post is the second in our series of entries submitted for the 1st Annual Lions Talk Science Blog Award. This piece is by Caitlin Millett, a 2nd year PhD candidate in the Neuroscience Graduate Program.
Image credit: Alan Levine (Flickr)
Have you ever heard a friend exclaim “I’m being so OCD right now!” when they can’t help but double check for their house keys before slamming the front door? It seems that this phrase has become a cultural colloquialism, it is used so often.
Luckily, most people who say “I am so OCD!” do not, in fact, have a debilitating anxiety disorder marked by uncontrollable obsessive thoughts and behavioral compulsions, the hallmark features of obsessive-compulsive disorder.
Though the term obsessive-compulsive is often misattributed to those of us who are perhaps too meticulous, prone to anxiety, or a combination thereof, we as a society have familiarized ourselves with the term through our exposure to literature and media to the extent that it is now a part of our lexicon.
The following post is the first in our series of entries submitted for the 1st Annual Lions Talk Science Blog Award. This piece is by Lina Jamis, a student in the Anatomy Graduate Program.
Image credit: FDA (Wikimedia Commons)
Researchers who study genetic interactions—of which there are thousands currently under study and billions more to be studied—often find themselves trying to explain their field to non-technical audiences.
And if there’s anything I’ve learned as a student who has taken various levels of human genetics as an undergraduate and now at the graduate level, it’s that the average person has many preconceived notions about genetics that are mostly inaccurate, if not altogether wrong. These misconceptions are often perpetrated and perpetuated by our educational systems and media that aim to simplify a field that is intrinsically un-simple.
There are few absolute truths when it comes to human genetics. Absolutely, there are disease genes, but there are also modifiers of disease genes, and modifiers of modifiers of disease genes. It goes on. Incomplete penetrance, genetic heterogeneity, pleiotropy, and gene-environment interactions—these are just some of the factors that make studies of relatively simple-seeming genetic diseases extremely challenging.