Imagine you are at your friend's party, and you are listening to a story about her last trip. Even though music is playing and other people are talking, you can probably understand what she is saying. But if you have hearing problems, you might find it hard to follow the conversation. Why is that? Our brains only pay attention to parts of the sound that we are trying to understand. In this case in your friend's voice there are some parts that help your brain listen to her instead of the music. I study how the parts of the brain that have the job of making you hear do exactly this. I want to help people with hearing problems to understand their friends voices even when there is loud music.

Sick people need making-better-stuffs to get well. We use computers to work out which making-better-stuffs should work best for different people. All people have slightly different small inside body things. Doctors want making-better-stuffs to stick to the right inside body things as well as possible to fix the problems that make people sick. In our computers we make pretend small inside body things just like those in different people and move them around like like they do really. We use them to find out which make-better-things stick the best without giving many making-better-stuffs to people which is slow and sometimes makes other things go wrong. We can also use our pretend small inside body things to help people put together new, better, making-better-stuffs.\cite{Wright_2014,Bhati_2016}

Cells move around inside us. They use tiny feet that stick to all the not-cell stuff around them. These tiny feet kind of help cells if they are alone. But not really that much. Do the tiny feet help cells if they are in a group? My work asked this question outside of a body. I put cells inside the same not-cell stuff from our body, and I watched if they moved in a group or not. They really needed the tiny feet in order to move through the not-cell stuff from our body. To make the tiny feet strong, cells use the same little bits that make a body strong to lift heavy things. Those little bits are in every cell in your body! They put together the tiny feet and hold them together. Without all that a group of cells can't move around inside our bodies. This is important for when cells don't stop growing and make a bad spot that keeps getting bigger.

The human body carries a lot of good tiny cells that are important for our well-being. One way that our tiny cells are good for us is that they stop bad tiny cells from growing in our bodies. However, how the good tiny cells stop bad tiny cells from growing and staying in our bodies is not well understood. When entering from the mouth and down the stomach, bad tiny cells and good tiny cells eventually find each other and have to fight for space and food inside our bodies. One type of bad tiny cell likes to grow by "breathing," much the same as we breathe air so that the cells in our bodies can live. However, "air" is low after entering the stomach. This is because in the normal body, the good tiny cells are always making things that keep the air low. After entering the stomach and moving down, bad tiny cells make things that hurt our bodies. Our bodies respond by making things that kill both good and bad tiny cells. However, the bad tiny cells have figured out ways to not die during the attack by our body, while the good tiny cells have not, and get killed. When the good tiny cells die, they can no longer keep the air low and the bad tiny cells are able to breathe and grow to very high numbers. So, one way that our good tiny cells keep us well is by stopping the bad tiny cells from breathing and growing in our bodies. However, some bad tiny cells have figured out a way to wipe out good tiny cells from our bodies. This is one way that bad tiny cells can make us sick.From \cite{Rivera_Ch_vez_2016}.

To make the most of bringing people together to talk about deciding something, you need to decide between different good ways of bringing people together, don't try to make all the good ways work for everyone at once. It is better to let people end with different thoughts than pretend everyone agrees. You should write down what people thought at the end and make it clear how that is used in deciding something.  Plan to share in open ways, so others can learn from what happened and what people thought at the end - others might use what you shared in ways you didn't plan, but that might help bringing people together mean more.

We take very many stories about what humans know to know. They are written in a way that is hard for a computer to study, so we move them to an easy-to-study way. We train the computer to learn to know what the pieces of the stories mean - their words and inner forms.Up-goer Five entry: herePhD proposal: Designing Definition Discovery - Read, Recognize, Reflect, Repeat

Up-goer Five EntryThe body is made up of lots of cells and cells have sticks that make them what they are. Normal cells have a normal number of cell sticks. Bad cells, which can kill a body, have the wrong number of cell sticks. More cell sticks in a cell can cause cell problems that can lead to even more cells sticks in a cell. When this happens more cells take over a body and kill it. Some cell sticks when added cause new changes to happen in a cell as well that can lead to a problem when all cell sticks have to be given to new cells.  Peer-Reviewed PublicationCancer cells display aneuploid karyotypes and typically mis-segregate chromosomes at high rates, a phenotype referred to as chromosomal instability (CIN). To test the effects of aneuploidy on chromosome segregation and other mitotic phenotypes we used the colorectal cancer cell line DLD1 (2n = 46) and two variants with trisomy 7 or 13 (DLD1+7 and DLD1+13), as well as euploid and trisomy 13 amniocytes (AF and AF+13). We found that trisomic cells displayed higher rates of chromosome mis-segregation compared to their euploid counterparts. Furthermore, cells with trisomy 13 displayed a distinctive cytokinesis failure phenotype. We showed that up-regulation of SPG20 expression, brought about by trisomy 13 in DLD1+13 and AF+13 cells, is sufficient for the cytokinesis failure phenotype. Overall, our study shows that aneuploidy can induce chromosome mis-segregation. Moreover, we identified a trisomy 13-specific mitotic phenotype that is driven by up-regulation of a gene encoded on the aneuploid chromosome. From \cite{Nicholson_2015}.

“If you can't explain it to a six year old, you don't understand it yourself.”Writing is hard. Writing about complex concepts is even harder. Writing about complex concepts with little writing training, that's research communication. And while research writing is difficult and often under-taught, it is critical to the success of a researcher and research. Implicit in the dictum publish or perish, is that you must write. Researchers write papers, syllabi, grants, progress reports and a variety of different documents on a daily basis. Yet researchers don't typically write for the public...or for fun. Today, we'd like to change that, with the Up Goer Five Challenge! A contest that challenges researchers to use only the ten hundred most common words to explain their research. We're offering everyone that participates in the Upgoer five challenge a free premium membership on Authorea for a year! We think such a challenge is great for PIs, postdocs, students, and anyone doing research and it is great for the community and public. We also think it's quite fun!To enter, follow these steps:Signup at authorea.com/signup to create an account.Upon signup, select the group "Up-Goer Five" to join the challenge.Describe your research using the ten hundred most common words with the Up-Goer five text editor. Copy and paste your entry into a public Authorea document.Hit "Publish" on the toolbar to publish your document to the Up-Goer five group.Assign a digital object identifier (DOI) to make it citable.Share it socially and challenge your friends! (#upgoerfive)